464 lines
34 KiB
Markdown
464 lines
34 KiB
Markdown
---
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title: "Mesial Temporal Sclerosis"
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docid: "3861ee73-c82c-49f2-a60f-8fd08f7e6165"
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authors:
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- key: "a25c450b-3d34-4f64-bba3-cc0834813df6"
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value: "Miral D. Jhaveri, MD, MBA"
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- key: "99e1aff7-f42c-43a0-95ae-d89c8551aa01"
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value: "Kevin R. Moore, MD"
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breadcrumbs:
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name: "Brain"
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slug: "brain"
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treeNodeId: "6d8829f1-14d7-45af-8675-255189aa526a"
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name: "Diagnosis"
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treeNodeId: "51c00394-446e-4a38-94af-d3b1d14d34e8"
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name: "Pathology-Based Diagnoses"
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slug: "pathology-based-diagnoses"
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treeNodeId: "d9d3a8ed-f21b-4831-8c77-591a3500ef77"
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name: "Acquired Toxic/Metabolic/Degenerative Disorders"
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slug: "acquired-toxicmetabolicdegenerativ-"
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treeNodeId: "ba3cfeaf-64d9-4117-91e8-d2ce58783fc5"
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name: "Toxic, Metabolic, Nutritional, Systemic Diseases With CNS Manifestations"
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slug: "toxic-metabolic-nutritional-system-"
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treeNodeId: "06bd883b-8269-4044-8411-70f7ab75bb7a"
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name: "Mesial Temporal Sclerosis"
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slug: "mesial-temporal-sclerosis"
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treeNodeId: null
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category: "Brain"
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cmeTopicId: "3cf4636d-0dca-4ef5-9436-e9548e51ffaa"
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documentVersionId: "50d12781-ca5e-4e04-95ef-7b0e6babf338"
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imageCount: 22
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lastUpdated: "07/31/20"
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pageDescription: "Mesial Temporal Sclerosis"
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pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Acquired Toxic/Metabolic/Degenerative Disorders, Toxic, Metabolic, Nutritional, Systemic Diseases With CNS Manifestations, Mesial Temporal Sclerosis"
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pageTitle: "Mesial Temporal Sclerosis | STATdx"
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enhancedTitle: "Mesial Temporal Sclerosis"
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type: "DX"
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references: true
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breadcrumbs:
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- "Brain"
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- "Diagnosis"
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- "Pathology-Based Diagnoses"
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- "Acquired Toxic/Metabolic/Degenerative Disorders"
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- "Toxic, Metabolic, Nutritional, Systemic Diseases With CNS Manifestations"
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- "Mesial Temporal Sclerosis"
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---
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# KEY FACTS
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- ## Terminology
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- Seizure-associated neuronal loss & gliosis in hippocampus & adjacent structures
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- ## Imaging
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- Primary features: Abnormal T2 hyperintensity, hippocampal volume loss/atrophy, obscuration of internal architecture
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- Secondary signs: Ipsilateral fornix & mammillary body atrophy, enlarged ipsilateral temporal horn, & choroidal fissure
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- ↑ hyperintensity on DWI (T2 shine-through)
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- ↓ NAA in hippocampus, temporal lobe
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- ## Top Differential Diagnoses
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- Status epilepticus
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- Low-grade astrocytoma
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- Choroidal fissure cyst
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- Hippocampal sulcus remnant
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- Focal cortical dysplasia
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- ## Pathology
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- Prolonged febrile seizures may produce acute hippocampal injury → subsequent atrophy
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- Coexistent 2nd developmental lesion in 15% of patients with mesial temporal sclerosis (MTS)
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- ## Clinical Issues
