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We found that glufosinate (DL-GLUF) was distributed in the spinal fluid in glufosinate poisoning. A 50-year old Japanese man (weighing 67 kg) attempted to commit suicide by ingesting about 100 ml of BASTA (containing DL-GLUF 18.5 g; ratio of D-GLUF to L-GLUF: 1 : 1). He was transported to our hospital, where serious respiratory depression was seen 26 h after ingestion, and management with artificial ventilation was initiated. The D-GLUF concentration 1 h after ingestion was 191.1 microg/ml, almost the same as that of L-GLUF 193.5 microg/ml, but by 3 h after ingestion, these levels had sunk to 60.3 microg/ml and 52.3 microg/ml, respectively, with the concentration of L-GLUF lower than that of D-GLUF. Later, at 27 and 35 h after ingestion, the D-GLUF level was still higher than the L-GLUF level, and the total amounts of urinary excretion were 2835 mg for D-GLUF and 2298 mg for L-GLUF, each variable thus showing a difference between the enantiomers. Cerebrospinal fluid taken from the patient 27 h after poison ingestion revealed the presence of DL-GLUF on CG-MS analysis, and quantitative HPLC analysis of the enantiomers indicated that the D-GLUF concentration was 0.48 microg/ml, and the L-GLUF concentration 0.12 microg/ml. The levels in blood collected at the same time were: D-GLUF, 1.44 microg/ml, and L-GLUF, 0.35 microg/ml. Also, the cerebrospinal fluid contained about one-third of the blood levels of both DL-GLUF enantiomers. He was discharged without any sequelae after 11 d of hospitalization.

Regional cerebral blood flow and amino acid concentration in the cerebrospinal fluid were studied in 12 cases of vascular dementia, 12 cases of Alzheimer's disease, 12 cases of chronic alcoholism, and 12 age-matched healthy controls. In vascular dementia, blood flows were decreased in the cerebral cortex, frontal white matter, thalamus, caudate nucleus, and putamen and alpha-aminobutyric acid and glutamic acid concentrations were increased in the cerebrospinal fluid. In Alzheimer's disease, blood flows were decreased in the frontal cortex, parietal cortex, temporal cortex, and frontal white matter and alanine concentration was increased in the cerebrospinal fluid. In chronic alcoholism, blood flows were decreased in the cerebral cortex, thalamus, and putamen and urea, alanine, and glycine concentrations were increased in the cerebrospinal fluid.

Effects of traditional Chinese medicine on dementia, P300, cerebral blood flow, and cerebrospinal fluid (CSF) examination were investigated. Ten patients with Alzheimer disease (AD) who agreed to take traditional Chinese medicine were studied. The traditional Chinese medicine was given for 3 months and the Mini-Mental State Examination (MMSE), P300 examination, cerebral blood flow examination, and CSF examination were performed before and after taking the traditional Chinese medicine. The scores of the MMSE, the P300 latency, and blood flow in the cerebral cortex in AD improved with treatment with the traditional Chinese medicine. The concentration of alpha-aminobutyric acid in the CSF decreased with treatment with the traditional Chinese medicine. The improvement is considered to be not a placebo effect. Key Words: T

Gamma-Aminobutyric acid (GABA) levels in cerebrospinal fluid were measured in seven patients with tension headache and 12 patients with migraine. GABA was detected only during the migraine attack. The results suggest disordered GABA metabolism in migraine.

We describe an automated amino acid analyzer with fluorescence detection (o-phthalaldehyde) which permits sensitive and rapid determinations of gamma aminobutyric acid in human cerebrospinal fluid. Concentrations as low as 50 nmol/liter can be accurately determined in 100 mul samples at the rate of one sample per hour. Concentrations in untreated cerebrospinal fluid increase rapidly after sampling by lumbar puncture. The concentration in immediately deproteinized samples from 38 patients with intervertebral disc disorders was 220 +/- 81 nmol/liter (mean +/- SD).

Neuropathologically, Huntington's disease is characterized by a profound reduction in neuronal cells originating in the corpus striatum and globus pallidus. Since one of these cell types utilizes gamma-aminobutyric acid (GABA) as a neurotransmitter, it may be possible to differentially diagnose this disorder on the basis of the CSF content of this amino acid. In order to determine the validity of this hypothesis, cerebrospinal fluid GABA was analyzed, using a recently developed radioreceptor assay procedure and was found to be significantly reduced in patients diagnosed as having Huntington's disease and also lower in patients with Alzheimer's disease, though no difference was noted between Parkinson patients and control subjects. The results suggest that analysis of cerebrospinal fluid GABA may have diagnostic, and perhaps predictive, value in certain neurological disorders.

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.

Gamma-aminobutyric acid (GABA) levels in the CSF were measured in 9 normal individuals, 17 drug-free schizophrenic patients and 10 of these same schizophrenic patients after neuroleptic treatment. There was no significant difference between CSF level of GABA in the control group compared to those in schizophrenic patients; however, 6 of the 7 lowest GABA levels were from schizophrenic patients. There was a significant decline of 12 per cent in mean GABA levels in the CSF after a mean of two months of neuroleptic treatment.

Cerebrospinal fluid gamma-aminobutyric acid (CSF GABA) was analyzed in 151 patients who underwent evaluation for central nervous system disease. CSF GABA was not detected in 19 of these patients, who had no evidence of neurologic disease and who served as controls. GABA was most frequently detected in patients with cerebrovascular disease, and was detected only in Parkinson's syndrome of atherosclerotic origin and dementia of multi-infarct type. CSF GABA was not detected in Alzheimer's disease or Huntington's disease. Patients with grand mal seizures exhibited CSF GABA elevation within 24 hours of the ictus. In patients with multiple sclerosis GABA detection was related to the presence or exacerbation of spinal cord lesions. Further study is necessary to evaluate the significance of elevated CSF GABA in central nervous system disease.