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1. It has been proposed that an increase in the concentration of the neuromodulator phenylethylamine at the post-synaptic dopamine receptor may be involved in the etiology of schizophrenia. If this increase is the case, a reduction in the CSF and/or serum concentrations of phenylacetic acid, its major metabolite, might be anticipated. 2. The authors have found in hospitalized Indian schizophrenic patients ingesting antipsychotic drugs, that the paranoid subgroup did indeed exhibit lower levels of unconjugated, conjugated and total phenylacetic acid in both serum and CSF.

Twenty-four psychotic patients were studied at two points during continuous neuroleptic treatment. Thirteen patients showed a tolerance pattern with respect to cerebrospinal fluid homovanillic acid following probenecid while 11 showed a nontolerance pattern. Patients who developed tolerance had significantly fewer symptoms and Parkinsonian side effects at approximately the fifth week of treatment.

Concentrations of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were significantly higher in CSF obtained after injection of air during pneumoencephalography (PEG) than in lumbar CSF, as drawn before the injection. There was a high correlation between levels in the `mixed' and lumbar samples of CSF in the case of each of the two acids. The concentration of lumbar HVA, but not that of 5-HIAA, was negatively correlated with CSF pressure. 5-HIAA levels were low in both samples of CSF in a group of epileptics, by comparison with controls. In two patients with Kufs disease and in one with Niemann-Pick disease, the concentration of HVA was very low in the lumbar sample. The application of a standardized PEG technique in the study of monoamine metabolism in man is suggested.

Using reversed-phase high-performance liquid chromatography and electrochemical detection with a rapid one-step purification on Sephadex G-10 column, we have developed a sensitive technique to measure p-hydroxyphenylacetic acid (PHPA), the oxidatively deaminated metabolite of p-tyramine, in cerebrospinal fluid (CSF). The method has been shown to offer simplicity, high sensitivity and low cost for the analysis of PHPA. By using this method PHPA can be measured concurrently with the dopamine metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in small amounts of CSF (0.5 ml or less). The concentrations of PHPA ranged 4.2 to 17.0 ng/ml with a mean value of 7.8 ng/ml+/-1.1 SEM in lumbar CSF of non-neurological control patients. PHPA value is consistent with the results of earlier studies using different methods. PHPA concentrations in both schizophrenic (4.7+/-0.6 ng/ml, n=11) and epileptic patients (5.8+/-0.4 ng/ml, n=28) were significantly lower than those in control patients. A concentration gradient of PHPA was found along the ventricular-lumbar axis. Probenecid markedly increased PHPA in lumbar CSF. These observations suggest that PHPA in lumbar CSF is derived at least in part from the brain and eliminated from CSF by a probenecid-sensitive transport mechanism. There was a significant correlation between PHPA and HVA concentrations in CSF. This is an interesting finding since a reciprocal relationship between dopamine turnover and p-tyramine concentrations has been found in the striatum of experimental animals. A number of recent studies suggest that p-tyramine may act as neurotransmitter or neuromodulator in specific neuronal systems. The present method should be useful in clinical investigations to clarify a functional role of p-tyramine in the brain.

The concentrations of the monoamine metabolites 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) have been determined by high-performance liquid chromatography in samples of lumbar cerebrospinal fluid from chronic therapy-resistant schizophrenics, both before and after either inactive or active hemodialysis for 10 weeks. A reasonable test-retest reliability was found for 5-HIAA during the inactive dialysis, but this was not found during active dialysis.

Phenylethylamine (PEA) is an endogenous substance with amphetamine-like stimulant properties. On the basis of this ability an abnormal brain PEA metabolism has been proposed as an etiological factor in some forms of schizophrenia. In the present study 28 schizophrenic patients and 15 healthy controls were investigated. No significant difference from control values was found in PEA concentration in cerebrospinal fluid (CSF) of either untreated of neuroleptic-treated schizophrenics. However, 2 schizophrenics with highest BPRS scores had extremely high PES concentrations. Free phenylacetic acid (PAA), the major metabolite of PEA, was significantly decreased in ummedicated but not in drug-treated schizophrenics. Because of the assumed neuromodulatory properties of PEA, it is suggested that lowered PAA concentrations and the tendency for PEA to be elevated may imply that altered central neurotransmission occurs in certain forms of schizophrenia.

