Fits are unrecognizable clinically in the presence of neuromuscular blockade, and persistent seizure activity leads to ischemic neuronal damage. Therefore EEG monitoring is mandatory to identify seizure activity if paralysis is used in status epilepticus. Many different protocols have been devised for the management of refractory status epilepticus; all require elimination of paroxysmal activity from the EEG, and some specify that sedation should be deep enough to produce a burst-suppression pattern in the EEG. Conventional EEG recording may be used, but a device such as the cerebral function monitor or cerebral function analyzing monitor is ideal for EEG monitoring in status epilepticus, since the marked increase in amplitude associated with seizure activity is clearly displayed and the burst-suppression pattern produced by deep sedation is readily identified ( Fig 1). Nursing staff must mark the EEG trace whenever the patient is turned, endotracheal suction applied, or any other nursing procedure is undertaken, so that the associated artifacts are not mistaken for fits. Seizure activity may occasionally appear without a marked increase in the EEG amplitude; therefore if monitoring is by cerebral function monitor or cerebral function analyzing monitor, the raw EeG should be inspected occasionally and full EEGs recorded at intervals.
Fig. 1 Refractory status epilepticus monitored by the cerebral function monitor. Repeated fits are associated with marked increase in amplitude. Bolus doses of thiopentone (T) suppressed the fits briefly, but could not be repeated because of hypotension. The fits were finally brought under control permanently by etomidate (E). Bolus doses were administered at the vertical arrows, and a continuous infusion is shown by the horizontal line. Calibration: vertical time markers every minute, and time trace reversed for 10 min every hour. Vertical lines on the graph paper are repeated every 5 min. The amplitude is logarithmic from 3 to 300 pV.
EEG monitoring sometimes fails to show any evidence of paroxysmal activity in a patient undergoing treatment for presumed convulsive status epilepticus. This indicates that the diagnosis is not status epilepticus, and some other condition should be considered. Important possibilities are decerebrate spasms, particularly after head injury, myoclonus status after cardiac arrest, or psychogenic 'pseudostatus', a potentially life-threatening condition which is being increasingly recognized.
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