Orgasmic aura--a report of seven cases.

We report on seven patients who experienced an orgasmic aura at the start of their seizures. The patients (five women, two men) were aged 36-58. Three of seven patients described the exact nature of their auras only many years after their appearance, when the epilepsy diagnostic procedure became more intensive due to drug resistance. Moreover, one patient even refused any new therapeutical options due to the reportedly positive role of the orgasmic aura in her life. All of our patients had temporal lobe epilepsy. The clinical picture, EEG, MRI or SPECT findings suggested a right temporal epileptic focus in six patients, while in one patient the epileptogenic region was localised in the left temporal lobe. In the latter case, the left hemisphere was speech-dominant, while in the other cases no Wada tests were done. Our results confirm that orgasmic aura could be considered as an ictal lateralising sign to the right hemisphere, however, it has no 100% lateralising value.

Concentration- and time-dependent effect of aminooxyacetic acid on cortical epileptogenicity.

In the present electrophysiological study the effect of aminooxyacetic acid (AOAA) on the cortical epileptogenicity, and on the basic electro-cortical activity was investigated in anesthetized rats. AOAA did not induce spontaneous epileptiform discharges but modified the somato-sensory evoked responses and the cortical epileptogenicity (induced by 4-aminopyridine) in the same manner depending on its concentration. AOAA at low concentrations increased the amplitude of evoked responses and the ipsilateral manifestation of epileptiform activity, however, at high concentrations significantly suppressed both the evoked responses and the induction and expression of seizures discharges. The anticonvulsive effect of AOAA was time-dependent (reached its maximum after 2h AOAA pre-treatment) and reversible. AOAA at low concentrations probably increases the efficacy of the NMDA excitatory system and decreases GABA-synthesis, resulting neuronal hyperexcitation. However, AOAA at high concentrations can lead to an effective cortical inhibition through intra- and extracellular accumulation of GABA. The gradual GABA accumulation - up to a certain level - at the synapses could also explain the time-dependency of the anticonvulsive effect of AOAA.

The effects of valproate on the arachidonic acid metabolism of rat brain microvessels and of platelets.

Long-term administration of the antiepileptic drug valproate can induce hematologic, hepatic and endocrine abnormalities and morphologic alterations in the brain capillaries and glial cells. Valproate elicits bone marrow suppression, reducing the number of red blood cells and platelets, and causes platelet functional abnormalities. Various data suggest that more than one mechanism of valproate-associated toxicity may exist, but the pathomechanism of cell function alterations elicited by valproate has not yet been elucidated. The reported ex vivo experiments were designed to investigate the effects of valproate on the arachidonic acid cascade of rat brain capillaries and platelets. Valproate was administered (300 mg/kg body weight/day) in the drinking water to male Wistar rats for 2 weeks. Isolated platelets and brain microvessels were labelled with [14C]arachidonic acid and the released [14C]eicosanoids were separated by overpressure thin-layer chromatography and determined quantitatively by liquid scintillation counting. Valproate treatment reduced the synthesis of cyclooxygenase and lipoxygenase products in rat platelets. In brain microvessels valproate stimulated the synthesis of lipoxygenase metabolites and attenuated the cyclooxygenase pathway. Modifications of the arachidonate cascade in platelets and brain microvessels may contribute to the cell function alterations caused by valproate.

Chronic low-dose maternal exposure to methylmercury enhances epileptogenicity in developing rats.

Effects of continuous low-dose maternal methylmercury intoxication on the induction and propagation of ictal epileptiform activity induced by 3-aminopyridine, were investigated on the neocortex of 4-weeks-old offspring rats. Epileptogenicity was significantly increased in offspring of mercury-treated animals compared to those of controls, characterized by more frequent occurrence of periodic ictal activity, a facilitated propagation of epileptiform discharges and a strong tendency to generalization. The latency of first ictal event was slightly shorter and the average duration of individual ictal periods slightly longer in treated animals. However, the amplitude of seizure discharges was significantly smaller in treated animals than in controls. We conclude, that the synaptic and membrane mechanisms responsible for initiation and propagation of paroxysmal activity were probably facilitated, while the efficacy of cortical inhibition, in preventing initiation and spread of epileptiform discharges was reduced by mercury treatment in the developing nervous system. The smaller amplitude of paroxysmal discharges could be a sign of a remarkable loss of cortical neurons.

Valproate treatment and platelet function: the role of arachidonate metabolites.

PURPOSE: Valproate (VPA) is an extensively used drug in the therapy of epilepsies. One of the most frequently reported side effects of VPA is hemorrhagic diathesis. Some authors emphasized the decreased platelet count as the basis of VPA-induced hemorrhagic diathesis, but some reports suggested that a significant proportion of patients with normal platelet count may still have an altered platelet function. The mechanism of the VPA-induced platelet dysfunction has not yet been elucidated. A determining element of platelet functions is the arachidonate cascade. Present ex vivo experiments were designed to determine whether a relation exists between the incidence of hemostasis caused by VPA and the effect of this drug on the arachidonate cascade of platelets. METHODS: Platelets were isolated from patients receiving long-term VPA treatment (serum level, 36.04+/-16.12 microg/ml; n = 10) or carbamazepine (CBZ) treatment (serum level, 5.24+/-2.67 microg/ml; n = 10) and were labeled with [14C]arachidonic acid. (CBZ-treated patients were chosen as a control group, because CBZ causes blood dyscrasias similar to those elicited by VPA, but there has been no report that CBZ induces a platelet dysfunction.) The 14C-eicosanoids were separated by means of overpressure thin-layer chromatography and determined quantitatively by liquid scintillation. RESULTS: Even when the mean plasma concentration of the drug was low, VPA treatment reduced the activity of the arachidonate cascade in platelets. VPA effectively inhibited the cyclooxygenase pathway and the synthesis of the strong platelet aggregator thromboxane A2. CONCLUSIONS: Inhibition of the platelet arachidonate cascade may contribute to the platelet-function alterations caused by VPA.