Three New Causes of Nonconvulsive Status Epilepticus
Three New Causes of Nonconvulsive Status Epilepticus
ABSTRACTS & COMMENTARY
Sources: Primavera A, et al. Aphasic status epilepticus in multiple sclerosis. European Neurology 1996;36:374-377; Blum A, Drislane F. Nonconvulsive status epilepticus in thrombotic thrombocytopenic purpura. Neurology 1996;47:1079-1081; Lukovits T, et al. Nonconvulsive status epilepticus after intravenous contrast medium administration. Epilepsia 1996;37:1117-1120.
Increased awareness among neurologists of the protean manifestations of nonconvulsive status epilepticus (SE), and our ability to confirm this diagnosis with the now widely available video-EEG monitoring, have led to a recent increase in the clinical settings recognized to be associated with nonconvulsive SE. Three recent reports indicate that aphasic SE can occur with multiple sclerosis (MS), generalized nonconvulsive SE can occur with thrombotic thrombocytopenic purpura (TTP), and complex partial SE can occur with injections of intravenous contrast medium for CT scanning.
Primavera and colleagues describe a 44-year-old woman with "remitting-progressive" MS who presented with acute onset of global aphasia, followed two hours later by a convulsion. An EEG showed continuous left hemispheral seizure activity. SE ultimately responded to gradually increasing doses of antiepileptic drugs over the next five days. The patient had a history of two generalized seizures four years previously and was on phenobarbital at the time she presented in aphasic status epilepticus.
Blum and Drislane describe an 87-year-old woman with TTP who became confused with downbeating nystagmus and limb twitching and was treated with phenytoin. Approximately 10 days later, she became unresponsive, and an EEG showed generalized nonconvulsive SE. Electrographic SE terminated over 48 hours with lorazepam and phenytoin, and the patient made a partial neurological recovery. Unfortunately, she died one week later of respiratory failure.
Lukovits et al report the case of a 52-year-old man who became globally aphasic after receiving intravenous ionic contrast medium for a cranial CT scan to evaluate a left parietooccipital glioblastoma multiforme. Simultaneously, he developed right homonymous hemianopia, right motor neglect, right hyperreflexia, and an extensor plantar sign on the right. An EEG showed left posterior temporal and parietal continuous ictal activity. He responded to treatment with lorazepam and phenytoin and recovered to his baseline functional level over the next 24 hours. He had no previous history of seizures.
COMMENTARY
Neurologists should keep in mind nonconvulsive SE when evaluating unexplained encephalopathic states, and even when evaluating new unexplained focal neurological deficits that localize to cerebral cortical dysfunction. In the first two cases described above, there was a history of convulsive seizure activity, which always raises the question of subsequent nonconvulsive seizure activity. On the other hand, in the third case (Lukovits et al), there was no seizure history and no convulsive activity, yet the EEG showed very definite ongoing electrographic ictal activity. Whether his prompt improvement related to the seizure control or merely the transient toxic nature of the contrast material cannot be discerned. Nevertheless, these case reports illustrate circumstances in which an emergency EEG can be diagnostic and should be performed promptly whenever nonconvulsive SE is even remotely considered.
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