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Biomedical subjects

B Adinoff

Publications and source records attributed to B Adinoff.

At least 55 records · Page 3Linked to original sources
PubMed1990

Cocaine abuse among schizophrenic patients.

Initial studies have indicated that stimulant abuse is prevalent among schizophrenic persons. To assess the phenomenon of cocaine abuse by patients with schizophrenia, 17 male cocaine-abusing schizophrenic patients were compared with 22 male schizophrenic patients who did not use cocaine. The cocaine-abusing subjects had been hospitalized more frequently, were more likely to be of the paranoid subtype, and were more likely to be depressed at the time of interview. It appears that cocaine abuse may influence both the psychopathologic presentation of schizophrenic patients and the intensity of care that they require.

Adult↗
PubMed1989

Lactate and hyperventilation substantially attenuate vagal tone in normal volunteers. A possible mechanism of panic provocation?

Many aspects of panic attacks, eg, palpitations, tremor, sweating, and an emotional sense of "fear," have been theorized to arise from sympathetic nervous system activation. However, most studies have not demonstrated clearly increased levels of catecholamines during an attack, which is contrary to this hypothesis. To explore another possible cause for the physiological changes known to occur during a panic attack, we assessed parasympathetic nervous system activity by measuring vagal tone during treatments known to produce panic symptoms: sodium lactate administration and hyperventilation. Our findings showed a marked reduction in vagal tone during both procedures. We postulate that withdrawal of parasympathetic activity may explain some of the physiological changes occurring in panic attacks and be contributing to the origin of panic.

Adult↗
PubMed1989

Effective pharmacotherapy of alcoholic amnestic disorder with fluvoxamine. Preliminary findings.

Ten patients with alcoholic chronic organic brain disease were categorized as having alcohol amnestic disorder, or Korsakoff's psychosis (n = 6), dementia associated with alcoholism (n = 3), or compensated alcoholic liver disease (n = 1). All patients had severe deficits in memory for recently acquired information (episodic memory). Patients with alcohol dementia also showed global intellectual decline, including decreased performance on measures of semantic (knowledge) memory and reduction in levels of cerebrospinal fluid somatostatin. In a 4-week double-blind crossover design, the serotonin-uptake blocker fluvoxamine maleate (100 to 200 mg/d) was found to improve episodic memory in only the patients with alcohol amnestic disorder. These improvements in memory were significantly correlated with reductions in levels of cerebrospinal fluid 5-hydroxyindoleacetic acid, suggesting that facilitation of serotonergic neurotransmission may ameliorate the episodic memory failure in patients with alcohol amnestic disorder.

Aged↗
PubMed1989

Benzodiazepines in the treatment of alcoholism.

This chapter comprises three sections that cover the main aspects of benzodiazepines and alcohol: (1) the basic pharmacology of benzodiazepines; (2) use of benzodiazepines in the treatment of withdrawal; and (3) the use of benzodiazepines in treating alcoholics. The basic studies suggest that a major site of action of alcohol may be the GABA/benzodiazepine receptor complex and that compensatory alterations in this complex may underly withdrawal. In the section on alcohol withdrawal, interactions between the GABA/benzodiazepine receptor complex, sympathetic nervous system, and hypothalamic-pituitary-adrenal axis are discussed. Use of benzodiazepines in the treatment of the alcohol withdrawal syndrome are reviewed, including the possibility that the benzodiazepines may prevent withdrawal-induced "kindling." Lastly, we review indications for, and efficacy of, benzodiazepines in long-term treatment of patients with alcoholism. Benzodiazepines are not indicated for the treatment of alcoholism. Furthermore, they have very few indications in alcoholics and their dependency-producing potency has to be appreciated when they are used in patients with alcoholism.

Alcohol Drinking↗
PubMed1989

CSF GABA and neuropeptides in pathological gamblers and normal controls.

We previously reported that pathological gamblers may have increased central noradrenergic activity. Neurons releasing gamma-aminobutyric acid (GABA) are known to be a part of an inhibitory system regulating the activity of central noradrenergic neurons. Therefore, we examined cerebrospinal fluid (CSF) levels of GABA in pathological gamblers and normal controls. There was no significant difference between the groups. Also, depressed and nondepressed gamblers did not differ significantly in their CSF levels of GABA. Among controls, however, there was a significant negative correlation between CSF levels of GABA and the norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) and a significant positive correlation between CSF levels of GABA and corticotropin releasing hormone (CRH). Also, CSF levels of CRH showed a significant positive correlation with CSF levels of adrenocorticotropic hormone in both pathological gamblers and controls.

Adult↗
PubMed1988

Pathological gambling. A psychobiological study.

We investigated psychobiological substrates of pathological gambling by measuring levels of norepinephrine, monoamine metabolites, and peptides in cerebrospinal fluid, plasma, and urine. Pathological gamblers had a significantly higher centrally produced fraction of cerebrospinal fluid levels of 3-methoxy-4-hydroxyphenylglycol as well as significantly greater urinary outputs of norepinephrine than controls. These results suggest that pathological gamblers may have a functional disturbance of the noradrenergic system. This system has been postulated to underlie sensation-seeking behaviors, aspects of which are thought to be abnormal among pathological gamblers.

