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title, docid, authors, breadcrumbs, category, cmeTopicId, documentVersionId, imageCount, lastUpdated, pageDescription, pageKeywords, pageTitle, enhancedTitle, type, references, anatomy, cases, breadcrumbs
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| Status Epilepticus | a058b733-4b80-46a1-8097-d68685ecf921 |
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Brain | 278eaa3d-09a7-46df-ade2-ce0997aab6eb | 02f328e2-8c74-4253-8ec4-2e6384af5444 | 30 | 06/06/20 | Status Epilepticus | Brain, Diagnosis, Pathology-Based Diagnoses, Acquired Toxic/Metabolic/Degenerative Disorders, Toxic, Metabolic, Nutritional, Systemic Diseases With CNS Manifestations, Status Epilepticus | Status Epilepticus | STATdx | Status Epilepticus | DX | true |
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title: "Status Epilepticus" docid: "a058b733-4b80-46a1-8097-d68685ecf921" authors:
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- "Brain"
- "Diagnosis"
- "Pathology-Based Diagnoses"
- "Acquired Toxic/Metabolic/Degenerative Disorders"
- "Toxic, Metabolic, Nutritional, Systemic Diseases With CNS Manifestations"
- "Status Epilepticus"
KEY FACTS
-
Terminology
- Seizure with ≥ 5 minutes continuous clinical &/or electrographic seizure activity, or recurrent seizure activity without recovery between seizures
- Synonyms: Transient seizure-related MR changes, reversible postictal cerebral edema
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Imaging
- T2/FLAIR hyperintensity in gray matter (GM) &/or subcortical white matter (WM) with mild mass effect - May involve hippocampus, corpus callosum, thalamus (particularly pulvinar nucleus) - Transient subcortical WM T2 hypointensity
- DWI: Restricted diffusion acutely
- T1WI C+: Variable gyriform or leptomeningeal enhancement
- PWI: Marked hyperemia, ↑ rCBF and rCBV in ictal state
- Interictal: Epileptogenic zone hypoperfusion/-metabolic
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Top Differential Diagnoses
- Cerebritis
- Cerebral ischemia-infarction
- Herpes encephalitis
- Astrocytoma
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Clinical Issues
- Active seizures &/or status epilepticus
- Other signs/symptoms: Location dependent
-
Diagnostic Checklist
- Acute seizures or status epilepticus may mimic other pathology, such as tumor progression or cerebritis
- Clinical information and follow-up imaging often differentiate from other etiologies
- Look for underlying mass that may have caused seizures/status epilepticus
- Seizure-related changes usually resolve within days to weeks
TERMINOLOGY
-
Abbreviations
- Status epilepticus (SE)
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Synonyms
- Transient seizure-related MR changes, reversible postictal cerebral edema
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Definitions
- Seizure with ≥ 5 minutes continuous clinical &/or electrographic seizure activity, or recurrent seizure activity without recovery between seizures
- MR changes associated with seizures likely related to transient cerebral edema
IMAGING
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General Features
-
Best diagnostic clue
- T2 hyperintensity in gray matter (GM) &/or subcortical white matter (WM) with mild mass effect - May focally involve hippocampus, corpus callosum, thalamus (particularly pulvinar nucleus) -
Location
- Supratentorial, related to epileptogenic focus - Typically cortex &/or subcortical WM - May involve focal structures - Hippocampus (febrile or partial complex seizures) - Splenium of corpus callosum - Pulvinar of thalamus - Occasionally cerebellar involvement
-
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CT Findings
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NECT
- Initial scans may be normal - Hypodensity in cortex &/or subcortical WM - Hippocampus, splenium of corpus callosum, thalamus (particularly pulvinar nucleus) may be involved - No hemorrhage -
CECT
