PubMed Health⌕ Search

Biomedical subjects

A S Chattha

Publications and source records attributed to A S Chattha.

16 recordsLinked to original sources
PubMed1984

Differential effect of antiepileptic and non-antiepileptic drugs on the reticular formation.

The effect of the antiepileptic drugs carbamazepine and phenytoin, and of the non-antiepileptic drug baclofen, was compared on various inhibitory and excitatory mechanisms in the feline trigeminal nucleus. Baclofen resembled carbamazepine and phenytoin in depressing segmental excitatory and facilitating segmental inhibitory mechanisms. However, baclofen facilitated the periventricular and periaqueductal inhibition of the trigeminal nucleus, while carbamazepine and phenytoin depressed these descending inhibitory mechanisms. Baclofen also resembles carbamazepine and phenytoin in its effectiveness in trigeminal neuralgia, but baclofen is not a clinically effective antiepileptic agent. Our experiments indicate that the ability to depress the reticular formation of the diencephalon and midbrain is an important characteristic of antiepileptic drugs. This suggests that the reticular core is involved in the spread and generalization of seizures.

Action Potentials↗
PubMed1984

Baclofen in the treatment of trigeminal neuralgia: double-blind study and long-term follow-up.

A double-blind crossover study of the effects of baclofen was conducted on 10 patients with typical trigeminal neuralgia. Baclofen significantly decreased the number of painful paroxysms in 7 of the 10 patients. An open trial in another 50 patients with trigeminal neuralgia refractory to or unable to tolerate carbamazepine showed that 37 (74%) were relieved of their attacks by baclofen, either alone (12 patients) or in combination with previously ineffective doses of carbamazepine or phenytoin (25). On long-term follow-up of one to five years (mean, 3.0 years), 18 of the 60 patients (30%) continued pain free while receiving baclofen; 10 (17%) went into remission after 3 to 6 months; 13 (22%) became refractory to baclofen after 1 to 18 months; and 2 (3%) elected operation despite a good response to baclofen. The results indicate that baclofen is a useful drug in the treatment of trigeminal neuralgia.

Adult↗
PubMed1983

Effect of cinromide on inhibitory and excitatory mechanisms.

The effect of the experimental anticonvulsant cinromide (3-bromo-N-ethylcinnamamide) on various inhibitory and excitatory mechanisms was investigated in the trigeminal nucleus of cats. Intravenous administration of 20-80 mg/kg cinromide depressed excitatory transmission and facilitated segmental inhibition to the same extent as phenytoin, but less than carbamazepine. These doses of cinromide also depressed periventricular inhibition, similar to valproate and ethosuximide. In addition, cinromide had a marked depressant effect on the EEG, suggesting a pronounced sedative effect. The serum levels of cinromide and of its active metabolites (3-bromocinnamamide and 3-bromocinnamic acid) were comparable to those in patients receiving long-term treatment with cinromide. Our results agree with those in other experimental models, which also suggest that cinromide is a broad-spectrum anticonvulsant, and with cinromide's effect in the clinical trials reported so far.

Animals↗
PubMed1982

Do phenytoin and carbamazepine depress excitation and/or facilitate inhibition?

The effect of phenytoin and carbamazepine on the segmental and the periventricular inhibition was investigated in interneurons of the spinal trigeminal nucleus oralis of cats. The segmental inhibition was elicited by delivering a conditioning stimulus to the maxillary nerve 100 ms prior to the test stimulus to the maxillary nerve, and the periventricular inhibition was elicited by delivering a conditioning stimulus to the periventricular gray matter. Therapeutic serum levels of phenytoin and carbamazepine facilitated the segmental inhibition, but depressed the periventricular inhibition, while also depressing the response of trigeminal nucleus neurons to an unconditioned maxillary nerve stimulus. These results indicate that the depression of neural activity by phenytoin and carbamazepine is selective, leaving some inhibitory pathways relatively untouched and thus greatly enhancing their effectiveness. It is suggested that the anticonvulsant properties of phenytoin and carbamazepine are due to their ability to produce a relative facilitation of inhibitory feedback mechanisms.

