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.

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.

A case of fever following antiepileptic treatment.

A 23-year-old female patient treated with 900 mg oxcarbazepine for complex partial seizures is presented. Good seizure control and slight fever were noted a few weeks after drug administration. Reduction of oxcarbazepine and replacement with valproate resulted in a transient normothermia. Because of fever reappearance, vigabatrin was added and valproate was gradually reduced. Seizures reappeared, but the body temperature fell below 37 degrees C. Substitution of valproate for lamotrigine resulted in seizure control but abnormal body temperature (37- 37.6 degrees C) was noted again. Repeated hospital admission for clinical and laboratory investigation before any change of treatment revealed no other abnormal findings. The patient's abnormal temperature possibly reflects a derangement of high-level temperature control.

Cognition in homozygous beta-thalassemia disease: a multichannel auditory event-related potential (P300) study.

Auditory Event-Related Potentials (AERP) were elicited in 25 beta-thalassemic patients, three days before and three days after a blood transfusion. The amplitude, latency and topographic distribution of P300 (P3) as well as N1, P2, N2 components were measured for the two assessment times. No significant differences in either amplitude, latency or topography were observed between the two situations, but thalassemic patients had significantly prolonged P3 latencies comparing to controls though none of them exceeded 3 standard deviations of the control mean values. Regarding P3 topography, 10 out of 25 patients showed a right centroparietal distribution area. It is concluded that information processing, as far as it is reflected in AERP components is impaired in thalassemic patients and blood transfusion have no significant influence in cognitive functions.

Cognition in relapsing-remitting multiple sclerosis: a multichannel event-related potential (P300) study.

Auditory event-related potentials (AERP) were elicited in 47 patients with relapsing-remitting (RR) multiple sclerosis (MS) and 24 age-matched controls. MS patients had significantly prolonged N2 and P3 latencies as well as low P3 amplitude compared with controls. Seven of them exceeded 3 standard deviations from the control mean values. The observed N2 and P3 alterations are associated with the patients' disability status as it is defined by the Kurtzke expanded disability status scale (EDSS), but are not related to the duration of the disease. A possible cognitive decline as reflected in the observed AERP components alterations in MS patients is subsequently discussed.

Neurophysiological and neuro-otological study of homozygous beta-thalassemia under long-term desferrioxamine (DFO) treatment.

This report presents data on visual evoked potentials (VEPs) and brainstem auditory evoked potentials (BAEPs), as well as neurologic, ophthalmologic and otologic assessments performed on 120 patients with beta-thalassemia major undergoing long-term DFO treatment. A total of 32 patients showed abnormal VEPs and 14 abnormal BAEPs; seven had both VEP and BAEP abnormalities; 12 had sensorineural hearing loss (SNHL); 18 had conductive hearing loss, while 14 showed a combination of SNHL and conductive hearing loss. After DFO administration was modified (taking in consideration the serum ferritin levels) patients with abnormal findings were retested. The values of 15 patients of 23 who underwent VEP examinations had been normalized. Eleven of 15 who repeated the BAEP test had also gained normal values. The audiogram had not returned to normal in any patient with SNHL. In a second repetition of the examinations, no change was observed. It is concluded that in a great percentage of thalassemics at least one of the above examinations shows abnormal values. These abnormalities are mostly reversible, and probably reflect a dysfunction of the visual or auditory system, due either to DFO neurotoxicity or to iron overload or both.