A liquid chromatographic assay for noradrenaline (NA), dopamine (DA), and 3,4-dihydroxyphenylacetic acid (DOPAC) in human and monkey cerebrospinal fluid (CSF) is described. The limits of sensitivity vary between 0.1-0.3 pmol/ml of each catechol. Within-day precision as indicated by mean coefficient of variation (CV) of five days varied between 8.0-14.8 for NA (3.0-0.1 pmol/ml), 6.9-27.4 for DA (6.0-0.1 pmol/ml), and 4.1-17.6 for DOPAC (30-1 pmol/ml). Between-day precision (CV) was estimated to be 12.3, 14.9 and 16.6 for 4 pmol/ml of NA, DA and DOPAC, respectively. The method was reproducible enough for reliable quantitation of CSF free NA and DOPAC levels at physiological concentrations while the sensitivity for DA was too low to measure the free amine in less than 3 ml of human lumbar CSF. After acid hydrolysis total (free + conjugated) DA can, however, be quantified in CSF. Ranges for CSF NA and DOPAC levels were 0.13-2.0 and 0.43-14.6 pmol/ml in normal volunteers (n = 72), 0.19-3.19 and 0.7-7.09 pmol/ml in untreated chronic schizophrenic patients (n = 52), and 1.1-3.2 and 9.8-22.7 pmol/ml in rhesus monkeys (n = 8), respectively.

Concentrations of norepinephrine, 3-methoxy-4-hydroxyphenylglycol, homovanillic acid, and 5-hydroxyindoleacetic acid (5-HIAA) were quantified in the CSF of 28 drug-free schizophrenic patients. Fifteen patients provided more than one drug-free sample on separate occasions. Considerable intraindividual variability over time was found in the concentrations of norepinephrine and these major monoamine metabolites in the repeated samples. This was not explained by assay errors or changes in the patient's global psychosis ratings. The variability in the present sample for CSF 5-HIAA concentrations was almost twice as wide as has been reported for patients with affective disorder. Variables that contribute much of the variability of norepinephrine and major monoamine metabolite concentrations in drug-free CSF samples from schizophrenic patients remain unknown and cannot be controlled.

In view of the central side effects of beta-adrenoceptor blocking agents and their alleged antipsychotic action in the absence of DA receptor blockade, it is important to establish which neurotransmitters are likely to be involved. Previous animal and patient studies have, however, produced conflicting data on this point. The changes in CSF HVA, 5HIAA and MHPG during treatment with propranolol (960 mg/day) in chronic schizophrenic patients were monitored on four occasions over 30 days. Clinical changes were monitored by the Wing and Krawiecka Scales and motor activity was assessed by pedometer. CSF HVA levels were significantly increased by propranolol and the rise continued throughout the 30 day period. There were no significant changes in the other metabolites. There was no evidence of any therapeutic benefit from propranolol treatment in these patients. These findings may explain the central side-effects and occasional reports of schizophreniform psychosis after propranolol, since an increase in DA turnover occurs without DA receptor blockade.

The effect of 1 mg dexamethasone on CSF levels of 5-hydroxyindoleacetic acid (5 HIAA), homovanillic acid (HVA) and cortisol (CS) was investigated in 100 psychiatric inpatients: 45 subjects had their lumbar punctures 1-4 days following dexamethasone administration, and the results were compared with those from 55 other patients investigated before drug ingestion. All patients were women, and none had received psychotropic medication for at least two weeks before the study. Seven subjects consented to two LPs both before and after dexamethasone. As expected, cortisol in the CSF significantly decreased after dexamethasone: the decrease was greatest 10 hours following the drug. HVA showed a weak and transient elevation after 10 hours only. CSF 5 HIAA was found to be significantly increased in postdexamethasone samples and high levels were still found even after 82 hours. Diagnostic differences (major or minor depression, schizophrenia, alcohol abuse or dependence) did not account for the observed differences. Repeated CSF examinations in seven subjects corroborated these findings: all cortisol values were decreased and all 5 HIAA values were increased after dexamethasone while HVA values showed random changes. The data may suggest that serotonergic mechanisms may be involved in dexamethasone action in the CNS. In addition, dexamethasone administration can alter CSF 5 HIAA level, a possible factor which should be taken into consideration in CSF studies.

