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C A Kaufmann

Publications and source records attributed to C A Kaufmann.

47 records · Page 3Linked to original sources
PubMed1986

Noradrenergic and neuroradiological abnormalities in tardive dyskinesia.

Previous studies suggest that catecholaminergic overactivity and structural brain damage may contribute to the pathogenesis of tardive dyskinesia (TD). Although dopaminergic (DA) mechanisms, specifically postsynaptic receptor supersensitivity, have been extensively studied, equally plausible noradrenergic (NE) changes have been all but ignored. Likewise, the interaction of neurochemical and neuroradiological abnormalities has received little attention. Over the past 6 years, 111 inpatients were studied with a battery of neurological, behavioral, biochemical, and neuroradiological measures. Forty-one patients met specific diagnostic criteria for TD, based in part on global ratings on the Abnormal Involuntary Movement Scale. Subgroups of patients were also evaluated with the Brief Psychiatric Rating Scale and were assayed for plasma dopamine-beta-hydroxylase (DBH) activity, platelet 3H-dihydroergocryptine (3H-DHE)-alpha 2 adrenergic receptor binding, lumbar cerebrospinal fluid (CSF) monoamines and metabolites [NE, 3-methoxy-4-hydroxyphenylglycol (MHPG), DA-sulfate, homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC)], and CT scan indices of brain atrophy, including ventricle/brain ratio (VBR), bifrontal/bicaudate ratio, and cortical atrophy. All patients were studied in the steady state, primarily when free of neuroleptics. Patients with TD had significantly greater DBH activity than those without TD. In addition, 3H-DHE binding and CSF NE were significantly correlated with the severity of TD when present. Finally, TD patients with low DBH activities (below the mean) had significantly larger ventricles than non-TD patients with low DBH activities. Other data suggested that subcortical, rather than cortical, atrophy was more likely to be responsible for the larger VBR in the low DBH TD group. These results suggest an association of NE overactivity and TD in a portion of patients. Moreover, the presence of neuroradiological abnormalities in TD patients with low DBH activity underscores the contribution of heterogeneous factors to the pathogenesis of this disorder and may provide one possible explanation for the discrepant biochemical findings in TD reported by earlier investigators.

Adult↗
PubMed1985

Abnormal cerebrospinal fluid protein indices in schizophrenia.

Determinations of albumin and immunoglobulin G (IgG) were performed in paired cerebrospinal fluid (CSF) and serum samples from 24 subjects with schizophrenia. These determinations allowed calculation of two indices, one that is an indicator of integrity of the blood-brain barrier and the other a measure of selective IgG production within the central nervous system (CNS). In comparison with previously determined reference values, 7 of 24 (29%) subjects showed increased blood-brain barrier permeability, and 8 of 24 (33%) demonstrated elevated endogenous CNS IgG production. One of these eight also demonstrated oligoclonal banding on high-resolution protein electrophoresis of the CSF.

Adolescent↗
PubMed1985

Eye-blink rate in Tourette's syndrome.

Gilles de la Tourette's syndrome is a hyperkinetic movement disorder in which an etiological role for dopaminergic hyperactivity has been proposed. Blink rate, a putative correlate of central dopamine activity, is commonly held to be elevated in Tourette's syndrome, a finding that would be consistent with the "dopamine" hypothesis of this disorder. In 19 patients who had Tourette's syndrome, however, blink rates during placebo treatment were identical with those of 49 index controls during reading and quiet sitting. Blink rate did correlate, however, with both the number and severity of tics. Pimozide treatment did not reduce blinking in the patients. It should be noted that nine of the patients were adolescents for whom there were not adequate age-matched controls, a fact which could obscure a blink rate elevation in this group. Insofar as blink rate is a putative correlate of central dopamine activity, these results are not consistent with elevated brain dopamine activity in adult patients who have Tourette's syndrome.

Adolescent↗
PubMed1984

Muscarinic binding in suicides.

