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May focal epileptic seizures be considered a marker of TIAs?
No full textLate-onset focal epileptic seizures occurred in 8 patients with ischemic cerebro-vascular disease (ICVD) and were associated with TIAs in 6 of them. History, physical, laboratory, ancillary examinations and follow-up revealed no other disease which might be responsible for the seizures. Moreover, time of onset and appropriate signs of ICVD suggested that transient cerebral ischemia was the most likely cause of seizures
Focal epilepsy as a possible sign of transient subclinical ischemia.
No full textLate-onset partial epileptic seizures occurred in 10 patients with symptoms and/or signs of ischemic cerebrovascular disease (ICVD) and were associated with transient ischemic attacks in 7 of them. History, somatic and neurological examinations, laboratory and ancillary investigations and follow-up revealed no other disease which might be responsible for the seizures. The anatomical and temporal proximity of signs of ICVD indicate the latter as the most likely cause of seizures. Although the available neuroimaging did not allow us to rule out the presence of silent cerebral infarctions in all patients, it is conceivable that jacksonian seizures, and more rarely complex partial seizures, might occasionally represent a clinical sign due to transient cerebral ischemia and thus herald major cerebrovascular events
Long-term observations on the clinical use of lamotrigine as add-on drug in patients with epilepsy
No full textMRI findings in epileptic patients on vigabatrin for more than 5 years.
No full textAlthough vigabatrin is a promising new antiepileptic drug, its safety has been challenged by the report of dose-dependent central nervous system myelin vacuolation in some preclinical animal studies. Since it has been shown that vacuolation is associated with specific magnetic resonance imaging (MRI) findings in rats and dogs, MRI of the brain was performed in 11 patients with complex partial seizures who had been receiving vigabatrin for 64-78 months (mean 74.0 +/- 5.0 sd) as additional treatment for epilepsy, with a cumulative exposure ranging 4200 to 9360 g. In no case did MRI show white matter changes similar to the pathological findings of microvacuolation observed in animals. These results would appear to confirm that current doses of vigabatrin do not cause myelin vacuolation in humans, even for treatment periods of longer than 5 years
Vigabatrin in chronic epilepsy: a 7-year follow-up study of responder patients.
No full textData on efficacy and safety of vigabatrin over very protracted treatment periods are still limited. This study reports the follow up of 23 responder epileptic patients who continued vigabatrin treatment after completion of the first year, to an overall long-term exposure ranging 21-84 months (median 60; mean 58.0 +/- 24.0 sd). The seizure frequency during the follow up was compared with that at the end of the first year on vigabatrin. The rates of patients who gained a further improvement and those who deteriorated were almost identical, ranging 33-45\% and 33-46\% respectively at individual time points. At the trial endpoint, nine patients (39\%) were improved, five (22\%) were unchanged and nine (39\%) showed some deterioration. All patients still had a 14-100\% decrease of seizure frequency as compared with pretreatment baseline. Two patients discontinued vigabatrin for occasional reasons. No patient experienced new adverse events during the follow up after the first year on vigabatrin. No significant effects were noted on any of the routine hematologic or metabolic screening assessments. Although reduction of concomitant treatment was rarely possible, the overall number of associated antiepileptic drugs dropped from 42 at entry to 40 at the trial endpoint. These findings indicate that vigabatrin retains its efficacy and safety in responder patients for periods up to 7 years
Levodopa and huntington's chorea"J. ." "J. Neuro0l. Neurosurg. Psychiat." ." 1976 39 "958-961"
No full textGABA and phosphatidylserine in human photosensitivity: a pilot study.
No full textPrevious experimental studies have shown that the simultaneous administration of gamma-aminobutyric acid (GABA) and phosphatidylserine (PS) can exert an anticonvulsant activity in different seizure models; moreover, a preliminary trial showed some effect of the association GABA-PS in patients with absence seizures. The aim of this study was to investigate the antiepileptic properties of GABA-PS in the model of human photosensitivity. Nine patients with epilepsy associated with an EEG pattern of photoconvulsive response at intermittent photic stimulation entered a 3-day study. The photosensitivity range (PSR) was determined at hourly intervals both in basal conditions and after the administration of a single oral dose of GABA (3000 mg) and PS (600 or 1200 mg). The administration of GABA-PS was not associated with any systematic changes of PSR, nor with any significant differences of time course profiles on each daily session. No correlation was found between PSR percent deviations from baseline and GABA serum levels. These results indicate that a single acute administration of GABA-PS has no effect in the human photosensitivity model, and suggest that the efficacy of GABA-PS in human epilepsy, as shown by a preliminary investigation, may possibly require chronic administration
Preliminary evaluation of the effect of GABA and phosphatidylserine in epileptic patients.
No full textThe effect of the combined administration of gamma-aminobutyric acid (GABA) and phosphatidylserine was evaluated in a pilot study of 42 patients with drug-resistant epilepsy. The group included patients with complex partial seizures, simple partial seizures and absence seizures. Patients with complex partial seizures and simple partial seizures showed no significant improvement; on the other hand, there was a remarkable decrease in absence seizures, linearly related to the dose of GABA and phosphatidylserine. Side effects occurred in 9 patients and were usually mild
The excitatory amino acid antagonist amino-phosphono-valeric acid (APV) provides protection against penicillin-induced epileptic activity in the rat.
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