- Variable enhancement: None to marked
-
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MR Findings
-
T1WI
- Hypointensity in cortex &/or subcortical WM - Swelling and ↑ volume of involved cortical gyri - Blurring of corticomedullary junction - Hippocampus, splenium of corpus callosum, thalamus (particularly pulvinar nucleus) may be involved - Rarely cerebellar involvement due to crossed cerebellar diaschisis - Delayed: Cortical laminar necrosis with T1 hyperintensity -
T2WI
- Hyperintensity in cortex &/or subcortical WM - Swelling and ↑ volume of involved cortical gyri - Transient subcortical WM hypointensity - Hippocampus, corpus callosum splenium, thalamus (particularly pulvinar nucleus) may be involved - Delayed: Focal brain atrophy, mesial temporal sclerosis -
FLAIR
- Hyperintensity in cortex &/or subcortical WM - Transient subcortical WM hypointensity - Mild edema and mass effect - Hippocampus, splenium of corpus callosum, pulvinar may be involved -
T2* GRE
- No hemorrhage - SWI: Focally diminished cortical veins in hyperperfused ictal regions -
DWI
- Restricted diffusion with decrease in ADC map acutely - ADC maps normal interictally, elevated in chronic seizures -
PWI
- Marked hyperemia in region of epileptic focus, elevated rCBF and rCBV maps - ASL: Elevated CBF ictal state -
T1WI C+
- Variable enhancement: None to marked - May see gyriform or leptomeningeal enhancement -
MRS
- Lipids &/or lactate shown in hippocampi of temporal lobe epilepsy (TLE) patients within 24 hours of last seizure - Follow-up MRS after seizures under control show no lipids/lactate
-
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Nuclear Medicine Findings
- Seizures: ↑ metabolism and perfusion
- PET: ↑ glucose metabolism and metabolic rate
- HMPAO SPECT: High uptake in affected cerebral lobe during or immediately after seizure
- Interictal: Epileptogenic zone hypoperfusion/-metabolic
-
Imaging Recommendations
-
Best imaging tool
- MR is most sensitive -
Protocol advice
- Contrast-enhanced MR with DWI and perfusion
-
DIFFERENTIAL DIAGNOSIS
-
Cerebritis
- T2-hyperintense "mass" with mass effect
- Typically DWI positive, patchy enhancement
-
- Typical vascular distribution (anterior cerebral artery, middle cerebral artery, posterior cerebral artery)
- Acute/subacute DWI positive
- Wedge-shaped, involves GM and WM
- Gyriform enhancement in subacute ischemia
-
- Confined to limbic system, temporal lobes
- Blood products, enhancement typical
- Acute onset, often with fever and seizures
-
Astrocytoma
- Infiltrating WM mass, may extend to cortex, variable enhancement
- May cause epilepsy
-
MELAS
- Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes
- Multifocal bilateral T2 hyperintensities
- Predominantly GM involvement, may involve subcortical WM
- Ischemia in > 1 vascular territory
- MRS shows lactate peak
-
- Abnormal T2 hyperintensity in mesial temporal lobe
- Hippocampal volume loss and architectural distortion
-
- Multiple small areas of T2 hyperintensity in deep and subcortical WM, often bilateral, ± enhancement
- GM involvement may be seen
-
- Multifocal WM lesions, deep gray nuclei
- Incomplete rim or horseshoe-shaped enhancement
PATHOLOGY
-
General Features
-
Etiology
- SE evolves through initiation phase to maintenance phase - Initiation phase: Triggering stimuli evoke discrete seizures, tend to abate as soon as stimulus is removed - Maintenance phase: Discrete seizures coalesce, triggering stimuli no longer required to sustain seizures - Intensity and duration of stimulation has direct influence on transition from initiation to maintenance phase - Persistent ictal activity → increase glucose utilization and oxygen extraction → uncoupling of blood flow-metabolism ratio → ↓ ADP and tissue hypoxia → anaerobic glycolysis - ↑ Glutamate and ↓ GABA , Na+/K+ pump failure, intracellular cytotoxic edema - Blood-brain barrier breakdown → vasogenic edema - MR signal abnormalities related to transient vasogenic &/or cytotoxic edema - Redistribution of intracellular and extracellular water, related to alteration in cell membrane permeability or cytotoxic edema - Hippocampus involvement by SE may result in mesial temporal sclerosis - Involvement of corpus callosum splenium, 2 theories - Transient focal edema related to transhemispheric connection of seizure activity - Reversible demyelination related to antiepileptic drugs -
