RESEARCH SUPPORT, NON-U.S. GOV'T
Focal motor seizures induced by alerting stimuli in critically ill patients.
Epilepsia 2008 June
PURPOSE: We have previously demonstrated that it is common for alerting stimuli to induce electrographic seizures and other periodic or rhythmic patterns in the critically ill; however, only 1 of the first 33 patients we reported with this phenomenon had a detectable clinical correlate.
METHODS: Review of charts and video EEG findings in critically ill patients in a neurological ICU at a tertiary care medical center in Manhattan.
RESULTS: We identified nine patients who had focal motor seizures repeatedly induced by alerting stimuli. All patients were comatose, and 8/9 had nonconvulsive status epilepticus at some point during their acute illness. Imaging abnormalities involved bilateral thalami in three patients, upper brainstem in one, and the perirolandic region in five.
DISCUSSION: We hypothesize that in encephalopathic patients, alerting stimuli activate the arousal circuitry, and, when combined with hyperexcitable cortex, result in epileptiform activity or seizures. This activity can be focal or generalized, and is usually nonconvulsive, as is true of seizures in general in the critically ill. However, when the cortex is hyperexcitable in a specific region only, focal EEG findings arise. If the electrographic seizure activity is adequately synchronized and involves motor pathways, this can present as focal motor seizures, as seen in these nine patients. Alerting can induce seizures in encephalopathic/comatose patients. The observation of clear focal clinical seizures removes the last remaining doubt that these stimulus-induced patterns are indeed seizures by any definition, not simply abnormal arousal patterns.
METHODS: Review of charts and video EEG findings in critically ill patients in a neurological ICU at a tertiary care medical center in Manhattan.
RESULTS: We identified nine patients who had focal motor seizures repeatedly induced by alerting stimuli. All patients were comatose, and 8/9 had nonconvulsive status epilepticus at some point during their acute illness. Imaging abnormalities involved bilateral thalami in three patients, upper brainstem in one, and the perirolandic region in five.
DISCUSSION: We hypothesize that in encephalopathic patients, alerting stimuli activate the arousal circuitry, and, when combined with hyperexcitable cortex, result in epileptiform activity or seizures. This activity can be focal or generalized, and is usually nonconvulsive, as is true of seizures in general in the critically ill. However, when the cortex is hyperexcitable in a specific region only, focal EEG findings arise. If the electrographic seizure activity is adequately synchronized and involves motor pathways, this can present as focal motor seizures, as seen in these nine patients. Alerting can induce seizures in encephalopathic/comatose patients. The observation of clear focal clinical seizures removes the last remaining doubt that these stimulus-induced patterns are indeed seizures by any definition, not simply abnormal arousal patterns.
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