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Biomedical subjects

T A Hare

Publications and source records attributed to T A Hare.

At least 55 records · Page 3Linked to original sources
PubMed1981

Isoniazid-induced elevation of CSF GABA levels and effects on chorea in Huntington's disease.

A randomized, double-blind, crossover, placebo-controlled clinical trial of oral isoniazid was undertaken in eight men with known Huntington's disease. Six completed the trial. Overall chorea scores indicated some amelioration, but clinical improvement was noticed in only two patients and was mild. Side effects included anorexia and elevation of liver enzyme levels. Cerebrospinal fluid (CSF) and plasma gamma-aminobutyric acid (GABA) concentrations were measured simultaneously. Mean CSF GABA increased threefold following treatment with isoniazid (414 +/- 52 SEM pmol/ml) compared to placebo (120 +/- 11 pmol/ml). No significant changes occurred in plasma GABA levels between the placebo and drug treatment phases. Reversal of central GABA deficiency appears not to correct extrapyramidal symptoms in Huntington's disease.

Adult↗
PubMed1980

Stability of GABA levels in CSF under various conditions of storage.

Measurement of GABA in human lumbar CSF specimens stored under various conditions showed that the concentrations remained stable in untreated frozen specimens stored at -20 degrees C and at -70 degrees C. In untreated liquid specimens the GABA concentrations approximately doubled during 2 h at room temperature but did not change significantly during 10 min at room temperature or 2 h at 2-4 degrees C. The GABA level was stable at -70 degrees C in deproteinized specimens but doubled during 11 months of storage at -20 degrees C. The level was stable in liquid deproteinized samples for 49 h at room temperature but increased 1.3-fold and 2.0-fold in deproteinized specimens stored for 3 weeks at 2-4 degrees C and room temperature, respectively. Amino acid analyses of homocarnosine standards in 0.1 N HCl revealed a similar increase of GABA during storage at room temperature and at -20 degrees C, suggesting that at least part of the increase seen in CSF specimens might result from breakdown of GABA containing peptides. This instability of GABA level may account for some of the discrepancies among the reports of CSF GABA levels.

Amino Acids↗
PubMed1980

Levels of gamma-aminobutyric acid in cerebrospinal fluid in various neurologic disorders.

Levels of gamma-aminobutyric acid (GABA) in CSF were measured by the ion exchange-fluorometric method in 136 patients who underwent evaluation for neurologic disorders. In 19 patients with no organic neurologic or mental disorders who acted as normal controls, the mean (+/-SD) GABA level in CSF was 239 +/- 76 picomoles/mL. Patients with acute hypoxic encephalopathy showed a mean GABA level in CSF higher than that of the controls, a difference that was statistically significant. In all the other disorders studied, the mean GABA level in CSF was either equal to or lower than that found in the controls. Statistically significant reductions of the GABA level in CSF were seen in patients with Huntington's disease, dementias, cerebellar cortical atrophy, multiple sclerosis, epilepsy, and Parkinson's disease.

Brain Chemistry↗
PubMed1980

Lack of effect of carbamazepine on gamma-aminobutyric acid in cerebrospinal fluid.

Carbamazepine was administered to nine patients with manic-depressive illness at doses ranging from 600 to 1600 mg per day, achieving blood levels between 6 and 11 microgram per milliliter. Compared to medication-free values, GABA levels in the cerebrospinal fluid (CSF) were not significantly altered by an average of 30 days' treatment with carbamazepine. These preliminary data do not support a major effect of carbamazepine on brain GABA as reflected in CSF as a mechanism for its anticonvulsant or psychotropic effects.

Adult↗
PubMed1979

Low cerebrospinal fluid gamma-aminobutyric acid content in seizure patients.

Gamma-Aminobutyric acid (GABA) has been implicated in the neurochemistry of epilepsy. Lumbar cerebrospinal fluid (CSF) GABA concentrations determined using an ion-exchange fluorometric assay reflect brain GABA content. The mean lumbar CSF GABA concentration among 21 medicated patients with intractable seizures was significantly lower (p less than 0.001) than that of 20 unmedicated normal volunteers. Patients with generalized tonic-clonic (grand mal) and complex partial (psychomotor) seizures had significantly lower (p less than 0.05) CSF GABA concentrations than those with simple partial (focal sensory/motor) seizures. Although lumbar CSF GABA levels in our seizure patients did not significantly correlate with serum concentrations of phenytoin, phenobarbital, or primidone, additional study of medication-free epileptic patients may be required to evaluate the possibility of anticonvulsant-drug-induced CSF GABA alterations.

Adult↗
PubMed1979

Gamma-aminobutyric acid in peripheral tissue, with emphasis on the endocrine pancreas: presence in two species and reduction by streptozotocin.

A screen of selected periphral organs of the rat found that gamma-aminobutyric acid (GABA) is generally present outside the central nervous system, and, of those organs examined, GABA was present at the highest concentration in the pancreas (approximately 40 pmol/mg wet wt). Furthermore, this putative inhibitory neurotransmitter was found to be present at even higher levels in islets of Langerhans tissue isolated from rat pancreas (190 pmol/mg). Administration of streptozotocin, a selective beta-cell toxin, decreased pancreatic GABA levels significantly, but had no or only small effects on the GABA content of other organs. Normal teleost (catfish) Brockmann body contains about the same level of GABA as normal rat islet tissue.

Animals↗
PubMed1978

Huntington's disease. Cerebrospinal fluid GABA levels in at-risk individuals.

Gamma-aminobutyric acid (GABA) was measured by the ion-exchange fluorometric method in CSF from 22 individuals at risk for Huntington's disease (HD), six individuals with HD, and five neurologically normal controls. The mean (+/- SD) GABA level in the specimens from patients with HD was 142 +/- 27 pmoles/ml, whereas that of the normal control specimens was 297 +/- 87 pmoles/ml. The mean GABA level of the specimens from the individuals at risk for HD was 209 +/- 79 pmoles/ml; however, nine of these were in the normal range with a mean value of 281 +/- 72 pmoles/ml, while the other 13 were below the normal range with a mean value of 159 +/- 27 pmoles/ml. The data indicate that low GABA levels in CSF are evident prior to the onset of symptoms of HD but a predictive value can only be determined by continued observation of the clinical course of these at-risk individuals.

Adolescent↗
PubMed1977

Cerebrospinal fluid GABA reductions in seizure patients evoked by cerebellar surface stimulation.

Lumbar cerebrospinal fluid (CSF) gamma-aminobutyric acid (GABA) levels determined by fluorometric assay in four seizure patients were found to be significantly lower during bilateral, continuous cerebellar stimulation than those determined after a 7-day period without stimulation. The CSF GABA concentrations during chronic unilateral, alternating cerebellar stimulation were reduced in three seizure patients but unchanged in a fourth patient. The percentage decrease in CSF GABA appeared to be independent of cerebellar stimulation frequency. These findings suggest that GABA-mediated neuronal transmission is depressed during cerebellar surface stimulation and this evoked reduction in GABA activity may compromise the efficacy of cerebellar stimulation in the treatment of epilepsy. Lumbar CSF cyclic guanosine monophosphate levels determined by radioimmunoassay were not significantly altered by either mode or frequency of cerebellar stimulation.

Aminobutyrates↗