Biogenic amine metabolites in cerebrospinal fluid of patients with affective disorders

Vestergaard, Per; Sørensen, Tanja Vibeke; Hoppe, E.; Rafaelsen, Ole J.; Yates, Celia M.; Nicolaou, Nicos

doi:10.1111/j.1600-0447.1978.tb06924.x

Cited by 97 publications

(16 citation statements)

References 26 publications

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“…The mean daily dose of risperidone in manic patients was 3.8 AE 1.1 mg/day in the present study, which is similar to a previous open study by Yatham et al (2003b). With regard to the catecholamine metabolites in manic patients, several reports have demonstrated that pretreatment cerebrospinal fluid (CSF) HVA is elevated in some groups of manic patients (Banki, 1977;Bowers and Heninger, 1977;Vestergaard et al, 1978;Swann et al, 1983). Mazure et al (1998) reported a significant relationship between elevated pretreatment plasma HVA and the response to antipsychotic drugs in manic patients.…”

Section: Discussionsupporting

confidence: 87%

Effect of risperidone on plasma catecholamine metabolites and brain‐derived neurotrophic factor in patients with bipolar disorders

Yoshimura

Nakano

Hori

et al. 2006

Human Psychopharmacology

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A combination treatment with a mood stabilizer and an antipsychotic drug is often used in as many as 90% of subjects with acute mania. Recently, augmentation therapy with atypical antipsychotics has been investigated in both the acute and long-term treatment of bipolar disorder with or without psychosis. In the present study, the authors investigated the efficacy of risperidone treatment for both acute manic and depressive episodes in bipolar disorder. Eighteen patients (M/F: 8/10, age: 34 +/- 15 yr) who met the DSM-IV criteria for bipolar I disorder (12 cases of manic episodes, 6 cases of depressive episodes) with risperidone treatment were evaluated regarding their clinical improvement using the Young Mania rating Scale (YMRS) and the Hamilton rating Scale for Depression (Ham-D). Plasma concentrations of HVA and MHPG were analyzed by HPLC-ECD and plasma brain-derived neurotrophic factor (BDNF) levels were detected by sandwich ELISA. The mean scores of the YMRS were 22, 18, 12, 8, and 5 at time points before and 1, 2, 3, and 4 weeks after the risperidone administration, respectively. The mean scores of the Ham-D were 24, 25, 21, 21, and 19 at time points before and 1, 2, 3, and 4 weeks after the risperidone administration, respectively. The plasma levels of HVA and 3-methoxy-4-hydroxyphenylglycol (MHPG) were observed to have decreased 4 weeks after risperidone administration in manic patients. The levels did not change in depressive patients. The plasma levels of BDNF were decreased in depressive patients compared with manic patients or healthy controls. However, the administration of risperidone did not alter plasma BDNF levels.

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Section: Discussionsupporting

confidence: 87%

Effect of risperidone on plasma catecholamine metabolites and brain‐derived neurotrophic factor in patients with bipolar disorders

Yoshimura

Nakano

Hori

et al. 2006

Human Psychopharmacology

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“…This difference may be related to the fact that we used a sample of depressed subjects without a history of alcoholism. Our finding appears to be consistent with the study by Vestergaard et al (1978), who reported significantly higher CSF HVA levels in depressed subjects than in healthy controls. It is possible that the variability in the rates of comorbid alcoholism and/or other comorbid disorders in different depressed populations plays an important role in the inconsistency of findings regarding CSF HVA levels in depressed subjects.…”

Section: Biological Findingssupporting

confidence: 83%

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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“…The most fruitful strategy is the measurement of the concentration of monoamine metabolites and precursors in the CSF (vanPraag 1977): although this technique can, in principle, supply information about the turnover of the transmitter amines, there are considerable difficulties in the interpretation (Post and Goodwin t975). It is therefore not surprising that human CSF amine metabolite studies on the metabolic differences between depressed patients and controls even resulted recently in a large, but controversial and confusing body of data (Vestergaard et al 1979;Berger et al, 1980). Several explanations have been proposed for this controversy.…”

Section: Introductionmentioning

confidence: 95%

Correlation of individual symptoms and other clinical variables with cerebrospinal fluid amine metabolites and tryptophan in depression

Bánki¹,

Molnár

Fekete

1981

Arch. F. Psychiatr. U. Z. Neur.

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Cerebrospinal fluid 5-hydroxyindoleacetic acid (5HIAA), homovanillic acid (HVA), and tryptophan in both CSF and plasma were measured in a carefully selected group of 33 depressed women. Strict and explicit inclusion and exclusion criteria were used, and CSF was taken under controlled circumstances. Seventeen operationally defined and uniformly rate psychiatric symptoms as well as global depression severity and 12 clinical background variables were correlated with the four biochemical parameters, using multivariate regression analysis based on Spearman's rank correlation coefficient according to the nature of the data. Global depression severity did not correlated with any of the biochemical variables; there were, however, significant correlations between CSF 5HIAA and anxiety, insomnia, and suicide on the one hand, and between CSF HVA and motor symptoms and paranoidity on the other hand. Background variables showed only a few--and much weaker--correlations. It was concluded that central monoamine metabolism does affect some particular psychiatric symptoms but is not parallel with the complex clinical construct of the depressive disease. Further studies using isolated psychopathological symptoms instead of nosological categories are suggested in clinical neurochemistry.

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Biogenic amine metabolites in cerebrospinal fluid of patients with affective disorders

Cited by 97 publications

References 26 publications

Effect of risperidone on plasma catecholamine metabolites and brain‐derived neurotrophic factor in patients with bipolar disorders

Effect of risperidone on plasma catecholamine metabolites and brain‐derived neurotrophic factor in patients with bipolar disorders

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

Correlation of individual symptoms and other clinical variables with cerebrospinal fluid amine metabolites and tryptophan in depression

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