Clinical measurements of central dopamine and 5-hydroxytryptamine metabolism: reliability and interpretation of cerebrospinal fluid acid monoamine metabolite measures

Mb, Bowers

doi:10.1016/0028-3908(72)90061-5

Cited by 98 publications

(35 citation statements)

References 39 publications

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“…We did not have a never depressed group with a history of alcoholism, however, we found that depressed subjects with alcoholism had significantly lower levels of HVA than depressed subjects who had never had alcoholism. CSF HVA reflects CNS dopamine turnover (Bowers, 1972;Stanley et al, 1985) and our finding suggests that less dopaminergic activity is associated with alcoholism among depressed persons.…”

Section: Biological Findingsmentioning

confidence: 64%

“…The cerebrospinal fluid (CSF) concentrations of the dopamine, serotonin, and to a lesser degree norepinephrine metabolites, homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG), respectively, are presumed to reflect the turnover of parent neurotransmitters in the central nervous system (Moir et al, 1970;Bowers, 1972;Stanley et al, 1985;Sharma et al, 1994;Reuster et al, 2002). Accordingly, measurements of these compounds in lumbar CSF have been employed in studies of brain function in vivo.…”

Section: Introductionmentioning

confidence: 99%

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Lower CSF Homovanillic Acid Levels in Depressed Patients with a History of Alcoholism

Sher

Oquendo

et al. 2003

Neuropsychopharmacol

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Major depression and alcoholism are often comorbid, resulting in more impairment and more suicidal behavior compared with either diagnosis alone. This study compared clinical features and cerebrospinal fluid (CSF) monoamine metabolites in depressed subjects with and without a history of alcoholism and healthy volunteers. We hypothesized that depressed subjects with a history of alcoholism would be more aggressive, impulsive, and suicidal than depressed subjects without a history of alcoholism, and would have lower CSF monoamine metabolite levels. We compared 63 subjects with a current major depressive episode (MDE) and a history of alcoholism, 72 subjects with a current MDE but without a history of alcoholism, and 22 healthy volunteers. Participants with a history of alcoholism were in remission for at least 6 months. All subjects were free from prescribed medications known to affect brain serotonin, dopamine, or norepinephrine systems for a minimum of 14 days. Depressive symptoms, lifetime aggression, impulsivity, Axis II disorders, and suicidal behavior were assessed. CSF was sampled and homovanillic acid (HVA), 5-hydroxyindolacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG) were assayed by high-performance lipid chromatography with electrochemical detection. Depressed subjects with a history of alcoholism did not differ from depressed subjects without a history of alcoholism in current severity of depressive symptoms, or in past suicidal behavior. Depressed subjects with a history of alcoholism had lower CSF HVA levels, and higher lifetime aggression and current suicide ideation scale scores and were more likely to be tobacco smokers compared with depressed subjects without a history of alcoholism. Low HVA was present after adjustment for sex, aggression and depression scores, cigarette smoking, antisocial and borderline personality disorders, psychomotor retardation, and delusions. Controls had CSF HVA levels intermediate between the two depressed groups. We found no group difference in CSF 5-HIAA and MHPG levels. In individuals with current MDE, those with a history of comorbid alcoholism had lower CSF HVA levels compared with those without a history of alcoholism. Low CSF HVA suggests that impaired dopaminergic activity is associated with a history of alcoholism in persons with current MDE.

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Section: Biological Findingsmentioning

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Lower CSF Homovanillic Acid Levels in Depressed Patients with a History of Alcoholism

Sher

Oquendo

et al. 2003

Neuropsychopharmacol

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“…These results have been confirmed by several others (cf. but not by all (Bowers, 1972). Furthermore, low values were found in only a fraction of even severe endogenous depressions by Van Praag and Korf (1973).…”

Section: Cerebrospinal Fluidmentioning

confidence: 99%

Biogenic Amines and Affective Disorders

Luchins¹

1976

Int Pharmacopsychiatry

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The evidence linking biogenic amines and affective disorders is critically reviewed. Surveyed are studies on the level of biogenic amines and their metabolites in the brain, blood, urine and cerebrospinal fluid of patients with affective conditions; the effects of biogenic amine precursors, depletors and blockers on affective states and the action of present methods of treatment of these disorders on the level of biogenic amines. Reference is also made to the existence of various disease states where abnormalities of biogenic amines exist in the absence of affective disorders. The review fails to uncover convincing evidence that affective disorders are related to abnormal levels of biogenic amines. Reasons are outlined why the 'catecholamine hypothesis' and related theories can neither be proven nor disproven with the available techniques.

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“…Marked accumulation suggests the reverse: high production of metabolites, a high degree of degradation and. therefore, a high turnover of the mother amines (Bowers, 1972;Goodwin et al, 1973;.…”

Section: Central Ma Deficiency In Depressive Patientsmentioning

confidence: 99%

Therapy-Resistant Depressions: Biochemical and Pharmacological Considerations

Vanpraag¹

1974

Psychother Psychosom

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Two statements are made: antidepressants increase the amount of MA at the central receptors; antidepressants are effective in some, but quite ineffective in other patients, even if they belong to the same diagnostic category. Three questions arise from these statements: (1) Does a central MA deficiency occur in depressive patients? (2) If so, is this disorder present in only a proportion of the patients? (3) If so, can this explain the apparent selectivity of antidepressants in the sense that MA-deficient patients benefit particularly from this type of therapy? Tentative answers are given to these three questions. In depressive patients the cerebral MA turnover can be diminished. These disorders do not occur in all patients but seem to be confined to certain categories of depression. Diminution or non-diminution of the central MA turnover is a (not the) factor which determines whether antidepressant medication will succeed or fail. The theoretical and practical implications of these answers are discussed.

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Clinical measurements of central dopamine and 5-hydroxytryptamine metabolism: reliability and interpretation of cerebrospinal fluid acid monoamine metabolite measures

Cited by 98 publications

References 39 publications

Lower CSF Homovanillic Acid Levels in Depressed Patients with a History of Alcoholism

Lower CSF Homovanillic Acid Levels in Depressed Patients with a History of Alcoholism

Biogenic Amines and Affective Disorders

Therapy-Resistant Depressions: Biochemical and Pharmacological Considerations

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