The cerebrospinal fluid homovanillic acid concentration in patients with Parkinsonism treated with L-dopa.

Curzon, G.; Godwin-Austen, R B; Tomlinson, E. B.; Kantamaneni, B. D.

doi:10.1136/jnnp.33.1.1

Cited by 54 publications

(21 citation statements)

References 18 publications

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“…15 The remaining portion was placed on Amberlite columns from which NE was eluted by 2/3 M boric acid and analyzed fluorometrically using the trihydroxyindole reaction according to modifications of the method of Renzini et al 16 and Valori et al 17 HVA and 5HIAA were organically extracted from CSF (usually 2.2 ml) using a modified combination of the methods of Ashcroft et al 18 and Gerbode and Bowers. 19 Both compounds were fluorometrically assayed, 5HIAA by the technique of Ashcroft and Sharman 20 and HVA according to Curzon et al 21 Cyclic AMP in CSF was analyzed by a protein binding assay similar to radioimmunoassay by a combination of the methods of Gilman 22 and of Brown et al 23 Glucose was measured in arterial and cerebral venous blood by an enzymatic spectrophotometric technique. 24 Lactate and pyruvate were measured by the enzymatic method of Rosenberg and Rush.…”

Section: Biochemical Methodologymentioning

confidence: 99%

Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients.

Meyer¹,

Miyakawa²,

Welch³

et al. 1976

Stroke

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SUMMARY Cerebral hemispheric blood flow and metabolism were measured before and after therapy with intracarotid infusion of combined PBZ and PPL in IS patients with recent cerebral infarction. HBF was unaltered despite decrease in cerebral perfusion pressure. Cerebral hemispheric oxygen consumption and carbon dioxide production decreased while cerebral hemispheric lactate production increased.Biphasic cerebral uptake of tyrosine was observed during and immediately after PBZ and PPL infusion. CSF HVA increased, indicating altered DA turnover. CSF SHIAA levels also increased, suggesting altered SHT turnover after PBZ and PPL. Release of cyclic AMP from ischemic brain into cerebral venous blood seen in the steady state was abolished after therapy.Cerebral hemodynamic studies suggest a functional balance between monoaminergic neurogenic influences in the control of cerebral circulation. Imbalance of such controlling factors in ischemic brain may lead to paradoxical vascular responses to induced hypertension and hypotension. PBZ and PPL enhance such responses perhaps by increasing central neurotransmitter turnover and release.Further shift toward cerebral anaerobic metabolism may occur in ischemic brain following the use of phenoxybenzamine and propranolol.Worsening of neurological deficit occurred in four cases. Combined therapy with PBZ and PPL does not appear beneficial in the therapy of patients with recent stroke.

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Section: Biochemical Methodologymentioning

confidence: 99%

Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients.

Meyer¹,

Miyakawa²,

Welch³

et al. 1976

Stroke

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“…This view is supported by the finding that levodopa treatment increased the concentration of dopa mine and its main metabolite, homovanillic acid (HVA) in the brain of experimental animals H yyppa et al, 1971], as well as in parkinsonian patients [Rinne et al, 1971;R inne and Sonninen, 1973;Y ahr, 1971; Davidson et al, 1971Davidson et al, , G reer et al, 1971 , There is experimental evidence that the metabolism of dopamine and 5-hydroxytryptamine (5-HT) in the brain can be reflected by the con centration of HVA and 5-hydroxyindoleacetic acid (5-HIAA), respec tively, in the cerebrospinal fluid (CSF), if the elimination of these acid monoamine metabolites from the brain and CSF is intact [Pletscher et al, 1967;Papeschi et al, 1970;M oir et al, 1970;R inne and Sonninen, 1972] , Indeed, significantly decreased concentrations of HVA and a less marked decrease in the concentration of 5-HIAA in the CSF of parkin sonian patients have been observed [Johansson and Roos, 1965;Bernheimer et al, 1966;Rinne andSonninen, 1968a, b, 1972]. On the other hand, increased values of HVA in the CSF have been reported during levodopa treatment [Weiner et al, 1969;Rinne et al, 1970;Anden et al, 1970;Curzon et al, 1970;van Woert and Bowers, 1970;Chase, 1970a;G odwin-A usten et al, 1971;Sharpless et al, 1971;Bertler et al, 1971;J equier and Dufresne, 1972;H interberger and Andrews, 1972]. However, it is not known to what ex tent the increased HVA levels in the CSF really reflect increased brain metabolism.…”

mentioning

confidence: 99%

Acid Monoamine Metabolites in the Cerebrospinal Fluid of Parkinsonian Patients Treated with Levodopa alone or Combined with a Decarboxylase Inhibitor