Anatomic considerations - Portions of brain most vulnerable to damage from SE - CA1, CA3 of hippocampus, amygdala, piriform cortex, cerebellar cortex, thalamus, cerebral cortex
-
-
Staging, Grading, & Classification
- SE classified broadly as convulsive and nonconvulsive - Convulsive SE further classified - Tonic-clonic, tonic, clonic, myoclonic - Nonconvulsive SE
-
Gross Pathologic & Surgical Features
- Acutely: Swelling of cortex &/or subcortical WM or hippocampus
- Chronic: Atrophy of involved cortex &/or subcortical WM
-
Microscopic Features
- Acutely - Reactive astrocytes with swollen cytoplasm and neuropil, consistent with cytotoxic edema
- Chronic - Marked neuronal loss with intense astrocytic reaction; reactive astrocytes replacing absent neurons
- Gliosis and neuronal loss affecting GM-WM junction with extension to cortex
CLINICAL ISSUES
-
Presentation
-
Most common signs/symptoms
- Active seizures &/or SE - Other signs/symptoms: Location dependent - Nonconvulsive SE: Abnormal mental status, unresponsiveness, ocular motor abnormalities -
Clinical profile
- EEG shows seizure activity
-
-
Demographics
-
Age
- Bimodal age distribution, peaks during infancy and in elderly -
Sex
- No sex predominance -
Epidemiology
- 7-40 cases/100,000 person-years
-
-
Natural History & Prognosis
- Typically complete resolution with treatment of seizures
- May be complicated by infarction related to hypoxemia
-
Treatment
- Treatment of underlying seizure disorder - Antiepileptic medicines primary therapy
- Surgical resection in patients with intractable epilepsy
DIAGNOSTIC CHECKLIST
-
Consider
- Acute seizures or SE may mimic other pathology, such as tumor or cerebritis
- Clinical information and follow-up imaging often differentiate seizure-related MR changes from other etiologies
-
Image Interpretation Pearls
- Look for underlying lesion that may have caused seizures/SE
- Seizure-related changes will usually resolve within days to weeks on follow-up imaging
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References
Selected References
- Husari KS et al: New-onset refractory status epilepticus in children: etiologies, treatments, and outcomes. Pediatr Crit Care Med. 21(1):59-66, 2020
- Guerriero RM et al: Imaging modalities to diagnose and localize status epilepticus. Seizure. 68:46-51, 2019
- Sculier C et al: New onset refractory status epilepticus (NORSE). Seizure. 68:72-8, 2019
- Strohm T et al: FDG-PET and MRI in the evolution of new-onset refractory status epilepticus. AJNR Am J Neuroradiol. 40(2):238-44, 2019
- Meletti S et al: Neuroimaging of status epilepticus. Epilepsia. 59 Suppl 2:113-9, 2018
- Betjemann JP et al: Status epilepticus in adults. Lancet Neurol. 14(6):615-24, 2015
- Cartagena AM et al: Reversible and irreversible cranial MRI findings associated with status epilepticus. Epilepsy Behav. 33:24-30, 2014
- Ohe Y et al: MRI abnormality of the pulvinar in patients with status epilepticus. J Neuroradiol. 41(4):220-6, 2014
- Di Bonaventura C et al: Diffusion-weighted magnetic resonance imaging in patients with partial status epilepticus. Epilepsia. 50 Suppl 1:45-52, 2009
- Goyal MK et al: Peri-ictal signal changes in seven patients with status epilepticus: interesting MRI observations. Neuroradiology. 51(3):151-61, 2009
- Katramados AM et al: Periictal diffusion abnormalities of the thalamus in partial status epilepticus. Epilepsia. 50(2):265-75, 2009
- Masterson K et al: Postictal deficit mimicking stroke: role of perfusion CT. J Neuroradiol. 36(1):48-51, 2009
- Milligan TA et al: Frequency and patterns of MRI abnormalities due to status epilepticus. Seizure. 18(2):104-8, 2009
