Acute psychosis due to treatment with phenytoin in a nonepileptic patient.

The development of psychosis related to antiepileptic drug treatment is usually attributed to the interaction between the epileptic brain substratum and the antiepileptic drugs. The case of a nonepileptic patient who developed psychosis following phenytoin treatment for trigeminal neuralgia is described. This case suggests that the psychotic symptoms that occur following phenytoin treatment in some epileptic patients may be the direct result of medication, unrelated to seizures.

Hemispheric predominance of abnormal findings in electroencephalogram (EEG).

The EEGs of 13,560 patients have been reviewed in order to determine whether abnormal findings, epileptiform or not, have a hemispheric dominance. We have included outpatients and hospitalized patients as well. Eight hundred and thirty-five EEGs had generalized abnormal findings, and 414 EEGs had lateralized abnormal findings. The EEGs of 322 patients (77.7%) had a left predominance, and those of 92 patients (22.3%) had a right predominance, of abnormal findings. A strong left predominance has been noted for the epileptiform discharges, i.e. 128 (79%) vs. 34 (21%). These results raise the possibility that the left hemisphere may be more vulnerable to nosological processes.

Area-selective stimulus-provoked seizures in post-anoxic coma.

We describe the case of a 70-year-old patient in whom hemiconvulsive seizures occurred during metabolic derangement, multiple stroke and post-anoxic coma following cardiac arrest. We employed the methods of clinical and EEG evaluation and CT brain scan. We found that hemiconvulsive seizures were provoked following a light tactile stimulus in the left-trigeminal area and occasionally a strong tapping in the right-trigeminal area. We conclude that this type of stimulus-provoked seizure is extremely rare and could be explained by diffuse and severe brain damage.

Area-selective stimulus-provoked seizures in post-anoxic coma.

We describe the case of a 70-year-old patient in whom hemiconvulsive seizures occurred during metabolic derangement, multiple stroke and post-anoxic coma following cardiac arrest. We employed the methods of clinical and EEG evaluation and CT brain scan. We found that hemiconvulsive seizures were provoked following a light tactile stimulus in the left-trigeminal area and occasionally a strong tapping in the right-trigeminal area. We conclude that this type of stimulus-provoked seizure is extremely rare and could be explained by diffuse and severe brain damage.

Convulsive status epilepticus following abrupt high-dose benzodiazepine discontinuation.

The misuse of benzodiazepines (BNZ)s may result in serious side effects. Three cases of convulsive status epilepticus (CSE) following abrupt discontinuation of long-term use of 25 mg of lorazepam in one patient and more than 20 mg of flunitrazepam in two patients are presented; they were non-epileptics and free of other high-risk factors for seizures. A favorable outcome for all three cases was noted. They remain free of seizures without antiepileptic treatment. Nevertheless, because of the extensive use of benzodiazepines, such rare high-risk side effects must be emphasized.

The usefulness of sleep and sleep deprivation as activating methods in electroencephalographic recording: contribution to a long-standing discussion.

Sedated sleep and sleep deprivation are commonly used methods to increase the diagnostic yield of the electroencephalogram (EEG), especially in the evaluation of people with epilepsy, but the rate of activation achieved by them is controversial, as is the issue of whether it is sleep itself, or sleep deprivation which is responsible for their alleged efficacy. We retrospectively studied the EEGs of epileptic patients, examined in our laboratory, who, after having undergone an inconclusive initial routine recording, had then been examined with a second recording. This was after either: (1) sleep deprivation with evidence of drowsiness in the recordings, (2) sleep deprivation without drowsiness (indicative of the effect which sleep deprivation per se has in eliciting abnormal patterns), or (3) drug-induced sedation. The activation rates found were (1) 22.5%, (2) 24% (22.6% for sleep deprivation collectively, regardless of the presence or not of subsequent drowsiness) and (3) 27% respectively. Only the sleep deprivation rate was statistically different from the 9.6% increased rate of abnormal patterns elicited by the simple repeating of a second routine recording, while the rate of drug-induced sleep was not. Although, sleep deprivation appeared to be more effective as an activating method of EEG compared with sedated sleep, no conclusions could be drawn about which stage of sleep, wakefulness or drowsiness, is primarily responsible for the method's efficacy.