Using gas chromatography-mass spectrometry, we developed a sensitive and reliable technique to measure phenylacetic acid (PAA), an oxidatively deaminated metabolite of beta-phenylethylamine (PEA), in small amounts of cerebrospinal fluid (CSF). In a preliminary analysis, PAA concentrations in depressive patients were significantly lower than those in controls, while there were no differences in PAA levels between schizophrenic patients and controls. This suggests a possible link between the decreased PEA metabolism in the brain and the etiology of depression. However, further studies are needed to clarify the effects of neuroleptics and antidepressants on PAA levels in CSF, since the samples were obtained without regard to medication in the present study. In control subjects, a U-shaped distribution was obtained when the values of PAA were plotted as a function of age. There were no sex differences and no significant concentration gradients in CSF PAA levels.

Cerebrospinal fluid (CSF) levels of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5HIAA) were determined in 40 drug-free schizophrenic patients and 21 healthy volunteers by a mass fragmentographic method. Twenty-one of the schizophrenic patients were first admissions who had never received neuroleptics. Significantly, lower levels of HVA but not 5HIAA were found in the patient group, and no difference was found between chronic, previously neuroleptic-treated and never-medicated patients. HVA levels correlated positively with social interest and total positive scores on the Nurses Observation Scale for Inpatient Evaluation (NOSIE-30) and negatively with lassitude and slowness of movements on the Comprehensive Psychopathological Rating Scale (CPRS). Low levels of 5HIAA were correlated to the CPRS items delusions and apparent sadness. There were slightly higher CSF levels of 5HIAA in patients with a family history of schizophrenia, but no such difference was seen for HVA. In both schizophrenic and control subjects CSF levels of HVA and 5HIAA showed a strong intraindividual correlation. The results indicate decreased central nervous system dopaminergic turnover in schizophrenia which seems to be associated with "negative" symptomatology.

Platelet monoamine oxidase (MAO) activity and amine metabolites in cerebrospinal fluid were compared in 22 schizophrenic patients, 8 of whom improved during a 30-day drug-free period. CSF 5-hydroxyindoleacetic acid and homovanillic acid did not distinguish between drug-free improvers and nonimprovers. However, drug-free improvers had lower platelet MAO activities than did normal controls. The authors suggest that looking at clinical variables in patients with low MAO activity might provide a means of biologically subtyping schizophrenic patients.

8 male schizophrenic patients participated in a double-blind, cross over study of the extrapyramidal side-effects of haloperidol and clozapine (acute dystonis, Parkinsonism and tardive dyskinesia), together with their effect on homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF). Haloperidol (9 mg/day) caused Parkinsonism, reduced tardive dyskinesias and increased the HVA concentration in the CSF. Clozapine (225 mg/day) had no effect on the neurological phenomena but reduced HVA and 5-HIAA concentrations in the CSF. During the discontinuation phase following the administration of haloperidol, tardive dyskinesia occurred or was aggravated; this did not occur after administration of clozapine. Accordingly, it is suggested that clozapine does not induce dopaminergic hypersensibility and, therefore, will not induce tardive dyskinesias.

Probenecid is used to block the transport of acid monoamine metabolites from cerebrospinal fluid (CSF), on the assumption that the resultant rise in CSF concentrations of the metabolites will reflect presynaptic "turnover" of the parent monoamine. However, CSF levels of probenecid correlate with CSF levels of the metabolite, suggesting that the blockade is incomplete at the probenecid levels obtained in human studies. This article reviews the literature on CSF probenecid-metabolite correlations and presents data demonstrating variations in the correlations across diagnostic groups. These cross-diagnostic variations may be due to group differences in membrane transport characteristics and and confound attempts to "correct for" CSF probenecid concentrations in studies of monoamine turnover.

Baseline concentrations of homovanillic acid (HVA), 5-hydroxyindole acetic acid (5-HIAA) and MHPG in the cerebrospinal fluid (CSF) were determined in 67 lobotomized and 30 non-lobotomized patients with chronic schizophrenia. In addition, in 69 of these patients the degree of brain atrophy was assessed by a pneumoencephalographic (PEG) technique. There were no significant differences in the concentrations of the monoamine metabolites in the CSF between the two patient groups studied despite the fact that the group of lobotomized schizophrenics had significantly more central and cortical brain atrophy than the group of nonlobotomized schizophrenic patients. The amine metabolite levels were also unrelated to the subtype of schizophrenia, duration of illness, or degree of mental incapacitation.