Supersensitive muscarinic cholinergic receptors may underlie mood, neuroendocrine, and sleep disturbances in depression. To test this hypothesis, we examined muscarinic binding sites in the brains of suicides and controls in a matched-pair design, using the radioligand 3H-quinuclidinyl benzilate (QNB) and focusing on regions (frontal cortex, hypothalamus, and pons) mediating those functions. Receptor densities and binding affinities did not differ between suicide and control brains in any brain region studied, although there was a trend for both density and affinity to be lower in hypothalami from suicides. We discuss the implications of these findings for the cholinergic-adrenergic balance hypothesis of depression and the methodological limitations of our preliminary study.

Acetylcholine↗
PubMed1984

Low dose bromocriptine: a study of acute effects in chronic mediated schizophrenics.

An acute low oral dose (2 mg) of bromocriptine was administered in a randomized double blind fashion to 11 chronic symptomatic mediated schizophrenic patients. There was an overall improvement for the group on the Brief Psychiatric Rating Scale (BPRS) following bromocriptine. Plasma homovanillic acid, 3-methoxy-4-hydroxyphenylglycol, and vanilloyl-mandelic acid concentrations were unchanged after bromocriptine. Bromocriptine concentrations in the plasma showed a large inter-individual variation. There was a significant inverse correlation between plasma bromocriptine concentration and total BPRS score at 60 minutes post-bromocriptine administration. These results suggest a need for further replication in a larger study population and a need for controlled studies with chronic administration of low dose bromocriptine in chronic medicated schizophrenic patients.

Adult↗
PubMed1984

Depression during methadone withdrawal: no role for beta-phenylethylamine.

An atypical depression, resembling beta-phenylethylamine (PEA) deficiency states, frequently complicates methadone withdrawal. We undertook a study of 24-h urinary free PEA excretion in steady-dosed and withdrawing methadone patients, hypothesizing that abstinent patients would excrete less PEA than controls and that methadone would show a dose-dependent effect on PEA turnover. As hepatic dysfunction, frequent in methadone patients, might affect PEA turnover, we also evaluated liver chemistries, [13C]aminopyrine excretion, 2-hydroxylation of estradiol, and 'blind', global severity ratings in each subject. PEA excretion did not significantly differ between eight fully detoxified methadone patients (median 4.76 micrograms/24 h) and seven normal controls (median 5.80 micrograms/24 h). Moreover, PEA excretion bore no relation to methadone dosage among 24 steady-dosed subjects. PEA excretion in seven withdrawing subjects each receiving 4-8 different doses of methadone similarly showed no relation to dose. Despite significant liver disease, several measures of impairment did not correlate with PEA excretion. These findings argue against a role for PEA deficiency in withdrawal depression.

2-Hydroxyphenethylamine↗
PubMed1983

Methadone, monoamine oxidase, and depression: opioid distribution and acute effects on enzyme activity.

Narcotic withdrawal is often accompanied by an atypical depression with responds to resumption of narcotics. We hypothesized that methadone might exert its antidepressant effects through monoamine oxidase (MAO) inhibition. The current study examined 3H-methadone distribution in rat brain and effects on regional MAO activity with acute doses (2.5 mg/kg) which approximate those found during chronic methadone maintenance in man. Limbic areas (amygdala, basomedial hypothalamus, caudate-putamen, hippocampus, preoptic nucleus), as well as pituitary and liver were assayed for MAO activity and methadone concentration. MAO activities did not differ significantly in acute methadone or saline-treated cage-mates at 1 or 24 hr. The concentrations of methadone at 1 hr ranged between 17 and 223 ng/100 mg wet wt tissue in the preoptic nucleus and pituitary, respectively. No significant correlation was found between change in MAO activity (MAO methadone/MAO saline) and methadone concentration in any region at 1 or 24 hr. This study does not support the hypothesis that methadone acts as an antidepressant through MAO inhibition, at least not following acute administration of this exogenous opioid.

Animals↗
PubMedDate not supplied

Abortion.

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Abortion, Induced↗