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diff --git a/docs_md/articles/brain_080771c2-02f3-408d-ad70-04a80d849500.md b/docs_md/articles/brain_080771c2-02f3-408d-ad70-04a80d849500.md
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+++ b/docs_md/articles/brain_080771c2-02f3-408d-ad70-04a80d849500.md
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+---
+title: "Brain"
+docid: "080771c2-02f3-408d-ad70-04a80d849500"
+authors:
+ - key: "961f3a7f-ad62-43bc-98f4-5116b17ab812"
+ value: "Paula J. Woodward, MD, FSRU"
+breadcrumbs:
+ -
+ name: "Ultrasound"
+ slug: "ultrasound"
+ treeNodeId: "517432cb-177e-4b78-bd9f-4c2e751d132e"
+ -
+ name: "Anatomy"
+ slug: "anatomy"
+ treeNodeId: "43bd9326-ab1c-493e-8d96-8ad0aa58c66a"
+ -
+ name: "Brain and Spine"
+ slug: "brain-and-spine"
+ treeNodeId: "615c6d75-0c7c-43e3-87a7-df4e7ac2304b"
+ -
+ name: "Brain"
+ slug: "brain"
+ treeNodeId: null
+category: "Ultrasound"
+documentVersionId: "22ef60d5-14ee-4367-99df-09df85fb9f88"
+imageCount: 77
+lastUpdated: "12/20/17"
+pageDescription: "Brain"
+pageKeywords: "Ultrasound, Anatomy, Brain and Spine, Brain"
+pageTitle: "Brain | STATdx"
+enhancedTitle: "Brain"
+type: "ANATOMY"
+breadcrumbs:
+ - "Ultrasound"
+ - "Anatomy"
+ - "Brain and Spine"
+ - "Brain"
+---
+## GROSS ANATOMY
+
+- ### Supratentorial Structures
+
+
+ - **Gyri**: Complex convolutions of brain cortex; hypoechoic on ultrasound (US)
+ - **Sulci**(fissure): CSF-filled grooves or clefts that separate gyri; echogenic on US
+ - Sulci separate gyri, **fissures** separate hemispheres/lobes
+ - **Frontal lobe**
+ - **Central sulcus separates frontal, parietal lobes**
+ - Precentral gyrus contains primary motor cortex
+ - Detailed topographically-organized map ("motor homunculus") of contralateral body
+ - Head/face lateral, legs/feet along medial surface
+ - Premotor cortex: Within gyrus just anterior to precentral gyrus (motor cortex)
+ - 3 additional major gyri: Superior frontal gyrus, middle frontal gyrus, & inferior frontal gyrus
+ - Superior sulcus separates superior & middle gyri
+ - Inferior sulcus separates middle & inferior gyri
+ - Orbital gyri cover base of frontal lobe; gyrus rectus medially
+ - **Parietal lobe**
+ - **Posterior to central sulcus**
+ - Separated from occipital lobe by parietooccipital sulcus (medial surface)
+ - Postcentral gyrus: Primary somatosensory cortex
+ - Contains topographical map of contralateral body
+ - Face, tongue, lips are inferior; trunk, upper limb superolateral; lower limb on medial aspect
+ - Superior & inferior parietal lobules lie posterior to postcentral gyrus
+ - Supramarginal gyrus lies at end of sylvian fissure
+ - Angular gyrus lies ventral to supramarginal gyrus
+ - Medial surface of parietal lobe is precuneus, in front of parietooccipital sulcus
+ - **Occipital lobe**
+ - **Posterior to parietooccipital sulcus**
+ - Primary visual cortex on medial occipital lobe
+ - Cuneus on medial surface
+ - **Temporal lobe**
+ - **Inferior to sylvian fissure**
+ - Superior temporal gyrus: Primary auditory cortex
+ - Middle temporal gyrus: Connects with auditory, somatosensory, visual association pathways
+ - Inferior temporal gyrus: Higher visual association area
+ - Includes major subdivisions of limbic system
+ - Parahippocampal gyrus on medial surface, merges into uncus
+ - **Insula**
+ - Lies deep in floor of sylvian fissure, overlapped by frontal, temporal, parietal opercula
+ - **Limbic****system**
+ - Includes amygdala, hippocampus, thalamus, hypothalamus, basal ganglia, & cingulate gyrus
+ - Cingulate gyrus extends around corpus callosum
+ - Tapers rostrally (anteriorly) into paraterminal gyrus, subcallosal area
+ - Hippocampus including dentate gyrus, Ammon horn (cornu ammonis)
+ - Important role in emotion, behavior, & long-term memory
+ - **White matter tracts**: 3 major types of fibers
+ - Association fibers: Interconnect different cortical regions in same hemisphere
+ - Cingulum is long association fiber, which lies beneath cingulate gyrus
+ - Commissural fibers: Interconnect similar cortical regions of opposite hemispheres
+ - **Corpus callosum** is largest commissural fiber, links cerebral hemispheres
+ - Projection fibers: Connect cerebral cortex with deep nuclei, brainstem, cerebellum, spinal cord
+ - Internal capsule is major projection fiber
+ - **Basal ganglia**
+ - Paired deep gray matter nuclei
+ - Caudate nucleus, lentiform nucleus (including putamen, globus pallidus)
+ - **Thalamus**
+ - Paired nuclear complexes, serve as relay station for most sensory pathways
+- ### Anatomy Relationships
+- ### Posterior Fossa (Infratentorial) Structures
+
+
+ - Protected space surrounded by calvarium & bounded by tentorium cerebelli superiorly & foramen magnum inferiorly
+ - Posterior fossa contents
+ - Brainstem (midbrain, pons, & medulla oblongata) anteriorly, cerebellum posteriorly
+ - Cerebral aqueduct & 4th ventricle
+ - CSF cisterns containing cranial nerves, vertebrobasilar arterial system & veins
+ - CSF cisterns suspend & cushion brainstem & cerebellum
+ - **Cerebellum**
+ - Integrates coordination & fine-tuning of movement, & regulation of muscle tone
+ - 3 surfaces: Superior (tentorial), inferior (suboccipital), anterior (petrosal)
+ - **2 hemispheres & midline vermis**
+ - Divided into lobes & lobules by transverse fissures
+ - Major fissures: Primary (tentorial), horizontal (petrosal), prebiventral/prepyramidal (suboccipital) cerebellar fissures
+ - Connected to brainstem by **3 paired peduncles**
+ - Superior cerebellar peduncle (brachium conjunctivum) connects cerebellum to cerebrum via midbrain
+ - Middle cerebellar peduncle (brachium pontis) connects to pons
+ - Inferior cerebellar peduncle (restiform body) connects to medulla
+ - **Brainstem**
+ - **3 anatomic divisions**
+ - **Midbrain (mesencephalon)**: Upper brainstem, connects pons & cerebellum with forebrain
+ - **Pons**: Bulbous midportion of brainstem, relays information from brain to cerebellum
+ - **Medulla**: Caudal (inferior) brainstem, relays information from spinal cord to brain
+ - Functional divisions
+ - Ventral part: Large descending white matter tracts; contains midbrain cerebral peduncles, pontine bulb, medullary pyramids
+ - Dorsal part: Tegmentum, common to midbrain, pons & medulla; contains cranial nerve nuclei & reticular formation
+ - **Midbrain (mesencephalon)**
+ - 3 main parts: Cerebral peduncles, tegmentum (cranial nerve nuclei, gray matter nuclei, white matter tracts), & tectum (quadrigeminal plate)
+ - Ventral: Cerebral peduncles (crus cerebri) containing corticospinal, corticobulbar & corticopontine tracts
+ - **Dorsal tegmentum**: Ventral to cerebral aqueduct
+ - White matter tracts: Medial longitudinal fasciculus, medial lemniscus, lateral lemniscus, spinothalamic tract, central tegmental tract
+ - Gray matter: Substantia nigra & red nucleus
+ - Upper midbrain: Contains CNIII nucleus, at superior colliculus level
+ - Lower midbrain: Contains CNIV nucleus, at inferior colliculus level
+ - **Tectum (quadrigeminal plate)**: Dorsal to cerebral aqueduct
+ - Superior & inferior colliculi, periaqueductal gray matter
+ - Cerebral aqueduct (of Sylvius) passes through dorsal midbrain between tectum posteriorly & tegmentum anteriorly, connecting 3rd & 4th ventricles
+ - **Pons**
+ - 2 main parts: Ventral (white matter tracts), dorsal tegmentum (continuation of midbrain tegmentum with cranial nerve nuclei, gray matter nuclei, white matter tracts)
+ - Ventral: Longitudinal fibers primarily from corticospinal, corticobulbar & corticopontine tracts
+ - Dorsal tegmentum: White matter tracts & CN nuclei
+ - White matter tracts: Medial longitudinal fasciculus, medial lemniscus, lateral lemniscus, trapezoid body, spinothalamic tract, central tegmental tract
+ - Upper pons: Contains main nuclei of CNV
+ - Lower pons: Contains nuclei of CNVI, VII & VIII
+ - **Medulla**
+ - Ventral: Olives & pyramids
+ - Dorsal tegmentum: White matter tracts & CN nuclei
+ - White matter tracts: Medial longitudinal fasciculus, medial lemniscus, spinothalamic tract, central tegmental tract, spinocerebellar tract
+ - CN nuclei: CNIX, X, & XI (bulbar portion) in upper & mid medulla; CNXII nuclei in mid medulla
+- ### Ventricular System & Subarachnoid Space
+
+
+ - Cerebral ventricles consist of paired lateral, midline 3rd, & 4th ventricles
+ - Communicate with each other as well as central canal of spinal cord & subarachnoid space
+ - Direction of CSF flow
+ - Lateral ventricles → foramen of Monro → 3rd ventricle → cerebral aqueduct → 4th ventricle → foramina of Luschka & Magendie → subarachnoid space
+ - Bulk of CSF resorption through arachnoid granulations in superior sagittal sinus
+ - **Lateral ventricles**
+ - Paired, C-shaped, curve posteriorly from temporal horns, arch around/above thalami
+ - Each has body, atrium, **3 horns (frontal, temporal, & occipital)**
+ - Occipital horn typically largest
+ - Asymmetry is common, often L > R
+ - Sizes change with maturity, more prominent in preterm infants
+ - **Atrium/trigone**: Confluence of horns
+ - Contains glomus of choroid plexus
+ - Lateral ventricles communicate with each other & 3rd ventricle via Y-shaped foramen of Monro
+ - **3rd ventricle**
+ - Thin, usually slit-like, between thalami
+ - May not see fluid, just bright echogenic line on US
+ - 80% have central adhesion between thalami (massa intermedia)
+ - Communicates with 4th ventricle via cerebral aqueduct (of Sylvius), passing through dorsal midbrain
+ - **4th ventricle**
+ - Infratentorial, diamond-shaped cavity (rhomboid fossa) along dorsal pons & upper medulla
+ - Fastigium: Blind ending, dorsally pointed midline outpouching from body of 4th ventricle
+ - Important marker for true midline vermian plane on US
+ - Communicates with subarachnoid space via foramina of Magendie & Luschka
+ - Terminates inferiorly at obex, which communicates with central canal of spinal cord
+ - **Choroid plexus**
+ - Produces CSF
+ - Glomus (enlargement of choroid plexus in atrium) thickest area
+ - Tapers & extends anteriorly to foramen of Monro & roof of 3rd ventricle
+ - Tapers laterally into roof of temporal horns
+ - Present in roof of 4th ventricle but **never extends into frontal or occipital horns**
+ - **Subarachnoid space/cisterns**
+ - CSF spaces between pia & arachnoid
+ - Numerous trabeculae, septa, membranes cross subarachnoid space & create smaller compartments termed cisterns
+ - **Supratentorial/peritentorial cisterns**: Suprasellar, interpeduncular, ambient (perimesencephalic), quadrigeminal cistern, & cistern of velum interpositum
+ - **Infratentorial (posterior fossa) cisterns**: Prepontine, premedullary, superior cerebellar, cisterna magna, & cerebellopontine
+ - All cisterns communicate with each other & with ventricular system
+ - Midline cystic structures (normal variants)
+ - **Cavum septi pellucidi**: Anterior to foramen of Monro, between anterior horns of lateral ventricles
+ - 85% closed by 3-6 months after birth, some remain open into adulthood
+ - Once closed called septum pellucidum
+ - **Cavum vergae**: Posterior to foramen of Monro, interposed between bodies of lateral ventricles
+ - Posterior extension of cavum septi pellucidi
+ - Begins to close from posterior to anterior from 6-month gestation; 97% closed by full term
+ - **Cavum velum interpositum**: Potential space above choroid in roof of 3rd ventricle & below fornices
+ - Typically seen in premature infants
+
+## ANATOMY IMAGING ISSUES
+
+- ### Imaging Approaches
+
+
+ - **Anterior fontanelle**most commonly used approach
+ - **Sagittal scans**
+ - Midline scan: Best view for corpus callosum, cerebellar vermis
+ - Sweep side-to-side from this position documenting key areas
+ - **Caudothalamic groove**: Most common site of germinal matrix hemorrhage
+ - Size of lateral ventricle
+ - Far lateral to assess degree of sulcal development
+ - **Coronal scans**
+ - Important to maintain symmetrical imaging of each 1/2 of brain
+ - Symmetrical structures (from anterior to posterior) include: Frontal horns, bodies & trigones of lateral ventricles; caudate nuclei, putamen, internal capsule, & thalami
+ - Midline structures (from anterior to posterior) include: Interhemispheric fissure, genu & anterior body of corpus callosum, cavum septi pellucidi, 3rd ventricle, brainstem
+ - **Posterior fontanelle**
+ - Best view to evaluate occipital horns for intraventricular hemorrhage
+ - Can misinterpret clot adherent to choroid plexus from anterior fontanelle approach alone
+ - **Mastoid fontanelle**
+ - Located at junction of squamosal, lambdoidal, occipital sutures
+ - Transducer placed about 1 cm behind helix of ear & 1 cm above tragus
+ - Allows assessment of brainstem & posterior fossa
+ - Best view for 4th ventricle, posterior cerebellar vermis, cerebellar hemispheres, & cisterna magna
+ - **Transtemporal**
+ - Temporal bone anterior to ear is thin, allowing imaging of brainstem even after sutural closure
+ - Best view for cerebral peduncles & 3rd ventricle
+- ### Imaging Pitfalls
+
+
+ - Need to know changing appearance with gestational age at birth; normal gyral pattern in 26-week preterm infant would be abnormal in term infant
+ - Slit-like lateral ventricles common in infants, not to be mistaken for cerebral edema
+ - Glomus of choroid plexus can be bulbous & irregular, not to be mistaken for blood clot
+ - Evaluate with color Doppler & posterior fontanelle view
+ - Echogenic material in frontal or occipital horns is clot; choroid does not extend into these horns
+
+ 55345e53-a3c9-4dfc-b082-0266dcaee622
+
+
+## Images
+
+
+### Gyri and Sulci
+
+
+*Lateral surface of the brain depicts the major gyri and sulci. The frontal lobe extends from the frontal pole to the central sulcus. The supramarginal and angular gyri are part of the parietal lobe. The superior temporal gyrus contains the primary auditory cortex, and also forms the temporal operculum. The insular cortex lies within the sylvian fissure beneath the frontal, temporal, and parietal opercula.*
+
+
+*Lateral surface of the brain depicts the major gyri and sulci. The frontal lobe extends from the frontal pole to the central sulcus. The supramarginal and angular gyri are part of the parietal lobe. The superior temporal gyrus contains the primary auditory cortex, and also forms the temporal operculum. The insular cortex lies within the sylvian fissure beneath the frontal, temporal, and parietal opercula.*
+
+
+*Lateral surface of the brain depicts the major gyri and sulci. The frontal lobe extends from the frontal pole to the central sulcus. The supramarginal and angular gyri are part of the parietal lobe. The superior temporal gyrus contains the primary auditory cortex, and also forms the temporal operculum. The insular cortex lies within the sylvian fissure beneath the frontal, temporal, and parietal opercula.*
+
+
+*Surface anatomy of the cerebral hemisphere, seen from above, shows the gyri and lobules on the left, and the sulci on the right. The central (Rolandic) sulcus separates the anterior frontal lobe from the posterior parietal lobe. The precentral gyrus of the frontal lobe is the primary motor cortex while the postcentral gyrus of the parietal lobe is the primary sensory cortex. On ultrasound, the sulci appear echogenic while the adjacent gyri are hypoechoic.*
+
+
+### Midline, Subarachnoid space
+
+
+*This midline sagittal graphic shows a medial view of the cerebral hemisphere. The corpus callosum represents the major commissural fiber. The fornix and cingulate gyrus are important in the limbic system. The cingulate gyrus is involved with emotion formation and processing, learning, and memory.*
+
+
+*Sagittal midline graphic through the interhemispheric fissure depicts subarachnoid spaces with CSF (blue) between the arachnoid (purple) & pia (orange). The central sulcus separates the frontal lobe (anterior) from the parietal lobe (posterior). The pia mater is closely applied to the brain surface, whereas the arachnoid is adherent to the dura. The ventricles communicate with the cisterns and subarachnoid space via the foramina of Luschka and Magendie. The cisterns normally communicate freely with each other.*
+
+
+### Ventricular System
+
+
+*Schematic 3D representation of the ventricular system, viewed in the sagittal plane, demonstrates the normal appearance and communicating pathways of the cerebral ventricles. CSF flows from the lateral ventricles through the foramen of Monro into the 3rd ventricle, and from there through the cerebral aqueduct into the 4th ventricle. CSF exits the 4th ventricle through the foramina of Luschka and Magendie to the subarachnoid space.*
+
+
+### Standard US Planes Via Anterior Fontanelle
+
+
+*Graphic shows the common coronal planes used in ultrasound brain scanning: Plane A to F from front to back. Cerebral cortex (CC); body of lateral ventricle (BV); frontal horn (FH); occipital horn (OH); massa intermedia (M); pineal recess (PR); 3rd ventricle (3); temporal horn (TH); supraoptic recess (SR); infundibular recess (IR); 4th ventricle (4); cerebellum (CB).*
+
+
+*Graphic shows the common sagittal planes used in ultrasound brain scanning: Plane A to C from midline to lateral. Cerebellum (CB); cerebral cortex (CC); corpus callosum (Coc); cavum septi pellucidi (CSP); frontal horn (FH); foramen of Monro (FM); occipital horn (OH); temporal horn (T); 3rd ventricle (3); 4th ventricle (4).*
+
+
+### Coronal US Via Anterior Fontanelle
+
+
+*The 1st of 9 coronal ultrasounds of the brain through the anterior fontanelle in a term infant shows the frontal lobes lie in the anterior cranial fossa with orbital cavities deep to the floor of the skull base.*
+
+
+*An image centered more posteriorly demonstrates a slightly more echogenic white matter region of the brain parenchyma known as the centrum semiovale. Parts of the skull base, including the sella turcica and anterior clinoid, can be seen.*
+
+
+*Image acquired just anterior to the foramen of Monro. The frontal horns of lateral ventricles are now seen. No choroid plexus should be present in the frontal horns. Any intraventricular echogenic material seen at this level should raise the suspicion of blood clot. The head of the caudate nucleus is inferior and lateral to the frontal horn and is separated from the lentiform nucleus by the internal capsule.*
+
+
+*The 4th of 9 coronal ultrasounds through the anterior fontanelle in a term infant is shown. This image is taken at the level of the foramen of Monro. The lateral ventricles are seen with the body of the caudate nucleus and anterior portions of the thalami below. It is not uncommon that the ventricles are asymmetric.*
+
+
+*Just slightly more posterior, the choroid plexus is present on the floor of the lateral ventricles and roof of the 3rd ventricle. The 3 echogenic foci of the choroid plexus, 1 on the roof of the 3rd ventricle and 2 located bilaterally on the floor of the lateral ventricles, are known as the 3-dot sign.*
+
+
+*A more posterior coronal image at the level of the quadrigeminal cistern is shown. Another ultrasound landmark, known as the echogenic star, is seen, which comprises the choroidal fissures as the upper limbs and tentorium cerebelli as the lower limbs. Inferiorly, the vermis appears echogenic, while the cerebellar hemispheres on both sides are hypoechoic.*
+
+
+*The 7th of 9 coronal ultrasounds obtained through the anterior fontanelle in a term infant is shown. This image is taken at the trigone of the lateral ventricles. The glomus of the choroid plexus appears highly echogenic, nearly occupying the whole trigone.*
+
+
+*This image, slightly posterior to the trigone, shows mildly echogenic white matter regions within the corona radiata, lateral and parallel to both trigones of the lateral ventricles. These regions are known as the periventricular halo, a normal finding, present in almost all normal mature and premature neonates. The echogenicity of the halo should be less than that of the choroid plexus and symmetrical in appearance.*
+
+
+*The most posterior coronal image shows the cortex of the occipital lobe with multiple echogenic sulci extending medially from the lateral margin of the brain. The falx is in midline.*
+
+
+### Coronal T1 MR
+
+
+*The 1st of 9 coronal T1 MR images through the cerebral hemispheres from anterior to posterior is shown. The images are taken through planes/levels corresponding to those commonly used for ultrasound scans through the anterior fontanelle. The 3 major frontal gyri are shown: Superior frontal gyrus, middle frontal gyrus, and inferior frontal gyrus, separated by the superior and inferior frontal sulci. The straight gyrus (gyrus rectus) is the most medial, covering the base of the frontal lobe.*
+
+
+*Slightly more posteriorly, the major white matter tracts, the centrum semiovale, are seen.*
+
+
+*This image shows the frontal horns. Immediately below each frontal horn is the caudate head, separated from the lentiform nucleus by the internal capsule.*
+
+
+*The 4th of 9 coronal T1 MR images through the cerebral hemispheres from anterior to posterior is shown. The images are taken through planes/levels corresponding to those commonly used for ultrasound through the anterior fontanelle. This image is taken at the level of the foramen of Monro where both lateral ventricles unite, becoming the 3rd ventricle in the midline.*
+
+
+*This image shows the thalami on either side of the 3rd ventricle.*
+
+
+*This image slightly more posterior shows the quadrigeminal cistern in the midline. Together with choroidal fissures and tentorium cerebelli on both sides, it gives rise to the characteristic echogenic star appearance on coronal ultrasound scanning.*
+
+
+*The 7th of 9 coronal T1 MR images through the cerebral hemispheres from anterior to posterior are shown. The images are taken through planes/levels corresponding to those commonly used for ultrasound scans through the anterior fontanelle. The glomus of the choroid plexus is prominent within the trigones of the lateral ventricles.*
+
+
+*More posterior image shows the posterior parietal lobes and occipital lobes. Cerebral hemispheres are separated by the interhemispheric fissure, which contains the falx cerebri. The ventricular system and cerebellum are no longer seen at this level. The primary visual cortex is on the medial aspect of the occipital lobe.*
+
+
+*This most posterior image shows gyri of the occipital lobe and a portion of the superior sagittal sinus, which arches posteriorly to the torcular Herophili.*
+
+
+### Sagittal US Via Anterior Fontanelle
+
+
+*The 1st of 6 sagittal ultrasounds of the brain through the anterior fontanelle in term infant is shown. This image, obtained in the midline, shows the corpus callosum as a hypoechoic curving line. Callosal and cingulate sulci are parallel to and above the corpus callosum. The midline also allows evaluation of the posterior fossa structures, including the brainstem anteriorly and the vermis posteriorly. The 4th ventricle is well seen in this plane and appears as a triangular fluid-filled structure at the level of the mid vermis.*
+
+
+*Parasagittal image obtained angling slightly lateral to midline: The thalamus and echogenic sulci can now be seen more clearly.*
+
+
+*Parasagittal image obtained by angling more laterally shows the caudothalamic groove, the junction between the caudate nucleus and the thalamus. This is the area of the vascular germinal matrix, which is vulnerable to hemorrhage in preterm infants.*
+
+
+*This parasagittal image shows the glomus of the choroid plexus in the trigone. The glomus tapers anteriorly as it courses along the floor of the lateral ventricle to the foramen of Monro and continues along the roof of the 3rd ventricle. It also tapers posteriorly from the trigone into the temporal horn of each lateral ventricle. Glomus may appear bulbous and irregular at the trigone and should not be mistaken as a blood clot.*
+
+
+*This parasagittal image is obtained just lateral to the lateral ventricle. The echogenic white matter of the brain just posterior and superior to the ventricular trigone is known as the peritrigonal blush or halo, representing radiating white fiber tracts (corona radiata). The peritrigonal blush is more prominent in premature than in term neonates.*
+
+
+*This is the last and most lateral sagittal image obtained, showing the mature sulcal pattern with hyperechoic sulci and hypoechoic gyri.*
+
+
+### Sagittal T1 MR
+
+
+*The 1st of 6 sagittal T1 MR images through the cerebral hemispheres from midline to lateral is shown. The images are taken through planes/levels corresponding to those commonly used for ultrasound scans through the anterior fontanelle. The midline sagittal image shows the corpus callosum, the largest commissural fiber connecting both cerebral hemispheres.*
+
+
+*Parasagittal image just off the midline is shown. The tentorium cerebelli is a dural fold separating the brain into supratentorial and infratentorial compartments.*
+
+
+*More lateral image shows the caudothalamic groove between the caudate head and thalamus. The parietooccipital sulcus is an important landmark, differentiating the parietal from the occipital lobes.*
+
+
+*This image shows a prominent choroid plexus within the atrium of the lateral ventricle, which tapers posteriorly and extends into the temporal horn.*
+
+
+*This parasagittal image shows the sylvian fissure bound superiorly by the frontal operculum and inferiorly by the temporal operculum. The central sulcus separates the frontal lobe anteriorly from the parietal lobe posteriorly.*
+
+
+*This image shows the most lateral portion of the sylvian fissure. The temporal lobe is inferior to the sylvian fissure. The superior temporal gyrus contains the primary auditory cortex. The middle temporal gyrus connects auditory, somatosensory, and visual association pathways. The inferior temporal gyrus is the higher visual association area.*
+
+
+### Premature Infant (23 weeks 6 days)
+
+
+*This coronal image of a very premature infant, born at 23-weeks 6-days gestational age, shows a very large, square, open sylvian fissure. The opercula have not yet grown to cover the insula.*
+
+
+*Sagittal image through the caudothalamic groove in the same case shows the parietooccipital sulcus. The cortex otherwise appears "flat" without gyri/sulcal formation.*
+
+
+*Another sagittal image further lateral shows similar findings with no cortical gyri/sulci seen.*
+
+
+### Sylvian fissure at different ages
+
+
+*A different infant born at 29 weeks 1 day shows more advanced development of the sylvian fissures. The frontal, temporal, and parietal lobes all have opercula, which have grown to cover the insula.*
+
+
+*At 31 weeks 6 days the opercula have grown to cover the insula.*
+
+
+*Another coronal image through the level of the sylvian fissure in a full-term infant shows multiple gyri and sulci over the convexities of the brain. It is important to understand the developmental anatomic changes; lack of cortical sulci may be normal for preterm infants, depending on the gestational age at delivery, but is very abnormal at term.*
+
+
+### Sagittal US Via Posterior Fontanelle
+
+
+*Although routine scanning is performed via the anterior fontanelle, the posterior fontanelle is another alternative, particularly when it is difficult seeing more posterior structures in the brain.*
+
+
+*This scan through the posterior fontanelle in a 26-week premature infant was performed to better evaluate the corpus callosum. The splenium is particularly well seen in this view.*
+
+
+*Color Doppler image shows flow within the choroid plexus of the glomus. The posterior fontanelle view can be helpful to differentiate bulky choroid from clot. The occipital horn does not contain choroid plexus, and any echogenic material in the occipital horn should raise the suspicion of intraventricular hemorrhage.*
+
+
+### Axial US Through Temporal Bone
+
+
+*Graphic of the transtemporal acoustic window is shown. The transducer is placed more anterior and superior than the mastoid fontanelle approach. The temporal bone anterior to the ear is thin enough to allow imaging of the brainstem even after closure of the temporosquamosal suture. This acoustic window allows the best assessment of cerebral peduncles and the 3rd ventricle.*
+
+
+*Transtemporal axial scan in a 29-week premature infant shows intracranial anatomy in a plane similar to CT or MR.*
+
+
+*The temporal bone anterior to the ear is thin, allowing imaging of the brainstem even after sutural closing. This is the best view for the cerebral peduncles and midbrain.*
+
+
+### Cerebellum and posterior fossa
+
+
+*Sagittal midline graphic of the posterior fossa shows the anterior brainstem and posterior cerebellum separated by the 4th ventricle. The brainstem consists of midbrain (mesencephalon), pons, and medulla. The cerebellum has superior (tentorial), inferior (suboccipital), and anterior (petrosal) surfaces. The primary (tentorial) fissure and horizontal (petrosal) fissures divide the vermis and cerebellar hemispheres into lobules.*
+
+
+*This midline sagittal view shows the brainstem. The pons is easily identified by its anterior bulge.*
+
+
+*A coronal image through the anterior fontanelle of a premature infant, born at 29 weeks 1 day, shows symmetric cerebellar hemispheres. The vermis is midline, covers the 4th ventricle, and is more echogenic than the rest of the cerebellum.*
+
+
+### Posterior fossa via mastoid approach
+
+
+*The mastoid/posterolateral fontanelle is located at the junction of temporosquamosal, lambdoidal, and occipital sutures. It allows assessment of brainstem and posterior fossa structures, which are not well demonstrated in the standard planes through the anterior fontanelle. The transducer is placed ~ 1 cm behind the helix of ear and 1 cm above the tragus. This acoustic window allows the best visualization of 4th ventricle, posterior cerebellar vermis, cerebellar hemispheres, and cisterna magna.*
+
+
+*The mastoid approach allows for detailed evaluation of the posterior fossa structures. This is a premature infant (27 weeks 5 days), which is evident by the lack of cortical gyri and cerebellar folia.*
+
+
+*Another mastoid view in an infant born at 37 weeks shows maturation with extensive folia on the surface of the cerebellum.*
+
+
+### Cavum Septi Pellucidi et Vergae
+
+
+*Coronal graphic with an axial insert shows a classic cavum septi pellucidi with a posterior extension, the cavum vergae. It creates a finger-like CSF collection between the lateral ventricles.*
+
+
+*The cavum septi pellucidi can be quite large, especially in premature infants and should not be confused with an elevated 3rd ventricle or intracranial cyst.*
+
+
+*Midline sagittal image in this 27-week premature infant shows a cavum septi pellucidi continuing posteriorly into the cavum vergae. This is a common finding in premature infants. The cavum vergae is closed in 97% of full-term infants and the cavum septi pellucidi is closed in 85% of infants by 3-6 months of age; however, it can remain open until adulthood.*
+
+
+### Cavum Velum Interpositum
+
+
+*Sagittal graphic with an axial insert shows a cavum velum interpositum. Note the elevation and splaying of the fornices. Also noted is the inferior displacement of the internal cerebral veins and 3rd ventricle.*
+
+
+*Midline sagittal ultrasound shown a mildly complex cavum velum interpositum.*
+
+
+*This premature infant has a cavum septi pellucidi, vergae, and interpositum. Like a cavum septi pellucidi and vergae, a cavum velum interpositum is more common in premature infants.*
+
+
+### Vascular anatomy
+
+
+*This graphic shows the arteries, sinuses, and veins, which can be seen seen on a routine midline sagittal view. The anterior cerebral artery and its 2 main branches, the pericallosal and callosomarginal arteries, are easily seen on midline color Doppler ultrasound. The basilar artery is also easily identified, running anterior to the brainstem. The middle cerebral and posterior cerebral arteries are better evaluated in an axial plane using a transtemporal or mastoid approach.*
+
+
+### Midline color Doppler
+
+
+*Midline sagittal color Doppler image, obtained via the anterior fontanelle, shows the pericallosal artery running in the callosal sulcus, just above the corpus callosum. In a normal newborn, the pericallosal artery should be close to the surface of the corpus callosum. While in callosal agenesis, this artery remains far from the 3rd ventricle and takes an upward oblique direction.*
+
+
+*The anterior cerebral artery divides into the pericallosal artery, which continues along the corpus callosum, and the callosomarginal artery, which courses superiorly to travel above the cingulate gyrus within the cingulate sulcus.*
+
+
+*Multiple cortical branches of the callosomarginal artery are seen traveling within cortical sulci.*
+
+
+### Circle of Willis
+
+
+*The circle of Willis illustrated in situ shows its intricate relationship to adjacent structures. It located in the suprasellar cistern just below the diencephalon. The hypothalamus, infundibular stalk, and optic chiasm lie in the middle of the circle. The horizontal (A1) anterior cerebral artery segment passes above the optic nerves (CNII); the posterior communicating artery passes above the oculomotor nerves (CNIII). The anterior communicating artery is near the midline, below the interhemispheric fissure.*
+
+
+*The circle of Willis is shown in isolation and turned 90° counterclockwise to match the plane of the ultrasound.*
+
+
+*Transtemporal axial color Doppler in a premature infant with ventriculomegaly from an intracranial hemorrhage shows the circle of Willis. The anterior and middle cerebral arteries are the terminal branches of the internal carotid artery. The posterior cerebral artery is the terminal branch of the basilar artery. These 3 crucial arteries communicate via the anterior and posterior communicating arteries in a complete circle of Willis. The transtemporal approach provides the best window for evaluating the circle of Willis.*
+
+
+### Cerebral Arteries
+
+
+*Doppler waveform of a cortical branch of the anterior cerebral artery shows a low-resistance waveform with abundant diastolic flow. Velocity of the cerebral artery is a reliable reflection of intracranial pressure.*
+
+
+*Doppler waveform of the middle cerebral artery in the coronal plane is obtained by angling the beam laterally toward the sylvian fissure. A low-resistance arterial waveform is again noted.*
+
+
+*Color Doppler ultrasound obtained by a parasagittal scan through the anterior fontanelle shows the thalamostriate arteries. Anteriorly, the caudate nucleus is supplied by the anterior thalamostriate artery while the thalamus posteriorly is supplied by the posterior thalamostriate artery. The thalamostriate arteries arise from the middle cerebral artery.*
+
+
+### Cerebral veins and sinuses
+
+
+*This graphic shows the the connections between the major dural sinuses and deep cerebral veins. The internal cerebral veins and basal veins of Rosenthal drain into the vein of Galen, which in turn drains into the straight sinus.*
+
+
+*Sagittal color Doppler scan through the anterior fontanelle shows a superficial cortical vein traversing the subarachnoid space and draining into the superior sagittal sinus.*
+
+
+*Spectral Doppler waveform of the superior sagittal sinus shows the waveform of the sinus to be pulsatile, under the effect of transmitted cardiac pulsations.*
+
+
+*Color Doppler ultrasound obtained by a midline sagittal scan through the anterior fontanelle shows the relationship of the vein of Galen and straight sinus. The vein of Galen is seen under the splenium of the corpus callosum. It receives drainage from the paired internal cerebral veins and basal veins of Rosenthal. The vein of Galen continues inferiorly into the straight sinus. The straight sinus, superior sagittal sinus, and transverse sinuses converge posteriorly, forming the torcular Herophili.*
+
+
+*In the angled coronal plane, the straight sinus is seen in the midline between the lateral ventricles.*
+
+
+*Other sinuses can be evaluated using different acoustic windows. The transverse sinus can be accessed via a mastoid fontanelle approach, as shown here. The cerebral venous system is valveless, and pulsed Doppler waveforms typically show cardiac pulsations.*
+
diff --git a/docs_md/articles/deep-cerebral-venous-thrombosis_056d86df-2bcb-4816-ace7-21f663d581f0.md b/docs_md/articles/deep-cerebral-venous-thrombosis_056d86df-2bcb-4816-ace7-21f663d581f0.md
new file mode 100644
index 0000000..ea75f3f
--- /dev/null
+++ b/docs_md/articles/deep-cerebral-venous-thrombosis_056d86df-2bcb-4816-ace7-21f663d581f0.md
@@ -0,0 +1,564 @@
+---
+title: "Deep Cerebral Venous Thrombosis"
+docid: "056d86df-2bcb-4816-ace7-21f663d581f0"
+authors:
+ - key: "8d5254e9-8dda-478b-8f08-bdee97a32c79"
+ value: "Karen L. Salzman, MD, FACR"
+ - key: "5cff4116-3654-4b3a-bb75-5ebe0b8c9850"
+ value: "Anne G. Osborn, MD, FACR"
+breadcrumbs:
+ -
+ name: "Brain"
+ slug: "brain"
+ treeNodeId: "0361042c-9c90-48e4-864e-a2e6428ee9c9"
+ -
+ name: "Diagnosis"
+ slug: "diagnosis"
+ treeNodeId: "948c6f1e-8e18-45f3-bd9d-7a04ab0b8708"
+ -
+ name: "Pathology-Based Diagnoses"
+ slug: "pathology-based-diagnoses"
+ treeNodeId: "d60fe914-7897-46a0-9cd2-f88ffb322f16"
+ -
+ name: "Stroke"
+ slug: "stroke"
+ treeNodeId: "7a135176-0a69-4fc9-b200-59569fbf5166"
+ -
+ name: "Cerebral Ischemia and Infarction"
+ slug: "cerebral-ischemia-and-infarction"
+ treeNodeId: "11d50e7d-f3e9-4071-b2b7-26b11ab40ea6"
+ -
+ name: "Deep Cerebral Venous Thrombosis"
+ slug: "deep-cerebral-venous-thrombosis"
+ treeNodeId: null
+category: "Brain"
+documentVersionId: "56aa1815-78a7-46e0-85f2-03f2113b0c2f"
+imageCount: 39
+lastUpdated: "09/16/25"
+pageDescription: "Deep Cerebral Venous Thrombosis"
+pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Deep Cerebral Venous Thrombosis"
+pageTitle: "Deep Cerebral Venous Thrombosis | STATdx"
+enhancedTitle: "Deep Cerebral Venous Thrombosis"
+type: "DX"
+references: true
+anatomy:
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+cases: 3
+breadcrumbs:
+ - "Brain"
+ - "Diagnosis"
+ - "Pathology-Based Diagnoses"
+ - "Stroke"
+ - "Cerebral Ischemia and Infarction"
+ - "Deep Cerebral Venous Thrombosis"
+---
+## KEY FACTS
+
+- ### Terminology
+
+
+ - Thrombotic occlusion of deep cerebral veins
+ - Usually both internal cerebral veins (ICVs) ± vein of Galen (VOG), straight sinus (SS)
+- ### Imaging
+
+
+ - NECT
+ - Hyperdense ICV ± VOG, SS
+ - > 62 HU (≥ 70 HU rarely normal)
+ - Hypodense thalami/basal ganglia (BG)
+ - Thalami seem to "disappear" into background white matter (WM) hypodensity
+ - ± hemorrhage (lobar, petechial)
+ - CECT
+ - Loss of ICV enhancement, presence of enlarged collateral channels
+ - ± "squiggly" deep WM veins, "shaggy" tentorium
+ - MR
+ - Acute clots hypointense on T2, bloom on T2*
+ - Deep (medullary) WM veins prominent, tortuous on SWI
+ - Protocol advice
+ - If CT/CECT/CTV scans negative → MR with MRV
+ - If MRV equivocal → DSA
+- ### Top Differential Diagnoses
+
+
+ - Bithalamic/BG lesions
+ - Neoplasm (e.g., bithalamic astrocytoma, lymphoma)
+ - Arterial ischemia (e.g., "top of basilar" or artery of Percheron infarct)
+ - Hypoxic-ischemic injury (HII)
+ - Toxic/metabolic disorders (e.g., PRES, CO poisoning)
+ - Acute necrotizing encephalopathy
+ - Influenza-associated
+ - COVID-19
+- ### Clinical Issues
+
+
+ - Venous thrombosis = 1-2% of strokes
+ - ICV thrombosis = 10% of venous "strokes"
+
+## TERMINOLOGY
+
+- ### Abbreviations
+
+
+ - Deep cerebral venous thrombosis (DCVT)
+- ### Definitions
+
+
+ - Thrombotic occlusion of deep cerebral veins
+ - Usually affects both internal cerebral veins (ICVs) ± vein of Galen (VOG), straight sinus (SS)
+ - Often with widespread dural sinus thrombosis (DST)
+
+## IMAGING
+
+- ### General Features
+
+
+ - #### Best diagnostic clue
+
+
+ - Hyperdense ICV ± VOG, SS ± bithalamic hypodensity
+ - Loss of deep gray matter-white matter (WM) interfaces
+ - Thalami seem to "disappear" into background WM hypodensity
+ - #### Location
+
+
+ - ICV ± VOG, SS, basal veins of Rosenthal
+ - Bilateral ICV thrombosis > > unilateral
+ - Edema (venous congestion)
+ - Deep gray nuclei, internal capsule, medullary WM
+ - Variable involvement of midbrain, upper cerebellum
+- ### CT Findings
+
+
+ - #### NECT
+
+
+ - Visual analysis highly specific but only moderately sensitive for diagnosis of CVT
+ - Hyperdense ICVs ± SS, DST by visual inspection ± accurate
+ - Measurements
+ - > 62 HU (normal very rarely ≥ 70 HU)
+ - HU:hematocrit (H:H) ratio 1.52
+ - HU in affected vs. unaffected sinus ratio = 1.3
+ - High specificity (97-100%) but low to moderate sensitivity (41-73%)
+ - Not sensitive enough to rule out CVT confidently
+ - Additional imaging (CTV, MR with MRV) when CVT suspected
+ - Variable parenchymal abnormalities
+ - Hypodense thalami/basal ganglia (BG), loss of gray matter-WM interfaces
+ - ± petechial hemorrhages
+ - #### CECT
+
+
+ - Empty delta sign (if DST)
+ - "Shaggy," irregular veins (collateral channels) in deep WM, around tentorium
+ - CTV
+ - Loss of ICV enhancement, presence of enlarged collateral channels
+ - Limited value in chronic cases as organizing thrombosis also enhances
+- ### MR Findings
+
+
+ - #### T1WI
+
+
+ - Clot: Early T1 isointense, later hyperintense
+ - Venous hypertension: Hypointense swelling of thalami, BG
+ - Venous infarct: Hypointense edema, may be hemorrhagic
+ - #### T2WI
+
+
+ - Acute thrombus hypointense, mimics flow voids
+ - Hyperintense swelling of thalami, BG common
+ - Corresponds to vasogenic ± cytotoxic edema
+ - Venous infarct: Parenchymal swelling, hyperintense edema, may be hemorrhagic
+ - #### FLAIR
+
+
+ - High signal in occluded veins
+ - Best demonstrates hyperintense BG edema
+ - #### T2* GRE
+
+
+ - Thrombus is hypointense, blooms
+ - SWI shows engorged, prominent deep WM (medullary) veins
+ - ± lobar &/or petechial hemorrhages
+ - #### DWI
+
+
+ - Variable findings
+ - BG/thalami may restrict early, normalize later
+ - Thrombus, hemorrhages may restrict
+ - #### T1WI C+
+
+
+ - Acute/early subacute clot: Peripheral enhancement outlines clot
+ - Late clot: Thrombus, fibrous tissue often enhances
+ - Venous stasis in deep WM (medullary) veins seen as linear enhancing foci radiating outward from ventricles
+ - Venous edema/hypertension: No enhancement
+ - Parenchymal venous infarct: Patchy enhancement
+ - #### MRV
+
+
+ - 2D time-of-flight (TOF) MRV shows "missing" ICVs, variably absent signal in VOG, SS
+ - May see abnormal collateral channels
+ - Contrast-enhanced MRV (CE-MRV)
+ - Faster; better depicts nonenhancing thrombus and small veins than TOF
+ - TOF limitations
+ - T1-hyperintense thrombus falsely appears as patent flow on MIP
+ - Always evaluate source images and conventional MR sequences
+ - Phase-contrast MRV: T1-hyperintense thrombus not misrepresented as flow
+ - #### MRS
+
+
+ - Reduced metabolites, lactate in infarcts may help differentiate from nonvascular pathology (bithalamic glioma) in equivocal cases
+ - MR perfusion
+ - T2* gadolinium perfusion may show extensive venous congestion but without perfusion deficits
+ - May play role in detecting venous congestion vs. venous infarction in cerebral venous thrombosis
+- ### Angiographic Findings
+
+
+ - DSA
+ - More accurate than MR
+ - Deep cerebral veins normally always present
+ - In DCVT, occluded ICVs do not opacify ("absent")
+ - Collateral venous channels (e.g., medullary veins) enlarge
+ - Interventional: Treatment with thrombolytics &/or mechanical declotting
+- ### Imaging Recommendations
+
+
+ - #### Best imaging tool
+
+
+ - NECT, CECT ± CTV venogram
+ - Conventional DSA if intervention planned
+ - #### Protocol advice
+
+
+ - If NECT/CECT/CTV scans negative → MR with 2D TOF MRV
+ - If MRV equivocal → DSA
+
+## DIFFERENTIAL DIAGNOSIS
+
+- ### Bithalamic Lesions
+
+
+ - **Arterial ischemia**
+ - "Top of basilar," artery of Percheron infarct
+ - DWI (+), acute onset
+ - **Deep venous thrombosis**
+ - Hyperdense veins
+ - May have associated edema, hemorrhage
+ - **Neoplasm** (glioma, primary CNS lymphoma)
+ - T2/FLAIR hyperintense, often enhancing
+ - **Hypoxic-ischemic injury (HII)**
+ - Acute onset, bilateral symmetric DWI (+)
+ - **Posterior reversible encephalopathy syndrome (PRES)**
+ - Patchy parietooccipital cortical/subcortical edema
+ - May affect deep gray nuclei; no DWI (+)
+ - **Acute necrotizing encephalopathy**
+ - T2-hyperintense lesions ± necrosis, hemorrhage
+ - Occurs after infection (i.e., influenza, COVID)
+ - **Creutzfeldt-Jakob disease (CJD)**
+ - DWI and FLAIR hyperintense lesions
+ - Often affect deep gray nuclei and cortex
+ - **Carbon monoxide (CO) poisoning**
+ - DWI (+), T2 hyperintensity in globus pallidus
+ - **Viral encephalitis**
+ - T2/FLAIR hyperintensity in deep gray nuclei
+
+## PATHOLOGY
+
+- ### General Features
+
+
+ - #### Etiology
+
+
+ - No cause identified in 20-25% of cases
+ - Wide spectrum of causes (> 100 identified)
+ - Trauma, infection, inflammation
+ - Pregnancy, peripartum period
+ - Metabolic (dehydration, thyrotoxicosis, cirrhosis, etc.)