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- Partial complex seizures
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- Often history of childhood febrile or medically intractable seizures
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- Surgical temporal lobectomy reserved for medically intractable seizures, intolerable drug side effects
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- ## Diagnostic Checklist
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- Most common cause of partial complex epilepsy in adult age group
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- Low-grade neoplasms & focal cortical dysplasia more common causes of partial complex epilepsy than MTS in pediatric age group
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# TERMINOLOGY
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- ## Abbreviations
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- Mesial temporal sclerosis (MTS)
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- ## Synonyms
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- Ammon horn sclerosis, hippocampal sclerosis (HS)
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- ## Definitions
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- Seizure-associated neuronal loss & gliosis in hippocampus & adjacent structures
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# IMAGING
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- ## General Features
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- ### Best diagnostic clue
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- Primary features: Abnormal T2 hyperintensity, hippocampal volume loss/atrophy, obscuration of internal architecture
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- Secondary signs: Ipsilateral fornix & mammillary body atrophy, enlarged ipsilateral temporal horn, & choroidal fissure
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- Additional findings: Loss of ipsilateral hippocampal head (pes) digitations, parahippocampal gyrus white matter (WM) atrophy, ↑ T2 signal in anterior temporal WM
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- ### Location
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- Mesial temporal lobe(s), 15-20% bilateral but usually asymmetric
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- Hippocampus > amygdala > fornix > mammillary bodies
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- ### Size
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- Slight to marked ↓ in hippocampal volume
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- ### Morphology
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- Abnormal shape, size of affected hippocampus
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- ## CT Findings
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- ### NECT
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- Usually normal; CT insensitive to MTS
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- ## MR Findings
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- ### T1WI
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- ↓ hippocampal size
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- Loss of normal hippocampal gray-white differentiation
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- ± ipsilateral fornix, mammillary body atrophy
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- Quantitative hippocampal volumetry: ↑ sensitivity of MTS detection (particularly bilateral MTS)
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- ### T2WI
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- Hippocampal atrophy
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- Obscuration of normal internal architecture
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- ↑ hippocampal signal intensity
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- ± ipsilateral fornix, mammillary body atrophy, dilatation of ipsilateral temporal horn
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- ± abnormal hyperintensity, volume loss in ipsilateral anterior temporal lobe
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- ### FLAIR
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- Hyperintense signal in abnormal hippocampus
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- ### DWI
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- ↑ hyperintensity on DWI (T2 shine-through)
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- ↑ diffusivity on ADC
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- DTI: ↓ fractional anisotropy affecting widespread WM tracts, extensive areas with ↑ radial diffusivities independent of disease side
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- ### T1WI C+
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- No enhancement
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- ### MRS
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- ↓ NAA in hippocampus, temporal lobe
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- ↓ NAA/Cho & ↓ NAA/Cho+Cr suggests MTS
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- ± lactate/lipid peaks after 24 hours of continual seizure
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- ## Angiographic Findings
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- Presurgical Wada testing: Neuropsychologic testing after intracarotid amobarbital (Amytal) injection
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- Lateralize memory & language functions
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- Predict postoperative memory loss, feasibility of surgery
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- May help lateralize seizure onset
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- fMRI mapping replacing Wada testing
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- ## Nuclear Medicine Findings