Concentrations of acid metabolites of dopamine and serotonin were measured in lumbar CSF of a diagnostically heterogeneous group of 154 psychiatric patients following oral probenecid loading. The patients ranged in age from 2 to 67 years old. No patients had received psychoactive medications for at least two weeks prior to the lumbar puncture. Children had higher mean CSF homovenillic acid (HVA) levels, higher mean CSF HVA-probenecid ratios, higher CSF HVA-log probenecid ratios, and lower mean CSF probenecid levels than adults. Age was negatively correlated with CSF HVA level and with CSF HVA-probenecid ratio. These correlations were more pronounced in male patients than in female patients.

The relationships between CSF monoamine metabolites (HVA and 5HIAA), nurses' ratings of clinical symptoms, and telemetered measures of motor movement of ten schizophrenic and ten depressed patients were investigated. There was a significant negative correlation between CSF 5HIAA and both agitation ratings and motor movement in the schizophrenics. CSF HVA correlated positively to anxiety and anger in the depressives. The schizophrenics had a significantly higher CSF HVA than the depressives which appeared unrelated to motor movement. The effects of serotonin turnover and arousal in schizophrenia and the association between CSF metabolite gradients, stress, motor movement, and biogenic amine levels in depression are discussed.

The monoamine metabolites 5-hydroxindoleacetic acid (5-HIAA), homovanillic acid (HVA) and 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) were measured in the lumbar cerebrospinal fluid (CSF) of 27 chronic schizophrenic patients who at some time had attempted suicide, and were compared with values from 27 chronic schizophrenic patients without a history of attempted suicide. There were no significant differences between either the violent or non-violent attempters and those without a history of attempted suicide in the mean lumbar CSF concentrations of the serotonin metabolite 5-HIAA, the dopamine metabolite HVA, or the norepinephrine metabolite MHPG. Significantly more of the suicide attempters had a previous major depressive episode, had received a course of ECT, and had significantly more psychiatric admissions than those who had never attempted suicide.

5-Hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) were measured in the lumbar cerebrospinal fluid of 57 drug-free female patients with DSM-III diagnoses of major unipolar or bipolar depression (n = 14), schizophrenic disorder (n = 18), alcohol dependence (n = 13) and a group of other disorders (n = 12). Following lumbar punctures all patients received a dexamethasone suppression test. Fourteen patients had attempted suicide immediately before admission, 4 of them by violent methods. Severity of depression, independent of the diagnosis, was assessed in every patient on the 24-item Hamilton scale. No significant differences in means and variances of amine metabolite or postdexamethasone plasma cortisol concentrations were found among the diagnostic subgroups. Suicidal patients, and in particular those who used violent methods, tended to have lower 5-HIAA, but not HVA, in their CSF; they also more often had non-suppression of cortisol after dexamethasone. Since correlation matrices in the diagnostic subgroups were homogeneous, we calculated partial correlations for the total group: here suicide attempts but not depression, seemed to be significantly correlated with CSF 5-HIAA. Thyrotropin stimulation tests were administered to 6 patients: maximal TSH responses showed a borderline significant correlation with CSF 5-HIAA, and a significant correlation with severity of depression. Neither suicide nor postdexamethasone cortisol levels showed any relation to maximal TSH changes.

Schizophrenic patients with high ventricle brain ratios and cortical brain atrophy, as shown by computerized tomography, had decreased spinal fluid concentrations of homovanillic acid and dopamine-beta-hydroxylase activity. These decreased cerebral spinal fluid concentrations in patients with brain atrophy support the proposal of disturbed noradrenaline and dopamine neurotransmission in a subgroup of schizophrenic patients.