- Nair PP et al: Role of cranial imaging in epileptic status. Eur J Radiol. 70(3):475-80, 2009
- Buracchio T et al: Restricted diffusion on magnetic resonance imaging in partial status epilepticus. Arch Neurol. 65(2):278-9, 2008
- Goyal MK et al: Role of MR imaging in the evaluation of etiology of status epilepticus. J Neurol Sci. 272(1-2):143-50, 2008
- Provenzale JM et al: Hippocampal MRI signal hyperintensity after febrile status epilepticus is predictive of subsequent mesial temporal sclerosis. AJR Am J Roentgenol. 190(4):976-83, 2008
- Yu JT et al: Diffusion-weighted magnetic resonance imaging demonstrates parenchymal pathophysiological changes in epilepsy. Brain Res Rev. 59(1):34-41, 2008
- Kuster GW et al: Hippocampal sclerosis and status epilepticus: cause or consequence? A MRI study. Arq Neuropsiquiatr. 65(4B):1101-4, 2007
- Parmar H et al: Acute symptomatic seizures and hippocampus damage: DWI and MRS findings. Neurology. 66(11):1732-5, 2006
- Calistri V et al: Visualization of evolving status epilepticus with diffusion and perfusion MR imaging. AJNR Am J Neuroradiol. 24(4):671-3, 2003
- Hicdonmez T et al: Reversible postictal MRI change mimicking structural lesion. Clin Neurol Neurosurg. 105(4):288-90, 2003
- Oster J et al: Diffusion-weighted imaging abnormalities in the splenium after seizures. Epilepsia. 44(6):852-4, 2003
- Cohen-Gadol AA et al: Transient postictal magnetic resonance imaging abnormality of the corpus callosum in a patient with epilepsy. Case report and review of the literature. J Neurosurg. 97(3):714-7, 2002
- Amato C et al: Transient MRI abnormalities associated with partial status epilepticus: a case report. Eur J Radiol. 38(1):50-4, 2001
- Castillo M et al: Proton MR spectroscopy in patients with acute temporal lobe seizures. AJNR Am J Neuroradiol. 22(1):152-7, 2001
- Kim JA et al: Transient MR signal changes in patients with generalized tonicoclonic seizure or status epilepticus: periictal diffusion-weighted imaging. AJNR Am J Neuroradiol. 22(6):1149-60, 2001
- Polster T et al: Transient lesion in the splenium of the corpus callosum: three further cases in epileptic patients and a pathophysiological hypothesis. J Neurol Neurosurg Psychiatry. 70(4):459-63, 2001
- Sagiuchi T et al: Transient seizure activity demonstrated by Tc-99m HMPAO SPECT and diffusion-weighted MR imaging. Ann Nucl Med. 15(3):267-70, 2001
- Men S et al: Selective neuronal necrosis associated with status epilepticus: MR findings. AJNR Am J Neuroradiol. 21(10):1837-40, 2000
- Kim SS et al: Focal lesion in the splenium of the corpus callosum in epileptic patients: antiepileptic drug toxicity? AJNR Am J Neuroradiol. 20(1):125-9, 1999
- Aykut-Bingol C et al: Reversible MRI lesions after seizures. Seizure. 6(3):237-9, 1997
- Chan S et al: Reversible signal abnormalities in the hippocampus and neocortex after prolonged seizures. AJNR Am J Neuroradiol. 17(9):1725-31, 1996
- Cox JE et al: Seizure-induced transient hippocampal abnormalities on MR: correlation with positron emission tomography and electroencephalography. AJNR Am J Neuroradiol. 16(8):1736-8, 1995
- Wasterlain CG et al: Pathophysiological mechanisms of brain damage from status epilepticus. Epilepsia. 34 Suppl 1:S37-53, 1993
Anatomy
Default Mode Network
Brain/ANATOMY:a29f7551-d39d-4deb-933e-b8d2816168c3
Gyral/Sulcal Anatomy
Brain/ANATOMY:849da2a0-4a32-4a07-8f00-c69291e59434
Language Overview
Brain/ANATOMY:40f2ed79-0d31-4943-aaa2-7c3244a7e87b
Functional Network Overview
Brain/ANATOMY:ef0be4c8-3d36-4ca9-b4c5-f22f66d2b367
Attention Control Network
Brain/ANATOMY:a1bedda5-6478-40b2-98e7-6c5f5363b06f
Limbic Network
Brain/ANATOMY:e1a20b61-b2c1-44c5-ba04-59843855bfef
Memory Overview
Brain/ANATOMY:40e2e25f-421b-4653-94e3-641b09b47e4d
Social Brain Anatomy
Brain/ANATOMY:0352d34a-5966-494e-b9c3-c26bde257bca
Cerebral Hemispheres Overview
Brain/ANATOMY:7006e397-5012-4027-aff8-e8d7158166ee
Gyral/Sulcal Anatomy
Brain/ANATOMY:299a5990-1805-4018-85b5-191d8416385b
Functional Network Overview