Adult↗
PubMed1988

High correlations of norepinephrine, dopamine, and epinephrine and their major metabolite excretion rates.

We have previously reported high correlations between norepinephrine and its metabolite outputs in depressed patients. In this article, we expand this finding to healthy volunteers and alcoholic patients. Furthermore, we find similar high correlations between urinary outputs of dopamine, norepinephrine, and their major metabolites. The same is true, to a lesser degree, for epinephrine and metanephrine outputs. There are implications of these findings for psychobiological research on the monoamine systems.

Adult↗
PubMed1988

Alcohol intoxication reduces visual sustained attention.

Effects of alcohol intoxication on visual sustained attention were studied using a vigilance task entailing detection of degraded target stimuli. Data were obtained in separate sessions under four ethanol doses, ranging from 0 (placebo) to 1.05 g/kg lean body weight, with periodic maintenance dosing of 0.12 g/kg. Intoxication lowered the overall level of detection performance, and in addition produced dose-related increases in the rate of performance decrement over time. Analysis of performance data using techniques derived from Signal Detection Theory indicated that the decrements were due specifically to alterations in perceptual sensitivity. Examination of eye movements and blinks indicated that the effects of ethanol were not mediated peripherally. Rather, alcohol appears to have deleterious effects on central processing capacity and the availability of capacity over time. The alcohol-related failure of sustained attention may contribute to increased accident risk in tasks requiring continuous performance.

Adult↗
PubMed1988

Acting out hostility in normal volunteers: negative correlation with levels of 5HIAA in cerebrospinal fluid.

We examined relationships in normal volunteers between cerebrospinal fluid (CSF) concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid (5HIAA) and scores on the Hostility and Direction of Hostility Questionnaire. There was a significant negative correlation between CSF 5HIAA levels and scores on the "urge to act out hostility" subscale, as well as a similar nonsignificant trend with CSF levels of homovanillic acid. These results suggest that among normal individuals reduced central serotonergic tone may be associated with impaired impulse control.

Adult↗
PubMed1988

Circadian rhythms of cortisol during alcohol withdrawal.

The authors have investigated the function of the hypothalamic-pituitary-adrenocortical (HPA) axis during and after withdrawal from alcohol. 24 hour rhythms of cortisol were abnormal in that elevated levels were seen throughout the day in patients with moderate to severe, but not mild, withdrawal. This abnormality of circadian secretion of cortisol, which is similar to that seen in Cushing's syndrome and post-operative trauma, returned to normal after a period of one week of abstinence on their in-patient ward. Such excessive secretion of cortisol may explain some of the complications of chronic alcoholism.

Adult↗
PubMed1988

Treatment of alcoholic organic brain syndrome with the serotonin reuptake inhibitor fluvoxamine: a preliminary study.

The chronic effects of fluvoxamine (200 mg per day for 4 weeks) were studied in ten alcoholic organic brain syndrome patients in a double-blind cross-over design. Complete neuropsychological evaluation was performed as well as measurement of neurochemical changes in CSF. Fluvoxamine produced a small but significant improvement in memory performance. An analysis of fluvoxamine minus placebo difference scores showed a significant correlation between memory functioning and CSF 5HIAA levels. Alcohol amnestic syndrome patients who had the highest blood levels of fluvoxamine demonstrated the largest changes in CSF 5HIAA and improvement in memory performance under fluvoxamine. These findings implicate a role of serotonergic mechanisms in alcoholic organic brain syndrome and suggest that with individual titration of the drug dose, fluvoxamine might be a clinically useful agent in the treatment of this syndrome.

Aged↗
PubMed1988

Acute effects of ethanol on motor performance and movement-related brain potentials.

The acute effects of ethanol on skilled motor functions were examined in male social drinkers, under four doses ranging from 0 (placebo) to 1.05 g/kg lean body weight. The movement entailed a forewarned choice transitive motion of the arm and hand, aimed at a flanking target. Performance measures disclosed only small effects of ethanol on speed and accuracy of movement. The simultaneously-recorded movement-related brain potentials disclosed decreased involvement of frontal and posterior brain areas, suggesting that ethanol disrupted the planning and regulation of movement despite the overall preservation of reaction speed.

Contingent Negative Variation↗
PubMed1987

NIH conference. Alcohol withdrawal and noradrenergic function.

Alcohol withdrawal syndrome is characterized by signs of overactivity of the sympathetic nervous system. Biochemical studies indicate that increased release of norepinephrine is associated with certain symptoms of alcohol withdrawal, and the severity of the withdrawal symptoms correlates positively with the amount of norepinephrine released. In the rat, the brain epinephrine concentration is reduced by alcohol, a phenomenon probably associated with both the intoxicating and rewarding effects of alcohol intake. Furthermore, intoxicating effects of alcohol can be reversed by inhibiting epinephrine synthesis in the rat brain. In this species, alcohol withdrawal is associated with profound depletion of epinephrine in the hypothalamus. When clonidine, a norepinephrine alpha-2-receptor agonist, was infused in alcoholics, these receptors were found to be subsensitive during alcohol withdrawal, and this subsensitivity may contribute to the syndrome. Repeated withdrawals may lead to "kindling" and thus further enhancement of noradrenergic overactivity. Pituitary responsiveness to corticotropin-releasing hormone, which is a central regulator of stress responses and increases the firing rate of brain noradrenergic neurons, is altered during alcohol withdrawal.