+ - Hematological (coagulopathy)
+ - Collagen-vascular disorders (e.g., APLA syndrome)
+ - Vasculitis (e.g., Behçet)
+ - Drugs (oral contraceptives, androgens, ecstasy)
+ - Ulcerative colitis
+ - Most common sequence
+ - Thrombus initially forms in dural sinus
+ - Clot propagates into cortical veins
+ - Venous drainage obstructed, venous pressure elevated
+ - Blood-brain barrier breakdown with vasogenic edema, hemorrhage
+ - Venous infarct with cytotoxic edema ensues
+ - #### Genetics
+
+
+ - Factor 5 Leiden mutation is most common cause of sporadic CVT
+ - Resistance to activated protein C
+ - Prothrombin (factor 2) gene mutation
+ - Protein S deficiency
+ - Antithrombin 3 deficiency
+ - #### Associated abnormalities
+
+
+ - May have thrombosis elsewhere
+ - Lower extremity DVT, pulmonary embolism
+- ### Staging, Grading, & Classification
+
+
+ - Venous ischemia
+ - Type 1: No abnormality
+ - Type 2: High signal on T2/FLAIR MR; no enhancement
+ - Type 3: High signal on T2/FLAIR MR; enhancement present
+ - Type 4: Hemorrhage or venous infarction
+- ### Gross Pathologic & Surgical Features
+
+
+ - ICVs occluded, distended by acute clot
+ - Venous hypertension ensues
+ - Adjacent thalami edematous with variable hemorrhage
+- ### Microscopic Features
+
+
+ - Thrombus in occluded vessels
+
+## CLINICAL ISSUES
+
+- ### Presentation
+
+
+ - #### Most common signs/symptoms
+
+
+ - Presentation highly variable
+ - Headache, nausea, vomiting
+ - ± focal neurologic deficit, seizure
+ - Altered mental status
+- ### Demographics
+
+
+ - #### Age
+
+
+ - Any
+ - Especially older, debilitated patients
+ - Pregnant, peripartum women, women on birth control pills
+ - #### Sex
+
+
+ - F > M
+ - #### Epidemiology
+
+
+ - Venous thrombosis causes 1-2% of strokes
+ - ICV thrombosis = 10% of venous "strokes"
+- ### Natural History & Prognosis
+
+
+ - Clinical diagnosis of CVT often elusive
+ - Outcome of CVT extremely variable, from asymptomatic to death
+ - Majority have no residual deficits at 16 months
+ - Subgroup (13%) have poor outcome
+ - Predictors of death/dependence
+ - Hemorrhage on admission CT
+ - DWI demonstration of cytotoxic edema (infarction)
+- ### Treatment
+
+
+ - Heparin ± rTPA
+ - Endovascular thrombolysis
+
+## DIAGNOSTIC CHECKLIST
+
+- ### Consider
+
+
+ - DSA in equivocal cases and for intervention
+- ### Image Interpretation Pearls
+
+
+ - Early imaging findings subtle, often overlooked
+ - Obtain NECT concurrently with CTV
+ - Flow voids on T2 do not rule out DCVT
+ - 2D TOF MRV should not be interpreted without benefit of standard imaging sequences
+ - Nonvisualization of deep venous system on CTA/MRA/DSA **always** abnormal
+
+ e796078b-3405-4713-8305-6e3abeec1135
+
+## References
+
+## Selected References
+
+1. [Gautam D et al: Endovascular treatment of cerebral venous sinus thrombosis: a systematic review and meta-analysis of efficacy based on technique. Interv Neuroradiol. 15910199251336946, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=40296709%5Bpmid%5D)
+1. [Kishi S et al: SWI brush sign of cerebral parenchymal veins in central nervous system diseases. Jpn J Radiol. 43(5):726-35, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=39730932%5Bpmid%5D)
+1. [Saposnik G et al: Diagnosis and management of cerebral venous thrombosis: a scientific statement from the American Heart Association. Stroke. 55(3):e77-90, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38284265%5Bpmid%5D)
+1. [Alajmi E et al: Prevalence of venous infarction in patients with cerebral venous thrombosis: baseline diffusion-weighted MRI and Follow-Up MRI. Stroke. 54(7):1808-14, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=37283035%5Bpmid%5D)
+1. [Boukerche F et al: Detection of cerebral cortical vein thrombosis with high-resolution susceptibility weighted imaging - a comparison with MR venography and standard MR sequences. Neuroradiology. 1-8, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=36720750%5Bpmid%5D)
+1. [Ranjan R et al: Pathophysiology, diagnosis and management of cerebral venous thrombosis: A comprehensive review. Medicine (Baltimore). 102(48):e36366, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=38050259%5Bpmid%5D)
+1. [Boukerche F et al: High-resolution susceptibility-weighted imaging of clots in cerebral venous thrombosis. Neuroradiology. 64(12):2267-75, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35821529%5Bpmid%5D)
+1. [Kuiper L et al: Association between dural AVFs and cerebral venous thrombosis. AJNR Am J Neuroradiol. 43(12):1722-9, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=36396334%5Bpmid%5D)
+1. [Cernera G et al: Molecular analysis of prothrombotic gene variants in venous thrombosis: a potential role for sex and thrombotic localization. J Clin Med. 9(4), 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32252449%5Bpmid%5D)
+1. [Dangi S et al: A case of deep cerebral venous thrombosis presenting like acute necrotizing encephalopathy. J Pediatr Neurosci. 15(1):54-6, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32435309%5Bpmid%5D)
+1. [Garaci F et al: Venous cerebral thrombosis in COVID-19 patient. J Neurol Sci. 414:116871, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32422428%5Bpmid%5D)
+1. [Komro J et al: Cerebral venous sinus thrombosis in adults with prothrombotic conditions: a systematic review and a case from our institution. Cureus. 12(4):e7654, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32411555%5Bpmid%5D)
+1. [Mazini B et al: Isolated superior striate vein thrombosis in adults. Interv Neuroradiol. 1591019919900825, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31969077%5Bpmid%5D)
+1. [Poillon G et al: Cerebral venous thrombosis associated with COVID-19 infection: causality or coincidence? J Neuroradiol. 48(2):121-4, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32437707%5Bpmid%5D)
+1. [Tan AP: Postoperative unilateral internal cerebral vein thrombosis with venous watershed infarcts: case report and review of the literature. World Neurosurg. 138:158-62, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32169620%5Bpmid%5D)
+1. [Aguiar de Sousa D et al: Brush sign is associated with increased severity in cerebral venous thrombosis. Stroke. 50(6):1574-7, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31035899%5Bpmid%5D)
+1. [Buyck PJ et al: Diagnostic accuracy of noncontrast CT imaging markers in cerebral venous thrombosis. Neurology. 92(8):e841-51, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30659138%5Bpmid%5D)
+1. [Kumar P et al: Deep cerebral vein thrombosis: a clinical masquerader. J Clin Diagn Res. 11(4):OD16-8, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28571198%5Bpmid%5D)
+1. [Barboza MA et al: Intracranial venous collaterals in cerebral venous thrombosis: clinical and imaging impact. J Neurol Neurosurg Psychiatry. 86(12):1314-8, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25589781%5Bpmid%5D)
+1. [Coutinho JM et al: Cerebral venous thrombosis in the absence of headache. Stroke. 46(1):245-7, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25378420%5Bpmid%5D)
+1. [Bonneville F: Imaging of cerebral venous thrombosis. Diagn Interv Imaging. 95(12):1145-50, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25465119%5Bpmid%5D)
+1. [Buyck PJ et al: CT density measurement and H:H ratio are useful in diagnosing acute cerebral venous sinus thrombosis. AJNR Am J Neuroradiol. 34(8):1568-72, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23471024%5Bpmid%5D)
+1. [Linn J et al: Noncontrast CT in deep cerebral venous thrombosis and sinus thrombosis: comparison of its diagnostic value for both entities. AJNR Am J Neuroradiol. 30(4):728-35, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19213820%5Bpmid%5D)
+
+## Anatomy
+
+### Basal Ganglia
+Brain/ANATOMY:a9de3815-ec59-4c78-adf0-94974065a7e3
+
+### Thalamus
+Brain/ANATOMY:b7f0cd6b-4ba2-4ed4-8dd0-5ca56d9ae92b
+
+### Limbic Network
+Brain/ANATOMY:e1a20b61-b2c1-44c5-ba04-59843855bfef
+
+### Deep Cerebral Veins
+Brain/ANATOMY:e426b06e-4b91-48ef-956b-78fb179b1de9
+
+## Cases
+
+- {'cases': [{'authors': [{'key': '07a2c087-6202-49e7-870b-7aa162d18f06', 'value': 'Bronwyn E. Hamilton, MD'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '1a6b9bc7-2048-4bbd-b099-184813b37b81', 'description': 'CT images (#1, 2) demonstrate enlargement and hyperdensity in the bilateral internal cerebral veins (arrows) and straight sinus (white open arrow), characteristic of venous thrombosis. Note normal density in the superior sagittal sinus (black open arrow, #2) for comparison. There is also hypodensity and mild mass effect in the bilateral thalami, basal ganglia, and left caudate head, consistent with associated edema &/or ischemia (curved arrows). Low density changes may represent vasogenic edema in venous occlusive disease; however severe cases can progress to cytotoxic edema and infarction (this distinction is best made with diffusion-weighted MR imaging and has prognostic value). \n\nComment: CT scans in very young infants and neonates can be more challenging to interpret because of the normally hypodense background of the brain parenchyma from unmyelinated fiber tracts. Vessels may normally appear quite dense, suggesting vascular occlusion. Comparison with other normal vascular structures provides an internal standard and is helpful to avoid this pitfall. Although the patient in this example is not a neonate, normal appearance of the relatively hypodense superior sagittal sinus (open black arrow, image #2) is illustrative of this point.', 'history': 'Patient had been dehydrated for 18 months prior to imaging.', 'imagePoolId': '6e0600c0-73bb-4692-ad8e-874b7be24bb0', 'name': 'Internal cerebral veins', 'teachingPoint': None}], 'caseType': 'Other', 'name': 'OTHER'}
+- {'cases': [{'authors': [{'key': '07a2c087-6202-49e7-870b-7aa162d18f06', 'value': 'Bronwyn E. Hamilton, MD'}], 'caseVersionId': '1166f713-bd94-45c8-9e4b-f5f1985deb90', 'description': 'MR imaging (#1) demonstrates hyperintense T2 signal and mild mass effect in the bilateral thalami, basal ganglia, and caudate nuclei (arrows). Note apparent flow voids in the bilateral internal cerebral veins (curved arrows).\n\nVenous phase image from diagnostic angiography (#2) shows complete absence of the deep venous system, confirming extensive deep vein thrombosis. \n\nComments: This case again illustrates a common pitfall with MR imaging. Flow voids on T2 imaging do not always imply vascular patency. Some stages of thrombus may appear T2 hypointense and mimic flow voids. Proton density sequences and flow sensitive studies (MR venography) are more reliable.\n\nExtensive signal abnormality in the deep nuclei can raise concern for a global hypoxic ischemic event, metabolic abnormality, or even neoplastic and inflammatory conditions, however the possibility of deep venous occlusion with resultant ischemia/infarction should be entertained.', 'history': None, 'imagePoolId': '4fad9ff2-a283-46d3-ade1-d611fc0bc02f', 'name': 'Extensive', 'teachingPoint': None}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'd4898616-f3a6-4802-8f8e-ec7a398b5d2a', 'description': "Lateral venous phase study of cerebral angiogram (#1) shows normal descending segment of superior sagittal sinus (arrow) and transverse/sigmoid sinus (open arrow). It is harder to note something that's missing: The straight sinus and internal cerebral veins show no filling. There are also very prominent frontal and temporal cortical veins with drainage into the cavernous sinus (curved arrow) and pterygoid venous plexus (immediately below cavernous sinus). AP view image (#2) shows these prominent cortical veins with no filling of either the internal cerebral veins or straight sinus. \n\nClassic angiographic findings of complete deep cerebral vein occlusion with nonvisualization of internal cerebral veins, vein of Galen, straight sinus.", 'history': 'Developed increasing headaches, decreasing mental status after long hike at high altitude with inadequate hydration.', 'imagePoolId': 'a56703cc-2c59-47e9-b564-6d42e0266a17', 'name': 'ICV, occlusion', 'teachingPoint': None, 'demographics': '22 Years old male'}], 'caseType': 'typical', 'name': 'TYPICAL'}
+- {'cases': [{'authors': [{'key': '07a2c087-6202-49e7-870b-7aa162d18f06', 'value': 'Bronwyn E. Hamilton, MD'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '1a8ba207-b684-4029-800f-c365092f8151', 'description': 'Head CT without contrast demonstrates typical findings of hyperdensity in the bilateral internal cerebral veins and straight sinus (arrows). Hypodensity in the bilateral thalami (open arrows) is consistent with edema and/or ischemia.\n\nSagittal T1 image (#2) reveals characteristic hyperintensity (curved arrow) in the straight sinus, consistent with slow flow and/or thrombosis, although the internal cerebral veins are less well visualized. Mixed signal on diffusion weighted imaging is common in venous occlusion, with variable degrees of cytotoxic and vasogenic edema. In this case, images show subtle diffusion restriction and corresponding ADC reduction (#3-4) in the thalami, supporting ongoing ischemia (arrows). \n\nFLAIR and T2 images (#5-6 respectively) demonstrate an important imaging pitfall: The internal cerebral veins are thrombosed, however the T2 hypointense acute thrombus has the appearance of normal or patent flow voids (open arrows). Proton density images (not shown) will resolve this concern, or MRV can be performed. Note that hemorrhage is a frequent accompanying feature of venous thrombosis, seen in the choroid plexus and ventricle in this case (curved arrows), although more typically hemorrhage is parenchymal. MRV MIP image (#7) confirms absent flow in the internal cerebral veins, inferior sagittal and straight sinuses (open arrows).', 'history': 'Patient presented with headache for one week prior to being found unresponsive by a family member. Subsequently, the patient was found to be heterozygous for the trait for factor V Leiden deficiency, which increases venous thrombosis risk by up to 10%. In addition, she had recently started taking oral contraceptives. \n', 'imagePoolId': '30b1cb48-ae27-43ab-8762-b04554569389', 'name': 'Thalamic infarcts, pseudo flow voids', 'teachingPoint': None, 'demographics': '25 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'e76dd47f-8303-48ec-b14b-11da653390ef', 'description': 'Sagittal imaging through the midline (#1) shows loss of the normal superior sagittal sinus flow void (arrows). Similarly, no definite flow voids are seen in the internal cerebral vein region (curved arrow) or vein of Galen (open arrow), suggesting occlusion or slow flow. \n\nAxial MR images (#2, 3) show abnormal T2 hyperintensity in the bilateral basal ganglia (arrows). Although a flow void is suggested in the vein of Galen (open arrow) on T2 imaging, it is important to remember that T2 images are not always reliable to insure vessel patency, as this case demonstrates. \n\nEnhanced images (#4-6) show extensive "cigar-shaped" filling defects in the bilateral transverse sinuses (curved arrows) and superior sagittal sinus (open arrow).Venous thrombi demonstrate a long cast-like morphology, which differentiates them from arachnoid granulations. Arachnoid granulations are also a cause of venous filling defects on enhanced studies, however they are typically round, and follow cerebrospinal fluid signal intensity on all sequences. \n\nAbnormal enhancement in both basal ganglia (arrows, #5, 6) corresponds to the areas of T2 signal abnormality, consistent with subacute infarction. All the deep nuclei are at risk for infarction when the deep cerebral veins thrombose, although in this case, abnormality was limited to the basal ganglia.\n\nMR venography (#7, 8) demonstrates flow in the left internal cerebral vein (arrow), however the contralateral internal cerebral vein is not seen on the AP view (#8). The vein of Galen, basal veins, and straight sinus are also thrombosed, in addition to several dural sinuses (posterior superior sagittal sinus and both transverse sinuses).', 'history': 'Unknown.', 'imagePoolId': 'e84067a8-faea-46d4-8a53-40b90d1f45d8', 'name': 'Severe', 'teachingPoint': None}, {'authors': [{'key': '07a2c087-6202-49e7-870b-7aa162d18f06', 'value': 'Bronwyn E. Hamilton, MD'}], 'caseVersionId': '9ba46d4a-1d12-4f73-9bb9-3b3021e36a41', 'description': 'Axial CT image (#1) shows subtle increased linear density in the expected location of the internal cerebral veins (arrow), which suggests thrombosis. Hypodensity and mild mass effect in the bilateral ventral thalami and basal ganglia (curved arrows) supports associated edema/ischemia (#1, 2). CT image (#2) also shows increased density in the straight sinus (open arrow), also suggesting occlusion. \n\nMR images (#3, 4) show T1 and T2 signal prolongation in the bilateral deep nuclei (arrows). T1 imaging (#3) shows increased signal in both internal cerebral veins (curved arrows), supporting deep venous occlusion. T2 imaging (#4) demonstrates hypointense signal in the internal cerebral veins (curved arrow) and right thalamostriate vein (open arrow), mimicking flow voids. This illustrates how T2 imaging can be unreliable to confirm vascular patency.\n\nEnhanced MR images (#5) show bilateral linear enhancement in the distribution of the medullary veins (arrows), consistent with venous congestion. Additional enhanced images (#6, 7) show marked enhancement of the deep nuclei (curved arrows). Although this might otherwise mimic a neoplastic or inflammatory process, the associated findings of central venous occlusion support breakdown of the blood brain barrier in the setting of subacute venous infarction. Diffusion imaging (not available in this case) would be confirmatory. \n\nVenous phase angiography (#8, 9) demonstrates occlusion of the central deep venous system. The internal cerebral veins, vein of Galen, basal veins, and straight sinus are absent, in addition to left transverse and sigmoid sinus occlusion.\n\nComments: Variations in the superficial venous system are common. Non-visualization of an isolated superficial cortical vein on venography may not necessarily be abnormal, and should be correlated with other findings. Absence of visualization of the deep cerebral venous system on venography however, is always pathologic. Clinical outcome in deep venous thrombosis varies; the majority have no significant deficits long term, however patients who go on to infarct or hemorrhage (13%) may die or have significant morbidity.\n\nEnhancement and edema in the deep nuclei can mimic neoplastic, metabolic, and inflammatory disorders. The diagnosis of deep venous thrombosis should always be entertained in such cases however, and can be confirmed by vascular imaging (to assess venous patency) and diffusion weighted imaging (to identify infarction). Cases which do not result in infarction typically show increased, rather than restricted diffusion, and have a better prognosis.', 'history': None, 'imagePoolId': '782c9718-1921-46ae-a734-e8bc4cab99dc', 'name': 'Deep venous infarcts', 'teachingPoint': None}], 'caseType': 'variant', 'name': 'VARIANT'}
+
+
+## Images
+
+
+### Selected Images
+
+
(red-orange). This consists of the paired internal cerebral veins (ICVs), vein of Galen, and straight sinus (SS). Deep cerebral venous thrombosis is a potentially life-threatening disorder with a combined mortality/disability rate of 25%; thus, early recognition on imaging studies is essential for patient treatment.](images/app.statdx.com_image_thumbnail_53a92cc1-f791-4220-a9e2-ba4bc556645c_annotated_true_size_900_quality_90_544e5779bee6adc7141b90f2572387d9944e2a0a.jpg)
+*Color-coded anatomic diagrams depict brain venous drainage territories at 4 different levels. Central core brain structures (basal ganglia, thalami, internal capsules, lateral and 3rd ventricle) and most of the corona radiata white matter (WM) are the territory drained by the deep "Galenic" venous system (red-orange). This consists of the paired internal cerebral veins (ICVs), vein of Galen, and straight sinus (SS). Deep cerebral venous thrombosis is a potentially life-threatening disorder with a combined mortality/disability rate of 25%; thus, early recognition on imaging studies is essential for patient treatment.*
+
+
+*Color-coded anatomic diagrams depict brain venous drainage territories at 4 different levels. Central core brain structures (basal ganglia, thalami, internal capsules, lateral and 3rd ventricle) and most of the corona radiata white matter (WM) are the territory drained by the deep "Galenic" venous system (red-orange). This consists of the paired internal cerebral veins (ICVs), vein of Galen, and straight sinus (SS). Deep cerebral venous thrombosis is a potentially life-threatening disorder with a combined mortality/disability rate of 25%; thus, early recognition on imaging studies is essential for patient treatment.*
+
+
with secondary hemorrhage in the choroid plexus and thalami 
. Edema in the thalami, basal ganglia, and deep cerebral WM are common findings. Linear WM medullary veins may become engorged and enhance.](images/app.statdx.com_image_thumbnail_118a0f9f-9cdc-4156-8434-364c5c824870_annotated_true_size_900_quality_90_87d9b9422f3c68fc665f6eca0913ecc7a6f50e45.jpg)
+*Axial graphic depicts thrombosis of both ICVs and the SS with secondary hemorrhage in the choroid plexus and thalami . Edema in the thalami, basal ganglia, and deep cerebral WM are common findings. Linear WM medullary veins may become engorged and enhance.*
+
+
, and the SS 
. The anterior aspects of the thalami appear isodense with the adjacent WM.](images/app.statdx.com_image_thumbnail_0fd52558-e2f8-42a1-91f0-e9baabec598e_annotated_true_size_900_quality_90_432aea110c1803db53e405bde5c99eb486451e59.jpg)
+*NECT shows hyperdensity in both ICVs , vein of Galen , and the SS . The anterior aspects of the thalami appear isodense with the adjacent WM.*
+
+
.](images/app.statdx.com_image_thumbnail_db09dc0e-bc1f-4db3-b569-12003b655227_annotated_true_size_900_quality_90_ad39eb7ba9681a90c7b17e89f0c812c01621c118.jpg)
+*Sagittal NECT in a 21 year old with severe headaches shows acute hyperdense thrombus in the ICVs , vein of Galen , and SS with enlargement of the SS. Additional thrombus is present in the superior sagittal sinus (SSS) .*
+
+
and SS 
. A large thrombus in the SSS is also illustrated. Thrombosis of the IVCs was better visualized on CT/CTA/CTV.](images/app.statdx.com_image_thumbnail_df788010-62c0-4d7e-a702-f9f1d4cfefc7_annotated_true_size_900_quality_90_13c567677602c1c6cb79878a0f0c5995400a72a4.jpg)
+*Sagittal T1 C+ MR in the same patient shows the acute thrombus in the vein of Galen and SS . A large thrombus in the SSS is also illustrated. Thrombosis of the IVCs was better visualized on CT/CTA/CTV.*
+
+
+*Axial NECT in a pediatric patient shows definite thrombus in both ICVs and SS and extensive hypodensity in the caudate, thalami, and putamen related to edema secondary to extensive deep cerebral venous occlusion.*
+
+
+*More cephalad axial NECT shows enlargement/hyperdensity in the ICVs, vein of Galen, and SS . Note the normal density in the SSS for comparison. There is hypodensity and mild mass effect in both the thalami and basal ganglia related to edema &/or infarction.*
+
+
+*Axial NECT in a 25-year-old man with headache and drowsiness shows hyperdense ICVs , SS , and transverse sinus . The thalami have faded into the background and are isodense with surrounding WM.*
+
+
+*Lateral CT venogram shows nonopacification of the thrombosed ICVs with filling defects in the vein of Galen . The SS and posterior 1/2 of the superior SS are also thrombosed. Deep cerebral venous thrombosis may be isolated in ~ 20% or occur with other venous thrombosis in ~ 80%.*
+
+
is hypointense and easily mistaken for normal flow voids. Note hyperintense edema in the thalami, more prominent on the left than right . Bilateral involvement of the deep gray nuclei is often asymmetric.](images/app.statdx.com_image_thumbnail_4ee7e835-94bf-4c51-8749-fd14106e2096_annotated_true_size_900_quality_90_02ddbba15ccf8286065c7af385f0a21fadf849a1.jpg)
+*Axial T2 MR in the same patient shows thrombus in the ICVs and SS , and confluence with the SSS is hypointense and easily mistaken for normal flow voids. Note hyperintense edema in the thalami, more prominent on the left than right . Bilateral involvement of the deep gray nuclei is often asymmetric.*
+
+
+*Axial T2* GRE MR shows blooming thrombus in both ICVs , vein of Galen , SS , and confluence with the SSS . Thrombosis of the entire deep venous system and SSS is shown.*
+
+
+*Axial NECT in a 58-year-old man shows hyperdense ICVs and SS . The left thalamus shows edema and hemorrhage related to a hemorrhagic infarct from the deep venous thrombosis.*
+
+
+*Axial T1 C+ MR in a 70-year-old with confusion shows enhancement in the left thalamus . Subtle enhancement is also present in the right thalamus. Biopsy was performed for concern for malignancy diagnosing a venous infarct. Venous infarcts may mimic arterial infarcts, tumors, or metabolic abnormalities.*
+
+
+*Axial NECT in an 80-year-old dehydrated man with altered mental status shows no abnormalities, except both thalami appear hypodense . Note the ICVs and SS do not appear hyperdense. The symmetric low density in the thalami raises concern for a metabolic process, infection, or ischemia.*
+
+
+*Sagittal T1 MR shows no definite abnormality, as the ICVs, vein of Galen, and SS are all isointense with the adjacent brain.*
+
+
+*Sagittal FLAIR MR shows symmetric hyperintensity in the basal ganglia, thalami, and deep periventricular WM. DWI sequences showed no restriction.*
+
+
+*Axial T2* GRE MR in the same patient shows blooming in both ICVs and junction of the vein of Galen with the SS . Note linear hypointensities in the septal veins , basal ganglia, and periventricular WM from deoxygenated blood and deep venous stasis.*
+
+
+*More cephalad T2* GRE MR shows hypointensity in the periventricular veins and distended medullary veins in the corona radiata . SWI often shows prominent deep WM medullary veins to better advantage, though is more limited by motion artifact.*
+
+
+*Axial NECT 2 days later shows the entire deep venous drainage territory is infarcted and hypodense . There is a small, focal hemorrhage in the left thalamus . Approximately 1/2 of all venous thrombosis cases results in ischemia &/or hemorrhage.*
+
+
+### Additional Images
+
+
+*Axial NECT shows bithalamic low-density edema/ischemia and increased density due to thrombosis in the IVCs and thalamostriate veins as well as the SS .*
+
+
+*Lateral DSA shows the absence of deep cerebral veins and SS, consistent with deep cerebral venous thrombosis. The deep venous system should always be seen on DSA.*
+
+
+*Axial T2 MR shows hypointense T2 signal, masquerading as flow voids in thrombosed ICVs . Bithalamic high signal reflects both cytotoxic and vasogenic edema.*
+
+
+*Axial T1 C+ MR in the same patient shows thrombosed, isointense, nonenhancing ICVs with extensive caudate nuclei enhancement and engorged deep medullary WM veins with contrast stasis .*
+
+
+*Axial T1 C+ MR shows enhancing striated vessels, characteristic of dilated medullary veins secondary to deep cerebral venous thrombosis.*
+
+
+*Lateral DSA shows nonfilling of deep cerebral veins, consistent with thrombosis. The deep venous system should always be seen on DSA. Note the increased flow within the petrosal sinuses .*
+
+
+*Axial DWI MR in a patient with ICV thrombosis and extensive bithalamic edema (not shown) reveals only mild diffusion restriction . Most of the abnormality was vasogenic edema secondary to venous hypertension.*
+
+
+*Axial gross pathology section shows hemorrhagic infarction in the bilateral thalami, left basal ganglia, and left hemisphere from bilateral ICV occlusion. (Courtesy J. Garcia, MD.)*
+
+
+*Axial FLAIR MR in a patient with deep venous system thrombosis shows hyperintensity in the caudate nuclei and thalami.*
+
+
+*Axial NECT in a 32-year-old woman with severe headache shows hyperdense ICVs . Both thalami are edematous and symmetrically isodense (normally hyperdense) compared to the surrounding WM.*
+
+
+*More inferior NECT in the same patient shows the vein of Galen and SS are also thrombosed and hyperdense (measured 70 HU).*
+
+
+*Axial FLAIR MR in a 70-year-old with confusion shows edema in the left thalamus . The lesion also enhanced. Biopsy was performed for concern for malignancy diagnosing a venous infarct. Venous infarcts may mimic arterial infarcts, tumors, or metabolic abnormalities.*
+
+
+*Sagittal T1 MR in a 21-year-old with headaches shows abnormal signal in the vein of Galen , SS , and SSS related to thrombosis. Subtle abnormal signal is also present in the inferior sagittal sinus .*
+
+
+*Sagittal NECT in a 23-year-old with ulcerative colitis and dehydration shows hyperdense acute thrombus in the vein of Galen and SS .*
+
+
+*Sagittal CTA in in the same patient shows the acute thrombus in the vein of Galen and SS .*
+
+
+*Sagittal CTA in a 58-year-old with headaches shows acute thrombus in the ICVs , vein of Galen , and SS . Note the normal enhancement in the SSS.*
+
+
+*Sagittal T1 MR in a 25-year-old with headaches and drowsiness shows acute thrombus in the superior sagittal and SSs and sinus confluence isointense with brain.*
+
+
+*Axial T1 MR in the same patient shows a missing flow void caused by thrombus in the SS and sinus confluence . The acute thrombus is isointense with brain.*
+
+
+*Sagittal NECT reformatted from the axial source data shows acute hyperdense thrombus in the ICVs , vein of Galen , and SS . The SS appears enlarged by the thrombus.*
+
+
+*Venous phase of lateral carotid DSA in the same patient shows normal cortical veins and SSS + a prominent vein of Labbé. The ependymal veins, ICVs, vein of Galen, and SS are unopacified because they are completely filled with thrombus.*
+
diff --git a/docs_md/articles/dural-sinus-and-aberrant-arachnoid-granulations_d7cc1586-8a57-431d-9566-ff51aebb338c.md b/docs_md/articles/dural-sinus-and-aberrant-arachnoid-granulations_d7cc1586-8a57-431d-9566-ff51aebb338c.md
new file mode 100644
index 0000000..a763745
--- /dev/null
+++ b/docs_md/articles/dural-sinus-and-aberrant-arachnoid-granulations_d7cc1586-8a57-431d-9566-ff51aebb338c.md
@@ -0,0 +1,511 @@
+---
+title: "Dural Sinus and Aberrant Arachnoid Granulations"
+docid: "d7cc1586-8a57-431d-9566-ff51aebb338c"
+authors:
+ - key: "b2e6dabb-ee1c-42a4-a332-9f0814c1c607"
+ value: "Surjith Vattoth, MD"
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+ name: "Dural Sinus and Aberrant Arachnoid Granulations"
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+pageDescription: "Dural Sinus and Aberrant Arachnoid Granulations"
+pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Dural Sinus and Aberrant Arachnoid Granulations"
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+cases: 2
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+ - "Stroke"
+ - "Cerebral Ischemia and Infarction"
+ - "Dural Sinus and Aberrant Arachnoid Granulations"
+---
+## KEY FACTS
+
+- ### Terminology
+
+
+ - Arachnoid granulation (AG)
+ - Defined as enlarged arachnoid villi projecting into major dural venous sinus (DVS) lumen
+ - Aberrant AG (AbAG): Arachnoid pit
+ - Defined as AG that penetrates dura, but fails to reach DVS, typically in sphenoid or temporal bone
+ - When large (1-1.5 cm in diameter) or occupy significant portion of dural sinus lumen → giant AG
+ - Vermiform giant AG: Giant AG with worm-like appearance
+- ### Imaging
+
+
+ - Intrasinus AG: Well-circumscribed, discrete, filling defect in venous sinus ± inner calvarial table erosion
+ - CECT: Nonenhancing; CSF density
+ - MR: T2 like CSF, often ↑ FLAIR, SWI isointense to brain
+ - AbAG: Multiple focal outpouchings in inner table
+ - Sphenoid bone location: Greater wing
+ - Temporal bone location: Posterior wall or tegmen
+ - CT: Multiple smooth pits in sphenoid or T-bone
+ - MR: T1 and T2 intensity follows CSF
+- ### Top Differential Diagnoses
+
+
+ - Brain herniations into DVS or calvarium
+ - Sternberg (lateral craniopharyngeal) canal
+ - Transverse-sigmoid sinus pseudolesion
+ - DVS thrombosis, dural arteriovenous fistula
+ - Dural sinus hypoplasia-aplasia
+- ### Pathology
+
+
+ - Normal variant enlarged arachnoid villi
+ - Giant AG could be consequence of benign intracranial hypertension (BIH), buffering CSF compartment
+ - Brain tissue may herniate into DVS; usually in giant AG
+- ### Clinical Issues
+
+
+ - AG: Asymptomatic; rarely **cause** or **consequence** of BIH
+ - AbAG: Mostly asymptomatic; may be seen in BIH
+ - If large with rupture, **CSF leak** ± meningitis possible
+ - Large AG may have associated **cephalocele** (± seizure)
+ - **Meningitis** may complicate CSF leak
+ - Treatment
+ - Intrasinus AG: No treatment required
+ - AbAG: No treatment unless CSF leak present
+- ### Diagnostic Checklist
+
+
+ - Sphenoid bone: CSF leak into sphenoid sinus → rhinorrhea
+ - T-bone: CSF leak into middle ear-mastoid → otorrhea
+
+## TERMINOLOGY
+
+- ### Abbreviations
+
+
+ - Arachnoid granulation (AG)
+ - Aberrant AG (AbAG)
+- ### Synonyms
+
+
+ - Pacchionian depressions, granulations, or bodies
+ - When large (1-1.5 cm in diameter) or occupy significant portion of dural sinus lumen → giant AG
+ - When in sphenoid bone and T-bone → AbAG (arachnoid pit)
+- ### Definitions
+
+
+ - Arachnoid villi: Term used to describe smaller AG
+ - **AG**: Enlarged arachnoid villi projecting from subarachnoid space (SAS) into major dural venous sinus (DVS) lumen
+ - **AbAG**: AG that penetrates dura but fails to reach DVS, typically in sphenoid or temporal bone
+ - Rarely other bones like parietal, occipital bone
+ - Also referred to as **arachnoid pits** or osteodural defects
+ - **Vermiform giant AG**: Giant AG with worm-like appearance
+ - Can mimic other pathology like DVS thrombosis, DVS cavernomas or brain tumors
+
+## IMAGING
+
+- ### General Features
+
+
+ - #### Best diagnostic clue
+
+
+ - Intrasinus AG: Discrete filling defect in DVS ± inner calvarial table erosion
+ - CECT: Nonenhancing; similar density to cerebrospinal fluid (CSF)
+ - MR: T1/T2 intensity like CSF; often ↑ FLAIR
+ - Signal intensity not following CSF on at least 1 sequence in 80%, usually FLAIR
+ - Brain tissue may herniate into DVS, usually as part of giant AG
+ - AbAG: Multiple focal outpouches in inner table of bone
+ - Bone CT: Multiple smooth arachnoid pits in bone
+ - MR: T1 and T2 intensity follows CSF
+ - #### Location
+
+
+ - Most common location: Transverse sinus
+ - Other locations: Sigmoid, sagittal, or straight sinus
+ - AbAG most common location
+ - Sphenoid bone, often greater wing, or lateral sphenoid sinus wall
+ - Temporal bone: Posterior wall or tegmen tympani
+ - #### Size