Animals↗
PubMed1981

Effect of anticonvulsant drugs on inhibitory and excitatory pathways.

A conditioning stimulus to the periventricular gray matter inhibits the response of spinal trigeminal neurons to maxillary nerve stimulation. Sodium valproate and ethosuximide decrease the periventricular inhibition without significantly affecting the response of these neurons to the unconditioned maxillary nerve stimulus. We have now found that carbamazepine and phenytoin decrease the response to the unconditioned maxillary nerve stimulus, and only depress the periventricular inhibition secondarily. These results further support the hypothesis that the ability to depress selectively inhibitory pathways in the CNS is an important characteristic of antiabsence drugs, and that absence seizures may represent paroxysmal discharges in inhibitory pathways.

Animals↗
PubMed1981

Role of inhibitory mechanisms in trigeminal neuralgia.

Segmental inhibition was elicited in the spinal trigeminal nucleus of cats by delivering a conditioning stimulus to the maxillary nerve 100 msec before the test stimulus. Carbamazepine, baclofen, and phenytoin markedly facilitated this segmental inhibition, as well as depressing the response to an unconditioned maxillary nerve stimulus. Phenobarbital, on the other hand, usually depressed the segmental inhibition. These results suggest that drugs that relieve trigeminal neuralgia both facilitate inhibitory mechanisms and depress excitatory mechanisms in the spinal trigeminal nucleus. The facilitation of inhibitory mechanisms appears to be at least as important as the depression of excitatory mechanisms and suggests that a failure of inhibitory mechanisms may play a significant role in the pathogenesis of trigeminal neuralgia.

Animals↗
PubMed1980

Baclofen in trigeminal neuralgia: its effect on the spinal trigeminal nucleus: a pilot study.

Experiments with cats showed that baclofen resembles carbamazepine and phenytoin sodium in its ability to depress excitatory synaptic transmission in the spinal trigeminal nucleus. Baclofen was, therefore, given to 14 patients with refractory trigeminal neuralgia. Ten patients were relieved of the paroxysms of tic douloureux while taking 60 to 80 mg/day of baclofen. A reduction in the dosage of baclofen in six of these patients resulted in a recurrence of painful paroxysms in five patients. Seven patients have been pain-free or almost pain-free on a regimen of baclofen for four to 12 months. Our results suggest that baclofen may be a useful drug in the treatment of trigeminal neuralgia and that our experimental model may successfully predict the efficacy of a drug in the treatment of this condition.

Adult↗
PubMed1980

Bicuculline and neuronal activity in motor cortex.

We have studied the effects of bicuculline applied in microgram quantities to the precruciate gyrus (motor cortex) of cat upon visually evoked and spontaneous single-unit and slow-wave activity. The bicuculline produced an increase in both the visually evoked and the spontaneous unit activity. A surface negative component of the slow-wave response was markedly enhanced by the bicuculline. This component was associated with an intense suppression of spontaneous single-unit activity. Therefore, we have found that bicuculline has a convulsant effect upon single-unit activity as previously reported by others. However, we also found that bicuculline potentiates a process which appears associated with an enhancement of inhibition.

Animals↗
PubMed1980

Antiabsence drugs and inhibitory pathways.

Conditioning stimuli to the coronal gyrus or periventricular gray matter inhibit the activity of spinal trigeminal neurons. Valproate decreased the corticofugal inhibition of the spinal trigeminal nucleus, as did ethosuximide, trimethadione, and imipramine. Valproate and ethosuximide also decreased the periventricular inhibition of the spinal trigeminal nucleus, indicating that antiabsence drug depress subcortical inhibitory pathways as well as pathways of cortical origin. These results support the hypothesis that ability to depress inhibitory pathways is an important characteristic of antiabsence drugs. The effect of valproate and ethosuximide on periventricular inhibition also suggests that these anticonvulsants may act by preventing the spread of seizure activity through subcortical pathways.

Animals↗
PubMed1978

Postnatal development of visually evoked activity within motor cortex of cat.