Alcoholism↗
PubMed1986

The benzodiazepine antagonist Ro 15-1788 does not antagonize the ethanol withdrawal syndrome.

It has been suggested that the signs and symptoms of the ethanol withdrawal syndrome may be due to the increased production of an "inverse agonist" that binds to the central benzodiazepine (BZ) recognition site in the brain. Ro 15-1788 (a potent antagonist at the central BZ recognition site), diazepam, and Ro 15-1788 plus diazepam were administered to groups of rats undergoing overt ethanol withdrawal. Ro 15-1788 did not alter the severity of the ethanol withdrawal reactions, but antagonized the ameliorative effect of diazepam. The results of our studies suggest that (1) the ethanol withdrawal syndrome is not produced by an endogenous ligand acting on the central BZ recognition site, and (2) diazepam decreases the severity of the ethanol withdrawal syndrome, at least in part, by its action at the central BZ recognition site.

Animals↗
PubMed1986

Alcoholic organic brain disease: nosology and pathophysiologic mechanisms.

Study of alcoholic chronic organic brain syndrome may have applicability to the large population of alcoholics with less severe cerebral dysfunction. Brain impairment in alcoholics may be conceptualized as two clinically and neuropathologically distinguishable organic brain syndromes: alcohol amnestic disorder or Korsakoff's psychosis (KP) and alcoholic dementia. Alcoholic organic brain disease may result from two interacting pathophysiological processes: nutritional (thiamine) deficiency and ethanol neurotoxicity. Subcortical periventricular lesions associated with KP result primarily from thiamine deficiency, whereas ethanol neurotoxicity and various secondary effects of alcoholism may contribute to the cortical neuropathological changes associated with alcoholic dementia. These two patterns of brain damage may be differentiable in individual alcoholics using cognitive tests and other measures of CNS function and, therefore, allow selection of a treatment strategy based on pathophysiological considerations. Studies in animals and humans suggest that a genetic predisposition to thiamine deficiency may contribute to alcoholism-associated dysfunction of brain and other organ systems and possibly have a causative role in the development of alcoholism.

Alcohol Amnestic Disorder↗
PubMed1983

Temporal integration deficit in visual information processing by chronic schizophrenics.

The primary objective of the present study was to evaluate speed of visual information processing of chronic schizophrenics and normal subjects. Retarded information processing by schizophrenics has been attributed to a dysfunction at the earliest stage of processing. In the present study, by using a backward-masking paradigm and varying target duration we were able to evaluate whether schizophrenic and normals conform to an iconic or visual persistence theory of processing. Also, we evaluated whether schizophrenic and normal information processing is a function of the total time a stimulus is available for viewing prior to disruption (stimulus onset asynchrony, SOA), or whether it is the time following the stimulus offset prior to disruption by the mask (interstimulus interval, ISI). The former conforms more closely to a visual persistence and the latter to an iconic notion of processing. The results indicate that schizophrenics and normals conform to the processing of information as a function of the SOA as opposed to ISI. However, schizophrenic processing during the period of temporal integration (i.e., up to 130 msec) was significantly retarded when compared to normal controls. These findings suggest that for chronic schizophrenics, visual signals associated with target processing during the temporal integration period have either decayed at a slower rate or are more unstable than those of normals. Also discussed is the compatability of these findings with a visual persistence as opposed to an iconic model of information processing.

Form Perception↗
PubMed1977

Effects of various neuroleptics on rabbit hyperthermia induced by N, N-Dimethyltryptamine (DMT) and d-amphetamine.

The effects of various neuroleptics were studied on N, N-dimethyltryptamine (DMT, 3.2 mg/kg) and d-amphetamine (3.2 mg/kg) induced hyperthermia in the rabbit. Complete dose-effect curves were obtained. The order of potency for antagonism of DMT-induced hyperthermia was: methiothepin greater than octoclothepin greater than or equal to oxyprothepin greater than perathiepin greater than dokloxythepin greater than mianserine greater than loxapine greater than oxypertine greater than chlorpromazine greater than pipamperone greater than fluphenazine greater than thiothixene greater than haloperidol greater than molindone. The order of potency for antagonism of d-amphetamine hyperthermia was: haloperidol greater than chlorpromazine greater than oxypertine greater than octoclothepin and methiothepin. For these five drugs, the order of potency for antagonism of amphetamine hyperthermia was the reverse of the order for antagonism of DMT hyperthermia. Methiothepin reduced d-amphetamine-induced hyperthermia effectively at a very high dose (0.32 mg/kg) and variably at lower doses. The results indicate that neuroleptics differ markedly in their specificity of antagonism of DMT and d-amphetamine which may act through different neurotransmitter mechanisms (tryptaminergic vs. adrenergic).

Animals↗