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Status epilepticus is an acute and prolonged seizure that persists for a sufficient length of time or is repeated frequently enough that recovery between attacks does not occur. It is a clinical emergency associated with high morbidity and mortality.
The estimated incidence of ~35 per 100,000, more common in poorer populations 1.
Although the definition of status epilepticus proposed by the International League Against Epilepsy does not provide a time-frame 8, a widely accepted seizure duration to qualify as status epilepticus is 5 minutes in length 7.
True status epilepticus needs to be differentiated from a non-epileptic attack (pseudostatus epilepticus), which has a psychological basis. Neuroleptic malignant syndrome and delirium tremens can occasionally have clinical presentations that mimic status epilepticus.
In patients with a known history of seizures, common causes of a status epilepticus are changes in anticonvulsant medication or withdrawal syndrome. About 50% of these events occur in patients without any history of epilepsy and are usually related to an underlying condition, such as 1,2:
- metabolic derangement
- toxicity (e.g. drugs)
- alcohol intoxication or withdrawal
- pregnancy-related, e.g. eclampsia
- infections accompanied by fever (the most important cause in children)
In most instances, unless one of the underlying conditions is visible (e.g. stroke), CT of the brain will be unremarkable.
The most common changes seen relate to an increased T2 signal (best seen on FLAIR) with some swelling. These regions may demonstrate corresponding diffusion abnormalities, with increased DWI signal and in some instances reduced ADC values 3,6.
These changes are believed to be due to excessive metabolic demands placed on tissues due to sustained seizure activity, resulting in vasogenic and/or cytotoxic edema. If severe enough, cell metabolism will fail resulting in eventual cell death 3,4.
Post-contrast T1 imaging is extremely variable, ranging from no enhancement to marked enhancement, which may be gyriform or leptomeningeal in distribution.
The locations involved are variable, including 3,5:
- cerebral cortex and subcortical white matter
- hippocampi and mesial temporal lobes
- thalamus, particularly the pulvinar region 5
- cerebellum 9
When T2 signal elevation is associated with significant (>10%) drop in ADC values, follow-up is likely to reflect permanent damage 3,6. In contrast, isolated T2 signal change, without ADC signal drop is likely to fully resolve 3.
It is important to note that diffusion needs to be assessed on ADC maps and not DWI as it is not possible to confidently distinguish true diffusion restriction from T2 shine through on DWI images only.
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