Brain/ANATOMY:7b97f239-0f6f-4809-ac44-594cdf4842d5
Brain
Ultrasound/ANATOMY:080771c2-02f3-408d-ad70-04a80d849500
Limbic System
Brain/ANATOMY:f2a117ed-9429-441d-baa0-5e99e05722ac
Cases
- {'cases': [{'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}, {'key': '2f45db48-acf1-4676-90d6-fe76257ce931', 'value': 'Michael Brant-Zawadzki, MD'}], 'caseVersionId': '29a86215-0920-4c14-863a-8e640ee14244', 'description': "NECT (#1) and CECT scans (#2) showed no abnormality so MR was obtained. T2WI (#3), FLAIR (#4) and DWI (#5) showed no abnormality. MRA (#6) showed no occluded vessels. MR perfusion was obtained and shows markedly increased cerebral blood flow and cerebral blood volume in the right parietal lobe (arrows, #7-9) compared to the normal left side.\n\nThe patient's left-sided weakness resolved over the next several hours. It was concluded he had had an unobserved seizure with Todd's paralysis. The markedly increased cerebral blood flow is from hyperperfusion induced by the seizure.", 'history': 'Elderly patient found down with left hemiparesis and was taken to ER.', 'imagePoolId': '07b96b17-d107-4e84-9fc0-e4d70f9d2e46', 'name': 'After seizure', 'teachingPoint': None}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '64b22fed-89da-4dff-91dd-2a19d04743f7', 'description': 'Sagittal (#1) and axial (#2) T2WIs show hyperintensity in corpus callosum splenium (arrows) caused by transient status epilepticus.', 'history': 'Imaged following status epilepticus.', 'imagePoolId': 'a73a8738-c191-434d-8d07-6dfef3fdcb7e', 'name': 'Seizure hyperperfusion', 'teachingPoint': None}, {'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': 'cae90331-1f21-443b-80dd-e30e2ce0e096', 'description': 'Typical case of MR hyperintensities related to status epilepticus. \n\nAxial diffusion image (#1) demonstrates a solitary round focus of increased signal (open arrow). Corresponding ADC map (#2) shows corresponding hypointensity, compatible with true restricted diffusion (arrow). Standard T2 weighted imaging (#3) shows a subtle focus of hyperintensity (curved arrow) in the area of diffusion abnormality. \n\nComments: Transient T2 hyperintense foci may be observed in patients during, or soon after, status epilepticus. Typical areas of involvement include gray matter and/or subcortical white matter, although isolated foci can affect the hippocampus or corpus callosum. Mild mass effect is common. When the corpus callosum is involved, there are two theories regarding pathophysiology: 1.) transient edema due to transhemispheric connectivity of seizure activity, or 2.) reversible demyelination from antiepileptic medications. \n\nDiffusion imaging of such foci usually shows restricted diffusion acutely. If perfusion imaging is performed, there is hyperemia ipsilateral to the epileptic focus, with rCBF elevation. Enhancement is variable; when present, it is typically gyriform or leptomeningeal. Many cases resolve completely in days to weeks. Imaging findings can overlap with infectious and inflammatory pathology such as cerebritis/encephalitis and demyelination (ADEM, MS), and cases of progressing tumor, some of which may also present with seizures, so the diagnosis is aided by clinical information and follow-up imaging.', 'history': 'Patient imaged after episode of status epilepticus. ', 'imagePoolId': 'a0aba9a0-aaf3-43c6-8061-76e61b2de68c', 'name': 'Splenium', 'teachingPoint': None, 'demographics': '58 Years old male'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}, {'key': 'c0f4b502-f859-48ff-87af-9a4545e51a72', 'value': 'Majda M. Thurnher, MD'}], 'caseVersionId': 'e849ee5f-0bbf-4fac-aaf1-0af9864210ff', 'description': 'Axial DWIs (#1-4) show no definite abnormality. The perfusion images (#5-8) tell another story. They show markedly elevated perfusion in the right temporal and parietal lobes (arrows) compared to the normal left side. PWI MR obtained a few days later on a different scanner (#9) shows almost complete normalization of cerebral perfusion. \n\nComment: Cerebral hyperperfusion