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- FDG PET: Hypometabolism in abnormal mesial temporal lobe
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- SPECT: Hypoperfusion (interictal) or hyperperfusion (ictal) in epileptogenic zone (EZ)
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- Sensitivity of ictal > interictal
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- ## Imaging Recommendations
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- ### Best imaging tool
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- High-resolution MR imaging
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- MRS, quantitative volumetry may help lateralize MTS in difficult cases
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- ### Protocol advice
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- Thin-section coronal T2WI & FLAIR (3 mm), coronal 3D SPGR (1-2 mm), angled perpendicular to long axis of hippocampus
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# DIFFERENTIAL DIAGNOSIS
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- [Status Epilepticus](/document/status-epilepticus/a058b733-4b80-46a1-8097-d68685ecf921)
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- Clinical history of multiple seizures or status epilepticus
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- Temporary T2 hyperintensity ± gyriform enhancement in affected cortex, hippocampus
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- ## Low-Grade Astrocytoma
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- Hyperintense temporal lobe WM mass (usually nonenhancing)
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- ± seizures, young adults typical
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- [Choroidal Fissure Cyst](/document/choroid-fissure-cyst/f60887bb-f021-401f-80b2-1d79e0a758e5)
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- Asymptomatic CSF signal cyst in choroidal fissure distorts normal hippocampus
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- Round on axial, coronal images
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- Oval, parallels temporal lobe long axis on sagittal imaging
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- No abnormal T2 hyperintensity in mesial temporal lobe
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- [Hippocampal Sulcus Remnant](/document/hippocampal-sulcus-remnant-cysts/3b54dc78-2c77-4cbb-9ab4-e5c6f5d8b228)
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- Failure of normal hippocampal sulcus involution → asymptomatic cyst between dentate gyrus, cornu ammonis (CA)
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- Common normal variant (10-15%)
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- [Cavernous Malformation](/document/cavernous-malformation/d6c0dfc6-25d3-4713-941f-373c68ca8f0d)
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- Heterogeneous hyperintense "popcorn" lesion with dark complete hemosiderin rim
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- ± seizures
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- ## Dysembryoplastic Neuroepithelial Tumor
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- [Demarcated "bubbly," variably enhancing cortical mass ± regional cortical dysplasia](/document/dnet/30baaad9-4835-4cf0-8b95-974d6517511e)
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- Partial complex seizures
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- [Focal Cortical Dysplasia](/document/focal-cortical-dysplasia/046564e0-5bb7-4f23-8a3e-010a68cfbafe)
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- Most common dual pathology associated with MTS
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- T2 hyperintensity in anterior temporal WM
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# PATHOLOGY
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- ## General Features
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- ### Etiology
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- Controversial whether acquired or developmental
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- Acquired: Follows complicated febrile seizures (FS), status epilepticus, encephalitis
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- Developmental: 2nd developmental lesion identified in 15%
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- 2-hit hypothesis: (1) Initial precipitating injury (like complicated seizures), (2) ↑ vulnerability (such as genetic predisposition or developmental anomaly)
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- Most likely MTS represents common outcome of both acquired & developmental processes
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- FS most common childhood seizure disorder (2-5%)
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- Prolonged FS may produce acute hippocampal injury → subsequent atrophy
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- ### Genetics
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- Familial cases of mesial temporal lobe epilepsy (TLE), FS reported
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- Recent studies suggest relationship between FS & later epilepsy development may be genetic
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- Syndrome-specific genes for FS (channelopathies) account for small proportion of FS cases
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- ### Associated abnormalities
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- Coexistent 2nd developmental lesion (15%)
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- ## Gross Pathologic & Surgical Features
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- Normal hippocampus divided anatomically into head (pes), body, tail