Using reversed-phase high-performance liquid chromatography and electrochemical detection with a rapid one-step purification on a Sephadex G-10 column, we have developed a sensitive technique to measure p-hydroxyphenylacetic acid, the oxidatively deaminated metabolite of p-tyramine. The metabolite was measured in cerebrospinal fluid with high recovery and precision. Concentrations of p-hydroxyphenylacetic acid ranged from 4.2 to 17.0 ng/ml with a mean value of 7.8 ng/ml +/- 1.1 SEM in lumbar cerebrospinal fluid of 11 control patients. In a preliminary analysis, the concentrations in schizophrenic patients were significantly lower than those in controls. Since p-hydroxyphenylacetic acid in cerebrospinal fluid seems to be derived from the brain, this finding may indicate a decrease in brain formation. The present method should be useful in clinical investigations to clarify a functional role of p-tyramine in the brain.

Tryptophan and 5-hydroxyindoleacetic acid (precursor and metabolite respectively of 5-hydroxytryptamine) were determined in ventricular CSF of psychiatric patients undergoing stereotactic subcaudate tractotomy. Tyrosine and homovanillic acid (precursor and metabolite respectively of dopamine) were also determined. Results suggest an association between affective state and the above precursor amino acids with lower concentrations in primary depression and higher ones when anxiety or agitation predominate. This leads to lower 5-hydroxyindoleacetic acid concentrations in depression and higher concentrations in anxiety and agitation.

Levels of HVA, MOPEG and 5-HIAA in cerebrospinal fluid (CSF) from psychotic men and women with a schizophrenic symptomatology were measured by mass fragmentography. Measurements were made before, 2 and 4 weeks after treatment with chlorpromazine (CPZ) which was given randomly in doses of 200, 400 or 600 mg per day. Before treatment there were positive correlations between the levels of HVA and 5-HIAA in both sexes. During CPZ treatment HVA was significantly elevated, whereas MOPEG and 5-HIAA were reduced. There was a tendency towards tolerance to CPZ's effect on HVA during treatment but a significant effect persisted after 4 weeks. No indication of tolerance to the effects on MOPEG or 5-hiaa was found. There were the same tendencies for the elevations of the HVA/MOPEG and HVA/5-HIAA ratios. The changes in HVA, MOPEG, 5-HIAA, HVA/MOPEG and HVA/5-HIAA were related to dose of CPZ in men but not in women. The bidirectional change of the different metabolites in CSF during CPZ treatment excluses a general and non-specific mechanism for the metabolite changes. The HVA elevation is in accordance with previous results in animals and man, and is presumably related to blockade of central dopamine receptors. Possible mechanisms for the effects on MOPEG and 5-HIAA are discussed.

Psychotic women with schizophrenic symptoms were treated with melperone 100 mg X 3 (n = 29) or thiothixene 10 mg X 3 (N = 34) USING A DOUBLE-BLIND PROCEDURE. Before and during treatment, levels of HVA, MOPEG, and 5-HIAA, the major metabolites of DA, NE, and 5-HT, were determined in lumbar cerebrospinal fluid by a mass fragmentographic technique. Both treatments resulted in an elevation of the HVA levels after 2 weeks, thiothixene having a more marked effect. The effect of thiothixene but not of melperone persisted after 4 weeks. Thiothixene did not influence the MOPEG level, but melperone reduced it after 4 weeks of treatment. The 5-HIAA levels were not significantly altered by the drugs. The HVA/MOPEG and the HVA/5-HIAA ratios were highly significantly elevated by both drugs after 2 as well as 4 weeks. Thiothixene induced a significantly greater change of these ratios than melperone. The results supply evidence that thiothixene accelerates central dopamine metabolism in man, presumably by blocking DA receptors. Melperone appears to act similarly, but has an effect which is weaker and/or of shorter duration. During long-term treatment with melperone the receptors develop tolerance to it. The acceleration in DA metabolism declines and the effect of melperone switches instead to central NA metabolism. The results indicate that both drugs cause long-term changes in the activity ratios of central monoamine systems. It is suggested that such changes in several systems rather than single biochemical events may be related to the antipsychotic effects of neuroleptic drugs. This study also demonstrated the versatility of using monoamine metabolite analysis of the CSF as a tool for the quantification of biochemical effects of neuroleptic drugs on the human CNS.