may occur after seizure (especially status epilepticus) or--less commonly--following carotid endarterectomy or stenting.', 'history': "Elderly female with high blood pressure, elevated cholesterol, brought to emergency unit after having seizure. Left hemiparesis (a Todd's paralysis) resolved slowly over the next week.", 'imagePoolId': '40bf73ac-3c14-44dd-a790-465b37f51572', 'name': 'Marked hyperperfusion on MR resolves', 'teachingPoint': None, 'demographics': '73 Years old female'}, {'authors': [{'key': '8d5254e9-8dda-478b-8f08-bdee97a32c79', 'value': 'Karen L. Salzman, MD, FACR'}], 'caseVersionId': 'da5cebc9-2f15-48c1-8b0c-1360d8d962fb', 'description': "Typical MR case of reversible seizure induced enhancement related to status epilepticus.\n\nAxial and coronal post-contrast images (#1-2) show gyriform and meningeal enhancement in the right parietal and occipital lobes. Ten days later, once the patient's seizures were well controlled, there is complete resolution of the previously seen enhancement on axial and coronal post-contrast images (#3-4).\n\nComment: MR changes associated with seizures are likely related to transient cerebral edema and/or hyperemia. Acute seizures or status epilepticus may mimic other pathology such as tumor progression or cerebritis.", 'history': 'Patient with a history of status epilepticus immediately prior to imaging. Imaging returned to normal after seizures became controlled.', 'imagePoolId': '9c5c0d2f-bd22-4543-b7c1-a48eba4702cf', 'name': 'Seizure induced enhancement, reversible', 'teachingPoint': None, 'demographics': '30 Years old male'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'e285f0f1-3428-4aaa-ba3b-392a3a6091e3', 'description': 'Sagittal T1WI (#1) shows absolutely classic "popcorn" lesion at the right temporal tip (arrow). Lesion has locules of mixed iso- and hyperintense fluid and is surrounded by complete hemosiderin rim, best appreciated on the coronal T2WI (#2) where the rim "blooms" (arrow). Findings are characteristic of Zabramski type 2 cavernous malformation. On T1C+ scans an associated enhancing developmental venous anomaly is present (arrows, #3,4). \n\nCavernous-venous is the most common type of histologically mixed vascular malformation.', 'history': 'Temporal lobe epilepsy.', 'imagePoolId': 'd311884f-c3a4-489f-b121-b25eb4b1d025', 'name': 'DVA', 'teachingPoint': None, 'demographics': '18 Years old male'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': '9bb600bd-fc5d-4421-b099-a36ff08c69f4', 'description': 'Axial NECT obtained in emergency department showed hyperdense lesion in the left temporal lobe (arrow, #1). An MR was obtained. Sagittal, axial T1WIs (#2-4) show multiple areas of T1 shortening (arrows). FLAIR scan shows a hyperintense ring around the left temporal lobe lesion (arrow, #5) which blooms on GRE (arrow, #6), indicating hemorrhage. T1C+ scans (#7-9) show dura-arachnoid lesions as well as other parenchymal lesions (arrows). \n\nComment: Biopsy of the left parietal dura-arachnoid lesion disclosed metastatic melanoma.', 'history': 'Patient with remote history of melanoma presented with first-time seizure.', 'imagePoolId': '0bc46271-cc7e-49e3-b728-7a60c2479408', 'name': 'Melanoma', 'teachingPoint': None}], 'caseType': 'typical', 'name': 'TYPICAL'}
- {'cases': [{'authors': [{'key': '07a2c087-6202-49e7-870b-7aa162d18f06', 'value': 'Bronwyn E. Hamilton, MD'}], 'caseVersionId': 'b6445eba-f87e-44e8-a6a5-2bfcf1e256af', 'description': "Typical MR imaging case of ictal hyperintensities with follow-up imaging showing resolution. \n\nInitial MR images (Figs. 1-4) performed shortly following a long episode of status epilepticus show increased T2 signal (Figs. 1-3) involving the left temporal lobe cortex and associated subcortical white matter
. Coronal FLAIR image (Fig. 3) shows high signal in the left thalamus also 
. Enhanced image (Fig. 4) shows edema and mild vascular congestion in the left parietal and temporal lobes 