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- Subdivision into Ammon horn, dentate gyrus, hippocampal sulcus, fimbria, alveus, subiculum, parahippocampal gyrus, collateral sulcus
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- Mesial temporal lobe atrophy: Hippocampal body (85-90%), tail (60%), head (50%), amygdala (10%)
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- Absence of hemorrhage or necrosis
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- HS described by gross pathologists as shrunken & hardened hippocampus with characteristic histologic neuronal loss, glial proliferation
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- ## Microscopic Features
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- Chronic astrogliosis with fine fibrillary background of bland astrocytic nuclei & ↓ residual neurons
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- Selective loss of inhibitory interneurons, abnormal axonal sprouting, reorganization of neural transmitter receptors, alterations in 2nd messenger systems, & hyperexcitability of granule cells
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- Ammon horn, CA, contains 4 zones of granular cells: CA1, CA2, CA3, CA4
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- CA1, CA4 pyramidal cell layers most susceptible to ischemia
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- All hippocampal regions may show varying neuronal cell loss
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# CLINICAL ISSUES
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- ## Presentation
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- ### Most common signs/symptoms
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- Partial complex seizures, automatisms
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- Simple at younger ages, increasingly complex & discrete with age
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- Motor manifestations ↓ with ↑ age; less abundant in adults
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- ### Other signs/symptoms
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- May progress to generalized tonic-clonic seizures
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- ### Clinical profile
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- Often history of childhood febrile or medically intractable seizures
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- History of complex or prolonged FS ↑ risk for development of hippocampal injury, MTS
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- Surface electro- (EEG) or magneto- (MEG) encephalogram helpful for localization (60-90%)
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- Intracranial EEG (subdural or depth electrodes) may be indicated if noninvasive studies discordant
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- ## Demographics
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- ### Age
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- Disease of older children, young adults
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- ### Sex
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- No sex predominance
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- ### Epidemiology
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- MTS accounts for majority of epilepsy patients undergoing temporal lobe seizure surgery
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- ## Natural History & Prognosis
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- Anterior temporal lobectomy 70-90% successful in MTS, 40-55% if MR normal
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- ↓ surgical success when amygdala involved
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- ## Treatment
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- Clinical management based on phenotypic features of initial febrile & subsequent seizures
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- Medical treatment initial approach
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- Surgical temporal lobectomy reserved for medically intractable seizures, intolerable drug side effects
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- Resection includes anterior temporal lobe, majority of hippocampus, variable portions of amygdala
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- Surgical resection of EZ
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- MR-guided laser interstitial thermal therapy (MRgLITT) less invasive option for stereotactic ablation of EZ
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# DIAGNOSTIC CHECKLIST
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- ## Consider
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- Most common cause of partial complex epilepsy in adults
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- Bilateral in 15-20%; difficult to detect without quantitative volumetry unless severe
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- MTS imaging findings not found in normal seizure-free patients (controversial)
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- ## Image Interpretation Pearls
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- Coronal high-resolution T2WI, FLAIR MR most sensitive for MTS; dual pathology in 15%
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- In pediatric age group, low-grade neoplasms & cortical dysplasia more common causes of partial complex epilepsy than MTS
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f1594712-2ab3-4d9e-9a3d-a75b51f1c879
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## References
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# Selected References
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1. [Hsu CCT et al: Imaging the patient with epilepsy. In Hodler J et al: Diseases of the Brain, Head & Neck, Spine 2020-23. Diagnostic Imaging. Springer, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32119252%5Bpmid%5D)
