Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of piracetam, a cyclical derivative of GABA, was compared with that of a placebo in a double-blind study of 60 patients with post-concussional syndrome of 2-12 months' duration. The daily dose of piracetam was 4,800 mg. After 8 weeks of treatment piracetam significantly reduced the occurrence and severity of the following symptoms: vertigo, headache, tiredness, decresed alertness, increased sweating and neurasthenic symptoms. No significant effect was observed on the following symptoms: tremor, orthostatic symptoms, and memory disorders. Side effect were reported by 64% of the patients under piracetam and by 32% under placebo. In the author's opinion, piracetam seems to be a promising new drug for the treatment of post-concussional syndrome.
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PMID:Piracetam in the treatment of post-concussional syndrome. A double-blind study. 34 47

A detailed presentation of 15 case-histories of subjects of both sexes, drawn from all decennies of life from the first to the eight, suggesting a syndrome originated from a possible GABA deficiency, is carefully made. Such syndrome is believed to be characterized by basic depressive state, loss of the habit of stretching oneself, sleep disorders, mostly with early morning awakening, constipation and nuchal headache. The above symptoms have been associated to a deficiency of GABA after noting the very speed recovery after administration of N-dipropylacetic acid, an inhibitor of GABA transaminase.
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PMID:A syndrome from a possible GABA deficiency. Clinical-therapeutic report on 15 cases. 35 28

Consumption of monosodium glutamate has long been considered to precipitate headaches in susceptible patients. In this study the direct effects of glutamate and its metabolite, glutamine, on arterial contractility were examined using rings of rabbit aorta. In a high concentration glutamate caused significant concentration-dependent contractions (EC50, 10(-1)M; maximum tension, 188.4 +/- 33.3 mg wt tension/mg tissue). Agonists and antagonists for alpha-adrenergic, histaminergic, serotonergic, cholinergic, and GABA-nergic receptors as well as inhibition of prostaglandin synthesis failed to influence glutamate contractions. At high concentrations (10(-5)M) the calcium channel blocker, verapamil, inhibited the glutamate response. Glutamate and glutamine both exhibited concentration dependent relaxation of norepinephrine (NE), phenylephrine (PE), histamine, serotonin (5-HT), and prostaglandin F2 alpha (PGF2 alpha)-induced contractions. Kainic acid (10(-4)M), an agonist of one subpopulation of central glutamate receptor, potentiated glutamate-induced vasoconstriction; a higher concentration (10(-3)M) produced an irreversible inhibition of glutamate contractility. Only the central glutamate receptor antagonist, ketamine (10(-4)-10(-2)M), induced a reversible, concentration dependent inhibition of glutamate-induced contractions. Glutamate contractility was not dependent on extracellular calcium, an intact endothelium or neuronal function. These results demonstrate a direct effect of glutamate on peripheral arterial tone. Dietary consumption of large quantities of MSG may represent a serious health hazard to certain individuals with pre-existing vascular disease.
Headache 1990 Sep
PMID:Vasospasm contributes to monosodium glutamate-induced headache. 226 10

Vigabatrin is a selective, irreversible suicide inhibitor of GABA transaminase and thus increases brain and CSF GABA. In 33 adult patients with long standing refractory epilepsy on treatment with one or two standard anti-convulsant drugs, the addition of vigabatrin up to 3g daily for eight weeks was associated with a 48.2% reduction in seizure frequency. Twenty patients who had exhibited a 50% or more reduction in frequency of one or more seizure types entered an eight week double-blind placebo controlled phase. Patients on vigabatrin maintained a 54.7% reduction of seizure frequency, whereas those on placebo showed an 18.6% increase in seizure frequency, a highly significant difference between the two groups. In the open phase, seven patients were withdrawn due to unacceptable and reversible adverse events. The commonest side effects were drowsiness, depression and mood instability, and headaches. Vigabatrin is a potentially valuable new treatment for chronic epilepsy, especially partial seizures with or without secondary generalisation.
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PMID:Vigabatrin: rational treatment for chronic epilepsy. 229 96

The alteration of amino acids content in cerebrospinal fluids (CSF) from 31 cases of epilepsy and 10 cases of headache (as control) was studied using high performance liquid chromatography (HPLC). In patients with epilepsy, it was found that the CSF levels of GABA and aspartic acid had a tendency to decrease, but these changes were not statistically significant. In simple partial seizures, the CSF levels of glutamic acid and glycine also showed a tendency to decrease. The decrease of CSF GABA found in epileptics had a tendency to normalize following treatment with valproic acid. At the same time, administration of valproic acid induced a decrease of aspartic acid in the CSF of epileptics. These results suggest that administration of valproic acid may induce an increase in GABA and a decrease in aspartic acid in the CSF of epileptics.
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PMID:Alteration of amino acid content of cerebrospinal fluid from patients with epilepsy. 322 34

