Fig. 1
Coronal T1-weighted magnetic resonance imaging (MRI) with gadolinium revealing a clot in the superior sagittal sinus (yellow arrow) and infarct in the left frontoparietal region (white arrow). This 50-year-old woman presented in focal status epilepticus
Fig. 2
Axial T2-weighted MR image of a 42-year-old woman with ongoing complex partial seizures, etiology was herpes simplex encephalitis. There are increased T2 signal and swelling of the right mesial temporal lobe (star)
Anoxic ischemic encephalopathy (AIE) is an uncommon cause of SE. Most cases of myoclonic seizures in AIE have a brainstem reticular formation origin and usually, but not invariably, a poor prognosis. AIE can also present with NCSE. A trial of antiepileptic drugs (AEDs) is usually warranted. Abnormal MRI findings in AIE include areas of restricted diffusion in the periventricular white matter, corpus callosum, internal capsule, and subcortically. These findings occur early after AIE [5]. Initial evidence suggested that cerebral gray matter is more vulnerable to global anoxia and ischemia due to its unique metabolic rate [6, 7]; however, white matter involvement has been found to occur early after the insult [5, 8]. The term “acute myelinopathy” caused by cerebral anoxia has been used and can be manifested as restricted diffusion with low ADC values on MRI. The usefulness of MRI in AIE with has been mainly for prognostic purposes. When diffusion-weighted imaging (DWI) or fluid attenuation inversion recovery (FLAIR) imaging reveals extensive cortical and subcortical damage, the prognosis for recovery is very poor.
Complications of SE and Subsequent MRI Changes
Often seizure-induced MRI abnormalities are left as a diagnosis of exclusion, and repeat imaging is necessary in order to exclude inflammatory or infectious etiologies as the cause of the MRI abnormalities. Examples of MRI abnormalities resulting from SE include areas of increased signal intensity on FLAIR, T2, or diffusion-weighted images, patchy cerebral contrast enhancement, leptomeningeal enhancement, and even cerebral swelling. Changes can be reversible or irreversible [9, 10]; even if the initial MRI findings disappear, often they will leave sequelae of mesial temporal sclerosis, focal and/or global atrophy [9, 11].
The most well-described changes are those that occur in the hippocampi [12, 13]. Other less well-described changes include involvement of the extratemporal cortex, subcortical structures, thalamus, and cerebellum and more widespread hemispheric atrophy [9, 10].
Hippocampal Changes
The magnetic resonance (MR) signal changes that can occur during SE most often involve the hippocampus, the most vulnerable region for SE-induced damage [14]. Histologically, the CA1, CA3, and hilus are the most affected regions. Hippocampal changes can often be pronounced. T2-weighted sequences will often demonstrate abnormally increased signal in the hippocampus, which can be followed by swelling and gliosis [12] (Figs. 3 and 4).
Fig. 3
A 40-year-old woman with a history of untreated complex partial seizures who presented in convulsive in status epilepticus. (a) Axial weighted T2 sequence reveals marked increased T2-weighted signal bilaterally in the hippocampal heads and bodies (yellow arrows). The hippocampi appear mildly swollen. (b) There is some mild associated restricted diffusion of the hippocampus on axial diffusion-weighted imaging (DWI) (yellow arrows)
Fig. 4
Follow-up of same patient (Fig. 3) several months after initial presentation. The hippocampi are hyperintense on coronal fluid attenuation inversion recovery (FLAIR) imaging and are now smaller than seen previously (white arrows)
Extratemporal Changes
Reversible and irreversible abnormalities have been described in the extratemporal cortex, basal ganglia, insula [9], and thalamic pulvinar [15]. Hemispheric atrophy is sometimes a consequence of prolonged focal status epilepticus (Fig. 5). Cerebellar changes as a consequence of a supratentorial epileptic focus have also been reported and are explained by crossed cerebellar diaschisis (Fig. 6a, b) [16]. The frequency with which various regions of the brain are involved during SE is shown in Table 1.
Fig. 5
A 28-year-old male with temporal lobe seizures and remote status epilepticus. The patient continues to have temporal lobe seizures. On coronal fluid attenuation inversion recovery (FLAIR) imaging, there is atrophy of the right hippocampus, as demonstrated with an enlarged temporal horn (white arrow). There are also increased signal within the right hippocampus (yellow star) and global right hemispheric volume loss compared to the left
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