5-Hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) were measured in the spinal fluid of 45 women hospitalized in a psychiatric department for major depression (14 cases), schizophrenia (18 cases) and alcohol dependence (13 cases). Dexamethasone suppression tests were performed following CSF examinations in all patients, and TRH stimulation tests were also made in six subjects. All biological examinations were carried out in a drug-free state. The Marke-Nyman Temperament scale was administered to all patients as soon as severe psychotic disturbances subsided and sufficient cooperation was achieved, but no later than 10 days following biological examinations. The MNT was repeated after recovery to check reliability of the test results during an episode of a psychiatric disorder. CSF amine metabolite concentrations did not differ significantly in the three patient groups; postdexamethasone average cortisol levels were above the critical level (5 micrograms/dl) in each group, the highest values being found in major depression. One of the three MNT factors was inhomogeneous among diagnostic groups (validity: low in depression and alcoholism), but the other two also differed from a healthy control population. Correlation structure between biological and psychological variables was homogeneous throughout the diagnoses and a significant inverse correlation was found only between CSF 5-HIAA and the validity factor of MNT. Maximal TSH response to TRH stimulation correlated with both solidity and stability in the MNT scale. Since MNT results proved to be stable even during an illness episode, a possible link is suggested between personality traits and central serotonin metabolism.

Research thus far indicates that CSF 5HIAA and HVA may be correlated with state components of psychotic syndromes. HVA may be positively correlated with a component of arousal or activity. The negative correlation between 5HIAA and state variables of activity or agitation in one study suggests an inhibitory deficit in some acute psychoses or a circulating psychotomimetic substance acting on 5HT receptors. Low CSF HVA values in some psychotic patients could be a manifestation of DA receptor supersensitivity which may antedate and promote the occurrence of acute psychosis. The low CSF HVA is also consistent with a Type B monoamine oxidase deficiency in chronic patients. Such a deficiency could theoretically play a role in either (or both) state or trait behavioral components of psychotic illnesses. Decreased CSF HVA could also be related to trait behaviors in psychoses as a possible reflection of MBD. An increasingly important aspect of biological research in psychotic states in the recognition that biological studies should relate to the component behaviors which make up particular psychotic disorders.

In 36 drug-free schizophrenic patients, lumbar CSF was analyzed by mass fragmentography for the major monoaminergic transmitter metabolites 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), and 3-methoxy-4-hydroxyphenylglycol (MHPG). High or deviant concentrations of 5-HIAA were significantly related to a family history of schizophrenia. For patients with deviant 5-HIAA levels, the probability for a family history of schizophrenia was eight times higher than in subjects with normal values. High concentrations of HVA also tended to be significantly related to a family history of schizoprenia. The majority of schizophrenic patients, who lacked family history for the disorder, had normal monoamine metabolite concentrations in CSF. The results suggest a coupling between biochemical variables related to central serotonin and dopamine metabolism and forms of schizophrenia that have a familial disposition.

Concentrations of the major monoaminergic transmitter metabolites HVA, MOPEG and 5-HIAA were determined in the cerebrospinal fluid (CSF) of untreated schizophrenic patients. Patients with aberrated concentrations of 5-HIAA and HVA in CSF had schizophrenia in their families in a frequency significantly higher than that of patients with normal concentrations. These results may indicate the existence of a subgroup of schizophrenic patients having a family disposition for the disorder and an aberrated transmission from central serotonin and dopamine neurons. In young healthy volunteers, aberrated monoamine metabolite concentrations in CSF were also related significantly to a history of psychiatric morbidity in the family. In psychotic patients treated with chlorpromazine significant correlations were obtained between therapeutic outcome on the one hand, and both biochemical effects related to central monoamine metabolism and chlorpromazine concentrations in the CSF on the other hand. Patients with chlorpromazine concentrations above 1 ng/ml in CSF or 40 ng/ml in plasma responded more favourably than patients with concentrations below those levels. The results indicate that biochemical and pharmacokinetic data may be of value for diagnostic classification and prediction of therapeutic outcome in drug-treated schizophrenic patients.

The authors completed ratings of premorbid sexual and social adjustment and assays of the CSF homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and probenecid concentrations in 108 psychiatric patients. Among the 30 patients diagnosed as schizophrenic, poor premorbid sexual adjustment was associated with higher accumulations of HVA in the CSF. No relationship between the estimated premorbid social adjustment and CSF HVA levels was observed. These findings suggest that 1) sexual and social premorbid adjustment are partially independent variables, and 2) one of the biological correlates of sexual adjustment in schizophrenic patients may be the functional maturity of central dopamine systems.