+
+
+ - 5-15 mm size range
+ - If > 10-15 mm, called giant AG
+ - #### Morphology
+
+
+ - AG project from SAS into major DVS lumen
+ - CSF core from SAS extends into AG and is separated from DVS endothelium by "arachnoid cap" cells
+ - Giant AGs often contain prominent venous channels and septations in CSF core
+ - Channels in arachnoid cap **drain CSF** into DVS
+ - Single or multiple ovoid lesions
+ - Focal osseous pits in inner table of calvarium
+- ### CT Findings
+
+
+ - #### NECT
+
+
+ - Intrasinus AG isodense with CSF
+ - CSF pulsations may result in erosion or scalloping of inner table
+ - AbAG: Focal osseous erosions in sphenoid bone
+ - If large, may be multilocular; mimic cystic bone lesion
+ - #### CECT
+
+
+ - Nonenhancing, ovoid focal filling defect within DVS
+ - Isodense to CSF
+ - AbAG: CSF density with subtle rim (dural) enhancement
+ - CT venogram
+ - Focal filling defect within DVS
+- ### MR Findings
+
+
+ - #### T1WI
+
+
+ - AG iso- to slightly more intense than CSF
+ - #### T2WI
+
+
+ - Hyperintense (like CSF)
+ - Surrounded by normal flow void of major DVS
+ - AbAG: High-signal outpouching into skull bone inner table
+ - If large, may see arachnoid pouch bulging into sphenoid sinus lumen
+ - Arachnoid strands: Low-signal lines within pouch
+ - Larger lesions may have **CSF leak** into sphenoid sinus
+ - Fluid levels seen in sphenoid sinus if leak present
+ - Larger lesions may have associated **cephalocele**
+ - #### DWI
+
+
+ - Facilitated diffusion: DWI hypointense and ADC bright, similar to CSF
+ - #### T1WI C+
+
+
+ - Intrasinus AG: Ovoid without enhancement surrounded by enhancing blood in dural sinus
+ - Veins, septa may enhance
+ - AbAG: Nonenhancing foci in sphenoid bone
+ - #### MRV
+
+
+ - Intrasinus AG
+ - Source images show focal signal loss in location of AG
+ - MRV reformation shows focal defect in affected sinus
+ - SWI
+ - Isointense to brain with internal venous flow voids
+- ### Imaging Recommendations
+
+
+ - #### Best imaging tool
+
+
+ - Intrasinus AG: Enhanced MR with 3D T1 sequences, such as MPRAGE, and MRV
+ - AbAG: Bone CT of skull base
+ - Enhanced MR and high-resolution 3D T2 MR sequences, such as CISS/SPACE/FIESTA focused to sphenoid bone area
+
+## DIFFERENTIAL DIAGNOSIS
+
+- [Brain Herniations With Surrounding CSF Into DVS or Calvarium](/document/intracranial-herniation-syndromes/e85ea6f9-0ff8-43ee-a79f-8b2698f5c7fd)
+ - Filling defects in DVS mimicking AG
+ - Asymptomatic with normal signal intensity of brain and CSF
+ - Temporal lobe → transverse sinus; cerebellum → skull; cerebellum → sigmoid sinus
+- ### Sternberg (Lateral Craniopharyngeal) Canal
+
+
+ - Membranous space in lateral sphenoid sinus wall
+ - Controversial extremely rare cause of lateral sphenoid sinus spontaneous CSF leak/cephalocele
+ - Should be medial to foramen rotundum (CNV2) in sphenoid sinus wall
+ - Arachnoid pits usually lateral to foramen rotundum, much more common with CSF leak/cephalocele
+- [Transverse-Sigmoid Sinus Pseudolesion](/document/jugular-bulb-pseudolesion/2bf19ff5-bfee-4764-9e2d-cea04ccce4ea)
+ - Asymmetric complex flow phenomenon in DVS
+ - Not present on all sequences; MRV sorts out
+- [Dural Sinus Thrombosis](/document/dural-sinus-thrombosis/9a1ac112-bd65-4306-92b0-022d16e360c3)
+ - Long-segment region of ↓ venous sinus flow
+ - NECT: Hyperdense if acute, later iso- to hypodense when subacute to chronic
+ - CECT: Nonenhancing clot in venous sinus lumen
+ - MR: Iso- to hyperintense on T1, or lack of flow void on T2
+ - SWI: Dark clot (vs. isointense to brain AG)
+ - T1 C+: Nonenhancing clot in venous sinus lumen
+ - Postcontrast MRV best to show nonenhancing clot as filling defect
+ - Phase contrast MRV (without gadolinium) also shows clot as filling defect
+ - Time of flight MRV may miss clot if it is hyperintense, mimicking normal flow signal
+- [Dural Arteriovenous Fistula](/document/dural-arteriovenous-fistula/99b59be6-df58-44a9-b14a-be194dfea1c7)
+ - MR: Recanalized, irregular transverse-sigmoid sinuses
+ - MRA: Enlarged, feeding external carotid artery branches; early venous drainage
+ - Angio: Enlarged, feeding external carotid artery branches
+- ### Dural Sinus Hypoplasia-Aplasia
+
+
+ - Congenital hypoplastic-aplastic transverse sinus
+ - "High-splitting" tentorium
+
+## PATHOLOGY
+
+- ### General Features
+
+
+ - #### Etiology
+
+
+ - Intrasinus AG: Normal variant enlarged arachnoid villi
+ - Penetrates dura overlying venous sinus
+ - Arachnoid cap cells in margin of AG responsible for CSF resorption
+ - Giant AGs can regress after therapeutic CSF removal in **benign intracranial hypertension (BIH)**
+ - Giant AG could be **consequence** of intracranial hypertension, buffering CSF compartment
+ - AbAG: AG that penetrates dura, but fails to reach venous sinus in sphenoid or temporal bone
+ - CSF pulsations enlarge AbAG → arachnoid pouch bulging
+ - Bulging arachnoid pouch penetrates subjacent structures (dura, then underlying bone)
+ - If pouch stretches and ruptures, CSF enters air cells
+ - Sphenoid bone-sphenoid sinus: CSF leak → sphenoid sinus fluid → rhinorrhea
+ - Temporal bone-air cells: CSF leak → middle ear-mastoid fluid → otorrhea
+ - Cephalocele possible in larger AbAG
+- ### Gross Pathologic & Surgical Features
+
+
+ - AG: Smooth AG projecting into venous sinus or subarachnoid space
+ - AbAG: Osteodural defects in lateral sphenoid sinus wall, greater wing of sphenoid or temporal bone
+- ### Microscopic Features
+
+
+ - Enlarged arachnoid villi
+ - Central core of loose connective tissue with CSF
+ - Peripheral zone of dense connective tissue
+ - Projects through dura of venous sinus wall
+
+## CLINICAL ISSUES
+
+- ### Presentation
+
+
+ - #### Most common signs/symptoms
+
+
+ - Intrasinus AG: Asymptomatic with rare exception
+ - If suspect giant AG in venous sinus **causing BIH** (venous hypertension) with headache, conventional angiography with pressure measurements needed
+ - In most cases, no pressure gradient across giant AG in DVS found
+ - AbAG: Mostly asymptomatic
+ - If CSF pulsations enlarge AbAG in sphenoid sinus or temporal bone wall, CSF leak ± meningitis possible
+ - Sphenoid sinus wall rupture: Rhinorrhea
+ - Temporal bone-air cell rupture: Otorrhea
+ - If significant cephalocele occurs, seizure possible
+ - #### Other signs/symptoms
+
+
+ - **BIH**in obese middle-aged females with rhinorrhea
+ - Look for AbAG (arachnoid pits) in sphenoid bone adjacent to sphenoid sinus
+- ### Demographics
+
+
+ - #### Age
+
+
+ - ↑ in frequency with ↑ age; ≥ 40 years
+ - #### Epidemiology
+
+
+ - Intrasinus AG: 25% CECT or T2 MR
+ - AbAG: Sphenoid bone: < 2%; temporal bone: < 1%
+- ### Natural History & Prognosis
+
+
+ - Intrasinus AG: Remains asymptomatic
+ - AbAG: May remain small
+ - If enlarge in response to CSF pulsations, may penetrate dura, bone, and air cells
+ - CSF leak, cephalocele, or meningitis may result
+- ### Treatment
+
+
+ - Intrasinus AG: No treatment required
+ - AbAG: No treatment needed unless enlarged with resulting CSF leak; if CSF leak → surgical dural repair
+ - If CSF leak present into sphenoid sinus or temporal bone, surgical dural repair necessary
+ - Surgical repair prevents meningitis possibility
+
+## DIAGNOSTIC CHECKLIST
+
+- ### Consider
+
+
+ - If **intrasinus giant AG** with history of headache, consider angiogram to look for intrasinus pressure gradient
+ - If **Ab****AG** presents in lateral wall **sphenoid bone**, look for fluid in sphenoid sinus as evidence for CSF leak
+ - MR to evaluate for possible associated cephalocele
+ - If **Ab****AG** found in posterior wall of **temporal bone**, look for fluid in mastoid air cells as evidence for CSF leak
+- ### Image Interpretation Pearls
+
+
+ - Intrasinus AG
+ - Confirm AG remains CSF density (on CECT or CT angiogram) and intensity (on T1 and T2 MR)
+ - Make sure proximal venous sinus and DVS are normal from imaging perspective
+ - AbAG in lateral sphenoid sinus wall or posterior wall temporal bone
+ - If large or multiple, look for evidence of CSF leak
+
+ 8da03d5e-91c3-4801-824f-9bc4824face4
+
+## References
+
+## Selected References
+
+1. [Guevara Tirado OA et al: Neuroimaging of vermiform giant arachnoid granulations in children. Children (Basel). 11(7), 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=39062213%5Bpmid%5D)
+1. [Mehta RI et al: Giant arachnoid granulations: a systematic literature review. Int J Mol Sci. 24(16), 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=37629195%5Bpmid%5D)
+1. [Freeman CW et al: Variations of the CNS venous system mimicking pathology: spectrum of imaging findings. J Neuroimaging. 29(6):673-88, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31529762%5Bpmid%5D)
+1. [Sade R et al: Brain herniation into the transverse sinuses' arachnoid granulations in the pediatric population investigated with 3 T MRI. Acta Neurol Belg. 119(2):225-31, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=29797238%5Bpmid%5D)
+1. [Taieb G et al: Reversible giant arachnoid granulations. Neurology. 91(24):1107-8, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30530555%5Bpmid%5D)
+1. [Battal B et al: Brain herniations into the dural venous sinuses or calvarium: MRI of a recently recognized entity. Neuroradiol J. 27(1):55-62, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24571834%5Bpmid%5D)
+1. [De Keyzer B et al: Giant arachnoid granulations mimicking pathology. A report of three cases. Neuroradiol J. 27(3):316-21, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24976198%5Bpmid%5D)
+1. [Settecase F et al: Spontaneous lateral sphenoid cephaloceles: anatomic factors contributing to pathogenesis and proposed classification. AJNR Am J Neuroradiol. 35(4):784-9, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24091443%5Bpmid%5D)
+1. [Alonso RC et al: Spontaneous skull base meningoencephaloceles and cerebrospinal fluid fistulas. Radiographics. 33(2):553-70, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23479713%5Bpmid%5D)
+1. [Barañano CF et al: Sternberg's canal: fact or fiction? Am J Rhinol Allergy. 23(2):167-71, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19401043%5Bpmid%5D)
+1. [La Fata V et al: CSF leaks: correlation of high-resolution CT and multiplanar reformations with intraoperative endoscopic findings. AJNR Am J Neuroradiol. 29(3):536-41, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18079188%5Bpmid%5D)
+1. [Lloyd KM et al: Imaging of skull base cerebrospinal fluid leaks in adults. Radiology. 248(3):725-36, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18710972%5Bpmid%5D)
+1. [Schuknecht B et al: Nontraumatic skull base defects with spontaneous CSF rhinorrhea and arachnoid herniation: imaging findings and correlation with endoscopic sinus surgery in 27 patients. AJNR Am J Neuroradiol. 29(3):542-9, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18079185%5Bpmid%5D)
+1. [Haroun AA et al: Arachnoid granulations in the cerebral dural sinuses as demonstrated by contrast-enhanced 3D magnetic resonance venography. Surg Radiol Anat. 29(4):323-8, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17483869%5Bpmid%5D)
+1. [Amlashi SF et al: Intracranial hypertension and giant arachnoid granulations. J Neurol Neurosurg Psychiatry. 75(1):172, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14707340%5Bpmid%5D)
+1. [Liang L et al: Normal structures in the intracranial dural sinuses: delineation with 3D contrast-enhanced magnetization prepared rapid acquisition gradient-echo imaging sequence. AJNR Am J Neuroradiol. 23(10):1739-46, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12427634%5Bpmid%5D)
+1. [Casey SO et al: Prevalence of arachnoid granulations as detected with CT venography of the dural sinuses. AJNR Am J Neuroradiol. 18(5):993-4, 1997](http://www.ncbi.nlm.nih.gov/pubmed/?term=9159387%5Bpmid%5D)
+1. [Leach JL et al: Normal appearance of arachnoid granulations on contrast-enhanced CT and MR of the brain: differentiation from dural sinus disease. AJNR Am J Neuroradiol. 17(8):1523-32, 1996](http://www.ncbi.nlm.nih.gov/pubmed/?term=8883652%5Bpmid%5D)
+1. [Roche J et al: Arachnoid granulations in the transverse and sigmoid sinuses: CT, MR, and MR angiographic appearance of a normal anatomic variation. AJNR Am J Neuroradiol. 17(4):677-83, 1996](http://www.ncbi.nlm.nih.gov/pubmed/?term=8730187%5Bpmid%5D)
+1. [Marukawa S et al: [Malignant hyperthermia - evaluation of serum creatine phosphokinase and lactate dehydrogenase.] Masui. 24(5):489-96, 1975](http://www.ncbi.nlm.nih.gov/pubmed/?term=1172024%5Bpmid%5D)
+
+## Differential diagnosis
+
+### Posterior Skull Base Lesion
+DDX:8a29ab23-43c8-4534-8af8-fdf252b88642
+
+### Dural Sinus Lesion, General
+DDX:2fbd9762-23d0-40cb-868f-ff7ef3304264
+
+### Intrinsic Skull Base Lesion
+DDX:563bc74a-c052-4fdb-a5f2-5a318578bb62
+
+## Anatomy
+
+### Dural Sinuses
+Brain/ANATOMY:deb22ea4-1ac5-4542-a85a-8945376ad725
+
+### Central Skull Base
+Brain/ANATOMY:2a489198-8130-4d47-8226-6970858ed6ed
+
+### Pterygopalatine Fossa
+Head and Neck/ANATOMY:8028d3aa-f348-48e4-b364-f793ca6aac88
+
+### Central Skull Base
+Head and Neck/ANATOMY:8887bf04-6027-42cb-9a34-3e15c6cc27ff
+
+### Intracranial Venous System Overview
+Brain/ANATOMY:fa5537f5-50aa-4a7d-abd1-a469b8a8b55f
+
+### Posterior Fossa Veins
+Brain/ANATOMY:7b5caf92-e4eb-4a23-ba29-45d1dbb1af65
+
+### Transcranial Doppler
+Ultrasound/ANATOMY:914fd68b-ddab-4640-bcc4-883c425d13f8
+
+## Cases
+
+- {'cases': [{'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '87325a1a-7e2e-4829-afd1-c4bc607f88af', 'description': 'Axial NECT scans with bone reconstruction (#1-3) show multiple well-delineated, sharply marginated lucent lesions (arrows) in the right occipital bone, adjacent to the location of the transverse sinus. The lesions are well-corticated and represent arachnoid granulations. \n\nComment: Arachnoid granulations are common in the dural venous sinuses and sometimes invaginate into the inner calvarium, causing bony "pits." The occipital bone is their most common location.', 'history': 'Fell. No loss of consciousness. Routine NECT scan obtained in ER. Bone windows showed "funny lesions" in the posterior skull base.', 'imagePoolId': '60ed45b0-2988-419a-9025-8b2f7b159112', 'name': 'Skull erosions', 'teachingPoint': None, 'demographics': '74 Years old male'}, {'authors': [{'key': '5b96b27c-fdf8-413b-9121-7f04ca185363', 'value': 'Joel K. Curé, MD'}, {'key': '6651ae1c-5f55-4d2e-9f68-46223037c90a', 'value': ' , '}], 'caseVersionId': 'dc486869-8470-417f-b096-79c0a96342cd', 'description': 'Typical MR imaging appearance of posterior fossa arachnoid granulations.\n\nAxial T2WI MR images demonstrate sharply marginated rounded foci of fluid signal intensity in the occipital bones, near the transverse sinuses (open arrows). Note that at least one of these appears to communicate with the adjacent subarachnoid space via a defect in its inner margin (the inner calvarial table, curved arrow). \n\nComment: Meninges or occasional meninges with contained brain tissue may project into the skull within prominent arachnoid granulations, forming an "intraosseous meningocele" or "meningoencephalocele".', 'history': None, 'imagePoolId': '364d54e6-cb52-42db-885b-ef033e1958c3', 'name': 'Calvarial defect', 'teachingPoint': None, 'demographics': '66 Years old female'}, {'authors': [{'key': '5b96b27c-fdf8-413b-9121-7f04ca185363', 'value': 'Joel K. Curé, MD'}], 'caseVersionId': '0c0b9c5d-a394-461d-9af7-5d4316c1b069', 'description': "Typical case of multiple arachnoid granulations invaginating into the occipital bone. \n\nImages 1-3 demonstrate a cluster of sharply marginated rounded foci with CSF-like signal intensity on both T2 (#1-2) and T1 (#3) weighted images, projecting though the inner table into the occipital bones within and to both sides of midline (open arrows). Note proximity to torcular herophili (curved arrow). An MRV (#4) demonstrates a cluster of prominent veins in the region of the arachnoid granulations (arrow). There is thin peripheral enhancement on post-contrast T1 weighted images (#5, open arrows).\n\nThese occipital arachnoid granulations were felt to be incidental and unrelated to the patient's symptoms.\n\nComment: Arachnoid granulations represent invaginations of arachnoid villi into the lumen of dural venous sinuses or through the inner table into the calvarium. They are often located adjacent to or within the transverse sinuses. In the latter case they appear as filling defects in the sinus on enhanced images or angiography. As seen in this case, they are sharply circumscribed and appear internally CSF-like on all MR imaging sequences. Intraosseous lesions may enhance very subtly along their periphery. The lesions are incidental and asymptomatic unless associated with erosion into the middle ears, mastoid air cells, or sphenoid sinuses in which case they may present with CSF otorrhea or rhinorrhea.", 'history': 'This patient had a history of insulin dependent diabetes mellitus, hypertension, cardiac disease, multiple falls, worsening dizziness and gait instability. \n\n', 'imagePoolId': '78aaa68d-677c-469d-b6c4-a939462f18c5', 'name': 'Multiple, occipital bone', 'teachingPoint': None, 'demographics': '56 Years old female'}, {'authors': [{'key': '5b96b27c-fdf8-413b-9121-7f04ca185363', 'value': 'Joel K. Curé, MD'}], 'caseVersionId': '5a13550c-fa7c-43b1-8ad7-a5b0779bb746', 'description': 'Typical case of an arachnoid granulation (AG) within the transverse sinus.\n\nThe arachnoid granulation (open arrow) is CSF-like on all imaging sequences and appears as a nonenhancing filling defect in the right transverse sinus on contrast-enhanced images. A prominent enhancing vascular structure (curved arrow), probably a vein, is evident in the AG.\n\nComment: Arachnoid granulations are common incidental findings on brain CT and MR studies (when intravascular, present as filling defects on the venous phase of angiographic examinations). They may project into the adjacent calvarium or dural venous sinus (or both). They should not be confused with thrombus given their imaging characteristics. They are commonly encountered in the transverse sinus near the insertion of the vein of Labbe, adjacent to the torcular Herophili, in the posterior superior sagittal sinus above the torcular Herophili, or in the straight sinus immediately posterior to the vein of Galen.', 'history': 'This patient complained of headaches and symptoms suggestive of trigeminal neuralgia. The finding in the right transverse sinus was felt to be incidental, and unrelated to her complaints.', 'imagePoolId': '1d08c086-9f20-44ba-96fa-dd696316a37b', 'name': 'Transverse sinus', 'teachingPoint': None, 'demographics': '48 Years old female'}, {'authors': [{'key': '5b96b27c-fdf8-413b-9121-7f04ca185363', 'value': 'Joel K. Curé, MD'}], 'caseVersionId': 'a918241d-4873-449b-ac70-ccab1c716023', 'description': 'Three images from an enhanced axial CT (#1-3) demonstrate a sharply marginated osseous defect due to an arachnoid granulation invaginating through the inner table of the right occipital bone (open arrows). This arachnoid granulation also invaginated into the adjacent right transverse sinus, producing a lucent filling defect here (#3, arrow).\n\nComment: A defect in the inner table is a common finding on CT in patients with arachnoid granulations that affect bone. Occasionally prominent venous channels will also be evident in the adjacent bone. An intimate relationship to an adjacent venous sinus supports this diagnosis.', 'history': 'This patient presented with dementia and worsening memory loss. The right occipital arachnoid granulation was felt to be incidental and not responsible for his dementia or memory loss.', 'imagePoolId': 'c1c48f5f-eafc-40e4-a10a-8773e2f12d4f', 'name': 'Solitary, large', 'teachingPoint': None, 'demographics': '68 Years old male'}], 'caseType': 'typical', 'name': 'TYPICAL'}
+- {'cases': [{'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '3ef952ad-ad01-41a3-9603-a045f9950ff2', 'description': 'Sagittal and axial T1WIs (#1,2) show a large mass in the descending aspect of the superior sagittal sinus (SSS) (arrows). Note that on this sequence, the mass appears slightly hyperintense to CSF. Sagittal and axial T2WIs (#3-5) show the mass (arrow) is hyperintense, similar to CSF, but contains some linear structures within it (open arrows). On FLAIR (#6,7), the mass (arrow) appears complex with internal structures (open arrow) and does not suppress. \n\nT1 C+ FS scans (#8-10) are very informative. Here the mass (white arrows) appears like CSF and contains enhancing structures (open arrows) that look like veins. A cortical vein (curved arrow, #9) can be seen passing into the SSS and entering the intrasinus mass directly (black arrow). The coronal scan (#10) shows "flow voids" of the SSS (black arrows) passing around the mass which is encased in enhancing dural leaves (white arrows). A "flow void" is seen within the mass (open arrow). DWI (#11) shows no restriction.\n\nDSA (#12-15) was performed. The SSS (arrows) can be seen splitting and curving around the mass. A cortical vein (open arrows) is seen entering and then coursing within the nonopacified mass. Pressure measurements were obtained through a microcatheter passed directly into the SSS (curved arrow, #15). Normal intrasinus pressures were present on both sides of the mass, indicating it did not cause elevated venous sinus pressure.\n\nComment: This interesting case is a giant complex arachnoid granulation. It does not completely parallel CSF on all sequences but does not enhance (as would a meningioma or possibly a Masson vegetant hemangioendothelioma) and contains veins which can be seen entering into it and then coursing through it.', 'history': 'Headaches.', 'imagePoolId': 'eeefe92b-ccb0-4986-963b-d948e3fc5539', 'name': 'Giant, complex', 'teachingPoint': None, 'demographics': '35 Years old male'}, {'authors': [{'key': '33151213-01b2-4542-9105-342e006b3915', 'value': 'H. Ric Harnsberger, MD'}, {'key': '94f835c8-fa13-4e8a-995b-53048e6b0605', 'value': 'Philip R. Chapman, MD'}], 'caseVersionId': '3ddec732-5bd7-4ce3-95eb-36e454237310', 'description': 'Variant CECT-MR-angiography case of a giant arachnoid granulation cluster in the transverse and sigmoid sinuses on the right.\n\nAxial CECT (#1-6) reveal multilobular low density lesion (arrow) in the right transverse and sigmoid sinuses. On T1 MR (#7) the lesion (arrow) is low signal, while T2 images (#8-9) show it to be high signal (arrow). FLAIR images (#10-11) demonstrate incomplete attenuation (arrow). \n\nInternal carotid angiogram images (#12-15) clearly depict the lesion to be a cluster of giant arachnoid granulations (arrow) within the transverse and sigmoid sinus lumen. There is no evidence that these arachnoid granulations are obstructing the flow of blood through the dural sinuses.\n\nComment: Giant arachnoid granulations within the dural sinus may mimic tumor or thrombosis. They rarely if ever cause significant pressure gradients in the affect sinus.', 'history': 'Patient presents with long term history of migraines.', 'imagePoolId': 'b9f28616-6664-4b4b-b984-38341bcbaffd', 'name': 'Giant arachnoid granulation cluster', 'teachingPoint': None, 'demographics': '45 Years old male'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'ab5658d7-bdef-40ef-8d01-9951b9d56976', 'description': 'Sagittal and axial T1WIs (#1,2), axial T2WI (#3), and axial FLAIR (#4) show a large filling defect in the superior sagittal sinus (arrows). Images (#2,3) show "flow voids" of the superior sagittal sinus (open arrows) which appear to split around the filling defect. The defect follows CSF signal intensity exactly and suppresses completely on FLAIR. Coronal T1 C+ scans (#5,6) show the enhancing superior sagittal sinus expanded around the CSF-like filling defect (arrows). Axial MRV (#7) shows the superior sagittal sinus (open arrows) contains the CSF-like cyst (arrow). Oblique AP DSA (#8) in another case with a large arachnoid granulation in this unusual location shows a very big filling defect in the middle of the superior sagittal sinus (arrows). \n\nComment: So-called "giant arachnoid granulations" can be found in virtually any dural venous sinus but are far more common in the transverse and sigmoid sinuses. They are round or ovoid and should not be mistaken for dural sinus thrombosis (most clots in dural venous sinuses are elongated and sausage-like, almost never perfectly round or ovoid).', 'history': 'Incidental finding.', 'imagePoolId': '8c082fcd-8651-4bf2-9d2f-348c0f62f820', 'name': 'Huge', 'teachingPoint': None}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '6aa0d198-2bd5-497b-928f-8dab15f44ccf', 'description': "Axial T1WI (#1-2) show large masses in both transverse sinuses (arrows). The masses are slightly hyperintense compared to CSF. They appear nearly CSF-like on T2WI (#3-4) and show multiple internal linear septations or vessels (open arrows). Both are inhomogeneously hyperintense compared to CSF on FLAIR (arrows, #5-6). T1 C+ FS scans (#7-8) are very interesting. They show that most of the mass does not enhance. However, the internal septations/veins do enhance (open arrows), and on image #7 there is a structure that appears to extend from the lesion into the skull (curved arrow).\n\nComment: These intrasinus lesions are giant arachnoid granulations. While the classic teaching is that arachnoid granulations (being filled with CSF) behave just like CSF on CT and MR, they often don't. The majority of giant AGs are hyperintense to CSF on FLAIR and finding some linear enhancement within AGs (veins or septations) is also common. Having 2 giant AGs in a single patient is unusual. These were felt to be incidental and unrelated to the patient's symptoms.", 'history': 'Dizzy, balance difficulties.', 'imagePoolId': '225aa912-8864-41c6-ac74-fe2f69b8fd4b', 'name': 'Two giant AGs', 'teachingPoint': None, 'demographics': '60 Years old male'}, {'authors': [{'key': '5b96b27c-fdf8-413b-9121-7f04ca185363', 'value': 'Joel K. Curé, MD'}], 'caseVersionId': '75d1a351-e693-467e-8076-d9824c903a31', 'description': 'This large solitary arachnoid granulation fills (but does not expand) the diploic space of the left occipital bone, thinning the inner and outer tables (open arrows). The lesion is CSF-like on all MR imaging imaging sequences (including FLAIR, #4) and enhances only very subtly along its periphery on gadolinium-enhanced T1 weighted images (#6, arrows).\n\nComment: Meninges and even tiny knuckles of brain may protrude into these lesions though a dural defect overlying the thinned inner table. Intradiploic epidermoids may mimic arachnoid granulations on CT. However, arachnoid granulations are CSF-like on all MR imaging sequences, while epidermoids tend to be brighter than CSF on FLAIR, proton density weighted, and diffusion weighted MR images and less intense than CSF on steady state free precession (SSFP) images.', 'history': 'This patient presented with headaches. The left occipital arachnoid granulation was felt to be incidental and not responsible for the headaches.', 'imagePoolId': '4cc1916a-8384-49eb-bbd4-5644bd211b81', 'name': 'Large, solitary', 'teachingPoint': None, 'demographics': '46 Years old male'}], 'caseType': 'variant', 'name': 'VARIANT'}
+
+
+## Images
+
+
+### Selected Images
+
+
+*Graphic shows giant arachnoid granulation (AG) projecting from subarachnoid space (SAS) into dural venous sinus (DVS) . CSF core extends into AG, separated by arachnoid cap cells from venous sinus endothelium . Giant AGs often have prominent veins and septations. Channels in the arachnoid cap drain CSF into DVS.*
+
+
+*Graphic shows giant arachnoid granulation (AG) projecting from subarachnoid space (SAS) into dural venous sinus (DVS) . CSF core extends into AG, separated by arachnoid cap cells from venous sinus endothelium . Giant AGs often have prominent veins and septations. Channels in the arachnoid cap drain CSF into DVS.*
+
+
+*Sagittal NECT shows AGs as CSF density filling defects in the slightly hyperdense superior sagittal sinus (SSS) and the straight sinus . Note linear internal venous strands in AGs.*
+
+
+*Sagittal T1 MPRAGE MR (top left) shows nonenhancing giant AG within the enhancing torcula. Note enhancing internal veins in AG. The AG shows bright CSF-like T2 (top right), iso- to bright FLAIR (bottom left) and brain isointense SWI (bottom right) signals with internal venous flow voids.*
+
+
+*Coronal T1 MPRAGE MR (top left) shows nonenhancing clot at the junction of a cortical vein with SSS. Clot shows dark T2 (top right), mixed bright FLAIR (bottom left), and dark SWI (bottom right) signals . Note other cortical vein clots.*
+
+
+*Lateral internal carotid angiogram shows giant AGs in transverse and proximal sigmoid sinuses. No intrasinus pressure gradient was present across the AG. Giant AG can rarely be a cause or consequence of benign intracranial hypertension.*
+
+
+*Coronal T2 MR shows an aberrant AG (AbAG) seen as a high-signal outpouching smoothly scalloping the inner table of left parietal calvarium . AbAG has penetrated the dura, but failed to reach the adjacent SSS DVS . Note the low-signal strands in AbAG due to veins and septations.*
+
+
+*Coronal CT cisternography shows contrast leaking from the SAS into multiple giant AbAGs in the left greater wing of sphenoid and basisphenoid.*
+
+
+*Coronal 3D CISS T2 MR shows a right tegmen tympani defect due to AbAG arachnoid pits eroding it with associated herniation of the inferior right temporal lobe and CSF into the right middle ear cavity (cephalocele) . Note the normal continuous hypointensity of left tegmen tympani and dark air-filled left middle ear cavity .*
+
+
+*Coronal bone CT shows left sphenoid sinus lateral wall defect , lateral to foramen rotundum (FR) , with sphenoid sinus cephalocele . Note another arachnoid pit scalloping the left greater sphenoid wing inferolaterally . Sternberg canal is controversial and should be medial to FR to comply with Sternberg's original description.*
+
+
+*Coronal T1 C+ MPRAGE MR (top) shows a filling defect in right transverse sinus , which is demonstrated to be due to brain herniation on coronal 3D FLAIR MR (bottom).*
+
+
+### Additional Images
+
+
+*Graphic shows a giant AG projecting from SAS into transverse sinus . CSF core extends into the AG and is separated by arachnoid cap cells from the venous sinus endothelium . Giant AGs often contain prominent venous channels and septations. Channels in the arachnoid cap drain CSF into the DVS .*
+
+
+*Axial CECT shows a giant AG cluster at the transverse-sigmoid venous sinus junction. Note contrast in sinus around the AG .*
+
+
+*Axial T2 MR shows multiple AGs projecting into the transverse sinus bilaterally. AGs were an incidental finding in this patient with siderosis.*
+
+
+*Axial T1 C+ MR demonstrates a classic example of an isolated right transverse venous sinus AG . Note the normal sinus venous enhancement on either side of the AG.*
+
+
+*Axial bone CT through the midsphenoid sinus shows multiple ovoid bony defects in the greater wing of sphenoid bone representing AbAGs (arachnoid pits). These AGs may enlarge from CSF pulsations.*
+
+
+*Axial left ear T-bone CT reveals an example of incidental AbAG in posteromedial tegmen mastoideum. No CSF in the mastoid is present.*
+
+
+*Axial bone CT reveals a multilocular lesion in the left greater wing of the sphenoid and basisphenoid . The most likely etiology of this lesion is CSF pulsations enlarging AbAGs.*
+
+
+*Axial T2 MR in the same patient demonstrates CSF signal within the greater wing of the sphenoid bone and basisphenoid . Arachnoid outpouching with arachnoid stranding can be seen within the giant AbAGs.*
+
+
+*Coronal T1 C+ MR in the same patient shows fluid within the expanded pterygoid wing of sphenoid . This represents CSF within an arachnoid pouch filling giant AbAGs.*
+
+
+*Coronal T1 C+ MPRAGE MR shows giant AG seen as filling defect in the enhancing SSS. Note prominent venous channel extending from SAS into AG.*
+
diff --git a/docs_md/articles/dural-sinus-thrombosis_9a1ac112-bd65-4306-92b0-022d16e360c3.md b/docs_md/articles/dural-sinus-thrombosis_9a1ac112-bd65-4306-92b0-022d16e360c3.md
new file mode 100644
index 0000000..86ab89e
--- /dev/null
+++ b/docs_md/articles/dural-sinus-thrombosis_9a1ac112-bd65-4306-92b0-022d16e360c3.md
@@ -0,0 +1,603 @@
+---
+title: "Dural Sinus Thrombosis"
+docid: "9a1ac112-bd65-4306-92b0-022d16e360c3"
+authors:
+ - key: "ab4396df-0647-4f6a-b534-995eda06646c"
+ value: "Nancy J. Fischbein, MD"
+ - key: "5cff4116-3654-4b3a-bb75-5ebe0b8c9850"
+ value: "Anne G. Osborn, MD, FACR"
+breadcrumbs:
+ -
+ name: "Brain"
+ slug: "brain"
+ treeNodeId: "0361042c-9c90-48e4-864e-a2e6428ee9c9"
+ -
+ name: "Diagnosis"
+ slug: "diagnosis"
+ treeNodeId: "948c6f1e-8e18-45f3-bd9d-7a04ab0b8708"
+ -
+ name: "Pathology-Based Diagnoses"
+ slug: "pathology-based-diagnoses"
+ treeNodeId: "d60fe914-7897-46a0-9cd2-f88ffb322f16"
+ -
+ name: "Stroke"
+ slug: "stroke"
+ treeNodeId: "7a135176-0a69-4fc9-b200-59569fbf5166"
+ -
+ name: "Cerebral Ischemia and Infarction"
+ slug: "cerebral-ischemia-and-infarction"
+ treeNodeId: "11d50e7d-f3e9-4071-b2b7-26b11ab40ea6"
+ -
+ name: "Dural Sinus Thrombosis"
+ slug: "dural-sinus-thrombosis"
+ treeNodeId: null
+category: "Brain"
+documentVersionId: "808615fe-d3b1-4f8a-a6bc-7f71384429ba"
+imageCount: 44
+lastUpdated: "08/19/25"
+pageDescription: "Dural Sinus Thrombosis"
+pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Dural Sinus Thrombosis"
+pageTitle: "Dural Sinus Thrombosis | STATdx"
+enhancedTitle: "Dural Sinus Thrombosis"
+type: "DX"
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+ddx: true
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+cases: 2
+breadcrumbs:
+ - "Brain"
+ - "Diagnosis"
+ - "Pathology-Based Diagnoses"
+ - "Stroke"
+ - "Cerebral Ischemia and Infarction"
+ - "Dural Sinus Thrombosis"
+---
+## KEY FACTS
+
+- ### Imaging
+
+
+ - General features
+ - Empty delta sign on CECT, contrast-enhanced MR
+ - CT
+ - Hyperdense sinus on NECT (usually > 70 HU)
+ - ± hyperdense cortical veins (cord sign)
+ - CTV: Filling defect (thrombus) in dural sinus
+ - MR
+ - Acute thrombus often blooms on T2* GRE
+ - Absence of flow in occluded sinus on 2D TOF MRV
+ - Filling defect on C+ 3D GRE T1-weighted imaging
+ - Protocol recommendations
+ - NECT/CECT ± CTV often done as initial screening
+ - If CT negative or for further evaluation: MR/MRV (T2*, DWI, MRV, 3D GRE T1 C+)
+ - Hyperdense sinus (65-70 HU) on NECT
+- ### Top Differential Diagnoses
+
+
+ - Normal (arteries, veins normally slightly hyperdense)
+ - High hematocrit (newborns, polycythemia)
+ - Dural sinus hypoplasia/aplasia
+ - No blooming; collaterals/venous infarcts absent
+ - Giant arachnoid granulations
+ - Round/ovoid, T2 bright, not elongated like thrombus