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1. [Strnad BS et al: An image processing algorithm to aid diagnosis of mesial temporal sclerosis in children: a case-control study. Pediatr Radiol. 50(1):98-106, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31578627%5Bpmid%5D)
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1. [Youngerman BE et al: Magnetic resonance imaging-guided laser interstitial thermal therapy for epilepsy: systematic review of technique, indications, and outcomes. Neurosurgery. 86(4):E366-82, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31980831%5Bpmid%5D)
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1. [Dahi F et al: Image processing to improve detection of mesial temporal sclerosis in adults. AJNR Am J Neuroradiol. 40(5):798-801, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30948379%5Bpmid%5D)
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1. [Mettenburg JM et al: Improved detection of subtle mesial temporal sclerosis: validation of a commercially available software for automated segmentation of hippocampal volume. AJNR Am J Neuroradiol. 40(3):440-5, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30733255%5Bpmid%5D)
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1. [Chong S et al: Surgical treatment of lesional mesial temporal lobe epilepsy. J Epilepsy Res. 8(1):6-11, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30090756%5Bpmid%5D)
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1. [Corrêa DG et al: Widespread white matter DTI alterations in mesial temporal sclerosis independent of disease side. Epilepsy Behav. 87:7-13, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30149360%5Bpmid%5D)
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1. [Azab M et al: Mesial temporal sclerosis: accuracy of NeuroQuant versus Neuroradiologist. AJNR Am J Neuroradiol. 36(8):1400-6, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25907519%5Bpmid%5D)
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1. [Hamelin S et al: Revisiting hippocampal sclerosis in mesial temporal lobe epilepsy according to the "two-hit" hypothesis. Rev Neurol (Paris). 171(3):227-35, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25748332%5Bpmid%5D)
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1. [French JA et al: Can febrile status cause hippocampal sclerosis? Ann Neurol. 75(2):173-4, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24443389%5Bpmid%5D)
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1. [Roessler K et al: Improved resection in lesional temporal lobe epilepsy surgery using neuronavigation and intraoperative MR imaging: favourable long term surgical and seizure outcome in 88 consecutive cases. Seizure. 23(3):201-7, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24355699%5Bpmid%5D)
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1. [Thom M: Review: Hippocampal sclerosis in epilepsy: a neuropathology review. Neuropathol Appl Neurobiol. 40(5):520-43, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24762203%5Bpmid%5D)
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1. [Kapina V et al: Hippocampal sclerosis and chronic epilepsy following posterior reversible encephalopathy syndrome. Epileptic Disord. 15(4):451-4, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=24515311%5Bpmid%5D)
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1. [Blümcke I et al: Defining clinico-neuropathological subtypes of mesial temporal lobe epilepsy with hippocampal sclerosis. Brain Pathol. 22(3):402-11, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22497612%5Bpmid%5D)
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1. [Bonilha L et al: Subtypes of medial temporal lobe epilepsy: influence on temporal lobectomy outcomes? Epilepsia. 53(1):1-6, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22050314%5Bpmid%5D)
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1. [Malmgren K et al: Hippocampal sclerosis--origins and imaging. Epilepsia. 53 Suppl 4:19-33, 2012](http://www.ncbi.nlm.nih.gov/pubmed/?term=22946718%5Bpmid%5D)
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1. [Kröll-Seger J et al: Non-paraneoplastic limbic encephalitis associated with antibodies to potassium channels leading to bilateral hippocampal sclerosis in a pre-pubertal girl. Epileptic Disord. 11(1):54-9, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19251579%5Bpmid%5D)
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1. [Bote RP et al: Hippocampal sclerosis: histopathology substrate and magnetic resonance imaging. Semin Ultrasound CT MR. 29(1):2-14, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18383904%5Bpmid%5D)
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1. [Chang YC et al: Long-term neuroplasticity effects of febrile seizures in the developing brain. Chang Gung Med J. 31(2):125-35, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18567412%5Bpmid%5D)
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1. [Focke NK et al: Voxel-based diffusion tensor imaging in patients with mesial temporal lobe epilepsy and hippocampal sclerosis. Neuroimage. 40(2):728-37, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18261930%5Bpmid%5D)
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1. [Carne RP et al: 'MRI-negative PET-positive' temporal lobe epilepsy (TLE) and mesial TLE differ with quantitative MRI and PET: a case control study. BMC Neurol. 7:16, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17588263%5Bpmid%5D)
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1. [Ray A et al: Temporal lobe epilepsy in children: overview of clinical semiology. Epileptic Disord. 7(4):299-307, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=16338672%5Bpmid%5D)