1. The development of visually evoked activity within motor cortex was studied in chloralose-anesthetized kittens of 3, 4, and 5 mo of age and adult cats. 2. The slow-wave response from motor cortex of the adult cat is a triphasic negative-positive-negative wave. In 3-mo-old kittens the response is only a long-duration negative wave, while at 4 mo the positive and late negative waves emerge, and at 5 mo of age the adult form of the response is present. 3. Single neurons in the adult respond to the light during the positive component of the slow-wave response. When only the negative wave is present in kittens of 3 and 4 mo of age, neurons do not respond to the photic stimulus. At 5 mo of age the correlation between unit activity and the positive component of the response is identical to the adult. 4. The laminar analysis of the positive component of the response suggests that it originates relatively superficially in cortex and migrates down toward the deeper layers. Its correlation with unit activity indicates that the positive component represents excitatory postsynaptic potentials. 5. These results are consistent with an excitatory drive on neurons within motor cortex undergoing development change until the 5th mo of life.

Aging↗
PubMed1977

Cerebral white-matter hypoplasia.

Twelve patients, including three sisters, with lifelong severe intellectual impairment and neurologic defects were found to have generalized hypoplasia of the cerebral white matter, with corresponding enlargement of the ventricular system. Gray-matter structures were remarkably intact. Reactive cellular changes (gliosis, phagocytosis, inflammation) were absent. To our knowledge, this particular syndrome has not previously been delineated in the extensive literature on cerebral palsy. The abnormalities in these cases could result from the effects of a selectively acting tissue-damaging factor, such as has been postulated in perinatal telencephalic leukoencephalopathy, but the factors underlying the disorder are still unknown.

Adolescent↗
PubMed1975

Sylvian aqueduct syndrome as a sign of acute obstructive hydrocephalus in children.

Eight cases of obstructive hydrocephalus manifesting palsy of upward gaze and other features of the Sylvian aqueduct syndrome are reported. During the crisis of intracranial hypertension, all of them developed upward gaze palsy and variable abnormalities of the convergence mechanism such as paralysis, spasm, and convergence nystagmus. The frequent apparent blindness was probably related to gaze paralysis, since visual evoked responses were present. All these ocular abnormalities disappeared after shunting. Periaqueductal dysfunction on the basis of raised intracranial pressure is postulated as the possible mechanism for the above ocular manifestations. The 'setting sun' sign is frequently seen in infants and children with hydrocephalus and has been considered in the past to result from displacement of eyeballs by pressure from the orbital roof plate. Our observations would suggest periaqueductal dysfunction rather than the mechanical displacement as the possible mechanism for this sign.

Acute Disease↗
PubMedDate not supplied

Comparison of progabide with other antiepileptic and GABAergic drugs.

The effect of the experimental antiepileptic gamma-aminobutyric acid (GABA) agonist drug progabide, [alpha-(chloro-4-phenyl)fluor-5-hydroxy-2-benzilideneamino]-4-buty ramide, on the trigeminal complex of cats was compared with the effect of established antiepileptic drugs and with the effect of various GABA agonists and antagonists. Intravenous administration of 10-40 mg/kg progabide depressed excitatory transmission and descending periventricular inhibition, similar to carbamazepine and phenytoin. However, progabide depressed, rather than facilitated, segmental inhibition. The serum levels of progabide were comparable with those in patients receiving long-term treatment with progabide. The GABA antagonist bicuculline had the opposite effect of progabide on our experimental model, but the other GABA agonists THIP (4,5,6,7-tetrahydroisoxazolo-5,4-C-pyridine-3-ol) and muscimol did not have the same effects as progabide. THIP had no effect on excitatory transmission, periventricular inhibition, or segmental inhibition, whereas muscimol facilitated periventricular inhibition and sometimes segmental inhibition and had no effect on excitatory transmission. Our experiments thus indicate that progabide, but not THIP or muscimol, should have antiepileptic properties, in agreement with the clinical experiences that have been reported. The reason for the differential effect of these three GABA agonists remains to be elucidated.

Animals↗