+ - Acute subdural hematoma
+ - Blood layering on tentorium can mimic thrombosis
+- ### Diagnostic Checklist
+
+
+ - NECT: Exclude dense thrombus as false-negative CECT/CTV
+ - Also, normal-appearing brain does not exclude dural sinus thrombosis
+ - Venous infarction may not be present
+ - Review MRV source images
+ - Exclude pseudoocclusions (e.g., hypoplastic transverse sinus)
+ - Review T1 images to exclude false-negative MRV
+ - Intrinsically T1-bright thrombus can mimic flow
+ - Consider giving MR contrast: Very useful sequence for dural sinus thrombosis is C+ 3D GRE T1
+ - High diagnostic accuracy for both partial and complete thrombosis; useful for diagnosis and follow-up
+ - Chronic thrombosis may enhance
+ - Recanalization or granulation tissue enhances
+ - Can look bizarre, mimic neoplasm
+
+## TERMINOLOGY
+
+- ### Abbreviations
+
+
+ - Dural sinus thrombosis (DST)
+- ### Definitions
+
+
+ - Thrombotic occlusion of intracranial dural sinuses
+
+## IMAGING
+
+- ### General Features
+
+
+ - #### Best diagnostic clue
+
+
+ - Hyperdense sinus (65-70 HU) on NECT
+ - **Empty delta sign** on CTA/CTV/CECT, C+ 3D GRE T1 MR
+ - #### Location
+
+
+ - Transverse sinus most common, followed by superior sagittal sinus, then sigmoid sinus and SS
+- ### CT Findings
+
+
+ - #### NECT
+
+
+ - Imaging findings can be subtle, overlooked
+ - Careful attention to window/level to distinguish thrombosed sinus from adjacent bone, brain
+ - Hyperdense sinus (compare to carotid arteries)
+ - Usually 65-75 HU in thrombosed dural venous sinus
+ - Density ≥ 70 HU should be presumed thrombus
+ - Distinguish thrombus vs. hyperdense sinus from high hematocrit (HCT)
+ - HU:HCT ratio in thrombus 1.9 ± 0.32 vs. 1.33 ± 0.12 nonthrombus
+ - ± associated hyperdense cortical veins (**cord sign**)
+ - ± associated bland or hemorrhagic venous infarct
+ - Edema, cortical/subcortical petechial hemorrhages, parenchymal hematoma
+ - Small volume subarachnoid hemorrhage may be present
+ - Straight sinus (SS) ± deep Galenic venous thrombosis/internal cerebral vein (ICV) occlusion
+ - Thalami/basal ganglia ± periventricular white matter hypodense, swollen; variably hemorrhagic
+ - #### CECT
+
+
+ - Look for **empty delta sign**
+ - Enhancing dura surrounds nonenhancing thrombus
+ - CTA/CTV
+ - Filling defect (thrombus) in dural sinus (empty delta)
+ - Caution: Acute clot can be hyperdense, obscured on CECT/CTV: Include NECT for comparison
+- ### MR Findings
+
+
+ - #### T1WI
+
+
+ - Signal intensity of thrombus varies with clot age, imaging method used
+ - Acute thrombus: Isointense to brain; subacute thrombus: Hyperintense; chronic thrombus: Isointense
+ - Normal anatomic variations in dural sinus size, flow may mimic thrombosis; jugular bulb common pitfall
+ - Transverse/sigmoid sinus hypoplasia common
+ - CTV/CECT or MRV/C+ MR to confirm suspected DST
+ - #### T2WI
+
+
+ - Acute thrombus: Hypointense
+ - Caution: Can mimic normal sinus flow void
+ - Look for sinus enlargement by clot to troubleshoot
+ - Subacute thrombus: Hyperintense
+ - Chronic thrombus: Variable signal intensity
+ - Longstanding thrombosed sinus appears isointense
+ - Venous infarct: Mass effect with mixed hypo-/hyperintense signal in adjacent parenchyma
+ - #### PD/intermediate
+
+
+ - Loss of normal flow voids
+ - May be more sensitive than T2WI
+ - #### FLAIR
+
+
+ - Clot signal varies but usually hyperintense
+ - Venous ischemia/infarction: Edema is hyperintense
+ - #### T2* GRE
+
+
+ - GRE/SWI: Hypointense thrombus usually **blooms**
+ - Caution: Subacute/chronic sinus occlusions may not exhibit gradient susceptibility
+ - GRE/SWI hypointensity may be seen in dilated adjacent cortical, parenchymal veins
+ - GRE/SWI sensitive to parenchymal hemorrhage
+ - #### DWI
+
+
+ - 40% have hyperintense clot in occluded vessel (usually T2 shine-through effect)
+ - DWI/ADC findings in parenchymal venous infarction variable, heterogeneous
+ - Mixture of vasogenic and cytotoxic edema ± blood products
+ - Cytotoxic edema may precede vasogenic edema
+ - Some parenchymal abnormalities may be reversible
+ - #### T1WI C+
+
+
+ - C+ 3D gradient-recalled echo T1-weighted sequence is preferred
+ - Superior diagnostic performance c/w spin-echo T1, unenhanced MRV
+ - Sensitive to partial as well as complete sinus thrombosis
+ - Acute, subacute DST: Dura enhances, clot does not → empty delta sign
+ - Chronic DST: Longstanding clot can enhance
+ - Organized fibrous tissue ± recanalization
+ - Potential source of false-negative interpretation
+ - Clue: "squiggly" collateral vessels (medullary veins)
+ - #### MRV
+
+
+ - 2D TOF, phase-contrast, or contrast-enhanced MRV (CE-MRV)
+ - Absence of flow in occluded sinus
+ - Frayed or shaggy appearance of venous sinus
+ - Abnormal collateral channels (e.g., enlarged medullary veins) may be present
+ - T1-hyperintense (subacute) clot can masquerade as flow on MRV; compare standard sequences, source images
+ - Potential cause of false-negative MRV
+ - Phase-contrast MRV not limited by T1-hyperintense thrombus; useful for noncontrast problem solving
+ - Flow gaps on MIPs must be reviewed on source images to exclude hypoplastic sinus variants
+ - Potential source of false-positive interpretation
+ - CE-MRV can show thrombus, small vein detail, collaterals better than 2D TOF
+ - MR perfusion
+ - May see hypoperfusion in area of brain drained by thrombosed sinus
+ - Also prolonged mean transit time, ↑ CBV due to venous congestion
+- ### Angiographic Findings
+
+
+ - Occlusion of involved sinus
+ - Slow flow in adjacent patent cortical veins
+ - Collateral venous drainage develops
+ - Chronic DST may show "squiggly" tortuous medullary veins
+- ### Imaging Recommendations
+
+
+ - #### Best imaging tool
+
+
+ - NECT, CECT ± CTV as initial screening
+ - MR with MRV if noncontrast study (include T2*/SWI, DWI, FLAIR)
+ - Optimal: Include C+ 3D GRE T1-weighted sequence
+ - #### Protocol advice
+
+
+ - If CT/CECT/CTV negative, consider C+ MR study
+ - Cerebral angiography is not 1st-line diagnostic modality but can be considered when noninvasive imaging inconclusive or detailed anatomical information is required
+
+## DIFFERENTIAL DIAGNOSIS
+
+- ### Normal
+
+
+ - Arteries, veins normally slightly hyperdense on NECT
+- ### High Hematocrit
+
+
+ - Common in newborns (low-density brain, physiologic polycythemia) and patients with dehydration
+ - Polycythemia vera (both arteries, veins equally hyperdense)
+- ### Dural Sinus Hypoplasia-Aplasia
+
+
+ - Congenital hypoplastic/aplastic transverse sinus
+ - Transverse sinus flow gaps (30%); nondominant sinus
+ - Right transverse sinus dominant (50-60%), left dominant (25%), codominant (20-25%)
+ - "High-splitting" tentorium
+- [Giant Arachnoid Granulations](/document/dural-sinus-and-aberrant-arachnoid-/d7cc1586-8a57-431d-9566-ff51aebb338c)
+ - Round/ovoid filling defect (clot typically long, linear)
+ - CSF density/signal intensity
+ - Commonly seen in > 85% of patients on thin-slice C+ MR
+ - Transverse sinuses, superior sagittal sinus are common locations
+- [Acute Subdural Hematoma](/document/acute-subdural-hematoma/06930a44-3a5e-460c-84b3-6a0ea4468037)
+ - Layering blood on tentorium cerebelli may mimic transverse sinus thrombosis: Assess multiplanar reformations
+
+## PATHOLOGY
+
+- ### General Features
+
+
+ - #### Etiology
+
+
+ - Wide spectrum of predisposing causes
+ - Trauma, infection, inflammation
+ - Pregnancy, oral contraceptives, other medications
+ - Metabolic (dehydration, thyrotoxicosis, cirrhosis)
+ - Hematologic (coagulopathy, genetic vs. acquired)
+ - Autoimmune (antiphospholipid antibody syndrome, connective tissue disease)
+ - Most common pattern
+ - Thrombus forms in dural sinus
+ - Clot propagates into cortical veins
+ - Venous drainage obstructed, venous pressure elevated
+ - Blood-brain barrier breakdown with vasogenic edema, hemorrhage
+ - Venous infarct with additional cytotoxic edema
+ - #### Genetics
+
+
+ - Resistance to activated protein C (typically due to factor 5 Leiden mutation): Most common cause of sporadic cerebral vein thrombosis
+ - Protein S deficiency
+ - Prothrombin (factor II) gene mutation
+ - #### Associated abnormalities
+
+
+ - Dural arteriovenous fistula: Venous occlusive disease may be underlying etiologic factor
+ - Nontraumatic subarachnoid hemorrhage: Can occur even in absence of hemorrhagic venous infarct
+- ### Staging, Grading, & Classification
+
+
+ - **Venous ischemia grading**
+ - Type 1: No abnormality
+ - Type 2: Hyperintense on T2/FLAIR; no enhancement
+ - Type 3: Hyperintense on T2/FLAIR; enhancement
+ - Type 4: Hemorrhage or venous infarction
+- ### Gross Pathologic & Surgical Features
+
+
+ - Sinus occluded, distended by acute clot
+ - Often thrombus in adjacent cortical veins
+ - Edematous adjacent cortex; petechial hemorrhage
+- ### Microscopic Features
+
+
+ - Thrombosis of veins; proliferative fibrous tissue in chronic thromboses
+
+## CLINICAL ISSUES
+
+- ### Presentation
+
+
+ - #### Most common signs/symptoms
+
+
+ - Nonspecific presentation makes diagnosis difficult
+ - Most common: Headache, 90% of cases
+ - Other: Nausea/vomiting, seizure, change in vision, focal neurologic deficit
+- ### Demographics
+
+
+ - #### Age
+
+
+ - > 75% of cases in patients < 50 years
+ - #### Sex
+
+
+ - Women are disproportionately affected
+ - #### Epidemiology
+
+
+ - Venous strokes: 0.5-1% of all strokes
+- ### Natural History & Prognosis
+
+
+ - Extremely variable: Asymptomatic (60-80%) to coma, death
+ - Venous infarction can be fatal: Brain swelling, herniation
+ - Mortality rate: ~ 8%
+ - Factors associated with poor prognosis: Older age, male, hemorrhage on admission CT
+- ### Treatment
+
+
+ - Anticoagulation is 1° approach: Usually IV heparin until clinically stabilized, then oral anticoagulation for 3-6 months (vs. lifelong if permanent risk factors)
+ - More severe cases: Consider endovascular thrombectomy ± local intrathrombus infusion of thrombolytic agent
+
+## DIAGNOSTIC CHECKLIST
+
+- ### Consider
+
+
+ - NECT: Check venous sinuses for hyperdensity
+ - Careful assessment of dural venous sinuses on all C+ 3D GRE T1-weighted images: Partial sinus thrombosis easy to miss on most other sequences
+ - Venous filling defects from arachnoid granulations are common: Typically round, may demonstrate vessel in their center
+ - Lack of parenchymal abnormality does not exclude DST
+- ### Image Interpretation Pearls
+
+
+ - Review MRV source images to exclude pseudoocclusions
+ - Transverse sinus common site for hypoplastic segment variations mimicking occlusion
+ - Review T1 images to exclude false-negative MRV
+ - Review NECT to exclude dense thrombus as false-negative CECT or CTV
+ - Consider DSA if noninvasive imaging inconclusive and clinical suspicion remains high
+ - Chronic thromboses may enhance on any contrast study due to recanalization or granulation tissue
+
+ da773eec-567c-4cd6-9e2c-67536c4a6088
+
+## References
+
+## Selected References
+
+1. [Saposnik G et al: Diagnosis and management of cerebral venous thrombosis: a scientific statement from the American Heart Association. Stroke. 55(3):e77-90, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38284265%5Bpmid%5D)
+1. [Vazqez S et al: Inpatient outcomes of cerebral venous thrombosis in patients with malignancy throughout the United States. J Stroke. 26(3):425-33, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=39266016%5Bpmid%5D)
+1. [Zhou Y et al: Venous stroke-a stroke subtype that should not be ignored. Front Neurol. 13:1019671, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=36277910%5Bpmid%5D)
+1. [Ropper AH et al: Cerebral venous thrombosis. N Engl J Med. 385(1):59-64, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=34192432%5Bpmid%5D)
+1. [Almqvist H et al: Radiological evaluation in patients with clinical suspicion of cerebral venous sinus thrombosis presenting with nontraumatic headache - a retrospective observational study with a validation cohort. BMC Med Imaging. 20(1):24, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32103735%5Bpmid%5D)
+1. [Ghoneim A et al: Imaging of cerebral venous thrombosis. Clin Radiol. 75(4):254-64, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31980184%5Bpmid%5D)
+1. [Medhi G et al: Mechanical thrombectomy for cerebral venous sinus thrombosis: a case series & technical note. World Neurosurg. 140:148-61, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32389866%5Bpmid%5D)
+1. [Neal E et al: Hypodense cerebral venous sinus thrombosis on unenhanced CT: a potential pitfall. Report of a case and review of the literature. Radiol Case Rep. 15(1):35-8, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31737143%5Bpmid%5D)
+1. [Zong C et al: Dural venous sinuses: what we need to know. Curr Med Imaging. 16(10):1259-70, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32101130%5Bpmid%5D)
+1. [Freeman CW et al: Variations of the CNS venous system mimicking pathology: spectrum of imaging findings. J Neuroimaging. 29(6):673-88, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31529762%5Bpmid%5D)
+1. [Hedderich DM et al: Diagnostic imaging in the management of patients with possible cerebral venous thrombosis: a cost-effectiveness analysis. Neuroradiology. 61(10):1155-63, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31292690%5Bpmid%5D)
+1. [Mahalingam HV et al: Imaging spectrum of cavernous sinus lesions with histopathologic correlation. Radiographics. 39(3):795-819, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30978149%5Bpmid%5D)
+1. [Azeemuddin M et al: Prevalence of subarachnoid haemorrhage among patients with cranial venous sinus thrombosis in the presence and absence of venous infarcts. Neuroradiol J. 31(5):496-503, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29890915%5Bpmid%5D)
+1. [Kouzmitcheva E et al: Anatomical venous variants in children with cerebral sinovenous thrombosis. Stroke. STROKEAHA118023482, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30580715%5Bpmid%5D)
+1. [Ozturk K et al: Dural venous sinus thrombosis: the combination of noncontrast CT, MRI and PC-MR venography to enhance accuracy. Neuroradiol J. 31(5):473-81, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29869561%5Bpmid%5D)
+1. [Gazioglu S et al: Cerebral venous sinus thrombosis: clinical features, long-term outcome and recanalization. J Clin Neurosci. 45:248-51, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28802797%5Bpmid%5D)
+1. [Coutinho JM et al: Cerebral venous thrombosis in the absence of headache. Stroke. 46(1):245-7, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25378420%5Bpmid%5D)
+1. [Bonneville F: Imaging of cerebral venous thrombosis. Diagn Interv Imaging. 95(12):1145-50, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25465119%5Bpmid%5D)
+1. [Gökçe E et al: Torcular Herophili classification and evaluation of dural venous sinus variations using digital subtraction angiography and magnetic resonance venographies. Surg Radiol Anat. 36(6):527-36, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24154635%5Bpmid%5D)
+1. [Buyck PJ et al: CT density measurement and H:H ratio are useful in diagnosing acute cerebral venous sinus thrombosis. AJNR Am J Neuroradiol. 34(8):1568-72, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23471024%5Bpmid%5D)
+
+## Differential diagnosis
+
+### Dural Sinus Lesion, General
+DDX:2fbd9762-23d0-40cb-868f-ff7ef3304264
+
+### Meckel Cave Lesion
+DDX:9c5ce268-caf8-4d2a-9735-9b415ad3c9c3
+
+## Anatomy
+
+### Accessory Nerve (CNXI)
+Brain/ANATOMY:9d50453e-c26a-46a3-826e-265736e43174
+
+### Glossopharyngeal Nerve (CNIX)
+Brain/ANATOMY:172680f5-d290-4a02-b07e-63c1da75e148
+
+### Hypoglossal Nerve (CNXII)
+Brain/ANATOMY:71012f02-fab7-42ed-bc60-e584dc229ccb
+
+### Vagus Nerve (CNX)
+Brain/ANATOMY:68b6ede4-c797-4d55-8d29-aed3df441741
+
+### Carotid Space
+Head and Neck/ANATOMY:627bdee1-4bde-46f2-b93d-958882586337
+
+### CNIX (Glossopharyngeal Nerve)
+Head and Neck/ANATOMY:2e74a767-3f28-49be-a50f-1dbcc10ce90f
+
+### CNXI (Accessory Nerve)
+Head and Neck/ANATOMY:18e60151-70bc-40a1-9b4f-4b86f8fd65c2
+
+### CNXII (Hypoglossal Nerve)
+Head and Neck/ANATOMY:f734d678-561c-47fd-afb5-dab6afacc1a8
+
+### CNX (Vagus Nerve)
+Head and Neck/ANATOMY:83868689-c995-4608-bed3-f59664cbd586
+
+## Cases
+
+- {'cases': [{'authors': [{'key': '07a2c087-6202-49e7-870b-7aa162d18f06', 'value': 'Bronwyn E. Hamilton, MD'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'a0624f7c-6f6c-4d24-85fa-44cd9f2211d6', 'description': 'Initial non-contrast head CT image (#1) shows hemorrhage in the left temporal lobe (arrow). MR images (#2-3) show mass effect with corresponding T1 and T2 signal prolongation (arrow). Dots of T1 hyperintense signal (image #2) in regional sulci suggest slow flow and/or thrombosis of cortical veins (#2, open arrows). \n\nPost-contrast T1 images (#4-5) demonstrate curvilinear enhancement due to venous congestion (curved arrows). Gradient (T2*) sequences (#6) can be helpful since intraluminal thrombus and/or parenchymal bleeds are often more conspicuous due to susceptibility artifact ("blooming"), depending on the stage of hemorrhage (open arrow). \n\nMRV MIP image (#7) reveals lack of flow-related enhancement in the left transverse and sigmoid sinuses and left internal jugular vein (curved arrows). Source image (#8) confirms the findings. Confirming suspected dural sinus occlusion on source images is always recommended. Reliance on MIP images alone may lead to the incorrect conclusion that a sinus is occluded rather than developmentally small in certain cases. Dural sinus asymmetry in the posterior fossa is extremely common, with the left sided venous system being most frequently nondominant. \n\nComment: Temporal lobe hemorrhage in this distribution without other explanation should prompt the radiologist to evaluate the intracranial venous system. This location of hemorrhage is classic for vein of Labbe thrombosis. Many patients will tolerate isolated transverse sinus thrombosis since collateral drainage pathways may exist. However if clot propagates into cortical draining veins, venous hypertension ensues, resulting in edema, ischemia and/or hemorrhage.', 'history': 'Patient four weeks postpartum who had sudden onset of headache and visual cloudiness. She subsequently had a generalized tonic clonic seizure. \n', 'imagePoolId': '463276f9-ef31-48bb-86ce-870d0019ac64', 'name': 'Temporal lobe hemorrhagic', 'teachingPoint': None, 'demographics': '22 Years old female'}, {'authors': [{'key': '07a2c087-6202-49e7-870b-7aa162d18f06', 'value': 'Bronwyn E. Hamilton, MD'}], 'caseVersionId': '34c6d830-7fcc-46c9-a56f-8d3b9b143fa3', 'description': 'Sagittal imaging (#1) demonstrates characteristic T1 hyperintense thrombus in the sigmoid sinus (arrow). Midline sagittal imaging (#2) demonstrates abnormal signal in the vein of Galen (curved arrow) and in the superior sagittal sinus (open white arrows). Unenhanced T1 images are one of the more sensitive sequences for the detection of dural thrombosis.\n\nAxial image (#3) shows abnormal high T2 signal intensity in the left transverse sinus instead of the expected flow void (arrow), concerning for occlusion. It is important to remember that this findings is less reliable due to common variations in flow in the venous sinuses. Slow flow, not only occlusion, can demonstrate high T2 signal. \n\nT2* images may be helpful (#4, 5), since thrombus often demonstrates susceptibility artifact, and can "bloom" or show dark signal intensity (curved arrow).\n\nTime of flight 2D MR venography source image (#6) shows lack of flow related enhancement in the torcular and bilateral transverse sinuses (open arrows), consistent with thrombosis. MRV maximum intensity projection image (#7) best shows the extensive nature of dural venous sinus thrombosis, with occlusion of the superior sagittal (arrows), transverse sinus (curved arrow), and vein of Galen (open arrow). This patient fortunately had adequate venous collaterals, and had no associated venous ischemia, infarction, or hemorrhage. Linear foci of signal in the transverse sinus region likely correlates with partial recanalization, which is not uncommon in later subacute and chronic venous occlusions.\n\nComments: Lack of flow voids on spin echo sequences (T1, T2) are an important part of the radiologists search pattern, and can reflect occlusive disease in the arterial or venous system. Lack of flow voids on proton density (PD) images are more reliable than on T1 or T2 for vascular occlusion.\n\nVenous occlusion can be challenging due to normal variations in flow patterns. Inherently slow flow in the venous system can be particularly confusing in areas of tortuosity such as the sigmoid sinus and at the jugular foramen. Flow sensitive sequences (MRV) and/or contrast-enhancement (including enhanced MRV) should always be considered to further assess suspected abnormalities.', 'history': 'Patient is 14 weeks pregnant with new onset severe headaches, nausea, and vomiting. Because of concurrent shortness of breath, CT pulmonary angiography was also performed (not shown), which demonstrated pulmonary emboli in addition to extensive intracranial venous thrombosis.', 'imagePoolId': '72b33429-1c0b-4f8b-8667-acb9f0b64139', 'name': 'Extensive', 'teachingPoint': None, 'demographics': '31 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '7029c6eb-1829-47e4-945b-10799615279a', 'description': 'Classic MR and DSA features of dural sinus and cortical vein thrombosis are demonstrated by this case.\n\nSagittal T1WIs (#1, 2) show absence of "flow voids" in the superior sagittal, straight, and transverse sinuses (arrows). The clot in the sinuses is mostly isointense with adjacent brain and appear hypointense on T2WIs (arrows, #3, 4). Note hyperintensity in the left basal ganglia and thalamus (open arrow, #3), indicating venous ischemia in the Galenic and internal cerebral vein drainage territory. \n\nSagittal (#5, 6), axial (#7) and coronal (#8) images beautifully show the enhancing dura around the nonenhancing clot (arrows). A nice MR "empty delta" sign is seen on images #6-8. Cortical vein thrombi can be appreciated on image #8 (open arrows) as they extend laterally from the occluded superior sagittal sinus.\n\nLateral (#9) and AP (#10) venous phase DSA shows absence of deep veins as well as the superior sagittal and straight sinuses. Image 10 shows the angiographic equivalent of the "empty delta" sign (open arrow) as well as thrombus in a prominent vein of Trolard (arrow). All cortical veins are unusually prominent and slow to empty, characteristic of multiple dural sinus occlusion.', 'history': 'Headaches, papilledema.', 'imagePoolId': '34f04b78-1136-4e23-8c14-8c509a109dab', 'name': 'Multiple dural sinuses, cortical veins thrombosed', 'teachingPoint': None}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'c73bcc10-dc48-4bfd-b296-2bd6fff6312b', 'description': 'NECT scans show hyperdense superior sagittal sinus (arrows, #1,2). Note slight asymmetry of cerebral sulci, with mild effacement on the left compared to the right. CTA was obtained as part of acute stroke protocol. Sagittal (#3,4) and coronal (#5) views show normal-appearing arteries. The anterior third of the superior sagittal sinus (open arrows) fills with contrast normally. However, the posterior two-thirds is filled with clot and does not enhance (arrows). Note empty delta sign on coronal scan (arrow, #5). \n\nMR was obtained and shows isointense clot in the SSS (arrows, #6). Note hyperintense left-sided CSF on the FLAIR scan (#7), presumably secondary to some subarachnoid hemorrhage. T2* (GRE) scan shows blooming clot within the SSS and left superficial cortical veins (arrows, #8). Coronal T1C+ scans show the isointense clot (arrows, #9,10) within the intensely enhancing dural leaves of the SSS.', 'history': '76 year old male with headache, transient right-sided weakness was evaluated for "acute stroke" in the ER.', 'imagePoolId': '80a5d43e-15fa-4c7d-a566-d470bb96a0ff', 'name': 'Hyperintense CSF on FLAIR', 'teachingPoint': None, 'demographics': '76 Years old male'}, {'authors': [{'key': '07a2c087-6202-49e7-870b-7aa162d18f06', 'value': 'Bronwyn E. Hamilton, MD'}], 'caseVersionId': 'f72fdadf-de75-4a19-84b5-4df4a8c8b1c6', 'description': 'Unenhanced CT image (#1) demonstrates left temporal lobe hemorrhage (white arrows). This location is characteristic for vein of Labbe thrombosis, and should raise suspicion for the diagnosis in the absence of other explanation.\n\nMR images (#2, 3) show isointense T1 and heterogeneous T2 signal characteristics consistent with acute blood (curved white arrows). Enhanced T1 image (#4) shows thrombus in the left transverse sinus (open white arrow).\n\nCoronal enhanced MR (#5) demonstrates a distended clot-filled left vein of Labbe (white arrow). Conventional angiography (#6) in late venous phase confirms thrombosis of the left vein of Labbe and left transverse sinus (open black arrows).\n\nComment: Isolated sinus thrombosis is often well tolerated by patients, however when cortical draining veins are involved as in this case, venous ischemia and hemorrhage usually follow.', 'history': 'Patient presenting with new onset seizures.', 'imagePoolId': 'cf1f25b0-4263-4667-ac13-19d62d8f7b2d', 'name': 'Infarct venous', 'teachingPoint': None, 'demographics': '40 Years old male'}, {'authors': [{'key': '07a2c087-6202-49e7-870b-7aa162d18f06', 'value': 'Bronwyn E. Hamilton, MD'}], 'caseVersionId': '43c48aa1-1de8-4361-808d-b8c1cc42e636', 'description': 'Enhanced CT image (#1) demonstrates a soft tissue attenuation filling defect ("delta sign") in the superior sagittal sinus (white arrow). MR images (#2, 3) show abnormal T1 hyperintensity in the occluded superior sagittal sinus (open white arrows). T2 imaging (#4) also shows hyperintense thrombus (curved white arrows), instead of the normally expected flow void.\n\nComment: Unenhanced T1 images are one of the most sensitive sequences for the detection of sinus occlusion. Contrast administration is useful, particularly if subacute or chronic thrombus is suspected. The lack of brain edema or venous ischemia in this case suggests that adequate venous collaterals are present.', 'history': 'Patient with a history of oral contraceptive use, presenting with new onset headaches.', 'imagePoolId': '350f2555-54d4-4082-aa18-88713b660e6a', 'name': 'Subacute classic', 'teachingPoint': None, 'demographics': '34 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '5dab99a2-06b9-467a-98bc-b6c3cfcfa166', 'description': 'Axial NECT scan (#1) shows hyperdense straight, transverse sinuses (arrows). Sagittal T1WI (#2) shows mostly isointense clot in both sinuses (arrows). T2WIs (#3, with close-up shown on #4) show the superior sagittal sinus clot is very hypointense, mimicking a flow void (arrows). Venous phase of DSA shows no filling of the superior sagittal sinus (arrows, #5), with prominent cortical veins that appear to "hang in space" because of slowed emptying.', 'history': 'Headaches.', 'imagePoolId': '404ef9bf-0358-4d17-9bca-35793d5a5388', 'name': 'Acute', 'teachingPoint': None, 'demographics': '26 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '79da32de-824e-4cf8-89d8-2971c5a83581', 'description': 'Axial NECT scans (#1, 2) show hyperdense straight sinus (arrows) and torcular herophili (curved arrow, #1). Note the gray matter of the right hemisphere appears somewhat swollen and the surface sulci are diminished compared to the left side. More superior images (#3, 4) show hyperdense superior sagittal sinus (open arrow) as well as several patchy areas of cortical and subcortical hemorrhage (arrows). Some subarachnoid blood can be seen on image 4 (curved arrow). \n\nComment: Dural sinus thrombosis is often accompanied by cortical venous thrombosis which in turn may cause one or more foci of parenchymal hemorrhage.', 'history': 'On birth control pills; developed 2d history of increasingly severe headaches. NECT scan requested to look for intracranial hemorrhage.', 'imagePoolId': 'ea065aca-42c0-424a-866a-a6b0001e7b02', 'name': 'With cortical vein thrombosis', 'teachingPoint': None, 'demographics': '23 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '8c57d3c7-c393-4339-97a8-7f14ac4e5e7f', 'description': 'Sagittal and axial T2WIs (#1,2) show absence of normal "flow void" in superior sagittal sinus (arrows). T2WI (#3) shows hypointense clot in right transverse sinus (arrows) extending into adjacent cortical veins (open arrow). Sagittal, axial T1C+ scans (#4-6) show enhancing veins and dura around nonenhancing clot in both superior sagittal, transverse sinuses (arrows), the MR equivalent of the "empty delta" sign on CECT.', 'history': 'Worsening headaches over 24 hours.', 'imagePoolId': 'fba45835-1667-444e-b760-6a25fa904fb8', 'name': 'Acute', 'teachingPoint': None}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'ad4df766-126a-4712-b0d8-9c3027c1973a', 'description': 'Axial NECT (#1) shows large left posterior temporal lobe hematoma (arrow) with edema, mass effect. Brain appears diffusely swollen, with obliterated sulci. Subtle subarachnoid hemorrhage present in left sylvian fissure (open arrow). Emergency MR was obtained. Axial T1WI (#2) shows a mixed signal intensity mass (arrows). Adjacent brain is swollen and there is evidence for early uncal and hippocampal herniation (open arrows). FLAIR scan (#3) shows moderate edema surrounding the clot (arrow) and confirms presence of subarachnoid hemorrhage (open arrows). Axial T1 C+ scan (#4) shows no abnormal enhancement. Coronal scan (#5) shows empty delta sign of nonenhancing thrombus surrounded by enhancing dura of left transverse sinus (arrow).', 'history': 'Postpartum headache, followed by seizure.', 'imagePoolId': '1c6e8746-a1f6-44d5-8651-02ba41ab1b8b', 'name': 'Large temporal lobe hematoma', 'teachingPoint': 'Dural sinus and cortical vein thrombosis are known risks in the postpartum hypercoagulable period. In this case, the thrombosed left transverse sinus caused a large spontaneous intracranial hemorrhage in the adjacent temporal lobe. These are often caused by concomitant occlusion of a dominant anastomotic vein of Labbe.', 'demographics': '24 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'b89cb94d-adcf-4f6f-8593-e4803a328830', 'description': 'Sagittal T1WI (#1) shows hyperintensity (arrow) in the left transverse sinus. Axial T2WI (#2) shows the left transverse sinus appears completely filled with hyperintense clot (arrow). A series of axial and coronal T1C+ (#3-6) images show the classic "empty delta" sign (arrows) of enhancing dura surrounding nonenhancing clot. On images (#5,6) you can clearly see the cigar-shaped, elongated clot within the transverse sinus (arrows).', 'history': 'Headaches for several days.', 'imagePoolId': 'b2c8ba4d-0110-4bed-82df-4e65c84c23a0', 'name': 'Subacute', 'teachingPoint': None}, {'authors': [{'key': 'e61f84c0-fe96-48cc-8bd4-294dd3bb3ae6', 'value': 'Kristine M. Mosier, DMD, PhD'}], 'caseVersionId': 'bd8317ec-cc36-4173-807c-3ac0f4edcb4b', 'description': 'Axial NECT scans (#1,2) demonstrate striking hyperdensity of the transverse (arrows, #1) and superior sagittal sinuses (arrows, #2). Two factors contribute to this normal appearance: (1) the physiologic polycythemia of newborns and (2) the low density of the adjacent, almost completely unmyelinated, brain. Circulating blood is always slightly hyperdense to even normal myelinated brain.', 'history': 'Premature infant born at 30 weeks gestation.', 'imagePoolId': 'fec87e76-b58b-48b0-ab2c-a91a1996efe0', 'name': 'Mimics DST', 'teachingPoint': None, 'demographics': '1 Days old '}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '088ce7c8-947c-45b9-a763-bb30add77af7', 'description': 'Series of axial NECT scans demonstrates hyperdense, expanded straight sinus (arrows, #1,2), clot in vein of Galen (black arrow, #1), involvement of torcular and superior sagittal sinus (curved arrows, #1-4), and clot within several cortical veins, seen best on images #3,4 (open arrows). The cortical vein clots represent classic examples of the "cord sign."', 'history': 'Headaches, papilledema, decreasing mental status.', 'imagePoolId': '9565e6d2-db22-4061-91b4-b6eced0cc77b', 'name': 'Great "cord sign"', 'teachingPoint': None}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '7635f470-8fbc-4b53-b9ed-590c2debb8c7', 'description': 'Close-up view of axial NECT scan shows subtle hyperdensity in left transverse sinus (arrow, #1). Axial T2WI (#2) and FLAIR (#3) show hypointense clot in the entire left transverse sinus (arrows). Note absence of any parenchymal abnormality in the adjacent brain despite evidence on the T2* scan that clot extends into the vein of Labbe (arrow, #4). MRA (#5) shows the entire left transverse and sigmoid sinus are occluded, as is the ipsilateral jugular vein.', 'history': 'Worsening headaches.', 'imagePoolId': '9cee31a7-c20a-4539-aec6-19d6c516e969', 'name': 'Acute with typical CT, MR', 'teachingPoint': None}], 'caseType': 'typical', 'name': 'TYPICAL'}