Rinne¹,

Sonninen²,

Siirtola³

1973

Eur Neurol

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Concentrations of homovanijlic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF) were studied before and during treatment of 151 parkinsonian patients with levodopa alone or combined with a decarboxylase inhibitor. A particular attempt was made in this study to determine whether any correlation exists between the concentrations of these acid monoamine metabolites in the CSF before and during treatment as well as after administration of probenecid and the therapeutic response and side-effects of the treatment. In patients with Parkinson’s disease the concentrations of HVA and 5-HIAA in the CSF before therapy and after administration of probenecid were found to be significantly lower than those in control subjects. Statistical analyses showed that these variables could not be used to predict the clinical response to treatment. Long-term treatment with levodopa alone or combined with a decarboxylase inhibitor induced an increase in the concentration of HVA in the CSF which correlated significantly with the dose of the drug but not with the clinical improvement. However, the concentrations of HVA during combined treatment were considerably lower than during treatment with levodopa alone, using therapeutically equivalent dosages. Obviously, a part of the HVA found in the CSF during levodopa treatment originates from the brain capillary walls. Treatment with levodopa and decarboxylase inhibitor decreased the concentration of 5-HIAA in the CSF. During treatment with levodopa alone, there was a significant negative correlation with the dose of levodopa as well as with libido and psychotic behavior after 6 and 12 months’ treatment, respectively.

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“…CSF HVA was determined by a modified combination of the methods of And6n, Roos, and Werdinius (1963) and Murphy, Robinson, and Sharman (1969) described previously (Curzon, Godwin-Austen, Tomlinson, and Kantamaneni, 1970) ,and 5-HIAAbyamodificationof the procedure of Korf and Valkenburgh-Sikkema (1969).…”

Section: Methodsmentioning

confidence: 99%

“…Increased dopamine turnover after L-dopa administration may cause alerting (Blaschko and Chrusciel, 1960) but also increases CSF HVA (Curzon et al, 1970). However, HVA formation requires two enzymes (Axelrod, 1966), the intraneuronal monoamine oxidase and the extraneuronal catecholamine-O-methyl transferase.…”

Section: Beforementioning

confidence: 99%

Effect of folic acid by mouth on cerebrospinal fluid homovanillic acid and 5-hydroxyindoleacetic acid concentration

Hunter

Barnes

Curzon

et al. 1971

Journal of Neurology, Neurosurgery & Psychiatry

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SUMMARY Administration of 30 mg folic acid by mouth caused a significant fall in cerebrospinal fluid homovanillic acid concentration in 11 subjects. There was no significant change of 5-hydroxyindoleacetic acid concentration. The fall was less marked in five patients on anticonvulsant medication and failed to reach statistical significance. Neither homovanillic acid nor 5-hydroxyindoleacetic acid concentrations changed significantly when 15 mg folic acid was given in divided dosage for one, two, and four weeks. The effect appeared to be related to the height of serum-folate levels reached and to be independent of cerebrospinal fluid-folate levels, which did not change significantly. Possible mechanisms and their potential therapeutic application are discussed.

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The cerebrospinal fluid homovanillic acid concentration in patients with Parkinsonism treated with L-dopa.

Cited by 54 publications

References 18 publications

Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients.

Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients.

Acid Monoamine Metabolites in the Cerebrospinal Fluid of Parkinsonian Patients Treated with Levodopa alone or Combined with a Decarboxylase Inhibitor

Effect of folic acid by mouth on cerebrospinal fluid homovanillic acid and 5-hydroxyindoleacetic acid concentration

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