The efficacy and tolerability of vigabatrin (gamma-vinyl GABA, GVG), given as add-on therapy to 23 adult outpatients with severe drug-resistant epilepsy (17 with partial seizures), were studied using a double-blind, placebo-controlled, crossover design. The study consisted of two 7-week periods during which vigabatrin and placebo were administered in random sequence. Dosage was 1.0 g twice daily for patients weighing less than or equal to 65 kg and 1.5 g twice daily for patients weighing greater than 65 kg. Three patients were dropped from the study, two for reasons unrelated to treatment and one because of the appearance of vertigo, headache, dysarthria, and ataxia, which subsided rapidly when vigabatrin was stopped (3 g daily). Sixteen of the 20 patients available for analysis showed a decrease in the total number of seizures as compared with the placebo period. Of these, 12 showed a greater than 50% reduction in seizure frequency and 4 of the 12 showed a greater than 75% reduction. Both the total number of seizures and the number of partial seizures were significantly reduced by vigabatrin (p less than 0.01). Only in the patient who dropped out were severe adverse effects seen. The most frequently reported unwanted effect was mild drowsiness, which developed in seven patients on vigabatrin and in one on placebo. Positive effects, however, were also seen with six patients who reported an improved sense of well-being while receiving vigabatrin as compared with only 1 during the placebo period. No consistent changes in electrocardiogram (ECG), electroencephalogram (EEG), and visual-, auditory-, and somatosensory-evoked potentials were seen during the study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vigabatrin in the treatment of epilepsy: a double-blind, placebo-controlled study. 353 69

The alteration of amino acids in cerebrospinal fluids (CSF) from 14 cases of Parkinson's disease, five cases of cerebellar degeneration and five cases of headache (control) was studied using high performance liquid chromatography. In patients with Parkinson's disease, it was found that the CSF level of GABA showed a significant decrease, while that of taurine had an increase. The degree of disability in Parkinson's disease and the decreased GABA levels had a positive correlation, especially at its advanced stages. In patients with cerebellar degeneration, it was also found that there was a significant decrease in CSF GABA. The present results suggest that the CSF level of GABA may be a good indicator of the severity of Parkinson's disease as well as the presence of cerebellar degeneration. Possible involvement of the increase of CSF taurine in the pathogenesis of Parkinson's disease is also suggested.
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PMID:Alteration of amino acids in cerebrospinal fluid from patients with Parkinson's disease and spinocerebellar degeneration. 370 20

The observation that migraine patients improve during pregnancy with return of headache upon commencement of breast feeding, led Authors to investigate the involvement of Pain Suppressor System (PSS) in pregnancy and after delivery. PSS is a complex system which utilizes neurotransmitters as beta-Endorphine-Like-Immunoreactivity (beta-ELI), 5-Hydroxytryptamine (5-HT), Dopamine (DA) and GABA. The Authors report preliminary results of beta-ELI behaviour in pregnancy and in the immediate post-partum period in rats.
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PMID:[The puerperium and dysnociception. I) Behavior of serum beta-endorphins in pregnant and post-partum animals]. 627 25

Recent debate concerning the interpretation of studies of regional cerebral blood flow in migraine has re-emphasized that cerebral ischaemia may occur during attacks of migraine with aura. In this article we suggest that the presence of ischaemia during attacks makes it possible that migraine with aura causes neuronal damage in the long term. We argue that damage is likely to occur in the primary visual cortex, given that a recent high-resolution rCBF study has found flow reductions confined to this area. Furthermore, we hypothesize that the extent to which rCBF is reduced in migraine with aura is sufficient to cause damage only to GABA-ergic inhibitory interneurons in layer IV of this cortex. In animal models, similar cells are known to be selectively vulnerable to damage as a result of hypoxic conditions. Evidence consistent with our hypothesis is provided by recent studies of visual function in migraine. Some clinical and pathophysiological implications of this hypothesis are discussed.
Cephalalgia 1994 Dec
PMID:Might migraine damage the brain? 769 2

The neuropsychological effects of the GABA-reuptake blocker, tiagabine-HCl, were tested in an open trial of 22 adult patients with refractory partial epilepsy followed by a double-blind, placebo-controlled, cross-over trial in 12 subjects. Nineteen patients completed the initial open titration and fixed-dose phase of the study and 11 patients completed the double-blind phase. The median daily tiagabine dose was 32 mg during the open fixed dose and 24 mg during the double-blind periods. Neuropsychological evaluation did not show any significant effect on cognitive function in the open or double-blind phases. In this group of patients no statistically significant difference in the frequency of the total number of seizures or complex partial seizures was found in the open or double-blind stages. Seizure severity was significantly less in the open fixed dose than in the baseline period, but was not significantly different between the two double-blind periods. Reported side effects were transient, most commonly aggression/irritability, lethargy, headache and drowsiness. No significant EEG changes were observed.
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PMID:Neuropsychological effects of tiagabine, a potential new antiepileptic drug. 804 51


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