+- {'cases': [{'authors': [{'key': '33151213-01b2-4542-9105-342e006b3915', 'value': 'H. Ric Harnsberger, MD'}], 'caseVersionId': '61217703-7937-4921-b4ae-83eb31d06a28', 'description': 'Variant MR-MRV case of acute superior sagittal sinus (SSS) thrombosis with cortical vein thrombosis and stroke.\n\nSagittal T1 MR image (#1) shows subacute clot in the thrombosed SSS (arrows). Coronal MRV MIP (#2) reveals an absent SSS and cortical veins along with proximal right transverse sinus thrombosis (open arrows). Notice the right vein of Labbe is large (curved arrow) as it tries to function as a collateral route for venous drainage. Axial GRE images of the superior aspect of the brain (#3-6) demonstrate blooming in the thrombosed SSS (arrows) and in the associated cortical veins (curved arrows). The associated stroke is visible with petechial hemorrhage blooming (open arrows, #3). Axial FLAIR (#7) better displays the left hemispheric ischemia (open arrow). Axial T1 enhanced fat-saturated images (#8-11) reveal diffuse meningeal enhancement, the "empty delta sign" of the thrombosed SSS (arrows) and the collateral veins (open arrows) adjacent to the SSS.', 'history': 'Patient presents with severe headache after prolonged bout of diarrhea. Physical examination revealed papilledema and right hemiparesis.', 'imagePoolId': '19307357-3b39-48b0-844d-3b818e527936', 'name': 'With cortical vein thrombosis and stroke', 'teachingPoint': None, 'demographics': '66 Years old male'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'd2e13a74-24e2-4560-bfb5-4d894fd088a3', 'description': 'AP and lateral venous phases (#1-3) of selective right internal carotid angiogram show striking, extremely prominent deep white matter (medullary) veins (arrows) draining into dilated thalamostriate, lateral atrial, and markedly enlarged internal cerebral veins (open arrows). Note filling of cavernous sinus (curved arrows), draining into pterygoid venous plexus. The superior sagittal sinus does not opacify but the straight and transverse sinuses fill normally. \n\nAP and lateral venous phase studies (#4-8) of the left internal carotid angiogram are even more striking. Again note the prominent medullary veins (arrows), dilated deep cerebral veins (open arrows), and lack of normal filling of the superior sagittal sinus (curved arrows). Another, slightly different angled, view of the left ICA venous phase study is shown on images #9-10 (same arrows). Thin, attenuated and incomplete parasagittal venous channels are seen on images #5-10 (curved arrows). AP and lateral venous phase of the left vertebral angiogram (#11, 12) again show prominent parasagittal venous channels but no normal SSS. \n\nComment: While the prominent medullary veins make this case look like blue rubber bleb nevus syndrome, the patient had no cutaneous stigmata. This is a very unusual case of chronic, longstanding superior sagittal sinus thrombosis with enlarged medullary and subependymal veins serving as collateral venous drainage pathways. MR was recommended but not obtained.', 'history': 'Presented in ER with severe headaches. Outside CT scan showed "funny vessels."', 'imagePoolId': '64dcd0f2-c240-4e82-bb7f-b2a4a609d5d3', 'name': 'Chronic; prominent medullary veins mimic BRBNS', 'teachingPoint': None, 'demographics': '23 Years old female'}, {'authors': [{'key': '07a2c087-6202-49e7-870b-7aa162d18f06', 'value': 'Bronwyn E. Hamilton, MD'}], 'caseVersionId': 'f0e985c1-822c-4c25-b0e0-3df520a85578', 'description': 'CT angiogram source image (#1) shows lack of enhancement of the left transverse sinus, consistent with occlusion (arrows). Also noted is a punctate focus of gas within the occluded sinus, suggesting a temporal bone fracture (open arrow). Bone windows at the same level (#2) confirm a skull base fracture (arrow) and corresponding sutural diastasis (open arrow).\n\nCT image (#3) performed a day after presentation shows significant cerebral edema and cisternal effacement (arrow), for which a right hemicraniectomy has been performed to decompress the brain. Note the abnormal density in the left transverse sinus (open arrow) on this unenhanced study, again consistent with occlusion. Subtle hemorrhage in the left temporal lobe (curved arrows) is new since the admission head CT, and is somewhat unusual in location for typical contusion or shearing injury. This location is classic for vein of Labbe thrombosis and resultant hemorrhagic venous infarction. \n\nFollow-up CT (#4) performed a week after admission better demonstrates left temporal and occipital hemorrhage (arrow) with surrounding vasogenic appearing edema (curved arrows), typical of vein of Labbe occlusion.\n\nComments: Many patients tolerate isolated transverse and sigmoid sinus occlusions, however if thrombus extends to involve the superficial cortical veins, venous infarction and/or hemorrhage are the usual sequelae.\n\nWhen skull base fractures are encountered, one should always consider the underlying regional anatomy and think of potential complications. Intimal injury, dissection, traumatic occlusion, and pseudoaneurysm formation are possible complications of arterial injury, while epidural hematoma or traumatic venous occlusion are possible complications of fractures traversing the dural sinuses.', 'history': 'Head trauma.', 'imagePoolId': 'f7769ecd-ef0f-4a07-a3f0-32b7d3c0dcff', 'name': 'Traumatic occlusion', 'teachingPoint': None, 'demographics': '25 Years old male'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '5d0a631b-e743-4fc3-b782-849caaefec6f', 'description': 'Axial NECT scans (#1,2) show thick calvarium and very prominent, thick ossification along the falx (arrows). Note thickened superior sagittal sinus (open arrow, #2). \n\nAn MR was obtained. Note high signal from fat-containing osseous metaplasia along the falx cerebri on T1WI (arrows, #3). Also note thick skull and enlarged, chronically thrombosed, superior sagittal and straight sinuses (open arrows). The brain appears "tight" with downward displacement of the midbrain and cerebellar tonsils. Sagittal T2WI with fat saturation shows suppression fat within the metaplastic bone and thick calvarium (arrows, #4). Compare to image 3, where the fat is hyperintense. Axial FSE T2WIs without fat saturation (#5,6) show the hyperintensity of the fatty marrow encased by hypointense cortical bone (arrows). FLAIR scan also shows the osseous metaplasia as hypointense plaques along the falx cerebri (arrows, #7).\n\nAsymptomatic ossified dural plaques in the brain and spine are commonly found at surgery and autopsy and generally have little clinical significance. Most are patchy, thin and isolated. The cause of larger plaques, such as seen in this case, is unknown. Various etiologies proposed include intradural hematoma, vascular shunting or pressure effects, etc. In this case, longstanding chronic dural sinus occlusion was present and may have contributed to its development.', 'history': 'Worsening chronic headaches, papilledema.', 'imagePoolId': 'cdcbb3c1-9be0-4d03-94cb-bbaae51d7dc2', 'name': 'Thick skull, striking dural metaplasia', 'teachingPoint': None, 'demographics': '25 Years old male'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '2714a63b-7d58-4563-bb37-5986dbcd5d01', 'description': 'Axial T1WI shows isointense clot in left transverse sinus (arrow, #1). FLAIR scan (#2) shows widespread hyperintensity, mass effect in left temporal lobe. Axial and coronal T1C+ scans (#3,4) show bizarre sulcal and parenchymal enhancement, raising the possibility of neoplastic involvement. Coronal MRA (#5) and DSA (#6) confirm thrombosis of the left transverse and sigmoid sinuses. Filling defect in the left transverse sinus can be seen on the DSA (arrow, #6). The bizarre enhancement is secondary to venous ischemia. Biopsy was performed and showed no evidence for neoplastic involvement of the sinuses, brain or meninges.', 'history': 'Known systemic neoplasm, coagulopathy, seizure.', 'imagePoolId': '44bf3cdf-4ff9-4fa9-833a-a0bd9cf7511a', 'name': 'Venous infarct mimics neoplasm', 'teachingPoint': None}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '989d9136-4a35-4ce2-9662-7c721d731fdf', 'description': 'Axial (#1) and coronal (#2) T1C+ scans show prominent "blush" in parieto-occipital white matter (arrows) with prominent dilated medullary veins (open arrows) draining into enlarged subependymal veins (curved arrows). Contrast stasis, dural enhancement along the left transverse sinus indicates it has not recanalized.\n\nCollateral venous drainage in the face of persisting dural sinus occlusion may become very prominent. It is unusual to have such striking deep collaterals with white matter medullary veins so prominent.', 'history': 'History of left transverse sinus occlusion. Followup MR obtained.', 'imagePoolId': '4ca2938d-b992-45b7-8b87-11453402b007', 'name': 'Mimics DVA', 'teachingPoint': None}], 'caseType': 'variant', 'name': 'VARIANT'}
+
+
+## Images
+
+
+### Selected Images
+
+
+*Sagittal graphic shows thrombosis of the superior sagittal sinus (SSS) and straight sinus . Inset in the upper left reveals a thrombus in the SSS in cross section (empty delta sign) seen on contrast-enhanced imaging. This results from enhancement of dural walls surrounding the central nonenhancing thrombosed lumen.*
+
+
+*Sagittal graphic shows thrombosis of the superior sagittal sinus (SSS) and straight sinus . Inset in the upper left reveals a thrombus in the SSS in cross section (empty delta sign) seen on contrast-enhanced imaging. This results from enhancement of dural walls surrounding the central nonenhancing thrombosed lumen.*
+
+
+*Axial NECT in a 27-year-old woman on oral contraceptives with sudden onset of severe headaches shows hyperdensity in the straight sinus and sinus confluence .*
+
+
+*CT venography in the same patient shows contrast enhancement of the dura surrounding the nonenhancing thrombosed lumen of the SSS. This forms the so-called empty delta sign of dural venous sinus thrombosis.*
+
+
+*Sagittal CT venography in the same patient shows extensive nonenhancing thrombus in the SSS and the straight sinus . The vein of Galen and internal cerebral veins are enlarged and intensely enhancing because outflow through the straight sinus is obstructed.*
+
+
+*Axial NECT in a 46-year-old man with a sudden, severe headache shows a left posterior temporoparietal hematoma with a moderate degree of surrounding vasogenic edema and mild local mass effect with compression of the adjacent ventricular atrium .*
+
+
+*More inferior NECT slice in the same patient shows a hyperdense left transverse sinus (TS) . An adjacent tubular hyperdensity likely represents an acutely thrombosed vein of Labbé (a.k.a. inferior anastomotic vein).*
+
+
+*Axial CT venography in the same patient shows a lack of contrast enhancement in the left TS , consistent with thrombosis. The right transverse/sigmoid sinus junction enhances intensely and normally.*
+
+
+*Coronal CT venography shows an empty delta sign in the left TS and thrombus extending into the proximal vein of Labbé as it empties into the TS. The right TS is normally opacified. The adjacent area of hemorrhagic venous infarction is again seen.*
+
+
+*Axial CECT shows cavernous sinus (CS) thrombosis, which can be a subtle diagnosis. Most cases occur as complications of sphenoid sinusitis and show a nonenhancing clot contained by enhancing dural walls .*
+
+
+*Axial T1 C+ FS MR in the same patient shows areas of nonenhancing clot enclosed by enhancing dural walls of the CS. Patients with CS thrombophlebitis typically have headache, cranial nerve palsies, and sphenoid sinusitis. High-dose IV antibiotics are the cornerstone of treatment.*
+
+
+*Axial NECT in a 66-year-old woman with several days of headache followed by seizure shows biparietal parenchymal hemorrhages with associated edema and a dense SSS .*
+
+
+*Midline sagittal NECT in the same patient shows a dense SSS , consistent with thrombosis. The acute thrombus measured 70 HU, while blood pool in the vein of Galen measured only 43 HU. The patient was subsequently diagnosed with a hypercoagulable state due to the JAK2 V617F mutation.*
+
+
+*A 21-year-old woman had 2 weeks of increasingly severe headache and moderate papilledema on presentation in the ER. The NECT was interpreted as normal; thus, CT venography was ordered for further evaluation. CT venography shows SSS thrombosis extending to the confluence of the sinuses as well as TS thrombosis (not shown).*
+
+
+*Sagittal T1-weighted SPGR MR in the same patient shows hyperintense subacute thrombus in the SSS and venous confluence .*
+
+
+*Axial FLAIR MR shows high signal in the right TS and a small vein of Labbé , consistent with venous thrombosis. Subacute thrombus is typically hyperintense on FLAIR MR. An additional small focus of hyperintensity may represent parenchymal hemorrhage or additional clot in a cortical vein.*
+
+
+*Axial T2* GRE MR shows blooming thrombus in tentorial veins , while the thrombosed TS shows mixed signal. Thrombus of varying ages can demonstrate heterogeneous signal intensity on T2* GRE.*
+
+
+*Axial CECT in a 23-year-old postpartum woman s/p seizure demonstrates a left parietal hemorrhagic venous infarct in the setting of SSS thrombosis with an empty delta sign .*
+
+
+*Axial T2* GRE MR in the same patient shows low signal intensity associated with the acutely thrombosed SSS and with dilated right parietal and left frontal venous structures, reflecting regional venous hypertension. The hemorrhagic venous infarct has enlarged in the interval from the prior CT.*
+
+
+*Midline sagittal T1 C+ SPGR MR in the same patient well delineates the extent of SSS thrombosis . Normal enhancement is well seen in the internal cerebral vein , vein of Galen , and straight sinus .*
+
+
+*Axial arterial spin label (ASL) perfusion map in the same patient demonstrates marked hypoperfusion in the region of the hemorrhagic venous infarct . Mildly reduced perfusion in the right parietal lobe likely reflects regional venous hypertension, as does mild asymmetry of the frontal lobes.*
+
+
+*MIP coronal view of a CT venogram in a patient with chronic dural sinus thrombosis shows innumerable tortuous corkscrew vessels extending from the cortex through the centrum semiovale and corona radiata.*
+
+
+*Sagittal 3D shaded surface display of the CTV in the same patient shows the hemispheres are filled with the corkscrew vessels, which are massively enlarged, tortuous medullary veins. Though segments of the dural sinuses are patent, bilateral chronic outflow obstruction has caused severe venous hypertension.*
+
+
+### Additional Images
+
+
+*Sagittal T1 MR reveals intermediate- to high-intensity clot filling the swollen SSS. This signal indicates that the thrombosis is subacute in age.*
+
+
+*Axial CTA demonstrates low-density clot in the left TS . The normal right TS is filled with contrasted blood .*
+
+
+*Axial CTA shows sigmoid sinus and jugular foramen thrombosis on the left. Note the normal right enhancing sigmoid sinus and jugular bulb .*
+
+
+*Axial CECT demonstrates double empty delta signs at the anterior and posterior margins of the SSS. Complete SSS thrombosis was present.*
+
+
+*Coronal MRV reveals SSS thrombosis with right TS thrombosis . Note that the right vein of Labbé is large as it provides collateral flow.*
+
+
+*Axial T2* GRE MR shows blooming (overly large low signal) in the thrombosed SSS and in the associated cortical veins . Cerebral infarction may result.*
+
+
+*Axial CT venography shows an occluded SSS with a classic empty delta sign .*
+
+
+*Axial T1 MR in the same patient shows the subacute clot is hyperintense.*
+
+
+*Subacute dural sinus thrombosis is typically very hyperintense on FLAIR MR.*
+
+
+*Note that on T2* GRE MR this subacute thrombus does not exhibit internal gradient susceptibility.*
+
+
+*Acute venous occlusion may be difficult to see on MR as thrombus is isointense with brain. Axial T1 MR shows isointense thrombus in the straight sinus and both internal cerebral veins .*
+
+
+*Coronal T1 MR shows extensive thrombus in the superior sagittal and both TSs .*
+
+
+*FLAIR MR in the same patient shows edema in both the basal ganglia and thalami. The right side is more severely affected than the left, but the left thalamus is clearly hyperintense.*
+
+
+*T2* (GRE/SWI) scans are very helpful in venous thrombosis. Here, thrombus in both internal cerebral veins and the straight sinus demonstrates blooming and appears very hypointense.*
+
+
+*More inferior T2* MR in the same patient also shows extensive blooming thrombus in the right TS and tributary tentorial veins as well as the vein of Labbé .*
+
+
+*T2* MR through the vertex in the same patient shows complete thrombosis of the SSS . The blooming clot also extends into several cortical veins .*
+
+
+*Axial CT venography in a patient with chronic dural sinus thrombosis shows innumerable enhancing corkscrew vessels interspersed throughout the white matter.*
+
+
+*Parasagittal CT venography through the corona radiata shows the corkscrew vessels exceptionally well.*
+
+
+*Parasagittal T1 MR in the same patient shows clusters of corkscrew flow voids caused by the enlarged medullary veins.*
+
+
+*Sagittal MR venography shows the anterior and middle segments of the SSS are occluded. The corkscrew collateral medullary veins are faintly visible.*
+
+
+*Axial T1 MR shows hyperintense thrombus in an occluded, enlarged right TS. Note thrombus in an adjacent tentorial vein .*
+
+
+*Axial T2 MR in the same patient shows the subacute thrombus is hyperintense.*
+
diff --git a/docs_md/articles/fat-emboli-cerebral-infarction_f202ed78-4256-4d0b-b15a-2af1088e7c51.md b/docs_md/articles/fat-emboli-cerebral-infarction_f202ed78-4256-4d0b-b15a-2af1088e7c51.md
new file mode 100644
index 0000000..cc69934
--- /dev/null
+++ b/docs_md/articles/fat-emboli-cerebral-infarction_f202ed78-4256-4d0b-b15a-2af1088e7c51.md
@@ -0,0 +1,323 @@
+---
+title: "Fat Emboli Cerebral Infarction"
+docid: "f202ed78-4256-4d0b-b15a-2af1088e7c51"
+authors:
+ - key: "8d5254e9-8dda-478b-8f08-bdee97a32c79"
+ value: "Karen L. Salzman, MD, FACR"
+ - key: "318f80ab-6abb-4067-a809-2ebdaa5a30c9"
+ value: "Kalen Riley, MD, MBA"
+breadcrumbs:
+ -
+ name: "Brain"
+ slug: "brain"
+ treeNodeId: "0361042c-9c90-48e4-864e-a2e6428ee9c9"
+ -
+ name: "Diagnosis"
+ slug: "diagnosis"
+ treeNodeId: "948c6f1e-8e18-45f3-bd9d-7a04ab0b8708"
+ -
+ name: "Pathology-Based Diagnoses"
+ slug: "pathology-based-diagnoses"
+ treeNodeId: "d60fe914-7897-46a0-9cd2-f88ffb322f16"
+ -
+ name: "Stroke"
+ slug: "stroke"
+ treeNodeId: "7a135176-0a69-4fc9-b200-59569fbf5166"
+ -
+ name: "Cerebral Ischemia and Infarction"
+ slug: "cerebral-ischemia-and-infarction"
+ treeNodeId: "11d50e7d-f3e9-4071-b2b7-26b11ab40ea6"
+ -
+ name: "Fat Emboli Cerebral Infarction"
+ slug: "fat-emboli-cerebral-infarction"
+ treeNodeId: null
+category: "Brain"
+documentVersionId: "a7e5f3e7-e8d0-4e84-8325-2b94fb1344e5"
+imageCount: 13
+lastUpdated: "08/21/25"
+pageDescription: "Fat Emboli Cerebral Infarction"
+pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Fat Emboli Cerebral Infarction"
+pageTitle: "Fat Emboli Cerebral Infarction | STATdx"
+enhancedTitle: "Fat Emboli Cerebral Infarction"
+type: "DX"
+references: true
+cases: 1
+breadcrumbs:
+ - "Brain"
+ - "Diagnosis"
+ - "Pathology-Based Diagnoses"
+ - "Stroke"
+ - "Cerebral Ischemia and Infarction"
+ - "Fat Emboli Cerebral Infarction"
+---
+## KEY FACTS
+
+- ### Terminology
+
+
+ - Acute stroke related to fat emboli
+- ### Imaging
+
+
+ - Acute ischemia with appropriate clinical history
+ - Long bone or pelvic fractures, cardiac surgery, joint replacement surgery
+ - Often mimics thromboembolic stroke
+ - Commonly affects gray matter and white matter (WM)
+ - May affect deep and periventricular WM
+ - May affect deep gray nuclei
+ - May show typical vascular territory or mimic "watershed" infarct
+ - NECT: Typically negative acutely
+ - Hypodense MCA sign related to fat within MCA
+ - T2/FLAIR: Multiple small, scattered hyperintense foci
+ - DWI: Multiple foci of + restriction: **Starfield pattern**
+ - T2* GRE/SWI: May show extensive petechial hemorrhages
+ - T1WI C+: May see faint enhancement of lesions
+- ### Top Differential Diagnoses
+
+
+ - Acute cerebral ischemia-infarction
+ - Posterior reversible encephalopathy syndrome (PRES)
+ - Vasculitis
+ - Septic emboli
+ - Diffuse axonal injury (DAI)
+- ### Pathology
+
+
+ - Fat emboli can pass through pulmonary capillaries without shunting lesions and result in systemic embolization (brain, kidneys most commonly)
+- ### Clinical Issues
+
+
+ - Fat embolism syndrome: Pulmonary, CNS, and cutaneous manifestations
+ - Hypoxia, deteriorating mental status, petechiae
+ - Neurologic dysfunction varies from confusion to encephalopathy with coma and seizures
+ - Uncommon but potentially life threatening
+ - Fat embolism syndrome after fractures: Up to 2.2%
+
+## TERMINOLOGY
+
+- ### Definitions
+
+
+ - Acute stroke related to fat emboli
+
+## IMAGING
+
+- ### General Features
+
+
+ - #### Best diagnostic clue
+
+
+ - Acute ischemia with appropriate clinical history
+ - Often mimics thromboembolic stroke
+ - Hypodense MCA sign related to fat within MCA
+ - #### Location
+
+
+ - Commonly affects both gray (GM) and white matter (WM)
+ - May affect deep and periventricular WM
+ - May affect deep gray nuclei (basal ganglia and thalamus)
+ - May involve typical vascular territory (MCA, PCA, ACA)
+ - May mimic "watershed" infarct
+ - #### Size
+
+
+ - Punctate to large vascular territory
+- ### CT Findings
+
+
+ - NECT: Typically negative acutely
+ - Hypodense MCA sign related to fat within MCA is rare
+- ### MR Findings
+
+
+ - T1WI: Typically normal
+ - T2WI: Multiple small, scattered hyperintense foci in WM and GM
+ - May affect only deep gray nuclei (BG and thalamus)
+ - FLAIR: Multiple small, scattered hyperintense foci in WM and GM
+ - DWI/DTI: Acute diffusion restriction
+ - Starfield pattern with innumerable tiny punctate foci of DWI restriction in multiple vascular distributions
+ - T2* GRE/SWI: Multiple foci of "blooming" common, related to petechial hemorrhages
+ - Some authors consider this feature pathognomonic
+ - T1WI C+: May see faint enhancement correlating with areas of DWI restriction and T2 hyperintensity
+- ### Imaging Recommendations
+
+
+ - #### Best imaging tool
+
+
+ - MR with DWI
+
+## DIFFERENTIAL DIAGNOSIS
+
+- [Acute Cerebral Ischemia-Infarction](/document/acute-cerebral-ischemiainfarction/7a3ed4a9-ae05-4d64-ae8e-6a30105501e1)
+ - Wedge-shaped T2 hyperintensity in typical vascular territory (MCA, PCA, ACA)
+ - DWI restriction
+ - PWI shows abnormal perfusion
+- [Acute Hypertensive Encephalopathy, PRES](/document/posterior-reversible-encephalopath-/84176f2c-fc9d-4497-8af9-1430b9f0187c)
+ - T2/FLAIR hyperintensity in cortex/subcortical WM of posterior circulation
+ - May affect BG and thalami
+ - Typically reversible
+- [Vasculitis](/document/miscellaneous-vasculitis/221f737a-6bfa-4331-b296-402e40973f7e)
+ - Irregularity, stenosis, and vascular occlusion of 2nd- and 3rd-order arterial branches
+ - T2/FLAIR subcortical and BG hyperintensities
+ - Patchy enhancement is common
+ - May see associated hemorrhage
+ - May be DWI + acutely
+- ### Septic Emboli
+
+
+ - Areas of DWI restriction in multiple vascular territories of variable size
+ - Will typically enhance
+ - Clinical history (endocarditis, cardiac vegetations, IV drug use, etc.) may be key differentiating feature
+- ### Diffuse Axonal Injury
+
+
+ - Trauma patient
+ - Punctate lesions at corticomedullary junction, corpus callosum, deep GM, brainstem
+ - Typically DWI + with T2*/SWI hypointense, "blooming"
+
+## PATHOLOGY
+
+- ### General Features
+
+
+ - #### Etiology
+
+
+ - Fat emboli can pass through pulmonary vasculature without shunting lesions, resulting in systemic embolization; most common in brain and kidneys
+ - Fat emboli often result from long bone or pelvic fractures
+ - May result as complication of cardiac surgery, intracardiac right-to-left shunt, or venous-arterial shunt
+ - Coronary artery bypass or valve replacement surgery
+ - May result from hip or knee replacement surgery
+ - Rarely reported as complication of sickle cell disease related to bone marrow necrosis
+ - Onset is typically 2 hours to 2 days after trauma or surgery
+ - Pathologic hallmark is arteriolar fat emboli with perivascular microhemorrhages
+
+## CLINICAL ISSUES
+
+- ### Presentation
+
+
+ - #### Most common signs/symptoms
+
+
+ - Fat embolism syndrome: Pulmonary, central nervous system, and cutaneous manifestations
+ - Main criteria: Hypoxia, deteriorating mental status, and petechiae
+ - Secondary signs: Tachycardia, fever, anemia, and thrombocytopenia
+ - Neurologic dysfunction varies from confusion to encephalopathy with coma and seizures
+ - Cerebral manifestations of fat embolism syndrome are variable: Headache, lethargy, irritability, delirium, stupor, seizures, coma
+ - #### Other signs/symptoms
+
+
+ - Many cases are subclinical and remain undiagnosed
+ - High-resolution chest CT findings of fat emboli: Bilateral ground-glass opacities and thickening of interlobular septa
+- ### Demographics
+
+
+ - #### Epidemiology
+
+
+ - Uncommon but potentially life threatening
+ - Incidence of fat embolism syndrome after bone fractures is 0.9-2.2%
+ - Reports of incidence up to 5-10% if multiple fractures
+- ### Treatment
+
+
+ - Supportive measures, including supplemental oxygenation, mechanical ventilation (if necessary) and fluid resuscitation, are mainstays of therapy
+
+## DIAGNOSTIC CHECKLIST
+
+- ### Consider
+
+
+ - Fat embolism as cause of stroke in patient with appropriate history
+ - In patient with hypoxia, skin petechia, and acute stroke, think fat emboli
+
+ da014c5b-868c-4cc4-a0b4-f9658a6a64d4
+
+## References
+
+## Selected References
+
+1. [Amseian G et al: Brain microbleeds resulting from presumed extensive fat emboli in a patient with bone marrow necrosis following a sickle cell disease vaso-occlusive crisis. Emerg Radiol. 32(1):125-9, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=39333401%5Bpmid%5D)
+1. [Salunkhe R et al: Unusual presentation of cerebral fat embolism syndrome post-femur fracture: a case study and diagnostic insights. Cureus. 16(7):e64819, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=39156416%5Bpmid%5D)
+1. [Kanda N et al: Prospective study examining the probability of cerebral fat embolism based on magnetic resonance imaging. Heliyon. 9(3):e14073, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=36915523%5Bpmid%5D)
+1. [Singh A et al: Cerebral fat embolism syndrome at a single trauma center. J Stroke Cerebrovasc Dis. 31(12):106794, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=36215903%5Bpmid%5D)
+1. [Gadde JA et al: Neuroimaging of patients in the intensive care unit: pearls and pitfalls. Radiol Clin North Am. 58(1):167-85, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31731899%5Bpmid%5D)
+1. [Uzelac A: Imaging of altered mental status. Radiol Clin North Am. 58(1):187-97, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31731900%5Bpmid%5D)
+1. [Bhatt AA et al: Beyond stroke-uncommon causes of diffusion restriction in the basal ganglia. Emerg Radiol. 25(1):87-92, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=28871382%5Bpmid%5D)
+1. [Skalski KA et al: Hemorrhagic and non-hemorrhagic causes of signal loss on susceptibility-weighted imaging. Emerg Radiol. 25(6):691-701, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30136160%5Bpmid%5D)
+1. [Rutman AM et al: T2*-weighted and diffusion magnetic resonance imaging differentiation of cerebral fat embolism from diffuse axonal injury. J Comput Assist Tomogr. 41(6):877-83, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28708729%5Bpmid%5D)
+1. [Zakhari N et al: Unusual cerebral emboli. Neuroimaging Clin N Am. 26(1):147-63, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=26610666%5Bpmid%5D)
+1. [Eriksson EA et al: Fat embolism in pediatric patients: an autopsy evaluation of incidence and Etiology. J Crit Care. 30(1):221.e1-5, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25306239%5Bpmid%5D)
+1. [Kosova E et al: Fat embolism syndrome. Circulation. 131(3):317-20, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25601951%5Bpmid%5D)
+1. [Kuo KH et al: Dynamic MR imaging patterns of cerebral fat embolism: a systematic review with illustrative cases. AJNR Am J Neuroradiol. 35(6):1052-7, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=23639561%5Bpmid%5D)
+1. [Kellogg RG et al: Massive cerebral involvement in fat embolism syndrome and intracranial pressure management. J Neurosurg. 119(5):1263-70, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23952720%5Bpmid%5D)
+1. [Medina FJ et al: Cerebral fat embolism detection with susceptibility-weighted images in sickle cell disease. Neuroradiol J. 25(4):411-4, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=24029033%5Bpmid%5D)
+1. [Abend NS et al: Hypodense middle cerebral artery with fat embolus. Neurocrit Care. 6(2):147-8, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17522799%5Bpmid%5D)
+1. [Koch S et al: Cerebral fat microembolism and cognitive decline after hip and knee replacement. Stroke. 38(3):1079-81, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17255544%5Bpmid%5D)
+1. [Aydin MD et al: Cerebral fat embolism: pulmonary contusion is a more important etiology than long bone fractures. Clin Neuropathol. 24(2):86-90, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=15803808%5Bpmid%5D)
+1. [Lee TC et al: The hypodense artery sign. AJNR Am J Neuroradiol. 26(8):2027-9, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=16155153%5Bpmid%5D)
+1. [Simon AD et al: Contrast-enhanced MR imaging of cerebral fat embolism: case report and review of the literature. AJNR Am J Neuroradiol. 24(1):97-101, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12533333%5Bpmid%5D)
+1. [Yoon SS et al: Acute fatal stroke immediately following autologous fat injection into the face. Neurology. 61(8):1151-2, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=14581689%5Bpmid%5D)
+1. [Parizel PM et al: Early diagnosis of cerebral fat embolism syndrome by diffusion-weighted MRI (starfield pattern). Stroke. 32(12):2942-4, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11740000%5Bpmid%5D)
+1. [Forteza AM et al: Transcranial doppler detection of fat emboli. Stroke. 30(12):2687-91, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10582998%5Bpmid%5D)
+1. [Wegener K et al: A case of cerebral fat embolism demonstrating no pathophysiological involvement of lung dysfunction. Eur Neurol. 42(1):65-6, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10523138%5Bpmid%5D)
+1. [Ghatak NR et al: Cerebral fat embolism following cardiac surgery. Stroke. 14(4):619-21, 1983](http://www.ncbi.nlm.nih.gov/pubmed/?term=6658941%5Bpmid%5D)
+
+## Cases
+
+- {'cases': [{'authors': [{'key': 'f184750a-90b4-47a7-907b-23b05d70357a', 'value': 'Chang Yueh Ho, MD'}], 'caseVersionId': 'b4123f39-01b7-4aee-84a9-2f7e1e765116', 'description': "Axial NECT (#1) shows bilateral occipital hypodensity with loss of the gray-white differentiation (black arrows) at the junction of the MCA and PCA vascular distributions. Note the scalp hematoma related to the patient's recent trauma (white arrows). Axial NECT (#2) shows multiple hypodensities (black arrows) with loss of the gray-white differentiation in the frontal lobes at the junctions between the ACA and MCA vascular distributions and posteriorly at the MCA and PCA vascular distributions.\n\nAxial T2WI MR (#3) and axial FLAIR MR (#4) show bilateral occipital hyperintensities (black arrows). The left-sided lesion shows heterogeneous T2 hypointensity (white arrows) suggesting acute blood products. Axial T1WI MR (#5) shows left occipital hypointensity (black arrow) with central isointensity (white arrow) again confirming blood products. Axial DWI MR (#6) shows hyperintensity of the left occipital lesion (arrow) indicating acute infarct. Axial ADC (#7) shows hypointensity of the left occipital lesion (arrow) from reduced diffusivity indicating infarct. Axial T2WI MR (#8) and FLAIR (#9) MR show multiple hyperintensities (arrows) in multiple vascular distributions indicating embolic phenomenon. Axial DWI MR (#10) demonstrates multiple foci of hyperintensity (arrows) in multiple vascular distributions indicating embolic infarction. Axial ADC (#11) demonstrates corresponding hypointensity from reduced diffusivity (arrows) in multiple vascular distributions confirming embolic infarction.\n\nSagittal reformat CT (#12) of the left knee shows fracture through the base of the tibial plateau (arrows).\n\nAP radiograph of the left humerus (#13) shows a comminuted fracture (curved arrow). Long bone fractures are a primary risk factor for fat emboli causing cerebral infarcts. Note the chest wall emphysema (arrow) from pneumothorax. AP radiograph of the right humerus (#14) shows an an olecranon avulsion fracture (arrow).\n\nComment: Fat emboli should be considered in post-traumatic cerebral ischemia with multiple vascular distributions and associated long bone fractures. These ischemic regions may have a propensity for blood products.", 'history': 'Go-karting accident, hit a parked truck; follow-up head CT demonstrates new infarcts not seen on head CT at admission; diagnostic angiogram (not included) was negative for dissection or other occlusion.', 'imagePoolId': '5a7c6a13-71f9-496c-bb4c-d36d2470e0b4', 'name': 'Multiple infarcts with long bone fractures', 'teachingPoint': None, 'demographics': '38 Years old male'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}, {'key': 'b049ee34-939e-4e28-8aad-f747a8f9efb0', 'value': 'Ulrich Rassner, MD'}], 'caseVersionId': 'cf0126cb-5324-47d2-8048-99999787613c', 'description': 'Typical MR case of acute stroke related to fat emboli in a patient status post hip surgery.\n\nAxial DWI images (#1-6) show extensive hyperintense foci related to acute fat emboli. The ADC map (#7) at the level of the lateral ventricles shows low signal in the areas of DWI hyperintense foci, indicating restricted diffusion related to acute ischemia. \n\nAxial FLAIR images (#8-10) show multiple areas of hyperintense foci (arrows) related to the multifocal areas of ischemia. \n\nAxial post-contrast images show subtle enhancement in some of the regions of ischemia (curved arrows, #11-12).\n\nComment: Fat embolism syndrome is rare and occurs in ~ 2% of patients with fractures. The fat emboli may pass through the pulmonary capillaries without a shunting lesion.', 'history': 'Patient with history of recent hip arthroplasty and acute neurologic symptoms.', 'imagePoolId': '645b0017-07e0-44da-893e-91ceb61e15bd', 'name': 'Multifocal emboli', 'teachingPoint': None, 'demographics': '68 Years old female'}], 'caseType': 'typical', 'name': 'TYPICAL'}
+
+
+## Images
+
+
+### Selected Images
+
+
+*Axial FLAIR MR in a 35-year-old with confusion after a femur fracture from a mountain biking injury shows abnormal hyperintensities in the bilateral corticomedullary junctions and subcortical white matter related to infarcts from fat emboli. Involvement of the basal ganglia was also present (not shown).*
+
+
+*Axial FLAIR MR in a 35-year-old with confusion after a femur fracture from a mountain biking injury shows abnormal hyperintensities in the bilateral corticomedullary junctions and subcortical white matter related to infarcts from fat emboli. Involvement of the basal ganglia was also present (not shown).*
+
+
+*Axial DTI trace MR in the same patient shows extensive punctate foci of diffusion restriction throughout the cortex and white matter in a starfield pattern typical of fat embolism.*
+
+
+*Axial SWI MR in a 35-year-old man with multiple fractures shows extensive foci of susceptibility artifact or "blooming" related to petechial hemorrhages. These hemorrhages are often seen in patients with cerebral fat emboli. Microhemorrhages persist from the acute to chronic phases of fat embolism.*
+
+
+*Axial SWI MR in the same patient shows extensive foci of susceptibility artifact in the cerebellum. These microhemorrhages are characteristic of cerebral fat emboli and help clarify the diagnosis.*
+
+
+### Additional Images
+
+
+*Axial DWI MR shows bilateral ischemia related to fat emboli. Imaging mimics other more typical causes of acute ischemia.*
+
+
+*Axial DWI MR shows innumerable punctate foci of restriction throughout the white matter and gray matter of this 68-year-old with mental status changes status post hip surgery. Note the extensive involvement of the basal ganglia and thalami.*