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1. [Ray A et al: Treatment options and paradigms in childhood temporal lobe epilepsy. Expert Rev Neurother. 5(6):785-801, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=16274336%5Bpmid%5D)
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1. [Sloviter RS: The neurobiology of temporal lobe epilepsy: too much information, not enough knowledge. C R Biol. 328(2):143-53, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=15771000%5Bpmid%5D)
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1. [Cendes F: Febrile seizures and mesial temporal sclerosis. Curr Opin Neurol. 17(2):161-4, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15021243%5Bpmid%5D)
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1. [Theodore WH: Recent advances and trends in epilepsy imaging: pathogenesis and pathophysiology. Rev Neurol Dis. 1(2):53-9, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=16400258%5Bpmid%5D)
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1. [Van Paesschen W: Qualitative and quantitative imaging of the hippocampus in mesial temporal lobe epilepsy with hippocampal sclerosis. Neuroimaging Clin N Am. 14(3):373-400, vii, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15324854%5Bpmid%5D)
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1. [Volcy Gómez M: [Mesial temporal lobe epilepsy: its physiopathology, clinical characteristics, treatment and prognosis] Rev Neurol. 38(7):663-7, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15098189%5Bpmid%5D)
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1. [Bocti C et al: The pathological basis of temporal lobe epilepsy in childhood. Neurology. 60(2):191-5, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12552029%5Bpmid%5D)
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1. [Sokol DK et al: From swelling to sclerosis: acute change in mesial hippocampus after prolonged febrile seizure. Seizure. 12(4):237-40, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12763472%5Bpmid%5D)
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1. [Benbadis SR et al: MRI evidence of mesial temporal sclerosis in subjects without seizures. Seizure. 11(5):340-3, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12076108%5Bpmid%5D)
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1. [Capizzano AA et al: Multisection proton MR spectroscopy for mesial temporal lobe epilepsy. AJNR Am J Neuroradiol. 23(8):1359-68, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12223379%5Bpmid%5D)
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1. [Kumlien E et al: Treatment outcome in patients with mesial temporal sclerosis. Seizure. 11(7):413-7, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12237065%5Bpmid%5D)
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1. [Kuzniecky RI et al: Neuroimaging of epilepsy. Semin Neurol. 22(3):279-88, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12528053%5Bpmid%5D)
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1. [Lewis DV et al: Do prolonged febrile seizures produce medial temporal sclerosis? Hypotheses, MRI evidence and unanswered questions. Prog Brain Res. 135:263-78, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12143347%5Bpmid%5D)
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1. [Scott RC et al: Magnetic resonance imaging findings within 5 days of status epilepticus in childhood. Brain. 125(Pt 9):1951-9, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12183341%5Bpmid%5D)
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1. [Spencer SS: When should temporal-lobe epilepsy be treated surgically? Lancet Neurol. 1(6):375-82, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12849399%5Bpmid%5D)
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1. [Castillo M et al: Proton MR spectroscopy in patients with acute temporal lobe seizures. AJNR Am J Neuroradiol. 22(1):152-7, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11158901%5Bpmid%5D)
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1. [Moore KR et al: Incidental detection of hippocampal sclerosis on MR images: is it significant? AJNR Am J Neuroradiol. 20(9):1609-12, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10543629%5Bpmid%5D)
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1. [Ho SS et al: Temporal lobe developmental malformations and epilepsy: dual pathology and bilateral hippocampal abnormalities. Neurology. 50(3):748-54, 1998](http://www.ncbi.nlm.nih.gov/pubmed/?term=9521268%5Bpmid%5D)
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1. [Lee DH et al: MR in temporal lobe epilepsy: analysis with pathologic confirmation. AJNR Am J Neuroradiol. 19(1):19-27, 1998](http://www.ncbi.nlm.nih.gov/pubmed/?term=9432153%5Bpmid%5D)
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1. [Bronen RA et al: Regional distribution of MR findings in hippocampal sclerosis. AJNR Am J Neuroradiol. 16(6):1193-200, 1995](http://www.ncbi.nlm.nih.gov/pubmed/?term=7677010%5Bpmid%5D)
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## Images
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### Selected Images
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*Coronal graphic depicts the characteristic appearance of mesial temporal sclerosis (MTS). The right hippocampus <img src='img/arrows/CO.png'/> is small (atrophic) with loss of normal internal architecture, reflecting neuronal loss and gliosis. Note concordant atrophy of the ipsilateral fornix <img src='img/arrows/CS.png'/> and widening of the ipsilateral temporal horn and choroidal fissure.*
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*Coronal T2 MR at 3.0T demonstrates normal bilateral hippocampal anatomy <img src='img/arrows/CC.png'/>, size, and signal intensity. Note distinct layers of gray and white matter in the hippocampus.*
