A comparative evaluation of the EEG provocative action of TRH and amitriptyline was performed on 15 epileptic patients. TRH slightly increased the EEG abnormalities of 6 patients without giving important side effects. Amitriptyline was effective on 11 patients, but in two instances, gave rise to an epileptic fit.

Adolescent↗

PubMed1980

Cefazolin experimental epilepsy: the effects of diazepam on the interictal ECoG.

Diazepam i.v. injected at the dose of 5 mg/Kg on a group of 14 Rhode-Island-Red chicks was able to antagonize and prevent the interictal EEG pattern induced by cefazolin i.v. Since cefazolin epilepsy is most probably dependent on a receptorial antagonism with GABA, these data seem to confirm the GABA-ergic nature of cefazolin epilepsy.

Animals↗

PubMed1980

[Determination of proteins with the Coomassie brilliant blue G 250 method. IV. Use with cerebrospinal fluid proteins and comparative analysis with the biuret and Lowry methods].

The method of Bradford with Coomassie Brillant Blue G 250 for protein assay has been applyed to CSF in comparison with biuret and Lowry's methods. The results of Coomassie method closely agree with Lowry, and are similar to those of biuret. It is suggested to replace the previously used methods for CSF protein assay by the Bradford's method, because it keeps the sensitivity of Lowry and the simplicity of biuret. It adds too the advantage of requiring less time.

Cerebrospinal Fluid Proteins↗

PubMed1980

Some clinical pharmacological aspects of n-dipropylacetamide.

The kinetics of the primary amide of valproic acid (VPA), i.e. dipropylacetamide, rapidly transformed into the corresponding acid in humans, are investigated and compared with valproate kinetics. In a group of healthy volunteers peak VPA concentration was reached within 5-14 hours of dipropylacetamide and within 1-2 hours of valproate administration. The plasma half-life appeared to be 8-12 hours for both compounds without significant differences. The relative bioavailability of the amide was 81.2% of valproate on average. In epileptics no correlation between plasma VPA levels and daily valproate or amide dose was observed; daily plasma valproic acid level fluctuations were significantly less wide during dipropylacetamide therapy. This compound seems to offer some advantages over sodium valproate, namely: slower absorption, stabler plasma levels through the day, 2 instead of 3 or 4 daily doses and hence less risk of drug defaulting.

Adult↗

PubMed1980

Cefazolin: a valid model of experimental epilepsy?

In various animal species (chicks, rats and rabbits) the intravenous injection of high doses of cefazolin, a cephalosporin not hitherto reported to produce epileptic seizures, was found to produce epileptiform electrocortrical changes similar to those evoked by intravenous benzylpenicillin. Similar phenomena as those reported after systemic injection were also observed after microinjection of cefazolin into the III cerebral ventricle. In fact, both in chicks and rats cefazolin given by the latter route produced wild running crisis, myoclonic jerks of the limbs and in some instances generalized clonic convulsions. Concomitantly, bilateral electrocortical high voltage bursts of spikes were observed, followed during the intercritic period by periodic bilateral or unilateral single spikes.

Animals↗

PubMed1980

Effects of intraventricular gamma-acetylenic-GABA on GABA concentrations, GABA-T and GAD in several areas of the chick brain.

The great interest in new compounds able to increase GABA concentration in the brain as potential antiepileptic drugs has led to the synthesis of powerful inhibitors of GABA transaminase (GABA-T) e.g. gamma-acetylenic GABA (GAG) and gamma-vinyl-GABA. Present experiments were aimed to study behavioral, electrocortical and biochemical effects of GAG after its intraventricular injection. It has been shown that in chicks the microinjection of GAG into the third cerebral ventricle produced a biphasic behavioral and electrocortical syndrome : an initial phase of behavioral and electrocortical sleep followed by a paradoxycal increase in motor activity and a very intense behavioral and ECoG arousal pattern. In addition intraventricular GAG (0.8 mumol) produced a significant increase 1 and 2 h later in GABA concentration in the diencephalon and brain-stem whereas no changes occurred in other brain areas e.g. cerebral hemispheres, optic lobes. Higher doses (1.6 mumol), produced after 1 h, concomitantly to the increased GABA concentration, a significant GABA-T inhibition and a profound inhibition of glutamate-decarboxylase in the diencephalon and brain-stem. Present experiments may explain the paradoxical behavioral, motor and electrocortical stimulation observed at the time of GABA increase concentration and suggest that a small functional neuronal pool of GABA, more than the whole absolute levels of GABA in a given area of the brain, seems to be involved in the control of GABAergic mediated inhibitory mechanisms.

4-Aminobutyrate Transaminase↗

PubMed1980