.\n \nImaging performed 1 month later (Figs. 5-7), after treatment and clinical improvement, show near-complete resolution of the previous imaging abnormalities. Subtle increased signal persists (Figs. 5-6) along the left insular cortex and left medial temporal cortex (, Fig. 7).", 'history': 'New onset atypical seizures.', 'imagePoolId': '7b4df45b-9cc7-41a6-a899-bf9f9648d087', 'name': 'Transient', 'teachingPoint': 'Status epilepticus can result in MR changes that are believed related to transient cerebral edema. T2 hyperintensity in affected areas is most typical with associated mass effect. Although the hippocampus and splenium of corpus callosum are commonly involved, the abnormalities can be quite extensive, as in this case. Cortical and subcortical white matter involvement is characteristic. Restricted diffusion can be present acutely, and enhancement varies from none to extensive gyriform or leptomeningeal enhancement. Perfusion MR shows marked hyperemia on the side of the epileptic focus acutely with elevated rCBF maps. Follow-up imaging can demonstrate complete resolution in days to weeks. If the clinical course was complicated by hypoxemia, secondary ischemia can occur however, with resultant atrophy &/or gliosis of involved areas.', 'demographics': '48 Years old female'}, {'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': '6175bd6a-35ab-49d0-8c7f-f1327aa34208', 'description': "MR imaging case of acute status epilepticus signal hyperintensities with lobar involvement mimicking encephalitis. \n\nAxial T1 images (Figs. 1-2) suggest mild thickening of the right temporal lobe cortex and right hippocampus . T2 imaging (Figs. 3-4) show to better advantage the cortical thickening, and demonstrates hyperintense T2 signal changes in the right temporal cortex and hippocampus .", 'history': 'Status epilepticus.', 'imagePoolId': 'a16619fc-9f09-4e05-97ea-ed2c5e2a9ff0', 'name': 'Temporal lobe', 'teachingPoint': 'Mild edema and mass effect with corresponding T2 hyperintensity are typical imaging findings, which may be seen in acute status epilepticus. FLAIR and T2 images are most sensitive to detect signal abnormalities. Enhancement is variably present, and is typically gyriform or leptomeningeal. MR spectroscopy has shown lipids &/or lactate acutely in the hippocampi of temporal lobe epilepsy patients within 24 hours of their last seizure; however, follow-up imaging has not shown persistence of the metabolic abnormalities. While imaging hyperintensities may be focal, commonly localized to the hippocampi &/or corpus callosum (particularly the splenium), more diffuse involvement can occur, as in this case. Cortical and subcortical white matter involvement is characteristic, and can mimic infectious/inflammatory and neoplastic conditions. Follow-up imaging in such cases usually shows resolution of the acute imaging abnormalities in treated patients, with development of atrophy in some cases. If the clinical course is complicated by hypoxemia, infarction can occur however.', 'demographics': '20 Years old female'}, {'authors': [{'key': '5cff4116-3654-4b3a-bb75-5ebe0b8c9850', 'value': 'Anne G. Osborn, MD, FACR'}], 'caseVersionId': 'f0ff580f-9f85-433f-8c03-4cf1ea7775aa', 'description': 'NECT scan (#1) shows faint hyperdensity in the left posterior temporal lobe (arrow). CECT scan (#2) shows mild enhancement (arrow) when compared to the normal right side. Follow-up scan two weeks later was normal. This case is unusual because edema is low density. Why the hyperdensity? Perhaps mild increase in cerebral blood volume? The enhancement would indicate some degree of blood-brain-barrier disruption.', 'history': 'Prolonged left temporal lobe seizure imaged 36 hours after ictus.', 'imagePoolId': '63956ca6-353e-4161-8da4-0b6c1c700630', 'name': 'Hyperemia seizure induced', 'teachingPoint': None, 'demographics': '30 Years old male'}], 'caseType': 'variant', 'name': 'VARIANT'}
Images
Selected Images
Axial DWI on day 1 in a patient presenting with status epilepticus (SE) demonstrates gyriform restricted diffusion 
.