+
+
+*Axial DWI in the same patient shows the extensive foci of restriction related to acute ischemia from the patient's fat emboli. Note the more focal involvement of the left MCA territory with frontal and temporal lobe involvement. Microhemorrhages are also common with fat emboli.*
+
+
+*Axial FLAIR MR in an unresponsive 43-year-old after surgery for a pathologic acetabular fracture related to metastatic breast cancer shows abnormal hyperintensities in the bilateral deep gray nuclei and periventricular and subcortical white matter related to fat emboli.*
+
+
+*Axial T1 C+ MR in the same patient shows patchy enhancement of the lesions within the deep gray nuclei and subcortical white matter , most prominent in the occipital lobes.*
+
+
+*Axial DWI trace MR shows extensive punctate foci of diffusion restriction throughout the cortex and white matter this 30-year-old with mental status changes status post femur fracture repair. These bright foci have been described as the starfield pattern in the setting of fat emboli.*
+
+
+*Axial SWI MR in the same patient shows extensive foci of susceptibility artifact or blooming related to extensive petechial hemorrhages. The microhemorrhages persist from the acute to chronic phases of fat embolism. Differential considerations include traumatic diffuse axonal injury (DAI), which is typically less severe and also shows linear and punctate foci. At times, differentiating between DAI and cerebral fat emboli may be difficult given the imaging overlap.*
+
+
+*Axial DTI trace MR in an 81-year-old with altered mental status after hip fracture repair shows multiple foci of hyperintensity involving the cortex and corticomedullary junctions related to fat embolism. Imaging mimics multiple embolic infarcts.*
+
+
+*Axial SWI MR in the same patient shows scattered foci of susceptibility artifact related to petechial hemorrhages . Petechial hemorrhages are often seen in patients with fat embolism.*
+
diff --git a/docs_md/articles/hydranencephaly_a8d006a4-4aba-4cc4-a375-979eb05e66ca.md b/docs_md/articles/hydranencephaly_a8d006a4-4aba-4cc4-a375-979eb05e66ca.md
new file mode 100644
index 0000000..00420a6
--- /dev/null
+++ b/docs_md/articles/hydranencephaly_a8d006a4-4aba-4cc4-a375-979eb05e66ca.md
@@ -0,0 +1,335 @@
+---
+title: "Hydranencephaly"
+docid: "a8d006a4-4aba-4cc4-a375-979eb05e66ca"
+authors:
+ - key: "47381de4-c9fd-4999-8dd0-1808cd72db6b"
+ value: "Luke L. Linscott, MD"
+ - key: "5cff4116-3654-4b3a-bb75-5ebe0b8c9850"
+ value: "Anne G. Osborn, MD, FACR"
+breadcrumbs:
+ -
+ name: "Brain"
+ slug: "brain"
+ treeNodeId: "0361042c-9c90-48e4-864e-a2e6428ee9c9"
+ -
+ name: "Diagnosis"
+ slug: "diagnosis"
+ treeNodeId: "948c6f1e-8e18-45f3-bd9d-7a04ab0b8708"
+ -
+ name: "Pathology-Based Diagnoses"
+ slug: "pathology-based-diagnoses"
+ treeNodeId: "d60fe914-7897-46a0-9cd2-f88ffb322f16"
+ -
+ name: "Stroke"
+ slug: "stroke"
+ treeNodeId: "7a135176-0a69-4fc9-b200-59569fbf5166"
+ -
+ name: "Cerebral Ischemia and Infarction"
+ slug: "cerebral-ischemia-and-infarction"
+ treeNodeId: "11d50e7d-f3e9-4071-b2b7-26b11ab40ea6"
+ -
+ name: "Hydranencephaly"
+ slug: "hydranencephaly"
+ treeNodeId: null
+category: "Brain"
+documentVersionId: "b088be79-5aee-46b2-a4fa-4eba38585670"
+imageCount: 13
+lastUpdated: "04/29/25"
+pageDescription: "Hydranencephaly"
+pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Hydranencephaly"
+pageTitle: "Hydranencephaly | STATdx"
+enhancedTitle: "Hydranencephaly"
+type: "DX"
+references: true
+anatomy:
+ - "{'authors': 'Paula J. Woodward, MD, FSRU', 'bookmarked': False, 'bookmarkUrl': '/document/bookmark/080771c2-02f3-408d-ad70-04a80d849500', 'category': 'Ultrasound', 'compareUrl': '/compare/document/080771c2-02f3-408d-ad70-04a80d849500/related-anatomy/treeNode?subContext=Brain', 'documentId': '080771c2-02f3-408d-ad70-04a80d849500', 'documentType': 'ANATOMY', 'documentUrl': '/document/brain/080771c2-02f3-408d-ad70-04a80d849500', 'enhancedTitle': 'Brain', 'entryDate': '12/20/17', 'imageCount': 77, 'imageUrl': '/image/thumbnail/244b60fe-e15f-4ffb-8a39-cdbfe64fb3c4?size=174&quality=85', 'inCompareCart': False, 'rank': 1, 'referenceCount': 0, 'showCompareButton': False, 'title': 'Brain'}"
+ - "{'authors': 'Karen L. Salzman, MD, FACR', 'bookmarked': False, 'bookmarkUrl': '/document/bookmark/7006e397-5012-4027-aff8-e8d7158166ee', 'category': 'Brain', 'compareUrl': '/compare/document/7006e397-5012-4027-aff8-e8d7158166ee/related-anatomy/treeNode?subContext=Cerebral Hemispheres Overview', 'documentId': '7006e397-5012-4027-aff8-e8d7158166ee', 'documentType': 'ANATOMY', 'documentUrl': '/document/cerebral-hemispheres-overview/7006e397-5012-4027-aff8-e8d7158166ee', 'enhancedTitle': 'Cerebral Hemispheres Overview', 'entryDate': '10/20/20', 'imageCount': 37, 'imageUrl': '/image/thumbnail/a1907844-1c5e-4021-ac09-6bf1f0e43014?size=174&quality=85', 'inCompareCart': False, 'rank': 2, 'referenceCount': 0, 'showCompareButton': False, 'title': 'Cerebral Hemispheres Overview'}"
+ - "{'authors': 'Farshid Sepehrband, PhD, MS, BS; Karen L. Salzman, MD, FACR', 'bookmarked': False, 'bookmarkUrl': '/document/bookmark/f2a117ed-9429-441d-baa0-5e99e05722ac', 'category': 'Brain', 'compareUrl': '/compare/document/f2a117ed-9429-441d-baa0-5e99e05722ac/related-anatomy/treeNode?subContext=Limbic System', 'documentId': 'f2a117ed-9429-441d-baa0-5e99e05722ac', 'documentType': 'ANATOMY', 'documentUrl': '/document/limbic-system/f2a117ed-9429-441d-baa0-5e99e05722ac', 'enhancedTitle': 'Limbic System', 'entryDate': '10/20/20', 'imageCount': 29, 'imageUrl': '/image/thumbnail/b5ce3c29-7c01-4c02-9739-edac1cf33e65?size=174&quality=85', 'inCompareCart': False, 'rank': 3, 'referenceCount': 0, 'showCompareButton': False, 'title': 'Limbic System'}"
+cases: 2
+breadcrumbs:
+ - "Brain"
+ - "Diagnosis"
+ - "Pathology-Based Diagnoses"
+ - "Stroke"
+ - "Cerebral Ischemia and Infarction"
+ - "Hydranencephaly"
+---
+## KEY FACTS
+
+- ### Terminology
+
+
+ - Absence of cerebral hemispheres with intact thalamus, brainstem, cerebellum, skull/meninges
+ - Associated space filled with CSF ("water bag" brain)
+ - Probably caused by in utero vascular occlusion, infection, or trauma after 1st trimester
+- ### Imaging
+
+
+ - Absent cerebrum with fluid-filled cranial vault
+ - Thalamus, cerebellum, brainstem, falx intact
+ - Temporal, occipital lobe remnants common
+ - Macrocephaly
+- ### Top Differential Diagnoses
+
+
+ - Severe hydrocephalus
+ - Alobar holoprosencephaly (HLE)
+ - Severe bilateral open-lip schizencephaly
+ - Cystic encephalomalacia
+- ### Pathology
+
+
+ - In utero compromise of anterior cerebral circulation
+ - Implicated: Anoxia, infection, thrombophilia, maternal toxin exposure, radiation, genetic factors, twin-twin transfusion
+- ### Clinical Issues
+
+
+ - Newborn with macrocephaly, developmental failure, calvarial transillumination
+ - Hyperirritability, hyperreflexia, seizures
+ - Neurologic function limited to brainstem
+ - Prognosis: Death in infancy; prolonged survival rare
+ - Ventricular shunt treats macrocephaly
+ - Choroid plexus cauterization: Alternative treatment to shunting
+- ### Diagnostic Checklist
+
+
+ - Intact falx distinguishes hydranencephaly from alobar HLE
+ - Thin cortical mantle along inner table distinguishes severe hydrocephalus from hydranencephaly
+
+## TERMINOLOGY
+
+- ### Definitions
+
+
+ - Absence of cerebral hemispheres with intact thalamus, brainstem, cerebellum, skull/meninges
+ - Associated space filled with CSF
+ - Probably caused by in utero vascular occlusion, infection, or trauma after 1st trimester
+ - Hemihydranencephaly: Rare unilateral form
+
+## IMAGING
+
+- ### General Features
+
+
+ - #### Best diagnostic clue
+
+
+ - Absent cerebrum with fluid-filled cranial vault
+ - Falx cerebri and posterior fossa structures intact
+ - #### Location
+
+
+ - Cerebral hemispheres
+ - #### Morphology
+
+
+ - "Water bag" brain
+ - Thalamus, cerebellum, brainstem, falx intact
+ - Medial temporal, occipital lobe remnants common
+- ### CT Findings
+
+
+ - Fluid-filled cranial vault; macrocephaly
+- ### MR Findings
+
+
+ - Absent cerebral mantle
+ - Falx cerebri partially/completely intact
+ - No gliosis in remaining brain structures
+- ### Ultrasonographic Findings
+
+
+ - Anechoic cranial vault
+- ### Other Modality Findings
+
+
+ - CTA, MRA: Atretic, stenotic, occluded, malformed or normal supraclinoid carotids and branch vessels
+ - Prenatal US/MR: Severe hemorrhage may precede hydranencephaly
+- ### Imaging Recommendations
+
+
+ - #### Best imaging tool
+
+
+ - Prenatal US allows therapeutic intervention
+ - Postnatal MR best delineates extent of destruction
+
+## DIFFERENTIAL DIAGNOSIS
+
+- ### Severe Hydrocephalus
+
+
+ - Thin cortical mantle compressed against inner table
+- [Alobar Holoprosencephaly](/document/holoprosencephaly/1bec8ee3-0ffc-4d3a-9cb8-d1dadbce2878)
+ - Fused midline structures; absent falx
+- [Severe Bilateral Open-Lip Schizencephaly](/document/schizencephaly/8e4d8e67-4878-4cf2-a640-602fce63655c)
+ - Perisylvian transmantle cleft lined by abnormal gray matter
+- ### Cystic Encephalomalacia
+
+
+ - Scattered cerebral cavities, gliosis
+
+## PATHOLOGY
+
+- ### General Features
+
+
+ - #### Etiology
+
+
+ - In utero compromise of anterior cerebral circulation
+ - Brain injury results in liquefactive necrosis by 20- to 27-weeks gestation
+ - Implicated: Anoxia, infection, thrombophilic states, maternal toxin exposure, radiation, genetic factors, twin-twin transfusion
+ - *COL4A1* mutations with large prenatal hemorrhages
+ - #### Genetics
+
+
+ - Sporadic
+ - Rare autosomal recessive syndromes
+ - Fowler: Hydranencephaly, fetal akinesia, CNS vasculopathy
+ - Microhydranencephaly: Hydranencephaly, microcephaly, small body (Chr 16p13.3-12.1)
+ - #### Associated abnormalities
+
+
+ - Few reports: Vascular malformations, renal dysplasia
+- ### Gross Pathologic & Surgical Features
+
+
+ - Leptomeningeal-lined, fluid-filled "sacs" in lieu of cerebral hemispheres
+- ### Microscopic Features
+
+
+ - Hemosiderin-laden macrophages over remnant brain
+
+## CLINICAL ISSUES
+
+- ### Presentation
+
+
+ - #### Most common signs/symptoms
+
+
+ - Microcephaly (initially) with development of macrocephaly over time (poor CSF regulation)
+ - #### Other signs/symptoms
+
+
+ - Hyperirritability, hyperreflexia, seizures
+ - #### Clinical profile
+
+
+ - Newborn with microcephaly/macrocephaly, developmental failure, calvarial transillumination
+- ### Demographics
+
+
+ - Age: Diagnosis usually made in 1st few weeks of life
+ - Epidemiology: < 1:10,000 births; 10x ↑ teenage mothers
+- ### Natural History & Prognosis
+
+
+ - Neurologic function limited to brainstem
+ - Progressive hydrocephalus requiring CSF diversion
+- ### Treatment
+
+
+ - Ventriculoperitoneal shunt treats macrocephaly → microcephaly after shunting
+ - Endoscopic coagulation of choroid plexus
+
+## DIAGNOSTIC CHECKLIST
+
+- ### Image Interpretation Pearls
+
+
+ - Intact falx distinguishes hydranencephaly from alobar holoprosencephaly
+ - Thin cortical mantle along inner table distinguishes severe hydrocephalus from hydranencephaly
+
+ d7ba8237-7a34-4baa-94db-64fa77de82aa
+
+## References
+
+## Selected References
+
+1. [Egger C et al: A forensic case of hydranencephaly in a preterm neonate fully documented by postmortem imaging techniques. Forensic Sci Res. 8(1):79-83, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=37415801%5Bpmid%5D)
+1. [Huang J et al: Systematic Approach to pediatric macrocephaly. Radiographics. 43(5):e220159, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=37104125%5Bpmid%5D)
+1. [Thiong'o GM et al: Hydranencephaly treatments: retrospective case series and review of the literature. J Neurosurg Pediatr. 26(3):228-31, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32413862%5Bpmid%5D)
+1. [Omar AT 2nd et al: Hydranencephaly complicated by central diabetes insipidus: report of two cases and systematic review of literature. Childs Nerv Syst. 35(7):1165-71, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30929071%5Bpmid%5D)
+1. [Kline-Fath BM et al: Fowler syndrome and fetal MRI findings: a genetic disorder mimicking hydranencephaly/hydrocephalus. Pediatr Radiol. 48(7):1032-34, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29541808%5Bpmid%5D)
+1. [Pedrosa HAR et al: Choroid plexus cauterization on treatment of hydranencephaly and maximal hydrocephalus. Childs Nerv Syst. 33(9):1509-16, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28597309%5Bpmid%5D)
+1. [Kim SY et al: Endoscopic coagulation of choroid plexus in hydranencephaly. J Korean Neurosurg Soc. 55(6):375-8, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25237437%5Bpmid%5D)
+1. [Pavone P et al: Hydranencephaly: cerebral spinal fluid instead of cerebral mantles. Ital J Pediatr. 40(1):79, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25326191%5Bpmid%5D)
+1. [Cecchetto G et al: Looking at the missing brain: hydranencephaly case series and literature review. Pediatr Neurol. 48(2):152-8, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23337012%5Bpmid%5D)
+1. [Sepulveda W et al: Prenatal sonography in hydranencephaly: findings during the early stages of disease. J Ultrasound Med. 31(5):799-804, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22535728%5Bpmid%5D)
+1. [Meuwissen ME et al: Sporadic COL4A1 mutations with extensive prenatal porencephaly resembling hydranencephaly. Neurology. 76(9):844-6, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21357838%5Bpmid%5D)
+1. [Bae JS et al: Prolonged survival to adulthood of an individual with hydranencephaly. Clin Neurol Neurosurg. 110(3):307-9, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18222607%5Bpmid%5D)
+1. [Merker B: Life expectancy in hydranencephaly. Clin Neurol Neurosurg. 110(3):213-4, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18201820%5Bpmid%5D)
+1. [Quek YW et al: Hydranencephaly associated with interruption of bilateral internal carotid arteries. Pediatr Neonatol. 49(2):43-7, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18947016%5Bpmid%5D)
+1. [Tsai JD et al: Hydranencephaly in neonates. Pediatr Neonatol. 49(4):154-7, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=19054923%5Bpmid%5D)
+1. [Jordan L et al: CT angiography in a newborn child with hydranencephaly. J Perinatol. 24(9):565-7, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15329738%5Bpmid%5D)
+1. [Sutton LN et al: Hydranencephaly versus maximal hydrocephalus: an important clinical distinction. Neurosurgery. 6(1):34-8, 1980](http://www.ncbi.nlm.nih.gov/pubmed/?term=7354898%5Bpmid%5D)
+
+## Anatomy
+
+### Brain
+Ultrasound/ANATOMY:080771c2-02f3-408d-ad70-04a80d849500
+
+### Cerebral Hemispheres Overview
+Brain/ANATOMY:7006e397-5012-4027-aff8-e8d7158166ee
+
+### Limbic System
+Brain/ANATOMY:f2a117ed-9429-441d-baa0-5e99e05722ac
+
+## Cases
+
+- {'cases': [{'authors': [{'key': '196f55e2-14b6-4728-8de3-a59e54a37434', 'value': 'Anna Illner, MD'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '0701dbd0-52ae-4f33-a442-671861669d7e', 'description': 'Axial NECT images through the inferior brain (#1, 2) demonstrate a normal appearance of the cerebellum, midbrain and thalami (arrows, #2). More superior images (#3, 4) demonstrate near complete absence of the telencephalic structures, including most of the cerebral hemispheres and the basal ganglia. In lieu of these structures, the calvarium is filled with CSF. Note brain remnants along the falx and in the posterior parietal/occipital lobes. Sparing of the posterior parietal/occipital lobes is typical given the more common origin of the posterior cerebral arteries from the basilar artery. The posterior circulation is unaffected in hydranencephaly. A case with severe destruction of anterior circulation structures may have the clinical finding of "transillumination".', 'history': None, 'imagePoolId': '38481b5b-f421-48d5-9ad7-8cc22412ce6a', 'name': 'Parietal/occipital lobe remnants', 'teachingPoint': None, 'demographics': '1 Days old male'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '5402627f-f38c-45b3-a45c-d17f7f4bd802', 'description': 'Hydranencephaly classically shows near complete absence of the cerebral hemispheres and ventricles. The falx is present and the basal ganglia are separated. NECT scans (images 1-3) show fluid-filled cranial vault. The basal ganglia appear separated (image 1). Small bilateral parietal lobe remnants can be identified (image 2, arrows). More cephalad section (image 3) shows the falx (open arrow) surrounded by nothing but CSF.\n\nAxial T1 (image 4) and T2 weighted (image 5) MR scans show the cortical remnants (arrows). Coronal T1WIs (images 6, 7) show the basal ganglia and falx cerebri appear to "float" in the CSF-filled cranial vault.', 'history': 'Large head that transilluminates.', 'imagePoolId': 'a6c0df7c-10bf-4daf-a3ea-4e9c3b78e318', 'name': 'Classic', 'teachingPoint': None, 'demographics': '1 Days old male'}, {'authors': [{'key': '196f55e2-14b6-4728-8de3-a59e54a37434', 'value': 'Anna Illner, MD'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '9889f24b-ea01-4c28-acf7-3a3379335c94', 'description': 'Sagittal T1W MR (#1) demonstrates the classic appearance of hydranencephaly. The brainstem and cerebellum are normal. There is conspicuous absence of the majority of the supratentorial brain with few basilar lobar remnants identified. The cranial vault appears somewhat expanded by CSF causing mild downward mass effect onto the brainstem. Coronal T1 and T2W MR (#2, 3, arrows) again demonstrate the CSF-filled, mildly expanded cranial vault. The majority of infants with hydranencephaly have macrocranium secondary to preservation of the choroid plexus which continues to secrete CSF. Shunting typically prevents gross head enlargement. Note complete lack of brain tissue along the inner table and falx allowing differentiation from severe hydrocephalus. Intact anterior and posterior falx (#4, arrows) allows differentiation from alobar holoprosencephaly.', 'history': None, 'imagePoolId': 'ef77010c-7dc9-4fd7-af6a-dd6d5c9aaab7', 'name': 'Classic', 'teachingPoint': None, 'demographics': '1 Years old female'}, {'authors': [{'key': '196f55e2-14b6-4728-8de3-a59e54a37434', 'value': 'Anna Illner, MD'}], 'caseVersionId': 'f72ca192-aaa7-4709-a729-3802e56b8f90', 'description': 'Sagittal and axial T1W images (#1-4) demonstrate typical findings of hydranencephaly. The brain has a "water bag" appearance with no identifiable cerebral hemispheres superiorly (#4). More inferiorly, posterior circulation remnants, left temporal lobe, thalami, brainstem and cerebellum are identified (#1-3). Note the diminutive appearance of the brainstem (arrow, #2) secondary to Wallerian degeneration. The "water bag brain" differential diagnosis includes hydranencephaly, alobar holoprosencephaly and severe hydrocephalus. Normal separation of midline structures and intact falx cerebri (#4) distinguish hydranencephaly from alobar holoprosencephaly. Lack of cortical mantle adjacent to inner table and falx (#4) distinguish hydranencephaly from severe hydrocephalus. Hydranencephalic patients typically have brainstem function only and survival beyond infancy, as in this is case, is very unusual. This rare disorder may be caused by hereditary thrombophilic states, intrauterine infection, and intrauterine anoxia or hypoperfusion states. It is a component of Fowler sequence with associated CNS vasculopathy.', 'history': 'Left on doorstep as newborn, parents never found. Severe neurological delay. EEG shows "no brain function". Alive at age 22.', 'imagePoolId': '62b0beee-936a-4f4d-a7ec-d4a635b7a7ce', 'name': 'Prolonged survival', 'teachingPoint': None, 'demographics': '22 Years old female'}], 'caseType': 'typical', 'name': 'TYPICAL'}
+- {'cases': [{'authors': [{'key': '196f55e2-14b6-4728-8de3-a59e54a37434', 'value': 'Anna Illner, MD'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '8cea00e8-7add-4707-8091-d7ce44f2bed2', 'description': 'Hemihydranencephaly is a rare variant of hydranencephaly caused by unilateral ICA disruption. The result is unilateral cerebral hemispheric destruction. Axial T1 and T2W MR images (#1-5) demonstrate conspicuous lack of much of the right cerebral hemisphere. Similar to hydranencephaly, brain remnants are often identified in the spared posterior circulation (#1, 3, 4, arrows). In contrast to hydranencephaly, brain remnants can also be identified in the distribution of the anterior and even middle cerebral artery secondary to cross-fill from the normal contralateral ICA branches (#3, open arrow). As with hydranencephaly, macrocranium is frequent secondary to persistent CSF secretion on the affected side from intact choroid plexus. In hemihydranencephaly, this manifests as unilateral cranial vault bulging (#2, 5) and compression of the contralateral hemisphere.', 'history': None, 'imagePoolId': '40644625-4a85-4fd4-a9ad-817571e33e36', 'name': 'Hemihydranencephaly', 'teachingPoint': None, 'demographics': '8 Years old male'}, {'authors': [{'key': '99e1aff7-f42c-43a0-95ae-d89c8551aa01', 'value': 'Kevin R. Moore, MD'}], 'caseVersionId': 'ecd4e059-3e9e-4354-951f-e3fc8b2d06a7', 'description': 'Case of hydranencephaly with minimal residual cortex. Anterior cortical remnant present, typically even that is absent.\n\nFour sequential axial NECT of the brain (#1-4) from caudal to rostral demonstrate only a small incomplete rim of cortex in the frontal and occipital poles. There is preservation of the posterior fossa and diencephalon structures supplied by the posterior cerebral circulation. A single posterior ventricular catheter was placed to control CSF accumulation (arrow, #3). Hydranencephaly may be sporadic or syndromic. Hereditary thrombophilic states and intrauterine ICA compromise should also be considered.', 'history': 'Patient with severe developmental delay who is nonverbal presents with increasing agitation for possible ventriculoperitoneal shunt failure. ', 'imagePoolId': 'd1531fa5-384c-43f0-827e-81001ad04173', 'name': 'Minimal residual cortex', 'teachingPoint': None, 'demographics': '1 Years old male'}], 'caseType': 'variant', 'name': 'VARIANT'}
+
+
+## Images
+
+
+### Selected Images
+
+
+*Coronal graphic shows the classic features of hydranencephaly. The cerebral hemispheres are nearly absent, but the thalami, brainstem, and cerebellum are intact. The falx cerebri appears to float in a CSF-filled rostral cranial vault.*
+
+
+*Coronal graphic shows the classic features of hydranencephaly. The cerebral hemispheres are nearly absent, but the thalami, brainstem, and cerebellum are intact. The falx cerebri appears to float in a CSF-filled rostral cranial vault.*
+
+
+*Coronal ultrasound in a newborn with hydranencephaly shows near-complete absence of the cerebral hemispheres with residual brainstem, thalami , and cerebellum supplied by the vertebrobasilar system. Note the presence of the falx .*
+
+
+*Axial T2 MR in a 1-month-old shows complete absence of brain parenchyma supplied by the internal carotid artery (ICA) with preservation of brain supplied by the vertebrobasilar system (thalami and posterior cerebral artery territories ).*
+
+
+*Sagittal T2 MR in the same patient shows absence of the brain parenchyma in the ICA territories and preservation of occipital lobes , brainstem , and cerebellum in the posterior cerebral artery territory. Note the macrocephaly, a common feature in hydranencephaly.*
+
+
+### Additional Images
+
+
+*Axial T2 MR in a 4-year-old with hydranencephaly shows complete absence of brain parenchyma supplied by the ICA with preservation of brain supplied by the vertebrobasilar system (thalami and posterior cerebral artery territories ).*
+
+
+*Coronal T2 MR in a 2-day-old with hydranencephaly shows near-complete absence of the cerebral hemispheres with a small amount of residual inferior temporal lobes & thalami supplied by the vertebrobasilar system. Note the presence of the falx .*
+
+
+*Axial NECT shows near-complete absence of the cerebral hemispheres and ventricles with small bilateral parietal lobe remnants . The falx cerebri is thin (no adjacent brain) but intact.*
+
+
+*Axial NECT shows only thalami, brainstem, cerebellum, and inferior temporal lobe remnants ; CSF fills the remaining cranial vault. Note a shunt catheter in the right subcutaneous tissue.*
+
+
+*Lateral CT scout shows the macrocranium and shunt catheter in an infant with hydranencephaly.*
+
+
+*Axial NECT shows cerebral hemispheres replaced by CSF with no cortical mantle appreciated except in the medial temporal lobes . The posterior fossa and diencephalic structures supplied by the posterior cerebral circulation are intact.*
+
+
+*Coronal T1 MR in the same patient shows the expanded, CSF-filled spaces with only tiny amounts of residual brain . Note that the CSF appears somewhat heterogeneous due to pulsation. (Courtesy A. Illner, MD.)*
+
+
+*Sagittal T1 MR in a newborn with macrocephaly shows hydranencephaly. No cortical mantle is visible. CSF fills virtually all of the expanded supratentorial spaces. The brainstem and cerebellum appear normal.*
+
+
+*Axial T2 MR of hemihydranencephaly shows a CSF-filled right hemicranium with a small occipital lobe remnant . This rare variant occurs from unilateral ICA compromise. As with hydranencephaly, a cortical mantle cannot be identified.*
+
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+---
+title: "Lacunar Infarction"
+docid: "03672bd8-67c2-4d2c-96fd-c21347f28cce"
+authors:
+ - key: "2bca6b86-1eca-4e93-b997-4e18913686a7"
+ value: "Hediyeh Baradaran, MD, MS"
+ - key: "8d5254e9-8dda-478b-8f08-bdee97a32c79"
+ value: "Karen L. Salzman, MD, FACR"
+breadcrumbs:
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+cases: 2
+breadcrumbs:
+ - "Brain"
+ - "Diagnosis"
+ - "Pathology-Based Diagnoses"
+ - "Stroke"
+ - "Cerebral Ischemia and Infarction"
+ - "Lacunar Infarction"
+---
+## KEY FACTS
+
+- ### Terminology
+
+
+ - Small, deep cerebral infarcts located in basal ganglia and thalamus, pons, or cerebral white matter (WM), ≤ 15 mm
+- ### Imaging
+
+
+ - Commonly deep gray nuclei, especially putamen, thalamus, caudate nuclei; internal capsule, pons
+ - Other locations include deep and periventricular WM
+ - Range in size from microscopic to 15 mm
+ - Because of small size, most acute lacunar infarcts are not seen on CT scans
+ - Acute: T2/FLAIR ↑ signal
+ - Chronic: FLAIR central low signal with ↑ peripheral signal (gliosis)
+ - DWI: Restricted diffusion (hyperintense) if acute/subacute
+ - May show small lesions otherwise undetectable
+ - Prominent perivascular spaces are main imaging differential diagnosis
+- ### Pathology
+
+
+ - Embolic, atheromatous, or thrombotic lesions in long, single penetrating end arterioles supplying deep cerebral gray matter
+ - Size of lacunar infarct depends on level of occlusion and anatomy of affected vessel
+- ### Clinical Issues
+
+
+ - Many different presentations, depending on size, location, number
+ - Most lacunar infarctions are clinically "silent," often subtle neurologic deficits that may go unnoticed by patient and physician
+ - Typical risk factors for cerebrovascular disease: Hypertension, diabetes, smoking history, obesity, hypercholesterolemia, etc.
+ - Lacunar infarcts account for up to 25% of all strokes
+ - Lacunar stroke is most common stroke subtype associated with vascular dementia
+
+## TERMINOLOGY
+
+- ### Synonyms
+
+
+ - Lacunar infarction (LI), lacunar stroke
+ - Lacunes
+- ### Definitions
+
+
+ - Small, deep cerebral infarcts typically located in basal ganglia (BG) and thalamus, pons, or cerebral white matter (WM), ≤ 15 mm in size
+ - From Latin word lacuna, meaning hole
+ - Used to describe small focus of encephalomalacia
+ - L'état lacunaire or lacunar state = multifocal BG lacunar infarcts with surrounding gliosis
+
+## IMAGING
+
+- ### General Features
+
+
+ - #### Best diagnostic clue
+
+
+ - Small, well-circumscribed areas of parenchymal abnormality (encephalomalacia) in BG, thalamus, WM
+ - #### Location
+
+
+ - Commonly deep gray nuclei, especially putamen, thalamus, caudate nuclei; internal capsule, pons
+ - Can be in other locations
+ - Cerebral WM in patients > 65 years
+ - Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) characteristically has subcortical lacunar infarcts
+ - #### Size
+
+
+ - Commonly 3-15 mm
+ - Majority < 8 mm
+ - #### Morphology
+
+
+ - Typically round or ovoid
+- ### CT Findings
+
+
+ - #### NECT
+
+
+ - When small, may not be seen on CT
+ - Small, well-circumscribed areas of low (CSF) attenuation
+ - Usually seen in setting of more extensive WM disease; often multiple
+ - #### CECT
+
+
+ - May enhance if late acute/early subacute
+- ### MR Findings
+
+
+ - #### T1WI
+
+
+ - Small, well-circumscribed, hypointense foci
+ - #### T2WI
+
+
+ - Small, well-circumscribed, hyperintense foci
+ - #### FLAIR
+
+
+ - Acute: ↑ signal
+ - Chronic: Central cystic portion suppresses (low signal) with ↑ peripheral signal (gliosis)
+ - #### DWI
+
+
+ - Restricted diffusion (hyperintense) if acute/subacute
+ - May show lesions not seen on standard sequences
+ - #### PWI
+
+
+ - Abnormal PWI seen in 2/3 of cases
+ - #### T1WI C+
+
+
+ - May enhance if late acute/early subacute
+ - #### MRA
+
+
+ - May be normal
+- ### Imaging Recommendations
+
+
+ - #### Best imaging tool
+
+
+ - NECT for chronic lacunes; MR with DWI for acutely symptomatic patient
+ - MR better to distinguish lacunar infarcts from perivascular spaces
+ - #### Protocol advice
+
+
+ - MR with DWI if acute
+
+## DIFFERENTIAL DIAGNOSIS
+
+- [Prominent Perivascular Spaces](/document/enlarged-perivascular-spaces/24c4b347-098b-48a2-9ff9-2b4ed9563cf8)
+ - Normal variant resulting from accumulation of interstitial fluid within enlarged Virchow-Robin spaces
+ - Found in all areas but tend to cluster around anterior commissure and in cerebral WM
+ - Similar to CSF signal on all pulse sequences
+ - Found in patients of all ages
+ - ↑ in size and frequency with advancing age
+ - Up to 25% have slight halo of ↑ signal on FLAIR or T2WI
+ - Can expand, occur in clusters (mimic neoplasm)
+- [État Criblé](/document/enlarged-perivascular-spaces/24c4b347-098b-48a2-9ff9-2b4ed9563cf8)
+ - Multiple, enlarged Virchow-Robin spaces most commonly in BG
+ - Blood vessels in état criblé are thickened, ectatic, with sclerotic walls
+ - Perivascular tissues may show reactive astrocytosis and isomorphic gliosis with glial fibers extending along degenerated axons
+- [Neurocysticercosis](/document/neurocysticercosis/fc7b01a2-45a4-432a-ad8e-c6bd999fa20a)
+ - May mimic benign intraparenchymal cysts
+ - Imaging findings vary with developmental stage of cyst as well as host response
+ - Solitary in 20-50%; when multiple, usually small number of cysts
+ - Inflammatory response around cyst may seal sulcus, making lesions appear intraaxial
+
+## PATHOLOGY
+
+- ### General Features
+
+
+ - #### Etiology
+
+
+ - Embolic, atheromatous, or thrombotic lesions in long, single penetrating end arterioles supplying deep cerebral gray matter and WM
+ - Size of LI depends on level of occlusion and anatomy of affected vessel
+ - Some studies suggest chronic endothelial dysfunction in cerebral small vessel disease and LI
+ - Subtle WM blood-brain barrier dysfunction in patients with LI but not with cortical ischemic strokes
+ - Endothelial prothrombotic changes may be important in mediating ischemic leukoaraiosis phenotype
+ - #### Genetics
+
+
+ - Usually sporadic
+ - May occur secondary to genetic disorder CADASIL
+ - CADASIL has been linked to mutation in *NOTCH3*gene locus (chromosome 19); genetic testing available for clinical diagnosis
+ - #### Associated abnormalities
+
+
+ - Most LIs are clinically "silent," often subtle neurologic deficits that may go unnoticed by patient and physician
+ - Small vessel cerebrovascular disease is important vascular cause of cognitive impairment
+ - **St**andards for **R**eport**I**ng **V**ascular changes on n**E**uroimaging (**STRIVE**)
+- ### Gross Pathologic & Surgical Features
+
+
+ - Similar to other types of cerebral infarction
+ - Earliest visible change is slight discoloration and softening of affected area
+ - Gray matter structures become blurred, and WM loses its normal fine-grained appearance
+ - Within 48-72 hours necrosis is well established and there is softening, disintegration of ischemic area with circumlesional swelling
+ - As resolution proceeds, liquefaction results in cyst formation; more apparent in lesions of larger size
+ - Cysts may be traversed by trabeculations of blood vessels and are surrounded by firm glial tissue
+- ### Microscopic Features
+
+
+ - Gliosis along margin of infarction
+ - Hypertensive hyalinization of supplying arterioles
+ - Pigmented macrophages can be found in some lacunes, suggesting possible hemorrhagic component
+
+## CLINICAL ISSUES
+
+- ### Presentation
+
+
+ - #### Most common signs/symptoms
+
+
+ - Many different presentations, depending on size, location, number
+ - Variable symptoms, ranging from clinically "silent" to focal neurologic deficit to cognitive impairment to dementia
+ - In study of patients ≥ 65 years, 23% had isolated lacunar infarcts
+ - 66% of these were single, 89% clinically silent
+ - Significant correlation between pure motor strokes and presence of LI in internal capsule
+ - ~ 1/4 of patients with classic lacunar syndrome have nonlacunar infarcts on MR
+ - Responsible LI seen in ~ 60% of cases in lacunar syndromes
+ - Symptoms depend on location of lacune
+ - Vascular lesions within thalami may produce "vascular syndromes" (sensorimotor and behavioral syndromes) depending on which nuclei are involved
+ - Reflect reciprocal cerebral cortical-thalamic connections that have been interrupted
+ - Tuberothalamic territory strokes produce impairments of arousal, orientation, learning, memory, personality, and executive function; superimposition of temporally unrelated information; emotional facial paresis
+ - Paramedian thalamic infarcts cause ↓ arousal (particularly if bilateral), impaired learning and memory
+ - Left paramedian and left tuberothalamic lesions that include ventrolateral nucleus result in language deficits
+ - Right thalamic lesions in both these vascular territories produce visual-spatial deficits, including hemispatial neglect
+ - Inferolateral territory strokes produce contralateral hemisensory loss, hemiparesis, hemiataxia, and pain syndromes; more common after right thalamic lesions
+ - Posterior choroidal lesions result in visual field deficits, variable sensory loss, weakness, dystonia, tremors, occasionally amnesia and language impairment
+ - #### Clinical profile
+
+
+ - Older adults, hypertensive patient
+ - Typical risk factors for cerebrovascular disease: Hypertension (HTN), diabetes (DM), smoking history, obesity, hypercholesterolemia, etc.
