Probenecid: Dosage, levels in plasma and cerebrospinal fluid (CSF) and influence upon CSF levels of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) in the rabbit

1975 ◽  
Vol 43 (3) ◽  
pp. 223-227 ◽  
Author(s):  
J. P. Muizelaar ◽  
J. I. Oberink
Keyword(s):  
Cerebrospinal Fluid ◽  
Homovanillic Acid ◽  
Hydroxyindoleacetic Acid ◽  
Csf Levels

Cerebrospinal Fluid Analyses in Migraine Patients and Controls

Cephalalgia ◽  
1995 ◽  
Vol 15 (6) ◽  
pp. 489-493 ◽  
Author(s):  
JF Rothrock ◽  
KR Mar ◽  
TL Yaksh ◽  
A Golbeck ◽  
AC Moore
Keyword(s):  
Amino Acids ◽  
Cerebrospinal Fluid ◽  
Homovanillic Acid ◽  
Divalproex Sodium ◽  
Transformed Migraine ◽  
Hydroxyindoleacetic Acid ◽  
Csf Levels ◽  
Baseline Values ◽  
Central Neurotransmitters

To investigate the role of central neurotransmitters in the pathogenesis of migraine, we measured cerebrospinal fluid (CSF) levels of certain amino acids (glycine, taurine, glutamine) and metabolites of biogenic amines (5-hydroxyindoleacetic acid and homovanillic acid) in 38 migraine patients and compared them with the levels from 10 headache-free controls. The levels of taurine, glycine and glutamine were significantly higher in the migraine patients (p < 0.0001 for taurine and glycine; p < 0.0009 for glutamine); there were no significant differences among the three migraine subgroups (infrequent migraine, frequent migraine and transformed migraine). In seven patients subsequently treated with divalproex sodium, CSF taurine levels decreased significantly from pretreatment baseline values. These data support the concept that migraine is at least in part a disorder of central neurotransmission.

Noradrenergic Overactivity in Chronic Schizophrenia: Evidence Based on Cerebrospinal Fluid Noradrenaline and Cyclic Nucleotide Concentrations

1980 ◽  
Vol 137 (4) ◽  
pp. 346-351 ◽  
Author(s):  
U. C. R. Gomes ◽  
B. C. Shanley ◽  
L. Potgieter ◽  
J. T. Roux
Keyword(s):  
Cerebrospinal Fluid ◽  
Cyclic Nucleotides ◽  
Homovanillic Acid ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Chronic Schizophrenia ◽  
Evidence Based ◽  
Chronic Schizophrenics ◽  
Hydroxyindoleacetic Acid ◽  
Lumbar Cerebrospinal Fluid

SummaryConcentrations of noradrenaline (NA), homovanillic acid, 5-hydroxyindoleacetic acid and cyclic nucleotides were determined in lumbar cerebrospinal fluid (CSF) from acute and chronic schizophrenics and various groups of psychiatric and non-psychiatric control subjects. Statistically significant increases in NA and cyclic adenosine monophosphate were found in CSF from chronic schizophrenics compared to all other groups. These results were shown by statistical analyses to be unrelated to medication. They may be interpreted as evidence for noradrenergic overactivity as a possible primary abnormality in chronic schizophrenia.

Low CSF Concentrations of Cyclic GMP in Schizophrenia

1983 ◽  
Vol 142 (3) ◽  
pp. 288-291 ◽  
Author(s):  
W. F. Gattaz ◽  
H. Cramer ◽  
H. Beckmann
Keyword(s):  
Cerebrospinal Fluid ◽  
Cyclic Gmp ◽  
Homovanillic Acid ◽  
Healthy Controls ◽  
Neuroleptic Treatment ◽  
Cholinergic Activity ◽  
Schizophrenic Patients ◽  
Csf Levels

SummaryIncreasing evidence suggests that the concentrations of cyclic guanosine 3′5′-monophosphate (cGMP) in the cerebrospinal fluid (CSF) may reflect central cholinergic activity. When the concentrations of this nucleotide in the CSF from 28 schizophrenic patients (13 without and 15 with neuroleptic treatment) and 16 psychiatrically healthy controls was determined the schizophrenics showed significantly lower CSF levels of cGMP as compared to controls.As dopamine and homovanillic acid concentrations were not altered in these CSF samples, this finding of reduced cGMP suggests a cholinergic-dopaminergic imbalance in schizophrenia, with a reduction of the former and consequently a relative dominance of the latter.

Association of Cerebrospinal Fluid Deficiency of 5-Methyltetrahydrofolate, but Not S-Adenosylmethionine, with Reduced Concentrations of the Acid Metabolites of 5-Hydroxytryptamine and Dopamine

1994 ◽  
Vol 86 (6) ◽  
pp. 697-702 ◽  
Author(s):  
Robert Surtees ◽  
Simon Heales ◽  
ANN Bowron
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Homovanillic Acid ◽  
Dopamine Turnover ◽  
Inborn Errors ◽  
Methyl Transfer ◽  
Hydroxyindoleacetic Acid ◽  
The Central Nervous System ◽  
Acid Metabolites

1. Folate deficiency, or inborn errors of folate metabolism, cause reduced turnover of 5-hydroxytryptamine (serotonin), and perhaps dopamine, in the central nervous system. The mechanism by which this occurs are not known. One possibility is that this is mediated by deficiency of the methyl-donor S-adenosylmethionine. 2. To test this in humans, we have measured cerebrospinal fluid concentrations of 5-hydroxyindoleacetic acid and homovanillic acid, metabolites of 5-hydroxytryptamine and dopamine, respectively, in children with inborn errors of the methyl-transfer pathway. These children are naturally deficient in 5-methyltetrahydrofolate, S-adenosylmethionine or both before treatment, and replete with S-adenosylmethionine, but not necessarily with 5-methyltetrahydrofolate, during treatment. 3. Children with subnormal cerebrospinal fluid concentrations of 5-methyltetrahydrofolate had significantly reduced concentrations of 5-hydroxyindoleacetic acid and homovanillic acid. Children with subnormal cerebrospinal fluid concentrations of S-adenosylmethionine did not have significantly reduced concentrations of these metabolites. 4. We conclude that the mechanism by which deficiency of 5-methyltetrahydrofolate causes reduced 5-hydroxytryptamine and dopamine turnover is unlikely to be mediated by S-adenosylmethionine.

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