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*Coronal T1 true inversion recovery MR at 3.0T shows asymmetric right hippocampal volume loss <img src='img/arrows/CS.png'/> and obscuration of normal internal gray-white differentiation. The ipsilateral fornix <img src='img/arrows/CC.png'/> is smaller than the normal left fornix.*
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*Coronal T2 MR at 3.0T in the same patient with right hippocampal sclerosis (HS) <img src='img/arrows/CS.png'/> shows hippocampal volume loss and obscuration of normal internal architecture but normal T2 signal intensity. FLAIR better shows the increase in signal intensity.*
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*Coronal T2 MR in a patient with epilepsy shows a vertical left collateral sulcus <img src='img/arrows/CS.png'/> and a globular hippocampus <img src='img/arrows/CC.png'/>. This common variation is due to failure of hippocampal inversion.*
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*Coronal T2 MR in a patient with temporal lobe epilepsy demonstrates primary and secondary imaging features of MTS. There is severe left hippocampal atrophy and hyperintensity <img src='img/arrows/CC.png'/>. Secondary features are atrophy of the left fornix <img src='img/arrows/CS.png'/> and mammillary body <img src='img/arrows/WS.png'/> as well as dilation of temporal horn <img src='img/arrows/CO.png'/>.*
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*Coronal T2-weighted MR at 3.0T in a patient with prolonged febrile seizure shows abnormal enlargement and T2 hyperintensity in the right hippocampus <img src='img/arrows/CS.png'/>. DWI (not shown) revealed reduced diffusion. The patient later developed HS.*
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*Coronal FLAIR MR in a patient with longstanding partial complex epilepsy shows bilateral hyperintense hippocampi <img src='img/arrows/CC.png'/> with loss of normal architecture, volume loss, R > L, consistent with bilateral mesial temporal sclerosis.*
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*Coronal T2WI MR in a patient with chronic seizures with large right temporal lobe cavernous malformation <img src='img/arrows/CO.png'/> demonstrates all 3 primary determinants of right HS <img src='img/arrows/CC.png'/> (volume loss, T2 hyperintensity, and loss of internal architecture).*
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*Coronal FLAIR MR in the same patient with right temporal lobe cavernous malformation <img src='img/arrows/CO.png'/> better shows HS <img src='img/arrows/CS.png'/>. Hyperintensity is usually more conspicuous on FLAIR, while T2 is better for depicting internal structure.*
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### Additional Images
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*Coronal T2WI MR shows classic left hippocampal sclerosis with abnormal T2 hyperintensity, ipsilateral atrophy, and loss of internal architecture.*
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*Coronal T1WI 3D SPGR demonstrates classic left HS with ipsilateral atrophy and loss of normal internal gray-white differentiation.*
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*Coronal FLAIR MR in a patient with complex partial epilepsy with left hippocampal sclerosis shows ipsilateral volume loss and conspicuous hyperintensity resulting from gliosis.*
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*Coronal T2WI MR in a 23 year old with complex partial seizures reveals abnormal hyperintensity and atrophy of the right hippocampus <img src='img/arrows/WS.png'/>. Loss of internal architecture is also seen, typical of MTS.*
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*Coronal T2WI MR shows abnormal hyperintense signal and atrophy of the right anterior temporal lobe related to prior injury.*
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*Coronal T2WI MR in a patient with acute complex partial seizures shows abnormal enlargement and hyperintensity of the right hippocampus <img src='img/arrows/BS.png'/>. Follow-up imaging 9 months later (not shown) confirmed subsequent development of right MTS.*
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*Coronal STIR MR at 3.0T in a normal nonepileptic patient shows a prominent left collateral sulcus <img src='img/arrows/WS.png'/> that changes the morphology of the adjacent normal hippocampus. This common anatomical variant can be mistaken for HS.*
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*Coronal STIR MR at 3.0T in an individual who had been born prematurely with developmental delay shows diffuse white matter volume loss (L > R) and concordant left hippocampal volume loss with the abnormal T2 hyperintensity <img src='img/arrows/WS.png'/> of HS.*
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*Coronal T2WI FS MR in a patient with longstanding partial complex epilepsy shows bilateral shrunken, hyperintense hippocampi <img src='img/arrows/WS.png'/> associated with diminished white matter volume in temporal lobes, consistent with bilateral HS.*
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*Coronal STIR MR at 3.0 T in a normal nonepileptic patient imaged for headaches demonstrates normal bilateral hippocampal anatomy <img src='img/arrows/CC.png'/>, size, and signal intensity.*
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*Coronal T2 MR in a patient with epilepsy shows a vertical left collateral sulcus <img src='img/arrows/CS.png'/> and a globular hippocampus <img src='img/arrows/CC.png'/>. This common variation can be mistaken for HS.*
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*Coronal T2 MR in a patient with longstanding partial complex epilepsy shows bilateral hyperintense hippocampi <img src='img/arrows/CC.png'/> with volume loss, R > L, consistent with bilateral MTS.*
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