An electroencephalogram (EEG) recorded after sleep deprivation (SDEEG) in epilepsy patients often discloses epileptiform discharges (ED) when routine EEG (REEG) does not, but since sleep alone activates ED, activation during SDEEG may result merely from the induction of sleep. We retrospectively investigated whether SDEEG is useful when REEG containing wakefulness and sleep fails to show ED. Subjects were patients with definite or highly probable epilepsy whose REEG lacked ED and who later underwent SDEEG. All had wakefulness and at least stage II sleep during both REEG and SDEEG. Patients with ED on REEG were specifically excluded to avoid including patients with activation due merely to the occurrence of sleep. Patient and EEG characteristics were studied, including duration of wakefulness and each sleep stage and timing and characteristics of ED. Fifteen of 29 patients (52%) had activation on SDEEG; exclusively during wakefulness in 1, exclusively during sleep in 6 and in both wakefulness and sleep in 8. Activation rates were not significantly different between wakefulness (9, 60%), stage I (11, 74%) and stage II (11, 74%). EEG characteristics were similar for REEG and SDEEG, except that total EEG duration and stage II sleep were longer in SDEEG than in REEG, which did not influence activation by a logistic regression model (p > 0.05). We conclude that sleep deprivation activates ED independent of the activating effects of sleep and therefore is useful in evaluation of suspected epilepsy even when REEG contains sleep.

We analyzed EEG characteristics comprehensively in a large series of nonconvulsive status epilepticus (NCSE) cases. Eighty-five ictal episodes in 78 patients were analyzed. The ictal discharges were generalized (group G) in 59 episodes (69%), diffuse with focal predominance (group GF) in 15 (18%), and focal (group F) in 11 (13%). The morphologies and patterns of persistence varied greatly. Frequency of ictal discharge was also variable and was almost always < 3 Hz. Demonstration of focal epileptic features in response to intravenous (i.v.) diazepam (DZP) and the presence of interictal focal epileptiform discharges in some cases in groups G and GF suggested possible focal onset secondarily generalized in these cases. This study suggests that electrographically NCSE is a highly heterogeneous epileptic state, and i.v. DZP may serve as a valuable diagnostic tool in differentiating generalized from focal onset NCSE.

Among patients with a prolonged confusional state after convulsive seizure, we diagnosed 8 cases as generalized nonconvulsive status epilepticus. Six had a history of seizures, and 2 had new onset. The convulsive seizures were generalized in 6 and focal in two. The postictal confusion lasted up to 36 hours in the most prolonged case, and a delayed response to anticonvulsant medications occurred in all cases. The clinical symptoms ranged from mild confusion to coma. Psychiatric manifestations or automatisms were rare. The presumed etiology was due to diverse causes, but a withdrawal state was the most common. EEG demonstrated continuous or nearly continuous generalized ictal discharges of variable morphology. These cases call attention to the fact that some prolonged confusional states following convulsive seizures are in fact due to persistent seizure activity that can be diagnosed by EEG.

Stupor is an unusual complication following the addition of valproic acid to other antiepileptic drugs. We report four such cases. Stupor occurred acutely in 3 patients and insidiously in the fourth. In the cases of acute toxicity, neither toxic levels of valproate nor significant elevations in blood levels of the other drugs occurred. In the fourth patient, stupor occurred concomitantly with a rise in the phenobarbital level. The electroencephalograms of all 4 patients revealed generalized high-amplitude rhythmic bisynchronous delta activity. Recovery occurred following discontinuation of valproic acid or other antiepileptic drugs. These observations suggest that stupor may occur as a result of drug interactions after the addition of valproic acid to other antiepileptic drugs.

Six patients ranging in age from 42 to 69 with no prior history of seizure disorder presented an acute prolonged or intermittent confusional state, with or without psychotic symptoms, as an ictal manifestation. The EEGs demonstrated protracted generalized spike and wave discharges, but full diagnostic evaluation disclosed no evident cause for the seizures. All promptly responded to small amounts of intravenous diazepam and subsequent oral phenytoin and phenobarbital. Three of the six patients had focal spike or sharp wave discharges on EEGs recorded subsequently, suggesting that the episodes may reflect secondary generalized seizures in some cases. These cases do not fit in the classic category of petit mal status and appear to be a distinct entity.