Axial DWI on day 1 in a patient presenting with status epilepticus (SE) demonstrates gyriform restricted diffusion .
Axial FLAIR MR in the same patient on day 1 shows cortical and subcortical edema 
with blurring of the gray matter-white matter interface. Postcontrast images (not shown) demonstrated gyriform enhancement. Prolonged ictal activity induces hypermetabolism with increased glucose utilization. MR signal abnormalities in SE are related to transient vasogenic &/or cytotoxic edema.
Axial FLAIR MR in the same patient on day 25 shows prominence of the sulci due to cortical volume loss. Note subcortical white matter hyperintensity 
due to gliosis.
Axial T1 MR in the same patient on day 25 shows cortical T1 hyperintensity due to laminar necrosis. Although SE-related imaging abnormalities may completely reverse following cessation of seizures, prolonged seizure activity can result in permanent abnormalities, as seen in this case.
Axial FLAIR MR in a patient with SE demonstrates extensive cortical and subcortical edema in the right posterior cerebral hemisphere with mass effect. DWI (not shown) demonstrated cortical restricted diffusion.
Axial rCBV map in the same patient shows increased CBV 
in the right posterior cerebral hemisphere compared with the left. Cerebral hyperperfusion may occur after seizures, particularly with SE.
Sagittal T1 C+ MR in the same patient demonstrates extensive gyriform enhancement . SE leads to increased glucose utilization and oxygen extraction as well as blood-brain barrier breakdown.
Axial DWI MR shows restricted diffusion in the splenium of the corpus callosum . Follow-up MR showed complete resolution. A transient splenial lesion can be seen with seizures, antiepileptic medications, PRES, viral infections, and hypoglycemia.
Axial FLAIR MR in a patient with SE shows right temporal and parietal cortex/subcortical hyperintensity . Note high signal in the pulvinar nucleus of right thalamus .
Axial FLAIR MR in the same patient after 1 year shows cystic encephalomalacia , gliosis , and volume loss in the same regions. Although in most cases imaging findings of SE are reversible, persistent imaging abnormalities, such as focal atrophy due to permanent neuronal damage, can occur, as in this case.
Additional Images
Axial T2WI MR shows hyperintensity in the right temporal cortex with mild gyral expansion and sulcal effacement in this 20 year old with SE and temporal lobe epilepsy. Repeat imaging was normal.
Axial T2WI MR shows focal hyperintensity in the splenium of the corpus callosum 
. The lesion completely resolved after the patient's seizures were treated. (Courtesy D. Mendelson, MD.)
that completely resolved on repeat MR in this 49-year-old man with temporal lobe epilepsy, poorly controlled by medication.
and subcortical white matter with mild mass effect.
in an SE patient. Cortical and subcortical white matter involvement is characteristic. Follow-up imaging in such cases usually shows resolution of the acute imaging abnormalities in treated patients. Atrophy may be seen chronically.
caused by transient SE. Hyperintensity within the splenium may be caused by the seizures or by the antiepileptic medications.
compared to the normal left side. Cerebral hyperperfusion may occur after seizures, particularly with SE.
, related to temporal lobe SE. Imaging 1 year later showed mesial temporal sclerosis.
. Imaging 1 month later showed near-complete resolution of the signal abnormalities. SE may result in MR changes that are likely related to transient cerebral edema.
.
. MR signal abnormalities are related to transient vasogenic &/or cytotoxic edema. Follow-up imaging in such cases usually shows resolution of the acute imaging abnormalities in treated patients. Atrophy may be seen chronically.
in a patient with SE. Transient diffusion changes related to seizures can involve the cortex/subcortical white matter, corpus callosum, hippocampus, and pulvinar nucleus of thalamus.
in the same region as the diffusion abnormality. Cerebral hyperperfusion may occur after seizures, particularly with SE.
related to SE. After treatment, the MR changes are completely resolved. This enhancement pattern is often seen in subacute stroke and encephalitis.