History and exam
Key diagnostic factors
common
persistent or repetitive tonic-clonic seizures with altered level of consciousness (generalized convulsive SE)
May have persistent tonic-clonic seizures with complete loss of consciousness or repetitive tonic-clonic seizures without regain of baseline consciousness.[2][34]
Although generalized convulsive SE is easily recognized by its motor manifestations (classified as overt SE), some patients may progress to have minimal or no apparent motor activity (classified as subtle SE). Motor activity may become asymmetric, asynchronous, and even discontinuous.[20] This motor activity might be limited to jerking or twitching of one muscle or limb. In this case, continuous electroencephalographic monitoring is warranted because it may confirm the diagnosis of persistent subtle generalized SE.[35]
altered awareness/confusion (nonconvulsive SE)
A patient with nonconvulsive SE can exhibit a wide variety of clinical manifestations, including coma, altered awareness or affect, somnolence, delusions, hallucinations, and paranoia.[2][20][34] Nonconvulsive SE is subdivided into generalized (absence) or focal (focal impaired consciousness) seizure types.
The diagnosis of nonconvulsive SE can be difficult and is dependent on electroencephalography (EEG).[35] Any patient with a prolonged change in personality or recent-onset psychosis should be investigated with EEG, as these may represent nonconvulsive SE. The physician must be aware of this situation, because aggressive treatment for this group (especially patients with focal impaired consciousness SE) is just as important as it is for the obviously convulsing patient.[38]
Other diagnostic factors
uncommon
focal SE without impaired consciousness
A patient with focal SE often presents with an isolated motor activity. This may involve jerking or twitching of one or more groups of muscles.
Less commonly, sensory symptoms such as tingling or numbness, or autonomic symptoms such as abdominal discomfort or nausea, can be the only complaints reported by the patient. There is no impairment of consciousness (aura continua, with autonomic, sensory, visual, olfactory, gustatory, emotional/psychic/experiential, or auditory symptoms).[7]
low oxygen saturation
Hypoxemia on pulse oximetry may be the result or the cause of SE.
Prompt treatment of this potentially lethal condition is crucial to avoid irreversible complications.
Risk factors
strong
nonadherence to anticonvulsant drugs
In a large retrospective study, poor anticonvulsant drug adherence was the single most common cause for SE in patients with a history of epilepsy.[9]
The possible mechanism is rebound seizures after acute withdrawal of anticonvulsant medication.
alcohol-use disorder
Alcohol-use disorder is a known risk factor for SE, which may be the first presentation of alcohol-related seizures. Alcohol withdrawal is also a risk factor for SE.[14]
Alcohol-related SE carries a more favorable outcome than SE of other causes, but recovery of these patients is usually marked by a prolonged postictal state.[28]
stroke
Stroke is the leading cause of SE among acute symptomatic cases, accounting for 14% to 22% of SE in adults.[29]
weak
refractory epilepsy
Chronic or refractory epilepsy is a risk factor for developing SE. This was observed in several clinical trials involving patients with pharmacoresistant epilepsy.[30]
toxic or metabolic causes
Examples include disturbances in water, glucose, and electrolyte metabolism.[14]
processes leading to direct cortical structural damage
drug use
This includes substance misuse of certain restricted or recreational drugs such as cocaine and some amphetamines. Also, certain prescription drugs (e.g., theophylline, bupropion, tramadol, or isoniazid) may in rare cases precipitate SE.[14]
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