+- ### Demographics
+
+
+ - #### Age
+
+
+ - Usually > 55 years, prevalence ↑ with age
+ - Patients with coronary artery or peripheral vascular disease are at risk for infarcts at younger age
+ - Patients with CADASIL present earlier, with TIA/stroke-like symptoms, beginning at ~ 45 years; cognitive decline can start as early as age 35 years
+ - #### Sex
+
+
+ - Not specific
+ - #### Epidemiology
+
+
+ - Lacunar infarcts account for up to 25% of all strokes
+ - Strong association with systemic hypertension
+ - Lacunar stroke is most common stroke subtype associated with vascular dementia
+ - Statistically significant incidence of isolated ipsilateral carotid stenosis in patients with LI located in carotid territory
+- ### Natural History & Prognosis
+
+
+ - Clinically "silent" to focal neurologic deficit
+ - HTN and DM are significant risk factors for recurrent LI
+ - Many patients with LI have good functional outcomes after 5 years
+ - ↑ risk of mortality, stroke recurrence, physical and cognitive decline with initial severe strokes and additional vascular risk factors
+ - **Early** mortality and stroke recurrence less common than nonlacunar infarcts; no difference after 1 month
+ - Silent infarcts more than double risk of subsequent strokes and dementia
+ - Presence of multiple LIs may be important prognostic indicator both for functional recovery as well as higher rate of recurrence
+- ### Treatment
+
+
+ - Typical treatment is targeted toward underlying etiology of vasculopathy
+ - More studies on mechanisms, prevention, and treatment are needed to provide specific guidance on long-term management of LI patients
+ - Risk-factor modification is likely to play large part in therapeutic interventions targeted at this stroke subtype
+
+## DIAGNOSTIC CHECKLIST
+
+- ### Consider
+
+
+ - Are lacunes really enlarged Virchow-Robin spaces
+ - Is there treatable embolic source
+- ### Image Interpretation Pearls
+
+
+ - To be classified as LI, location must be end-artery territory and lesion must be smaller than 15 mm
+
+ 64442d6a-1ea0-4fea-83c9-e538f9486441
+
+## References
+
+## Selected References
+
+1. [Grosset L et al: MRI-proven incident ischemia: a new marker of disease progression in small vessel diseases. Stroke. 56(1):39-45, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=39569496%5Bpmid%5D)
+1. [Hassani S et al: MRI predictors of cognitive function after lacunar infarction. Stroke. 56(7):1722-9, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=40365674%5Bpmid%5D)
+1. [Hainsworth AH et al: Cerebral small vessel disease, hypertension, and vascular contributions to cognitive impairment and dementia. Hypertension. 81(1):75-86, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38044814%5Bpmid%5D)
+1. [Koohi F et al: Does thrombosis play a causal role in lacunar stroke and cerebral small vessel disease? Stroke. 55(4):934-2, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38527140%5Bpmid%5D)
+1. [Markus HS et al: Cerebral small vessel disease: recent advances and future directions. Int J Stroke. 18(1):4-14, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=36575578%5Bpmid%5D)
+1. [Anand SS et al: Reduced cognitive assessment scores among individuals with magnetic resonance imaging-detected vascular brain injury. Stroke. 51(4):1158-65, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32126938%5Bpmid%5D)
+1. [Finn C et al: The association between carotid artery atherosclerosis and silent brain infarction: a systematic review and meta-analysis. J Stroke Cerebrovasc Dis. 26(7):1594-601, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28318958%5Bpmid%5D)
+1. [Gupta A et al: Silent brain infarction and risk of future stroke: a systematic review and meta-analysis. Stroke. 47(3):719-25, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=26888534%5Bpmid%5D)
+1. [Dhamoon MS et al: Long-term disability after lacunar stroke: secondary prevention of small subcortical strokes. Neurology. 84(10):1002-8, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25663222%5Bpmid%5D)
+1. [Sandset EC et al: Effects of blood pressure-lowering treatment in different subtypes of acute ischemic stroke. Stroke. 46(3):877-9, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25657183%5Bpmid%5D)
+1. [Hart RG et al: Predictors of stroke recurrence in patients with recent lacunar stroke and response to interventions according to risk status: secondary prevention of small subcortical strokes trial. J Stroke Cerebrovasc Dis. 23(4):618-24, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=23800503%5Bpmid%5D)
+1. [Kitagawa K et al: Association between carotid stenosis or lacunar infarction and incident dementia in patients with vascular risk factors. Eur J Neurol. 22(1):187-92, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25164480%5Bpmid%5D)
+1. [Palacio S et al: Lacunar strokes in patients with diabetes mellitus: risk factors, infarct location, and prognosis: the secondary prevention of small subcortical strokes study. Stroke. 45(9):2689-94, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25034716%5Bpmid%5D)
+1. [Staals J et al: Stroke subtype, vascular risk factors, and total MRI brain small-vessel disease burden. Neurology. 83(14):1228-34, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25165388%5Bpmid%5D)
+1. [Poppe AY et al: Normal magnetic resonance perfusion-weighted imaging in lacunar infarcts predicts a low risk of early deterioration. Cerebrovasc Dis. 28(2):151-6, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19546542%5Bpmid%5D)
+1. [Wardlaw JM et al: Lacunar stroke is associated with diffuse blood-brain barrier dysfunction. Ann Neurol. 65(2):194-202, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19260033%5Bpmid%5D)
+1. [De Reuck J et al: The classic lacunar syndromes: clinical and neuroimaging correlates. Eur J Neurol. 15(7):681-4, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18452543%5Bpmid%5D)
+1. [Arboix A et al: Recurrent lacunar infarction following a previous lacunar stroke: a clinical study of 122 patients. J Neurol Neurosurg Psychiatry. 78(12):1392-4, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17615167%5Bpmid%5D)
+1. [Vermeer SE et al: Silent brain infarcts: a systematic review. Lancet Neurol. 6(7):611-9, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17582361%5Bpmid%5D)
+1. [Appelros P et al: Lacunar infarcts: functional and cognitive outcomes at five years in relation to MRI findings. Cerebrovasc Dis. 20(1):34-40, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=15942172%5Bpmid%5D)
+1. [Jackson C et al: Are lacunar strokes really different? A systematic review of differences in risk factor profiles between lacunar and nonlacunar infarcts. Stroke. 36(4):891-901, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=15761206%5Bpmid%5D)
+1. [Arboix A et al: New concepts in lacunar stroke etiology: the constellation of small-vessel arterial disease. Cerebrovasc Dis. 17 Suppl 1:58-62, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14694281%5Bpmid%5D)
+1. [Giele JL et al: Silent brain infarcts in patients with manifest vascular disease. Stroke. 35(3):742-6, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14963273%5Bpmid%5D)
+1. [Lee SH et al: Comparative analysis of the spatial distribution and severity of cerebral microbleeds and old lacunes. J Neurol Neurosurg Psychiatry. 75(3):423-7, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14966159%5Bpmid%5D)
+1. [Aharon-Peretz J et al: Progression of dementia associated with lacunar infarctions. Dement Geriatr Cogn Disord. 16(2):71-7, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12784030%5Bpmid%5D)
+1. [O'Sullivan M et al: Frequency of subclinical lacunar infarcts in ischemic leukoaraiosis and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. AJNR Am J Neuroradiol. 24(7):1348-54, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12917126%5Bpmid%5D)
+1. [Schmahmann JD: Vascular syndromes of the thalamus. Stroke. 34(9):2264-78, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12933968%5Bpmid%5D)
+1. [Tejada J et al: Does a relationship exist between carotid stenosis and lacunar infarction? Stroke. 34(6):1404-9, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12738897%5Bpmid%5D)
+1. [Vermeer SE et al: Silent brain infarcts and the risk of dementia and cognitive decline. N Engl J Med. 348(13):1215-22, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12660385%5Bpmid%5D)
+1. [Longstreth WT Jr et al: Lacunar infarcts defined by magnetic resonance imaging of 3660 elderly people: the Cardiovascular Health Study. Arch Neurol. 55(9):1217-25, 1998](http://www.ncbi.nlm.nih.gov/pubmed/?term=9740116%5Bpmid%5D)
+
+## Anatomy
+
+### White Matter Tracts
+Brain/ANATOMY:846101a2-e892-4c70-9a32-c9fa887d073a
+
+### Basal Ganglia
+Brain/ANATOMY:a9de3815-ec59-4c78-adf0-94974065a7e3
+
+### Language Overview
+Brain/ANATOMY:40f2ed79-0d31-4943-aaa2-7c3244a7e87b
+
+### Limbic Network
+Brain/ANATOMY:e1a20b61-b2c1-44c5-ba04-59843855bfef
+
+### Brainstem Overview
+Brain/ANATOMY:bf889ffb-646b-429d-8699-d9bd34e8e193
+
+### Cerebellar Overview
+Brain/ANATOMY:b624e76f-15b9-4c1f-910e-8f5581ac2cfe
+
+### Pons
+Brain/ANATOMY:fc185efd-1f7a-4804-95f6-a49d0fa8aefb
+
+### Cerebellum
+Brain/ANATOMY:277bd2bc-3694-4712-a040-f69956b0b4ff
+
+### Brain
+Ultrasound/ANATOMY:080771c2-02f3-408d-ad70-04a80d849500
+
+## Cases
+
+- {'cases': [{'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'f2d2f750-602c-40b4-82c3-2dd2588aa42a', 'description': 'Sagittal T1WI (#1) shows well-delineated hypointense thalamic lesion (arrow). Axial T2WIs (#2,3) show lesion is hyperintense (arrows) and does not bloom on GRE (arrow, #4), indicating no hemorrhage. Lesion does not enhance on T1C+ studies (arrows, #5,6).\n\nComment: MR is "supernormal" for 71 year old patient except for the chronic solitary lacune. Unfortunately, its position is exactly "right" for causing Parkinson-like tremors.', 'history': 'Right >> left upper extremity tremor. Otherwise normal neurological examination.', 'imagePoolId': 'd9cfcd0d-c541-433d-98e2-02d243967ada', 'name': 'Solitary subthalamic lacune', 'teachingPoint': None, 'demographics': '71 Years old male'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '8b1c6a6c-83e0-4f2e-b31e-a459d6172ca2', 'description': 'Typical MR case of an acute lacunar infarction involving the corticospinal tract in the internal capsule and cerebral peduncle.\n\nAxial T2 and FLAIR MR images (#1-2) show abnormal hyperintensity within the left cerebral peduncle (curved arrow) involving the corticospinal tract. There is mild associated expansion of the left cerebral peduncle. DWI MR images (#3-4) show diffusion restriction in the left cerebral peduncle (curved arrow) and internal capsule (arrow) indicating this is an acute lacunar infarct.\n\nComment: Lacunar infarctions typically occur in the deep gray nuclei, specifically the basal ganglia and thalamus, and account for up to 20% of all strokes.', 'history': 'Patient with acute onset of left sided weakness.', 'imagePoolId': '2d0cea85-2d45-48fa-87ea-801537f13c80', 'name': 'Acute, cerebral peduncle, DWI', 'teachingPoint': None, 'demographics': '60 Years old male'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'd50767bf-1a4d-4013-9616-76c1904680d1', 'description': 'Typical MR case of an acute periventricular white matter lacunar infarction with DWI.\n\nAxial FLAIR MR image (#1) shows multiple nonspecific periventricular and subcortical white matter hyperintensities. In a patient of this age, they are likely related to chronic small vessel ischemia. Axial DWI MR (#2) image shows one of these lesions is an acute lacunar infarction. DWI allows identification of the acute lesion from the surrounding chronic disease.\n\nComment: Lacunar infarcts are more common in patients with hypertension and are associated with vascular dementia.', 'history': None, 'imagePoolId': '2d43f81c-3822-4aa0-8532-06261b5337a2', 'name': 'Acute, periventricular, DWI', 'teachingPoint': None, 'demographics': '83 Years old female'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '081eaf34-07af-4979-a2d9-aad5ce630b07', 'description': 'Typical MR case of an acute, embolic lacunar infarction in the periventricular white matter with DWI images.\n\nAxial DWI MR images (#1-2) show focal restricted diffusion in the periventricular white matter (arrows) related to an acute lacunar infarct. Axial T2 and FLAIR MR images (#3-6) show very subtle increased signal in the area of DWI signal abnormality (curved arrows) indicating this is an acute infarct. Without DWI images, the acute lacunar infarct would be indistinguishable form the other chronic white matter disease.', 'history': 'Unknown.', 'imagePoolId': 'e0278b82-d35b-4a82-a5a5-029843da5bc2', 'name': 'Acute, embolic, periventricular, DWI', 'teachingPoint': None, 'demographics': '52 Years old female'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '40c0101d-49c1-43ad-ada1-b041cd18c2c4', 'description': 'Typical MR case of a hyperacute lacunar infarct in the periventricular white matter seen only on DWI image.\n\nAxial T2 (#1) and FLAIR (#2) MR images show nonspecific periventricular hyperintensity (arrows), likely related to chronic small vessel disease in this patient with hypertension. Axial DWI (#3) image shows a focal ovoid area of diffusion restriction in the periventricular white matter (open arrow). This focal abnormality is related to a hyperacute lacunar infarct which is less than 6 hours old, as it is only seen on DWI images.', 'history': 'Patient with hypertension and acute onset of neurologic symptoms.', 'imagePoolId': 'd31e3b21-2d24-4045-b402-75a69603e939', 'name': 'Hyperacute, periventricular, DWI', 'teachingPoint': None, 'demographics': '65 Years old female'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}], 'caseVersionId': '2c5a1d8c-a182-4b39-b711-65b39cfc576a', 'description': "Typical MR case of an acute thalamic lacunar infarct with DWI.\n\nAxial FLAIR and T2 MR images (#1-2) show a focal small, less than 1 cm, hyperintensity within the right thalamus (arrows). Note the abnormal periventricular hyperintensity related to the patient's small vessel ischemia (open arrows). DWI (#3) shows restricted diffusion confirming the acute nature of this lacunar infarct (curved arrow). The MRA image (#4) of the right carotid is normal which is common in patient's with acute lacunar infarcts.", 'history': 'Patient with acute onset of focal neurologic deficit.', 'imagePoolId': '96084d71-beea-4b00-873d-d9f3ce03b2a9', 'name': 'Acute, DWI', 'teachingPoint': None, 'demographics': '70 Years old male'}], 'caseType': 'typical', 'name': 'TYPICAL'}
+- {'cases': [{'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '0c72ab91-8d32-46a2-8f84-09a54206ce1c', 'description': 'Series of axial T2WIs (#1-5) shows large left cerebellar territorial infarct (arrow, #1), midbrain infarct (arrow, #2), infarcts in both medial thalami (arrows, #3,4), as well as several cortical infarcts (open arrows, #2-5). The lesions all show acute restriction on DWI (#6-10). Note lesion in left cerebral hemisphere (curved arrow, #10) that was inapparent on the T2WI (#5). \n\nComment: Multiple embolic infarcts from cardiac thrombus was diagnosed. The central midbrain lesion and bilateral medial thalamic infarcts are classic for so-called "artery of Percheron" infarction. In this rare infarct, a single dominant perforating artery (the artery of Percheron) arises from the top of the basilar artery and supplies the midbrain and medial thalami (multiple small thalamoperforating arteries are the common vascular pattern in this area).', 'history': 'Multiple embolic infarcts following anterior wall myocardial infarction.', 'imagePoolId': '7e8ed955-5d20-4232-9e32-9b5d79b87305', 'name': 'Also bilateral thalamic infarcts', 'teachingPoint': None, 'demographics': '45 Years old male'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '94970483-3120-4afb-b11b-e5b203aa11d0', 'description': 'Sagittal, coronal T1WIs (#1-3) show multifocal lacunar infarcts in deep cerebral white matter, basal ganglia (arrows). Note that thalamic pulvinar is well seen (#1) and appears normal. T2WIs (#4-11) show multifocal discrete and confluent white matter hyperintensities in cerebellum, basal ganglia, and deep cerebral white matter (arrows). T2* GRE scans (#12-18) show multiple blooming foci in the pons, cerebellum and basal ganglia (arrows), with very few lesions in centrum semiovale or cortex. MRA (#19) shows major vessels are normal (left transverse sinus is hypoplastic).\n\nComment: The multiple lacunar infarcts are characteristic for Fabry disease. Whether the multiple hypointensities on GRE are caused by the microvasculopathy of Fabry disease or are secondary to hypertension is unclear. Fabry disease does cause cerebral hemorrhages and this patient never had severe hypertension.', 'history': 'Has had "abnormal spots" on hands, abdomen since age 10 years, called HHT by a number of physicians. No epistaxis or migraines. Had a brother who died in his 40\'s with "some type of heart disease." Has renal disease for which he had a cadaveric renal transplant 20 years ago and has done well. Treated for hypertension with persisting mildly elevated BP. No history of MI or stroke.\n\nPhysical examination disclosed numberous punctate lesions from umbilicus to groin and on both hands. Lesions are flat, tiny red lesions not typical for HHT. Dermatology consult confirmed Fabry\'s disease.', 'imagePoolId': '23afa666-de7a-4d11-a9ac-599961958f0d', 'name': 'Multiple lacunes, black dots on GRE', 'teachingPoint': None, 'demographics': '50 Years old male'}], 'caseType': 'variant', 'name': 'VARIANT'}
+
+
+## Images
+
+
+### Selected Images
+
+
+*Axial graphic illustrates numerous bilateral lacunar infarcts within the thalami and basal ganglia , the most common locations. Also shown are prominent perivascular (Virchow-Robin) spaces , a common normal variant.*
+
+
+*Axial graphic illustrates numerous bilateral lacunar infarcts within the thalami and basal ganglia , the most common locations. Also shown are prominent perivascular (Virchow-Robin) spaces , a common normal variant.*
+
+
+*Axial FLAIR MR shows multiple chronic lacunar infarcts bilaterally with central T2-/FLAIR-hypointense encephalomalacia and mild peripheral hyperintense gliosis. Lacunar infarctions are often seen in older patients with chronic hypertension.*
+
+
+*Axial DWI MR shows focal diffusion trace hyperintensity in the right thalamus, a common location for lacunar infarcts. Risk factors for lacunar infarcts include older age, hypertension, diabetes, smoking history, obesity, and hypercholesterolemia.*
+
+
+*Axial FLAIR MR shows a chronic lacunar infarct in the right thalamus with central encephalomalacia and mild peripheral gliosis. The surrounding gliosis and typical location can help differentiate a chronic lacunar infarct from a perivascular space.*
+
+
+*Axial FLAIR MR shows extensive confluent white matter signal abnormality related to chronic small vessel ischemia (arteriolosclerosis). There are also multiple chronic lacunar infarcts in this young adult with CADASIL.*
+
+
+*Axial DWI MR shows hyperintensity related to an acute lacunar infarct involving the posterior limb of the right internal capsule. While the majority of lacunar infarcts are clinically "silent," infarcts in this location have a high association with motor deficits.*
+
+
+*Axial FLAIR MR shows multiple remote lacunar infarctions in this patient with a background of extensive white matter hyperintensities of presumed vascular origin.*
+
+
+*Axial FLAIR MR shows multiple lacunar infarctions in the deep periventricular white matter . This patient was completely asymptomatic without known neurologic deficits or prior events.*
+
+
+*Axial T2 MR shows a classic appearance of multiple chronic lacunar infarcts in the basal ganglia, the most common location for this type of infarct. Note the bilateral involvement of the caudate heads and the left putamen .*
+
+
+*This 66-year-old woman with longstanding hypertension presented with acute right-sided paresthesias. DWI shows focal restricted diffusion (ADC not shown) in the left thalamus , consistent with acute lacunar infarct.*
+
+
+### Additional Images
+
+
+*Axial DWI MR shows acute, moderate to large lacunar infarction in right caudate head and anterior internal capsule .*
+
+
+*Axial FLAIR MR shows an acute lacunar infarct in the caudate body which was DWI positive (not shown), and Virchow-Robin spaces .*
+
+
+*Axial FLAIR MR shows multiple subcortical and periventricular hyperintense lesions. FLAIR imaging alone cannot distinguish the acute lesion from surrounding chronic lesions.*
+
+
+*Axial DWI MR confirms which lesion is acute in this patient with numerous subcortical and periventricular, FLAIR T2-hyperintense, chronic lacunar infarctions.*
+
+
+*Axial FLAIR MR shows hyperintensity in the right thalamus in a patient with acute sensory symptoms. DWI showed diffusion restriction indicating acute ischemia. Lacunar infarcts are typically < 1.5 cm in diameter and classically located in the basal ganglia, thalamus, and penetrating artery distributions, including the lenticulostriate arteries and thalamoperforating arteries.*
+
+
+*Axial FLAIR MR shows multiple chronic left basal ganglia lacunar infarcts with surrounding hyperintense gliosis.*
+
+
+*Axial DWI MR shows multiple foci of diffusion restriction related to multiple acute lacunar infarcts in this young adult with a drug abuse history. Lacunar infarcts are highly associated with systemic hypertension. (Courtesy N. Fischbein, MD.)*
+
+
+*Axial CT shows focal low attenuation in the left thalamus, consistent with lacunar infarction . Lacunar infarctions can be difficult to distinguish from perivascular spaces on CT.*
+
+
+*Axial FLAIR MR showing multiple lacunar infarctions, predominantly in the right corona radiata . Note T2/FLAIR hyperintensity in the right middle cerebral artery (MCA) vascular territory from acute ischemic stroke .*
+
+
+*Axial NECT shows a chronic lacunar infarction in the anterior limb of the right internal capsule . This patient also has a small, chronic left MCA distribution infarct . Risk factors for lacunar infarcts include hypertension, diabetes, smoking history, obesity, and hypercholesterolemia.*
+
+
+*Axial DWI MR shows multiple foci of diffusion restriction related to multiple acute lacunar infarcts in this young adult with a drug abuse history. Drug abuse and arterial dissections are common risk factors for acute strokes in young patients.*
+
+
+*Axial FLAIR MR shows bilateral periventricular hyperintensity as well as focal hyperintensity along the lateral thalamus related to an acute lacunar infarction. Lacunar infarcts are highly associated with vascular dementia.*
+
+
+*Axial DWI MR in the same patient shows hyperintensity related to acute ischemia. Without diffusion-weighted imaging, it would be impossible to distinguish this acute lacune from an area of chronic small vessel disease, which commonly coexist.*
+
diff --git a/docs_md/articles/multiple-embolic-cerebral-infarctions_6dfc36d2-a561-49d5-a391-e740ba94e5d7.md b/docs_md/articles/multiple-embolic-cerebral-infarctions_6dfc36d2-a561-49d5-a391-e740ba94e5d7.md
new file mode 100644
index 0000000..3a6a3c5
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+++ b/docs_md/articles/multiple-embolic-cerebral-infarctions_6dfc36d2-a561-49d5-a391-e740ba94e5d7.md
@@ -0,0 +1,342 @@
+---
+title: "Multiple Embolic Cerebral Infarctions"
+docid: "6dfc36d2-a561-49d5-a391-e740ba94e5d7"
+authors:
+ - key: "cdbaaa96-a7b4-4498-a355-a2823a7d9e26"
+ value: "Kelly A. Dahlstrom, DO"
+ - key: "8d5254e9-8dda-478b-8f08-bdee97a32c79"
+ value: "Karen L. Salzman, MD, FACR"
+breadcrumbs:
+ -
+ name: "Brain"
+ slug: "brain"
+ treeNodeId: "0361042c-9c90-48e4-864e-a2e6428ee9c9"
+ -
+ name: "Diagnosis"
+ slug: "diagnosis"
+ treeNodeId: "948c6f1e-8e18-45f3-bd9d-7a04ab0b8708"
+ -
+ name: "Pathology-Based Diagnoses"
+ slug: "pathology-based-diagnoses"
+ treeNodeId: "d60fe914-7897-46a0-9cd2-f88ffb322f16"
+ -
+ name: "Stroke"
+ slug: "stroke"
+ treeNodeId: "7a135176-0a69-4fc9-b200-59569fbf5166"
+ -
+ name: "Cerebral Ischemia and Infarction"
+ slug: "cerebral-ischemia-and-infarction"
+ treeNodeId: "11d50e7d-f3e9-4071-b2b7-26b11ab40ea6"
+ -
+ name: "Multiple Embolic Cerebral Infarctions"
+ slug: "multiple-embolic-cerebral-infarcti-"
+ treeNodeId: null
+category: "Brain"
+documentVersionId: "1f5c5ba9-48bd-4ad3-86c7-e806d1846d98"
+imageCount: 16
+lastUpdated: "08/15/25"
+pageDescription: "Multiple Embolic Cerebral Infarctions"
+pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Multiple Embolic Cerebral Infarctions"
+pageTitle: "Multiple Embolic Cerebral Infarctions | STATdx"
+enhancedTitle: "Multiple Embolic Cerebral Infarctions"
+type: "DX"
+references: true
+cases: 2
+breadcrumbs:
+ - "Brain"
+ - "Diagnosis"
+ - "Pathology-Based Diagnoses"
+ - "Stroke"
+ - "Cerebral Ischemia and Infarction"
+ - "Multiple Embolic Cerebral Infarctions"
+---
+## KEY FACTS
+
+- ### Terminology
+
+
+ - Infarcts in multiple arterial distributions from embolic source, often from atherosclerotic carotid plaque or cardiac origin
+- ### Imaging
+
+
+ - Diffusion restriction in multiple vascular distributions
+ - **NECT**: Multiple regions of low attenuation, loss of gray-white differentiation
+ - **T2/FLAIR**: Multiple supratentorial and infratentorial regions of hyperintensity, often in vascular distribution (potentially varying ages)
+ - Embolic infarcts tend to involve terminal cortical branches → wedge-shaped infarcts
+ - Cardiac echocardiography may show valve vegetations, intracardiac filling defect, or atrial/ventricular septal defect
+ - Most helpful: MR with DWI, FLAIR, SWI > T2*GRE, T1WI C+
+ - Evaluate CTA for vulnerable carotid plaque features
+- ### Top Differential Diagnoses
+
+
+ - Hypotensive cerebral infarction
+ - Vasculitis
+ - Multiple sclerosis
+ - Parenchymal metastases
+- ### Clinical Issues
+
+
+ - Multiple focal neurologic complaints not conforming to singular vascular distribution
+ - Peripheral signs of emboli, such as splinter hemorrhages or paradoxical emboli
+ - **Cardiac**source most common etiology of multiple bilateral embolic infarcts
+ - May be septic or bland emboli
+ - Carotid artery disease may cause multiple embolic infarct, if associated with variant posterior cerebral artery (PCA) origin
+ - CTA/MRA to evaluate craniocervical vasculature
+ - Cardiac and vascular evaluation → treat underlying disease
+
+## TERMINOLOGY
+
+- ### Definitions
+
+
+ - Infarcts in multiple arterial distributions from embolic source, often from cardiac origin or atherosclerotic carotid plaque
+
+## IMAGING
+
+- ### Imaging Anatomy
+
+
+ - Embolic infarcts tend to involve terminal cortical branches, producing wedge-shaped infarcts
+- ### General Features
+
+
+ - #### Best diagnostic clue
+
+
+ - Multiple areas of ischemia, infarct, or encephalomalacia within multiple arterial distributions
+ - #### Location
+
+
+ - Variable
+ - #### Size
+
+
+ - Variable
+ - #### Morphology
+
+
+ - Wedge-shaped or arterial distribution ischemia, infarct, or encephalomalacia
+- ### CT Findings
+
+
+ - #### NECT
+
+
+ - Multiple regions of low attenuation, loss of gray-white differentiation, or encephalomalacia
+- ### MR Findings
+
+
+ - #### T2WI
+
+
+ - Multiple foci of hyperintensity
+ - #### FLAIR
+
+
+ - Multiple supratentorial and infratentorial regions of hyperintensity, often in arterial distribution
+ - #### T2* GRE
+
+
+ - May see microhemorrhages as blooming
+ - #### DWI
+
+
+ - Diffusion restriction in various arterial distributions
+ - May be of different ages or synchronous
+ - #### T1WI C+
+
+
+ - Enhancement of subacute embolic infarcts
+- ### Ultrasonographic Findings
+
+
+ - Cardiac echocardiography may show valve vegetations, intracardiac filling defect, or atrial or ventricular septal defect
+- ### Imaging Recommendations
+
+
+ - #### Best imaging tool
+
+
+ - MR with DWI, FLAIR, GRE/SWI, T1WI C+
+ - #### Protocol advice
+
+
+ - Contrast enhancement if patient has history of malignancy or infection
+
+## DIFFERENTIAL DIAGNOSIS
+
+- [Hypotensive Cerebral Infarction](/document/hypotensive-cerebral-infarction/a3d3dd38-629e-42fc-9d0d-9a03a39781eb)
+ - Watershed pattern typical, at junctions of major arterial distributions
+ - DWI restriction acutely
+- [Vasculitis](/document/primary-arteritis-of-cns/490b3aed-37e2-4ec6-95dd-76efc734490f)
+ - Multifocal DWI restriction acutely
+ - Subarachnoid hemorrhage may be present
+ - DSA shows multifocal narrowing and dilatation
+- [Multiple Sclerosis](/document/multiple-sclerosis/abe95a5e-394f-411b-aca6-72ab160a1d0d)
+ - Multifocal T2 hyperintensities at typical locations, callososeptal interfaces
+ - Young patients
+ - No diffusion restriction
+- [Parenchymal Metastases](/document/parenchymal-metastases/2cf0bd40-4597-4c0b-83e4-74340304b98f)
+ - Multiple enhancing foci, typically at corticomedullary junctions
+ - Tumor history often known
+
+## CLINICAL ISSUES
+
+- ### Presentation
+
+
+ - #### Most common signs/symptoms
+
+
+ - Multiple neurologic complaints not conforming to singular vascular distribution
+ - May be synchronous or asynchronous
+ - Large middle cerebral artery (MCA) defect may clinically mask contralateral superior cerebellar artery (SCA) deficit
+ - #### Other signs/symptoms
+
+
+ - Splinter hemorrhages, paradoxical emboli, valve vegetations
+- ### Demographics
+
+
+ - #### Epidemiology
+
+
+ - Cardiac source very common (15-25% of major strokes)
+ - May be septic or bland emboli
+ - Commonly arise from carotid artery atherosclerotic plaques
+ - Vulnerable plaque features: plaque ulcerations and intraplaque hemorrhage
+- ### Natural History & Prognosis
+
+
+ - Evolution of multiple infarcts
+ - Sequential emboli may be associated with diminishing mental capacity or multiple infarct dementia
+- ### Treatment
+
+
+ - Symptomatic
+ - Cardiac and vascular evaluation, treat underlying disease
+
+## DIAGNOSTIC CHECKLIST
+
+- ### Consider
+
+
+ - CTA, MRA, cardiac and vascular ultrasound
+- ### Image Interpretation Pearls
+
+
+ - Use DWI, FLAIR, and T1WI C+ MR to determine age of multiple infarcts
+
+ 13c70c2a-adf5-4064-9aaf-7bf783744dbe
+
+## References
+
+## Selected References
+
+1. [Nio SS et al: High-risk embolic sources on cardiac computed tomography in patients with acute ischemic stroke: a case-control study. Stroke. 56(2):420-6, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=39704069%5Bpmid%5D)
+1. [Semerano A et al: Cerebral thrombus analysis as a useful diagnostic tool for infective endocarditis in ischemic stroke patients. Eur Stroke J. 23969873251320449, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=39957015%5Bpmid%5D)
+1. [Song JW et al: Prevalence of high-risk CTA-based carotid plaque-RADS subtypes in patients with embolic stroke of undetermined source. Stroke. 56(3):737-40, 2025](http://www.ncbi.nlm.nih.gov/pubmed/?term=39851043%5Bpmid%5D)
+1. [Alshaer QN et al: Symptomatic carotid webs and patent foramen ovale: RoPE score in competing stroke etiologies. Clin Neurol Neurosurg. 245:108437, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=39067194%5Bpmid%5D)
+1. [Antal SI et al: Examining the prevalence of left atrial appendage thrombus in a cohort of acute stroke patients with an extended computed tomography angiographic protocol. Eur Neurol. 87(3):105-12, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38749403%5Bpmid%5D)
+1. [Ntaios G et al: Embolic strokes of undetermined source: a clinical consensus statement of the ESC Council on Stroke, the European Association of Cardiovascular Imaging and the European Heart Rhythm Association of the ESC. Eur Heart J. 45(19):1701-15, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38685132%5Bpmid%5D)
+1. [Uchida K et al: Prevalence of ipsilateral "vulnerable carotid plaques with <50 % stenosis" on CT angiography in embolic stroke of undetermined source. J Neurol Sci. 467:123316, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=39580929%5Bpmid%5D)
+1. [Xiao J et al: MRI in the evaluation of cryptogenic stroke and embolic stroke of undetermined source. Radiology. 311(1):e231934, 2024](http://www.ncbi.nlm.nih.gov/pubmed/?term=38652031%5Bpmid%5D)
+1. [Jiang J et al: Clot-based radiomics model for cardioembolic stroke prediction with CT imaging before recanalization: a multicenter study. Eur Radiol. 33(2):970-80, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=36066731%5Bpmid%5D)
+1. [Larson AS et al: Nonstenotic carotid plaques and embolic stroke of undetermined source: a multimodality review. AJNR Am J Neuroradiol. 44(2):118-24, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=36549844%5Bpmid%5D)
+1. [Sharma M et al: Frequency and patterns of brain infarction in patients with embolic stroke of undetermined source: NAVIGATE ESUS trial. Stroke. 53(1):45-52, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=34538089%5Bpmid%5D)
+1. [Patel TR et al: Increased perviousness on CT for acute ischemic stroke is associated with fibrin/platelet-rich clots. AJNR Am J Neuroradiol. 42(1):57-64, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=33243895%5Bpmid%5D)
+1. [Boodt N et al: Stroke etiology and thrombus computed tomography characteristics in patients with acute ischemic stroke: a MR CLEAN registry substudy. Stroke. 51(6):1727-35, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32404040%5Bpmid%5D)
+1. [Goebel J et al: Is histologic thrombus composition in acute stroke linked to stroke etiology or to interventional parameters? AJNR Am J Neuroradiol. 41(4):650-7, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32193192%5Bpmid%5D)
+1. [Maurer CJ et al: Endovascular thrombectomy of calcified emboli in acute ischemic stroke: a multicenter study. AJNR Am J Neuroradiol. 41(3):464-8, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32029470%5Bpmid%5D)
+1. [Soize S et al: Fast stent retrieval improves recanalization rates of thrombectomy: experimental study on different thrombi. AJNR Am J Neuroradiol. 41(6):1049-53, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32409312%5Bpmid%5D)
+1. [MRI predicts intracranial hemorrhage in patients who receive long-term oral anticoagulation. Neurology. 93(10):465, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31477619%5Bpmid%5D)
+1. [Guglielmi V et al: Collateral circulation and outcome in atherosclerotic versus cardioembolic cerebral large vessel occlusion. Stroke. 50(12):3360-8, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31658903%5Bpmid%5D)
+1. [Potter CA et al: CT for treatment selection in acute ischemic stroke: a code stroke primer. Radiographics. 39(6):1717-38, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31589578%5Bpmid%5D)
+1. [Chen Z et al: Prediction of the multisegment clot sign on dynamic CT angiography of cardioembolic stroke. AJNR Am J Neuroradiol. 39(4):663-8, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29449280%5Bpmid%5D)
+1. [Baradaran H et al: Association between carotid plaque features on CTA and cerebrovascular ischemia: a systematic review and meta-analysis. AJNR Am J Neuroradiol. 38(12):2321-6, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=29074638%5Bpmid%5D)
+1. [Fonseca AC et al: Cryptogenic stroke. Eur J Neurol. 22(4):618-23, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25597418%5Bpmid%5D)
+1. [Hasegawa H et al: Emergent intracranial surgical embolectomy in conjunction with carotid endarterectomy for acute internal carotid artery terminus embolic occlusion and tandem occlusion of the cervical carotid artery due to plaque rupture. J Neurosurg. 1-9, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25574571%5Bpmid%5D)
+1. [Kim SK et al: Histologic analysis of retrieved clots in acute ischemic stroke: correlation with stroke etiology and gradient-echo MRI. AJNR Am J Neuroradiol. 36(9):1756-62, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=26159515%5Bpmid%5D)
+1. [Meila D et al: Subcallosal artery stroke: infarction of the fornix and the genu of the corpus callosum. The importance of the anterior communicating artery complex. Case series and review of the literature. Neuroradiology. 57(1):41-7, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25280444%5Bpmid%5D)
+1. [Emiru T et al: Thrombolytic treatment for in-hospital ischemic strokes in United States. J Vasc Interv Neurol. 7(5):28-34, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25566339%5Bpmid%5D)
+1. [Müller H et al: Embolic and hemodynamic transcranial doppler characteristics in patients with acute ischemic stroke due to carotid occlusive disease: contribution to the different infarct patterns on MRI. J Neuroimaging. 25(5):766-75, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25512057%5Bpmid%5D)
+1. [Park KY et al: Incidence and risk factors for diffusion-weighted imaging (+) lesions after intracranial stenting and its relationship with symptomatic ischemic complications. Stroke. 45(11):3298-303, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25300970%5Bpmid%5D)
+1. [Saremi F et al: Paradoxical embolism: role of imaging in diagnosis and treatment planning. Radiographics. 34(6):1571-92, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25310418%5Bpmid%5D)
+1. [Abenza-Abildua MJ et al: Stroke due to septic embolism resulting from Aspergillus aortitis in an immunocompetent patient. J Neurol Sci. 284(1-2):209-10, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19442990%5Bpmid%5D)
+1. [Christian BA et al: Showered calcific emboli to the brain, the 'salted pretzel' sign, originating from the ipsilateral internal carotid artery causing acute cerebral infarction. Stroke. 40(5):e319-21, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19286589%5Bpmid%5D)
+1. [Emond H et al: From amaurosis fugax to asymptomatic bithalamic infarct. J Neurol. 256(6):1007-8, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19252800%5Bpmid%5D)
+1. [Iwanaga T et al: Paracentral strip infarcts of the middle cerebral artery: borderzone ischaemia or cortical artery occlusion? Cerebrovasc Dis. 27(3):215-22, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19176953%5Bpmid%5D)
+1. [Khetarpal V et al: Calcific aortic valve and spontaneous embolic stroke: A review of literature. J Neurol Sci. 287(1-2):32-5, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19712938%5Bpmid%5D)
+1. [Ralea IC et al: Acute stroke and heart attack management within a four-hour time window. J Stroke Cerebrovasc Dis. 18(2):167-70, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19251195%5Bpmid%5D)
+1. [Barber PA et al: Cerebral ischemic lesions on diffusion-weighted imaging are associated with neurocognitive decline after cardiac surgery. Stroke. 39(5):1427-33, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18323490%5Bpmid%5D)
+1. [Kang SY et al: Anterior cerebral artery infarction: stroke mechanism and clinical-imaging study in 100 patients. Neurology. 70(24 Pt 2):2386-93, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18541871%5Bpmid%5D)
+1. [Li Q et al: Repeated embolism and multiple aneurysms: central nervous system manifestations of cardiac myxoma. Eur J Neurol. 15(12):e112-3, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=19049534%5Bpmid%5D)
+1. [Alfke K et al: Magnetic resonance imaging of individual cerebral perfusion territories improves the diagnosis of embolic stroke. J Comput Assist Tomogr. 31(6):894-5, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=18043352%5Bpmid%5D)
+1. [Gezer S: Antiphospholipid syndrome. Dis Mon. 49(12):696-741, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=14679358%5Bpmid%5D)
+1. [Provenzale JM et al: Brain infarction in young adults: etiology and imaging findings. AJR Am J Roentgenol. 169(4):1161-8, 1997](http://www.ncbi.nlm.nih.gov/pubmed/?term=9308483%5Bpmid%5D)
+
+## Cases
+
+- {'cases': [{'authors': [{'key': '7cc3ba75-2642-4233-b9f6-0ce69ffe28f3', 'value': 'Sheri L. Harder, MD, FRCPC'}], 'caseVersionId': '50a8bbd0-b3a1-47e5-acaa-f26544b32ca1', 'description': 'NECT (#1-3) demonstrate a hyperdense right MCA (white arrow), an acute right MCA infarct (curved arrows) and remote left MCA and cerebellar infarcts (black arrows). Axial T2WI (#4) shows corresponding T2 hyperintensity in the right MCA distribution (curved arrow). Axial DWI (#5) and ADC map (#6) confirm the acute right MCA infarct with evidence of diffusion restriction with corresponding ADC hypointensity (curved arrow). MRA (#7) shows absence of the right ICA, in keeping with occlusion from thrombus. Pulmonary CTA (#8) demonstrates thrombi in the pulmonary arteries (open arrows). Pulmonary CTA (#9-11) also reveal a large pulmonary arteriovenous fistula (arrow). Lower extremity ultrasound without compression (#12) and with compression (#13) demonstrates thrombus in the right peroneal vein (curved arrows).', 'history': 'This patient with known hereditary hemorrhagic telangiectasia (HHT) presents with sudden onset left sided weakness and dysarthria. Imaging reveals a large pulmonary AV fistula and DVT/PE resulting in multiple thromboembolic infarcts (acute and chronic).', 'imagePoolId': '961f590b-d387-4f00-93ee-25663acb056a', 'name': 'Pulmonary AVF', 'teachingPoint': None, 'demographics': '51 Years old female'}, {'authors': [{'key': 'bf7af3a5-468c-48d0-8aea-4f6e808af979', 'value': 'Bryson Borg, MD'}], 'caseVersionId': '76aa2a58-90fb-4c31-bc2e-67573294fa8d', 'description': 'There is dissection of the V3 segment of the right vertebral artery, seen on TOF (curved arrow, #1) and FS T1WI (curved arrow, #3). There is also dissection of the proximal V2 segment of the left vertebral artery, seen on TOF (curved arrow, #2) and FS T1WI (curved arrow, #4). Both are seen on 3D rendering of the axial TOF data (arrows, #5). Small infarcts are seen in the cerebellum and left pons (#6-7).', 'history': 'Patient presented with onset of right facial numbness, dizziness, right arm weakness, and had had chiropractic manipulation of her cervical spine several days earlier.', 'imagePoolId': '68ea4918-f82d-4a07-a68a-2f264689d1c7', 'name': 'With cerebellar infarct(s)', 'teachingPoint': None, 'demographics': '29 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'e003a794-5072-4080-a303-44ebcf603fee', 'description': 'Axial NECT scans (#1-6) obtained on admission show multiple hypodense infarcts. Bilateral large early subacute territorial infarcts in multiple vascular distributions (white arrows) as well as small cortical infarcts (open arrows, #6) are present. Note presence of thrombus in an M3 branch (curved arrow, #3) and some foci of early hemorrhagic transformation (black arrows, #4-6).', 'history': 'Mitral valve regurgitation with multiple emboli.', 'imagePoolId': '373c646a-49b7-4b40-bf49-513c8a236d04', 'name': 'Large territorial, small cortical', 'teachingPoint': None, 'demographics': '22 Years old male'}], 'caseType': 'typical', 'name': 'TYPICAL'}
+- {'cases': [{'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}, {'key': '94f835c8-fa13-4e8a-995b-53048e6b0605', 'value': 'Philip R. Chapman, MD'}], 'caseVersionId': '876550df-a013-4627-88c1-2ccd6b62ad7f', 'description': 'Axial T2WI (#1) shows no definite abnormalities. However, FLAIR scans (#2-4) show multiple cortical and subcortical hyperintensities that enhance strongly following contrast administration (#5-7). DWI (not shown) was only mildly positive for cortical linear and punctate areas of restricted diffusion.\n\nIngestion of even a small amount of concentrated hydrogen peroxide can result in cerebral air gas embolism. Hyperbaric oxygen may be helpful in some cases.', 'history': 'Deliberately drank a bottle of hydrogen peroxide, possibly in suicide attempt.\n', 'imagePoolId': 'f51cf6c9-35a4-41a4-b4d1-1d9925d64bd5', 'name': 'Multiple cortical infarcts', 'teachingPoint': None, 'demographics': '63 Years old female'}], 'caseType': 'variant', 'name': 'VARIANT'}
+
+
+## Images
+
+
+### Selected Images
+
+
+*Axial DWI MR shows multiple bilateral cerebral infarcts in different vascular territories and of various ages in this patient with uncontrolled atrial fibrillation presenting with right-sided weakness. DWI is helpful in determining age of infarcts.*
+
+
+*Axial DWI MR shows multiple bilateral cerebral infarcts in different vascular territories and of various ages in this patient with uncontrolled atrial fibrillation presenting with right-sided weakness. DWI is helpful in determining age of infarcts.*
+
+
+*Axial FLAIR MR in the same patient with a wedge-shaped area of encephalomalacia in the right anterior MCA territory , consistent with old embolic infarct, is shown. Involvement of the terminal cortical branches produces the wedge-shaped morphology.*
+
+
+*Coronal T1 C+ MR in an IV drug user with infective endocarditis and multiple supratentorial and infratentorial septic emboli/abscesses is shown. Cardiac source is the most common etiology of multiple embolic infarcts.*
+
+
+*Axial SWI MIP in the same patient with infective endocarditis shows multiple scattered bilateral cerebral "blooming" foci related to microhemorrhage-microemboli. Superficial siderosis is also noted coating the sulci.*
+
+
+### Additional Images
+
+
+*Axial T2 MR displays chronic-appearing encephalomalacia within bilateral MCA distributions, consistent with multiple infarcts. Always consider cardiac sources if multiple arterial distributions are involved.*
+
+
+*Axial NECT shows right parietal occipital encephalomalacia and subtle left insular ribbon effacement . This suggests ischemia of different ages.*
+
+
+*Axial FLAIR MR in the same patient demonstrates encephalomalacia with peripheral FLAIR hyperintensity in the region of right parietal occipital remote infarct . There is diffuse FLAIR hyperintensity in the left insular region in the MCA territory . FLAIR and CT changes suggest left ischemia for > 12 hours.*
+
+
+*Axial NECT shows extensive bilateral hypodense infarcts in multiple vascular distributions and varying ages, typical of multiple embolic infarcts. Cardiac evaluation is important in these cases as the etiology is usually cardiac, either bland or septic emboli.*
+
+
+*Axial DWI MR shows bilateral areas of restriction related to acute ischemia in this patient with cardiac valve vegetations. DWI is helpful to determine the age of the infarcts as they may be of varying ages.*
+
+
+*Axial T1 C+ FS MR shows multiple enhancing lesions in this patient with a history of septic emboli from a cardiac source. Imaging mimics metastatic disease. DWI is often helpful to differentiate infarct from neoplasm.*
+
+
+*Axial DTI trace image shows multiple regions of diffusion hyperintensity related to acute MCA distribution ischemia in bilateral hemispheres in a patient with embolic disease from a cardiac source.*
+
+
+*Axial DTI trace image shows acute ischemia in the left hemisphere in multiple vascular distributions. Note the involvement of the recurrent artery of Heubner from the ACA distribution (head of caudate) as well as the MCA and PCA territories) in this patient with severe internal carotid artery atherosclerotic disease and a fetal origin PCA.*
+
+
+*Axial DTI trace image shows multiple regions of diffusion hyperintensity related to acute MCA infarcts in a patient with embolic disease related to mitral valve vegetations. Note the wedge-shaped infarct , typical of an embolic infarct from involvement of the terminal cortical branches.*
+
+
+*Axial FLAIR MR in a patient with septic emboli shows multiple cortical and subcortical white matter hyperintensities related to acute infarcts in both MCA distributions. Diffuse leptomeningeal hyperintensity is related to associated meningitis.*
+
+
+*Axial FLAIR MR shows bilateral chronic MCA distribution infarcts related to untreated atrial fibrillation. Note the areas of encephalomalacia with surrounding gliosis , typical of chronic infarcts.*
+
+
+*Axial T1 C+ FS MR shows multiple foci of enhancement in bilateral hemispheres related to septic emboli in a patient with cardiac valve vegetations. A cardiac source is the most common etiology of multiple embolic infarcts.*
+
diff --git a/docs_md/articles/neonatal-hypoxic-ischemic-injury_e3e9538d-fac5-4a1f-8c7a-c989c692ff39.md b/docs_md/articles/neonatal-hypoxic-ischemic-injury_e3e9538d-fac5-4a1f-8c7a-c989c692ff39.md
new file mode 100644
index 0000000..00bc4c2
--- /dev/null
+++ b/docs_md/articles/neonatal-hypoxic-ischemic-injury_e3e9538d-fac5-4a1f-8c7a-c989c692ff39.md
@@ -0,0 +1,498 @@
+---
+title: "Neonatal Hypoxic-Ischemic Injury"
+docid: "e3e9538d-fac5-4a1f-8c7a-c989c692ff39"
+authors:
+ - key: "47381de4-c9fd-4999-8dd0-1808cd72db6b"
+ value: "Luke L. Linscott, MD"
+breadcrumbs:
+ -
+ name: "Brain"
+ slug: "brain"
+ treeNodeId: "0361042c-9c90-48e4-864e-a2e6428ee9c9"
+ -
+ name: "Diagnosis"
+ slug: "diagnosis"
+ treeNodeId: "948c6f1e-8e18-45f3-bd9d-7a04ab0b8708"
+ -
+ name: "Pathology-Based Diagnoses"
+ slug: "pathology-based-diagnoses"
+ treeNodeId: "d60fe914-7897-46a0-9cd2-f88ffb322f16"
+ -
+ name: "Stroke"
+ slug: "stroke"
+ treeNodeId: "7a135176-0a69-4fc9-b200-59569fbf5166"
+ -
+ name: "Cerebral Ischemia and Infarction"
+ slug: "cerebral-ischemia-and-infarction"
+ treeNodeId: "11d50e7d-f3e9-4071-b2b7-26b11ab40ea6"
+ -
+ name: "Neonatal Hypoxic-Ischemic Injury"
+ slug: "neonatal-hypoxic-ischemic-injury"
+ treeNodeId: null
+category: "Brain"
+documentVersionId: "4ff8fc17-48ee-4ccf-ad65-a346122ffb42"
+imageCount: 30
+lastUpdated: "06/08/25"
+pageDescription: "Neonatal Hypoxic-Ischemic Injury"
+pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Stroke, Cerebral Ischemia and Infarction, Neonatal Hypoxic-Ischemic Injury"
+pageTitle: "Neonatal Hypoxic-Ischemic Injury | STATdx"
+enhancedTitle: "Neonatal Hypoxic-Ischemic Injury"
+type: "DX"
+references: true
+cases: 3
+breadcrumbs:
+ - "Brain"
+ - "Diagnosis"
+ - "Pathology-Based Diagnoses"
+ - "Stroke"
+ - "Cerebral Ischemia and Infarction"
+ - "Neonatal Hypoxic-Ischemic Injury"
+---
+## KEY FACTS
+
+- ### Terminology
+
+
+ - Brain injury in neonate caused by hypoxic-ischemic insult
+- ### Imaging
+
+
+ - US may be used for screening, particularly in acute setting or with concern for hemorrhage
+ - MR best imaging test for parenchymal injury
+ - Acute profound (a.k.a. "deep") pattern
+ - Basal ganglia, thalami, ± perirolandic cortex, ± hippocampi
+ - Partial prolonged (peripheral) pattern of injury
+ - Injury to cortex, especially watershed regions
+ - Mixed pattern common, especially in severe hypoxic-ischemic injury (HII)
+ - **T1WI & T2WI**: Usually normal in 1st day(s) following injury
+ - T1WI: ↑ or ↓ signal in affected regions
+ - T2WI: ↑ or ↓ signal in affected regions
+ - **DWI**: Best sequence to define extent of injury
+ - ↑ DWI, ↓ ADC; pseudonormalization at ~ 8-10 days
+ - **MRS**: ↓ NAA & ↑ lactate in affected areas
+ - **PWI**:**** ↑ ASL in affected deep gray nuclei during 1st week
+- ### Pathology
+
+
+ - Acute profound (deep) pattern: Short duration severe HII
+ - Injury to regions of greatest metabolic demand
+ - Partial prolonged (peripheral) pattern: Less severe hypoxia, longer time period
+ - Regions of greatest metabolic demand protected
+ - Preterm infants more susceptible to equivalent ischemic injury compared to term infants
+ - Preterm neonates likely to have associated white matter injury & gray matter hemorrhage
+- ### Clinical Issues
+
+
+ - Symptoms vary depending on severity of hypoxic-ischemic encephalopathy
+ - Sarnat grading based on signs, seizures, & duration
+ - Most common outcome: Cerebral palsy
+- ### Diagnostic Checklist
+
+
+ - Findings may be inapparent/subtle in first 24 hours
+ - Image at 4-5 days for best MR evaluation of injury extent
+
+## TERMINOLOGY
+
+- ### Synonyms
+
+
+ - Hypoxic-ischemic injury (HII)
+ - Neonatal asphyxia or birth asphyxia
+- ### Definitions
+
+
+ - Hypoxic-ischemic encephalopathy (HIE): Constellation of clinical & imaging findings resulting from neonatal brain injury secondary to perinatal hypoxic-ischemic insult
+
+## IMAGING
+
+- ### General Features
+
+
+ - 2 main patterns of injury have been described
+ - Acute profound pattern (a.k.a. deep or central pattern)
+ - Injury to deep gray nuclei (basal ganglia & thalami), ± perirolandic cortex, ± hippocampi
+ - Profound HII (e.g., asystole)
+ - Associated with more severe encephalopathy
+ - Partial prolonged pattern (a.k.a. peripheral pattern)
+ - Injury to cortex & associated white matter (WM), usually most severely affecting watershed regions
+ - Prolonged partial ischemia (e.g., fetal bradycardia)
+ - Associated with seizures & less severe encephalopathy
+ - Mixed pattern also frequently encountered
+ - Involvement of both cortex & deep gray nuclei
+ - Usually seen in most severe cases of HIE
+ - Chronic findings: Atrophy, gliosis/encephalomalacia
+- ### CT Findings
+
+
+ - Acute
+ - Loss of gray-white differentiation
+ - Indistinct, hypodense deep gray nuclei
+ - Bright cerebellum sign due to supratentorial edema/ischemia
+ - Chronic
+ - Parenchymal Ca⁺⁺ & volume loss months after injury
+ - ± ↑ ventricles & ↑ extraaxial CSF spaces
+- ### MR Findings
+
+
+ - #### T1WI
+
+
+ - Usually normal during 1st day(s) following injury
+ - ↑ or ↓ signal in areas of injury depending on anatomy involved
+ - ↑ signal in deep gray nuclei & cortex (cortical laminar necrosis) may develop
+ - Loss of normal bright T1 signal in posterior limb of internal capsule
+ - #### T2WI
+
+
+ - Usually normal during 1st day(s) following injury
+ - Indistinct deep gray nuclei & loss of cortical ribbon
+ - ↑ signal in affected areas becomes more conspicuous over days
+ - Some areas of injury may show ↓ signal beginning in latter 1/2 of 1st week
+ - Late findings: ↑ signal & volume loss in affected areas
+ - #### PD/intermediate
+
+
+ - ↑ signal in affected areas
+ - May be more conspicuous than T1 & T2
+ - #### T2* GRE
+
+
+ - Term neonates: Hemorrhage less common
+ - Preterm neonates: Associated germinal matrix/intraventricular hemorrhage common
+ - #### DWI
+
+
+ - Most important sequence
+ - Restricted diffusion within 1-10 days, depending on anatomic area
+ - Anatomic areas with diffusion restriction evolves over time
+ - e.g., primary cortical injury & secondary WM injury
+ - Pseudonormalization begins at ~ 8-10 days in most areas
+ - Pseudonormalization (DWI & ADC similar to normal brain)
+ - May be delayed in patients (> 10 days) treated with hypothermia
+ - #### PWI
+
+
+ - ↑ ASL in affected deep gray nuclei during 1st week
+ - ↑ ASL correlates with more severe injury
+ - Cerebral oxygen metabolism more disturbed in severe vs. moderate HIE
+ - #### MRS
+
+
+ - ↓ NAA & ↑ lactate in affected areas
+ - ↑ lactate:NAA ratio correlates with more severe injury
+- ### Ultrasonographic Findings
+
+
+ - Findings often less conspicuous compared to MR
+ - Patchy ↑ echogenicity in WM
+ - Accentuated gray matter-WM differentiation
+ - ↑ echogenicity in deep gray nuclei
+ - Slit-like lateral ventricles & sulcal effacement: Not indicative of injury
+ - Typical appearance for newborn who has undergone labor &/or born vaginally, so not helpful to suggest HIE
+- ### Imaging Recommendations
+
+
+ - #### Best imaging tool
+
+
+ - MR with DWI & MRS
+ - #### Protocol advice
+
+
+ - Findings may be inapparent/subtle in first 24 hours
+ - Image at 4-5 days for best MR evaluation of injury extent
+ - ADC changes peak at ~ 4-5 days
+
+## DIFFERENTIAL DIAGNOSIS
+
+- ### Metabolic Disorders
+
+
+ - Nonketotic hyperglycinemia
+ - Sulfite oxidase deficiency
+ - Molybdenum cofactor deficiency
+- ### Urea Cycle Disorders
+
+
+ - Ornithine transcarbamylase deficiency
+ - Elevated ammonia, present at 24-28 hours
+- [Maple Syrup Urine Disease](/document/maple-syrup-urine-disease/3a260d42-504b-4e53-bb38-a0df76b3670b)
+ - Edema in myelinated areas
+ - Brainstem, perirolandic, & cerebellar WM
+- [Kernicterus](/document/kernicterus/1c0c7b6a-574a-4dcc-bfe9-9b0530b14386)
+ - Hyperbilirubinemia ± sepsis, hypoxia
+ - Mimics profound deep injury on T1WI
+ - Globus pallidus (not putamen or thalamus)
+- [Hypoglycemia](/document/pediatric-hypoglycemia/af0be376-e7f1-420b-b09d-0a5d636ac628)
+ - Characteristic occipital cortex injury
+ - May potentiate HII
+- [Perinatal Arterial Ischemic Stroke](/document/childhood-stroke/fbfddb67-5d7e-4979-9a22-85ff72665a91)
+ - Focal arterial territory injury without hypoxic event
+- [Venous Injury](/document/deep-cerebral-venous-thrombosis/056d86df-2bcb-4816-ace7-21f663d581f0)
+ - Edema, hemorrhage, or ischemia in venous distribution
+- [TORCH Infections](/document/torch-infections/3b509e1c-83cf-4793-8307-e0afa70781ce)
+ - May mimic chronic findings of HIE
+ - Microcephaly, migration anomalies, Ca⁺⁺
+- ### Human Parechovirus Meningoencephalitis
+
+
+ - Symmetric WM & posterior thalami diffusion restriction
+ - Typically presents after 1st week of life
+
+## PATHOLOGY
+
+- ### General Features
+
+
+ - #### Etiology
+
+
+ - Acute profound (deep) pattern associated with severe hypoxia of relatively brief (10-25 minutes) duration
+ - Causative (sentinel) event usually identifiable
+ - Injury to regions of greatest metabolic demand
+ - Partial prolonged (peripheral) pattern associated with less severe hypoxia over longer period (15 minutes, up to hours)
+ - Causative event may be cryptic
+ - Regions of greatest metabolic demand protected
+ - Watershed regions most susceptible
+ - Preterm infants more susceptible to equivalent ischemic injury as compared to term infants
+ - Preterm neonates more likely to have associated WM injury & germinal matrix hemorrhage
+ - Asphyxia triggers cascade of cellular biochemical events → abnormal function, edema, or cell death
+ - Extracellular glutamate accumulates, activates postsynaptic excitatory amino acid receptors
+ - Postsynaptic receptor distribution changes with ↑ age; different injury patterns based on age
+ - Multiple phases & causes of brain injury
+ - Primary neuronal (death at time of insult)
+ - Reactive cell death (reperfusion injury hours or days later)
+ - Seizure-related cell injury
+ - #### Associated abnormalities
+
+
+ - Maternal: Infection, preeclampsia, diabetes, drug use
+ - Infant: Anemia, growth restriction, hypoglycemia, sepsis, seizures
+ - Placental abnormalities: Chorioamnionitis, placental abruption
+ - Ischemia, often multiorgan (e.g., cardiac, renal, liver)
+- ### Staging, Grading, & Classification
+
+
+ - Sarnat stage (based on clinical & EEG findings)
+ - I (mild): Hyperalert/irritable, mydriasis, ↑ heart rate, EEG normal
+ - II (moderate): Lethargy, hypotonia, miosis, ↓ heart rate, seizures common
+ - III (severe): Stupor, flaccid, reflexes absent, seizures uncommon
+- ### Gross Pathologic & Surgical Features
+
+
+ - Acute profound pattern: Hippocampal, basal ganglia, thalamic, perirolandic atrophy
+ - Partial prolonged pattern: Ulegyria, gliosis, & atrophy with spared perirolandic region
+
+## CLINICAL ISSUES
+
+- ### Presentation
+
+
+ - #### Most common signs/symptoms
+
+
+ - Symptoms depend on severity of HIE
+ - Altered consciousness
+ - Abnormal muscle tone
+ - Respiratory & heart rate changes
+ - Cranial nerve dysfunction
+ - Seizures
+ - #### Other signs/symptoms
+
+
+ - Low Apgar scores
+ - Laboratory findings
+ - Cord blood gases: Metabolic acidosis (↓ pH, ↓ HCO₃⁻)
+ - ± abnormal renal, liver, & heart labs
+ - EEG findings
+ - Mild: Normal/↓
+ - Moderate: ↓ voltage (delta & theta waves), focal seizures
+ - Severe: Isopotential or infrequent periodic discharges
+- ### Demographics
+
+
+ - #### Age
+
+
+ - Ischemia may occur in immediate prenatal, intrapartum, & immediate postnatal periods
+ - #### Sex
+
+
+ - M > F
+ - #### Epidemiology
+
+
+ - 1-8/1,000 live births in resource-rich countries & ≤ 26/1,000 live births in resource-limited countries
+- ### Natural History & Prognosis
+
+
+ - Deep pattern associated with dyskinetic cerebral palsy
+ - Indicates involvement of subthalamic nucleus
+ - Peripheral pattern associated with spastic cerebral palsy
+ - Burst suppression EEG is poor prognostic factor
+- ### Treatment
+
+
+ - Resuscitation, correction of fluid & electrolyte imbalance
+ - Therapeutic hypothermia
+ - Treat seizures
+ - Erythropoietin (EPO) therapy may improve outcome
+
+## DIAGNOSTIC CHECKLIST
+
+- ### Image Interpretation Pearls
+
+
+ - DWI is most critical sequence but evolves over time
+ - Can be normal < 1 day, ↑ in severity over days, then pseudonormalization begins at ~ 8-10 days
+ - US: Slit-like lateral & 3rd ventricles are normal in 1st days of life following labor
+ - Should not be mistaken for cerebral edema
+
+ 08fecb97-1789-4ada-b108-a9f361deb471
+
+## References
+
+## Selected References
+
+1. [Guarnera A et al: Predictive value of MRI in hypoxic-ischemic encephalopathy treated with therapeutic hypothermia. Children (Basel). 10(3):446, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=36980004%5Bpmid%5D)
+1. [Parmentier CEJ et al: Magnetic resonance imaging in (near-)term infants with hypoxic-ischemic encephalopathy. Diagnostics (Basel). 12(3):645, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35328199%5Bpmid%5D)
+1. [Bach AM et al: Early magnetic resonance imaging predicts 30-month outcomes after therapeutic hypothermia for neonatal encephalopathy. J Pediatr. 238:94-101.e1, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=34237346%5Bpmid%5D)
+1. [Brocard C et al: Brain MRI after therapeutic hypothermia in asphyxiated newborns: predictive value at one year of imaging features. Eur J Radiol. 139:109724, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=33932716%5Bpmid%5D)
+1. [Chang PD et al: Predictive values of location and volumetric MRI injury patterns for neurodevelopmental outcomes in hypoxic-ischemic encephalopathy Neonates. Brain Sci. 10(12):991, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=33339156%5Bpmid%5D)
+1. [Razak A et al: Erythropoietin in perinatal hypoxic-ischemic encephalopathy: a systematic review and meta-analysis. J Perinat Med. 47(4):478-89, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30789826%5Bpmid%5D)
+1. [Salas J et al: The role of diffusion tensor imaging in detecting hippocampal injury following neonatal hypoxic-ischemic encephalopathy. J Neuroimaging. 29(2):252-9, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30325083%5Bpmid%5D)
+1. [Shetty AN et al: Cerebral oxygen metabolism during and after therapeutic hypothermia in neonatal hypoxic-ischemic encephalopathy: a feasibility study using magnetic resonance imaging. Pediatr Radiol. 49(2):224-33, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30402807%5Bpmid%5D)
+1. [Salas J et al: Head ultrasound in neonatal hypoxic-ischemic injury and its mimickers for clinicians: a review of the patterns of injury and the evolution of findings over time. Neonatology. 114(3):185-97, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29936499%5Bpmid%5D)
+1. [Weeke LC et al: A novel magnetic resonance imaging score predicts neurodevelopmental outcome after perinatal asphyxia and therapeutic hypothermia. J Pediatr. 192:33-40.e2, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29246356%5Bpmid%5D)
+1. [Heursen EM et al: Prognostic value of the apparent diffusion coefficient in newborns with hypoxic-ischaemic encephalopathy treated with therapeutic hypothermia. Neonatology. 112(1):67-72, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28351039%5Bpmid%5D)
+1. [Sánchez Fernández I et al: Prognostic value of brain magnetic resonance imaging in neonatal hypoxic-ischemic encephalopathy: a meta-analysis. J Child Neurol. 32(13):1065-73, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28925315%5Bpmid%5D)
+1. [Trivedi SB et al: A validated clinical MRI injury scoring system in neonatal hypoxic-ischemic encephalopathy. Pediatr Radiol. 47(11):1491-9, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28623417%5Bpmid%5D)
+1. [Charon V et al: Comparison of early and late MRI in neonatal hypoxic-ischemic encephalopathy using three assessment methods. Pediatr Radiol. 45(13):1988-2000, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=26209958%5Bpmid%5D)
+1. [De Vis JB et al: Arterial spin-labelling perfusion MRI and outcome in neonates with hypoxic-ischemic encephalopathy. Eur Radiol. 25(1):113-21, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25097129%5Bpmid%5D)
+1. [Douglas-Escobar M et al: Hypoxic-ischemic encephalopathy: a review for the clinician. JAMA Pediatr. 169(4):397-403, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25685948%5Bpmid%5D)
+1. [Shankaran S et al: Neonatal magnetic resonance imaging pattern of brain injury as a biomarker of childhood outcomes following a trial of hypothermia for neonatal hypoxic-ischemic Encephalopathy. J Pediatr. 167(5):987-93.e3, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=26387012%5Bpmid%5D)
+1. [Cavalleri F et al: Prognostic value of diffusion-weighted imaging summation scores or apparent diffusion coefficient maps in newborns with hypoxic-ischemic encephalopathy. Pediatr Radiol. 44(9):1141-54, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24715056%5Bpmid%5D)
+1. [Ancora G et al: Prognostic value of brain proton MR spectroscopy and diffusion tensor imaging in newborns with hypoxic-ischemic encephalopathy treated by brain cooling. Neuroradiology. 55(8):1017-25, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23703033%5Bpmid%5D)
+1. [Harteman JC et al: Placental pathology in full-term infants with hypoxic-ischemic neonatal encephalopathy and association with magnetic resonance imaging pattern of brain injury. J Pediatr. 163(4):968-95.e2, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23891350%5Bpmid%5D)
+1. [Jose A et al: Correlation of EEG, CT, and MRI brain with neurological outcome at 12 months in term newborns with hypoxic ischemic encephalopathy. J Clin Neonatol. 2(3):125-30, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=24251256%5Bpmid%5D)
+1. [Srinivasakumar P et al: Therapeutic hypothermia in neonatal hypoxic ischemic encephalopathy: electrographic seizures and magnetic resonance imaging evidence of injury. J Pediatr. 163(2):465-70, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23452588%5Bpmid%5D)
+1. [Bednarek N et al: Impact of therapeutic hypothermia on MRI diffusion changes in neonatal encephalopathy. Neurology. 78(18):1420-7, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22517107%5Bpmid%5D)
+1. [Mulkey SB et al: Quantitative cranial magnetic resonance imaging in neonatal hypoxic-ischemic encephalopathy. Pediatr Neurol. 47(2):101-8, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22759685%5Bpmid%5D)
+1. [Glass HC et al: Seizures and magnetic resonance imaging-detected brain injury in newborns cooled for hypoxic-ischemic encephalopathy. J Pediatr. 159(5):731-735.e1, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21839470%5Bpmid%5D)
+1. [Izbudak I et al: MR imaging of the term and preterm neonate with diffuse brain injury. Magn Reson Imaging Clin N Am. 19(4):709-31; vii, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=22082734%5Bpmid%5D)
+1. [Griffiths PD et al: Anatomic localization of dyskinesia in children with "profound" perinatal hypoxic-ischemic injury. AJNR Am J Neuroradiol. 31(3):436-41, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=19875467%5Bpmid%5D)
+1. [Logitharajah P et al: Hypoxic-ischemic encephalopathy in preterm infants: antecedent factors, brain imaging, and outcome. Pediatr Res. 66(2):222-9, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19390490%5Bpmid%5D)
+1. [Okereafor A et al: Patterns of brain injury in neonates exposed to perinatal sentinel events. Pediatrics. 121(5):906-14, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18450893%5Bpmid%5D)
+1. [Winter JD et al: Apparent diffusion coefficient pseudonormalization time in neonatal hypoxic-ischemic encephalopathy. Pediatr Neurol. 37(4):255-62, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17903669%5Bpmid%5D)
+1. [Barkovich AJ et al: MR imaging, MR spectroscopy, and diffusion tensor imaging of sequential studies in neonates with encephalopathy. AJNR Am J Neuroradiol. 27(3):533-47, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=16551990%5Bpmid%5D)
+1. [Miller SP et al: Patterns of brain injury in term neonatal encephalopathy. J Pediatr. 146(4):453-60, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=15812446%5Bpmid%5D)
+
+## Cases
+
+- {'cases': [{'authors': [{'key': 'e8af6d26-3aad-47c9-9083-5128aab09af2', 'value': 'Susan I. Blaser, MD, FRCPC'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'b5bd7feb-83a5-44a8-a41e-f85b86bd7a95', 'description': 'Axial images demonstrate loss of the normal myelin "stripe" of the posterior limb of the internal capsules (arrows, #1). There is hazy increased signal of the deep grey structures on both T1W (#1) and T2W (#5, 6) images. Subcortical "U-fiber" signal increase is present diffusely on FLAIR images (curved arrows, #3, 4) suggesting early laminar necrosis. The cortical ribbon remains intact on T2WIs (#5, 6). DWI (#7, 8) demonstrate involvement of the cortex, the subcortical "U-fibers" and the white matter diffusely. This combination of deep grey injury (as reflected by the deep gray structures) and the diffuse white matter and cortical injury (as demonstrated on DWI) is typical of a mixed pattern injury. The posterior prominence of restricted diffusion suggests that there may have been an additional component of neonatal hypoglycemia.', 'history': None, 'imagePoolId': '9776b96d-c77f-44d2-93f8-2962b9e2c408', 'name': 'Severe', 'teachingPoint': None}, {'authors': [{'key': 'e8af6d26-3aad-47c9-9083-5128aab09af2', 'value': 'Susan I. Blaser, MD, FRCPC'}, {'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '01f01567-a670-48fe-9b90-5b151e393add', 'description': 'Late imaging in this 1 year old shows gliosis and atrophy of the posterior putamina (arrows), thalami (curved arrow) and the cortical spinal tracts as they extend into the Rolandic cortex (open arrows) on T2WIs (#1-4). This particular constellation of findings is typical of infants who have survived an acute, profound insult in the perinatal period. Acute profound events may happen when there is a severe event, such as uterine rupture or a knot in the umbilical cord, leading to a profound event of hypoperfusion. When there is no time to shift cerebral blood flow to these areas of highest metabolic demand, they are damaged.', 'history': None, 'imagePoolId': '38ea2b3a-7942-493b-9618-1bfacb5e7afa', 'name': 'Neonatal Asphyxia BG PVL', 'teachingPoint': None, 'demographics': '1 Years old '}], 'caseType': 'Other', 'name': 'OTHER'}
+- {'cases': [{'authors': [{'key': '815f3e98-b5da-43c7-8f99-d3db52947320', 'value': 'Hank Baskin, MD'}], 'caseVersionId': '379da878-4081-4657-a7a7-b1b18e29b841', 'description': 'Axial T2 image through the cerebral hemispheres (#1) demonstrates extensive encephalomalacia with abnormal fluid signal and volume loss in the periventricular white matter of the occipital lobes (arrows).\n\nSagittal T1 weighted image (#2) demonstrates a decreased craniofacial proportion consistent with microcephaly. There is thinning of the body and splenium of the corpus callosum, reflecting hemispheric injury and volume loss (arrows).\n\nCoronal FLAIR images (#3-7) demonstrate abnormal signal intensity and volume loss in the periatrial white matter (straight arrows, #3-5) with cystic change and ulegyria (curved arrows).', 'history': 'Patient with history of HIE underwent evaluation for seizure\n', 'imagePoolId': '7108c5f6-460a-4ccd-8327-20b8a25e159b', 'name': 'Chronic findings, watershed pattern', 'teachingPoint': None, 'demographics': '15 Years old male'}], 'caseType': 'typical', 'name': 'TYPICAL'}
+- {'cases': [{'authors': [{'key': '99e1aff7-f42c-43a0-95ae-d89c8551aa01', 'value': 'Kevin R. Moore, MD'}], 'caseVersionId': '00894247-a336-4c04-a78a-ab2a69c9d80d', 'description': 'Variant case of multiple sutural craniosynostosis secondary to poor brain growth. \n\nAxial bone CT (#1) shows symmetric normal appearance of the skull-base. Axial bone CT image of the calvarium (#2) shows closure and fusion of the right coronal suture (white arrow), overlap of the closely approximated metopic (open arrow) and left coronal (curved arrow) sutures, and close approximation of both lambdoid sutures (black arrows). Axial bone CT (#3) at the vertex shows fusion of the abnormal sagittal suture anteriorly and abnormal straight configuration of the parietal sagittal suture. Lateral 3D bone CT reformats (#4-5) show closure of the right coronal suture (arrow, #4) and close approximation and overlap of the patent left coronal suture (curved arrow, #5) and metopic suture (open arrow, #5). Anteroposterior bone CT 3D reformats (#6-7) confirm ridging along the closed right coronal (arrow) and sagittal (open black arrow) sutures and the closely approximated, overlapping metopic (open white arrow) and left coronal (curved arrow) sutures. Axial NECT (#8-9), T1WI (#10), and T2WI (#11) images of the brain confirm severe brain parenchymal injury in this microcephalic infant, strongly supporting poor brain growth as the etiology for early sutural closure.', 'history': 'Former term infant with microcephaly, premature sutural closure, and history of severe birth depression. ', 'imagePoolId': '0864d1b3-32f4-4e83-860d-2dfc1a5822a4', 'name': 'Multiple suture fusion, poor brain growth', 'teachingPoint': None, 'demographics': '8 Weeks old female'}, {'authors': [{'key': 'e8af6d26-3aad-47c9-9083-5128aab09af2', 'value': 'Susan I. Blaser, MD, FRCPC'}], 'caseVersionId': '6664ad90-fa9e-4973-9351-9687afa3c912', 'description': 'Axial T1WI (#1) reveal intensely increased signal intensity within the posterior putamina (curved arrows) and lateral thalami (arrow). The posterior limbs of the internal capsules, however, are identified. Similar changes are seen on FLAIR (#2). Increased signal is present on T2WI (#3, 4), although the abnormal signal is more diffusely seen within the thalami and there is focal asymmetry (arrow). Note that the cortical ribbon (open arrows) is largely intact throughout. MRS (#5) reveals an inverted lactate doublet (curved arrow). Note that the DWI image (#6) is normal, despite the extensive abnormalities seen on routine imaging. DWI performed after 6 days from HIE insult may appear normal. The window for identifying changes on DWI in neonatal HIE is short, ranging from approximately day 2 to day 6. While restriction may be identified earlier or later, the extent will be grossly underestimated.', 'history': 'Full term with profound asphyxial event. Now 8 days old.', 'imagePoolId': 'f71386c3-0223-4b6d-8e0b-5144a40c1d04', 'name': 'Missed DWI window', 'teachingPoint': None, 'demographics': '8 Days old male'}, {'authors': [{'key': 'e8af6d26-3aad-47c9-9083-5128aab09af2', 'value': 'Susan I. Blaser, MD, FRCPC'}], 'caseVersionId': 'c54764c3-8e8f-4fae-b237-9b192cdbfbe1', 'description': 'Coronal sonography (#1) performed under 24 hours of age demonstrates abnormal echogenicity (arrows) and relatively normal sized anterior horns. Hypoxic ischemic encephalopathy occurring at birth usually leads to a pattern of small ventricles due to edema and relatively normal echogenicity in the first 24 hours of life. MRI was performed at 5 days of life. There is marked increase in basal ganglia and lateral thalamic signal intensity (curved arrows) on T1WI (#2). The posterior limb of internal capsule myelin (PLIC) is difficult to see, an additional feature of damage to the deep grey nuclei. FLAIR (#3) shows cystic changes (open arrows) of the frontal lobe white matter and mild ventricular dilatation. DWI (#4) and ADC (#5) show extensive diffuse restriction, particularly of the cortex. The basal ganglia demonstrate little restriction at this time. T2W axial (#6) and Coronal (#7) images confirm extensive loss of cortical ribbon (black arrow) and low signal intensity deep grey nuclei. MRS (#8) reveals extremely low NAA peak (curved arrow) and a large inverted lactate doublet (open arrow). CT 2 days later shows continued volume loss and marked white matter edema.\n\nFindings related to HIE were already well developed on day 1 of life in this neonate, and progressed in a pattern which corresponded with an injury occurring before birth. Basal ganglia were no longer restricted, but were very abnormal on routine imaging. White matter and cortex were restricted, but already demonstrating evidence of cystic change and volume loss. Timing of an hypoxic injury is becoming easier with MRI and, in particular, DWI. Evaluation of such findings, however, should not be performed in the absence of knowledge about clinical findings and history.', 'history': 'This infant presented with early seizures.', 'imagePoolId': '36f7d883-ef38-459c-9823-4a9c1b04ec73', 'name': 'Prenatal event', 'teachingPoint': None, 'demographics': '1 Days old male'}, {'authors': [{'key': 'e8af6d26-3aad-47c9-9083-5128aab09af2', 'value': 'Susan I. Blaser, MD, FRCPC'}], 'caseVersionId': 'ee63c06a-dad1-4603-85ce-06a8e4524fec', 'description': 'T1W axial images reveal bright signal within putamen, globus pallidus and lateral thalamus. The posterior limb of internal capsule (PLIC) has lost the normally increased signal of mature myelin (arrow). T2W image reveals a normal cortical ribbon, but signal change within the deep gray structures is extremely subtle.\n\nDWI shows striking restricted signal within the posterior putamina and lateral thalami (curved arrows) and within the Rolandic cortex (open arrows).\n\nMRS spectroscopy reveals a doublet (arrow), simulating lactate. Note, however, the location at 1.1ppm. The doublet, therefore, represents propan-1,2-diol, the injection carrier for anticonvulsants. There is mild irregularity adjacent to this at 1.3ppm, the location for lactate.\n\nThe imaging pattern is typical for profound acute hypoxic ischemic encephalopathy (HIE), seen when there has been an profound, acute event such as uterine rupture or cord prolapse.', 'history': 'Ventilated term infant with seizures and abnormal movements. Suffered umbilical cord prolapse during birth.', 'imagePoolId': '5a754c74-cb75-4389-98b4-2ad0e77db9f5', 'name': 'Profound', 'teachingPoint': None, 'demographics': '2 Days old female'}], 'caseType': 'variant', 'name': 'VARIANT'}
+
+
+## Images
+
+
+### Selected Images
+
+
+*Axial ADC MR in a 3-day-old term infant boy delivered via emergent C-section (with Apgar scores of 1, 1, & 1) shows diffusion restriction in the thalami & putamina , consistent with the deep injury pattern of profound HIE.*
+
+
+*Axial ADC MR in a 3-day-old term infant boy delivered via emergent C-section (with Apgar scores of 1, 1, & 1) shows diffusion restriction in the thalami & putamina , consistent with the deep injury pattern of profound HIE.*
+
+
+*Axial T1 MR in a 31-weeks premature infant 11 days following placental abruption shows irregular hyperintense signal in the bilateral thalami & globus pallidus. Also note germinal matrix hemorrhage & small layering interventricular blood , findings often seen in premature infants with HIE.*
+
+
+*Axial DWI in a 4-day-old with neonatal seizures shows symmetric diffusion restriction in the bilateral cerebral hemispheres, most severely affecting the watershed regions . The diffusion restriction in the corpus callosum represents secondary neuronal injury.*
+
+
+*Axial DWI in a 4-day-old term neonate shows asymmetric (R > L) diffusion restriction in the bilateral temporal-occipital regions. Most HII are fairly symmetric, but asymmetry does occur & may reflect differences in cerebrovascular anatomy.*
+
+
+*Coronal US performed at ~ 1 hour of life in a newborn with polyhydramnios & mother with previous term stillborn shows mild ↑ echogenicity in the thalami & white matter . The presence of these findings at 1 hour of life suggests a global HII occurred many hours or days prior to birth.*
+
+
+*Axial DWI MR in the same newborn at 4 days of life shows symmetric marked diffusion restriction in the cerebral hemispheres , basal ganglia , & thalami , consistent with a severe mixed pattern of HII.*
+
+
+*Axial T2 MR in the same 4-day-old shows ↑ T2 signal within the affected cerebral hemispheres with loss or decrease of gray-white differentiation . Note the ↑ signal in the basal ganglia & thalami as well.*
+
+
+*Single-voxel short echo MR spectroscopy centered in the left basal ganglia & thalami shows a markedly ↑ doublet lactate peak at 1.3 ppm & ↓ NAA peak at 2.0 ppm. These findings support the diagnosis of HII.*
+
+
+*Axial FLAIR in a 2-week-old with HIE shows early evolution of cystic encephalomalacia in a symmetric watershed pattern.*
+
+
+*Axial T2WI MR in the same patient at 10 years of age shows the significant encephalomalacia & gliosis in a symmetric watershed pattern with relative preservation of the perirolandic cortex . This anatomic distribution of injury suggests a partial prolonged pattern of HII.*
+
+
+### Additional Images
+
+
+*Axial DWI in an 8-day-old term neonate shows a typical partial-prolonged pattern of HII with symmetric involvement of frontal & parietooccipital watershed zones. Diffusion restriction in the corpus callosum suggests secondary neuronal injury.*
+
+
+*Axial T2WI MR in a 4-day-old term infant boy delivered by emergent C-section for fetal bradycardia shows ↑ signal with loss of cortical differentiation in the left occipital lobe + ↑ signal in the thalami.*
+
+
+*Axial DWI MR in the same 4-day-old boy best demonstrates the full extent of injury with definite involvement of the bilateral thalami & the left occipital lobe , suggesting a more severe injury with components of both the central & peripheral patterns.*
+
+
+*Axial DWI MR in a 4-day-old term girl with seizures (who was born to a febrile mother with chorioamnionitis) shows extensive cortical injury . Secondary injury in the genu of the corpus callosum is also noted. There is subtle ↑ signal in the caudate heads & ventral medial thalami.*
+
+
+*Short-echo MR spectroscopy in the left basal ganglia in the same 4-day-old term girl with seizures shows ↓ NAA & a large lipid-lactate peak , confirming injury to the basal ganglia.*
+
+
+*Axial T1WI MR in a 3-day-old term neonate with suspected severe HIE (after 18 minutes of cardiac arrest following birth) shows possibly ↑ signal intensity in the cortex & brainstem, but it is difficult to confidently define the extent of injury.*
+
+
+*Axial DWI MR in the same 3-day-old term neonate with suspected severe HIE (after 18 minutes of cardiac arrest following birth) shows uniform cortical diffusion restriction as well as restricted diffusion in the brainstem . Involvement of the brainstem can be seen in profound HIE & is a poor prognostic sign.*
+
+
+*Axial ADC MR map in the same 3-day-old term neonate with suspected severe HIE shows severe diffusion restriction in the brainstem , a very poor prognostic sign. Regions of restricted diffusion are also seen in the right frontal lobe . This patient was unresponsive on clinical examination & did not survive.*
+
+
+*Axial DWI MR in a 3-day-old term boy delivered via emergent C-section with Apgar scores of 1, 1, & 1 shows marked diffusion restriction in the thalami & posterolateral putamina , consistent with the deep injury pattern seen with profound HIE.*
+
+
+*Single-voxel short-echo MRS in the same 3-day-old term boy delivered via emergent C-section with Apgar scores of 1, 1, & 1 shows a lipid lactate doublet at 1.3 ppm. Despite a relatively normal appearance of the left basal ganglia on DWI, this lactate suggests more diffuse deep gray matter injury. The patient did not survive.*
+
+
+*Axial ADC MR in a 31-week premature infant at 11 days following placental abruption shows ↓ signal in the bilateral thalami, consistent with a profound injury. Involvement of the thalami carries a poor prognosis.*
+
+
+*Axial T2WI MR in a 4-day-old term girl with seizures (who was born to a febrile mother with chorioamnionitis) shows loss of gray matter-white matter differentiation in the left temporal & bilateral parietooccipital lobes, suggesting a peripheral pattern of injury. However, there is subtle ↑ signal in the deep gray nuclei as well.*
+
+
+*Axial NECT in the same patient with neonatal seizures & severe HIE at 4 months of age shows severe brain parenchymal volume loss & areas of encephalomalacia . A few small Ca⁺⁺ are noted in the right frontal white matter. A left subdural collection has developed.*
+
+
+*Axial NECT in a 3-day-old term girl with HIE shows hypoattenuating deep gray nuclei that cannot be distinguished from adjacent white matter, a reliable CT finding of HIE.*
+
+
+*Axial T2 MR in a term neonate with severe perinatal asphyxia shows irregular signal & poor definition in the ventrolateral thalami & basal ganglia . The peripheral cortical ribbon appears normal.*
+
+
+*Axial DWI MR from the same exam shows restricted diffusion in the ventrolateral thalami . This pattern of injury is associated with brief but profound degrees of hypoxia, & it often causes dyskinetic cerebral palsy.*
+
+
+*Axial T2 MR in a term neonate with hypoplastic left heart syndrome shows loss of the defined cortical ribbon in a parasagittal distribution . This pattern of injury is associated with more prolonged but milder degrees of ischemia, which may be clinically inapparent.*
+
+
+*Coronal T1WI MR in the same infant several months later shows atrophy in the affected cortex & subcortical white matter , a finding typically associated with spastic cerebral palsy.*
+
+
+*Axial NECT shows Ca⁺⁺ of the thalami & posterior basal ganglia from status marmoratus. There is diffuse atrophy & a collapsed calvarium following remote mixed HIE.*
+
+
+*Coronal NECT with 3D reconstruction shows microcephaly & overlapping fused sutures in an infant with craniostenosis due to the failure of brain growth following mixed HIE.*
+
diff --git a/results.json b/results.json
index 5b035bf..1fa5218 100644
--- a/results.json
+++ b/results.json
@@ -1,111 +1,64 @@
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- "path": "docs_md/articles/intracranial-hemorrhage_3a9cbed6-aa2c-45a0-88bf-b39f1523ee85.md",
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- "docid": "3a9cbed6-aa2c-45a0-88bf-b39f1523ee85",
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- "title": "Epilepsy, Child",
- "docid": "a342e5b5-5b98-4003-a437-6d42a483b40e",
+ "path": "docs_md/articles/hypotensive-cerebral-infarction_a3d3dd38-629e-42fc-9d0d-9a03a39781eb.md",
+ "title": "Hypotensive Cerebral Infarction",
+ "docid": "a3d3dd38-629e-42fc-9d0d-9a03a39781eb",
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+ "Stroke",
+ "Cerebral Ischemia and Infarction",
+ "Hypotensive Cerebral Infarction"
],
"authors": [
{
- "key": "47381de4-c9fd-4999-8dd0-1808cd72db6b",
- "value": "Luke L. Linscott, MD"
+ "key": "cdbaaa96-a7b4-4498-a355-a2823a7d9e26",
+ "value": "Kelly A. Dahlstrom, DO"
+ },
+ {
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- "snippet": "# KEY FACTS - ## Terminology - Abusive head trauma (AHT) - Traumatic injury inflicted on infants & children by adults...",
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+ "title": "White Matter Tracts",
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},
{
- "title": "Anatomy Document",
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+ "title": "Basal Ganglia",
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{
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+ "title": "Language Overview",
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