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Biomedical subjects

B Eichelman

Publications and source records attributed to B Eichelman.

At least 19 recordsLinked to original sources
PubMed1992

Aggressive behavior: from laboratory to clinic. Quo vadit?

This article sets forth two theses: (1) that animal models of aggressive behavior have utility in fostering and guiding human aggression research; and (2) that clinical violence research should now focus on the severely and repetitively aggressive patients for study and therapeutic research. Animal models are reviewed in terms of typology; studies of temperament; the role of sensory cues; neuroanatomy, neurochemistry, and neuroendocrinology; studies of stress; and studies of social conditions. Examples are presented that have implications and potential utility for human research. Clinical approaches to the study of human aggressive behavior are examined and five suggestions are made to enhance the efficacy and utility of clinically relevant aggression research.

Aggression↗
PubMed1992

Management of behavior disturbance in Alzheimer disease: current knowledge and future directions.

Assessment and treatment of behavior problems in patients with Alzheimer disease and related disorders is a seriously neglected area of study. Despite the fact that such problems are integral to the disorder, little is known about effective management. This article summarizes the current thinking on five areas of prime importance to patients, care providers, and health care professionals: agitation, assault/aggression, screaming, wandering, and depression/apathy/withdrawal. Methodological guidelines for studying these disorders are provided. Emphasis is on recognizing that behavior problems are important areas of study in their own right as well as in conjunction with studies of cognition.

Activities of Daily Living↗
PubMed1991

Diltiazem suppresses quinpirole-induced oral stereotypies in haloperidol withdrawn rats.

1. Tardive dyskinesia (TD) is one of the most serious untoward effects of chronic neuroleptic therapy. Dopaminergic receptor sensitization is assumed to be involved in its pathogenesis. 2. Male Wistar rats were administered (b.i.d.) intragastrically haloperidol (2 mg/kg), diltiazem (5 mg/kg), diltiazem plus haloperidol, and water (controls), for 21 days. 3. Forty eight hours after withdrawal the rats were injected ip with 0.3 mg/kg of quinpirole and observed for stereotypic behaviors (rearing, grooming, licking, and tongue protrusions). 4. There was a significant overall between-group difference in the duration of grooming and the number of tongue protrusions. The haloperidol withdrawn rats scored markedly higher than control and diltiazem alone treated rats. 5. Conjoint treatment with diltiazem and haloperidol prevented the increase of tongue protrusion episodes. 6. We conclude that concurrent diltiazem and haloperidol administration can prevent the occurrence of some behavioral manifestations of dopaminergic receptor supersensitivity, including a lingual dyskinesia.

Analysis of Variance↗
PubMed1991

Decreased hyperthermic effect of MK-801 in selectively bred hypercholinergic rats.

The Flinders Sensitive Line (FSL) of rats has been selectively bred to have increased sensitivity to cholinergic agonists. However, these rats exhibit altered responsiveness to a number of noncholinergic agents, such as apomorphine, buspirone and ethanol. This study compared the FSL and control Flinders Resistant Line (FRL) rats in terms of their hyperthermic response to the phencyclidine (PCP) receptor agonist, MK-801 (0.2 mg/kg SC) and their MK-801 binding characteristics. We have found that FSL rats react with a delayed hyperthermia, having a significantly lower hyperthermia for the first 120 min of observation. Thereafter the response does not differ in FSL and FRL rats. Both groups had similar affinities and numbers of [3H]MK-801 binding sites in the hippocampus/cerebral cortex. Pretreatment with scopolamine (1 mg/kg SC) failed to affect MK-801-induced hyperthermia in either line of rats. These findings suggest that selective breeding of FSL rats attenuated the secondary mechanisms involved in the PCP receptor-mediated hyperthermic response. However, by itself cholinergic supersensitivity does not appear to be a major factor in the blunted responsiveness of FSL rats to MK-801.

Animals↗
PubMed1991

Nicardipine protects against chronic ethanol- or haloperidol-induced supersensitivity to apomorphine-induced aggression.

Affective apomorphine-induced aggression was induced in originally nonaggressive rats after withdrawal from prolonged ethanol or haloperidol treatment. If the animals were co-administered Ca(2+)-channel blockers like diltiazem or verapamil the aggressive response to apomorphine was markedly decreased. Nicardipine (2 and 5 mg/kg b.i.d.) significantly attenuated the aggression-enhancing effect of chronic ethanol or haloperidol withdrawal in nonaggressive rats. Chronic nicardipine, alone, did not enhance aggressive behavior in the nonaggressive rats. Acutely, it suppressed apomorphine-induced aggression but did not alter open field activity when injected into aggressive rats. These results demonstrate that a Ca(2+)-channel blocker of the dihydropyridine type can prevent the development of an ethanol or haloperidol-withdrawal supersensitivity to apomorphine-induced aggression. It attenuates the aggression-inducing effect of apomorphine without impairing general activity.

Aggression↗
PubMed1990

The Carolina Nosology of Destructive Behavior (CNDB).

This article sets forth a multiaxial system for cataloging individuals who manifest destructive behavior toward themselves, others, or property. An initial codification to describe the characteristics of the destructive behavior of the individual is presented, followed by a description of a quaternary axial system which catalogs in a clinically relevant manner, individuals engaging in destructive behavior. The four axes presented and developed are Axis A--a medical diagnosis axis, Axis B--an axis of psychological correlates, Axis C--an axis of biological correlates, and Axis D--an axis of moral/cultural correlates. This nosology is proposed in order to standardize the coding of human destructive behavior. It is intended to be used by members of the clinical and research communities in order to compare patient types and their relationship to treatment interventions.

Aggression↗
PubMed1990

Ethical issues in selecting patients for treatment with clozapine: a commentary.

Three ethical constructs of distributive justice--utilitarianism, Marxism, and the theories of John Rawls--are applied to selection of patients for treatment with clozapine. Elements of an ethical selection process include a means of monitoring the clinical effectiveness of the drug so that it is not wasted and procedures for ensuring that patients' rights to advocacy and due process are met. The authors suggest that a disproportionate number of patients with tardive dyskinesia may receive clozapine because clinicians and hospitals risk litigation if these patients continue to receive standard neuroleptics and experience worsening side effects.

Chronic Disease↗
PubMed1988

Toward a rational pharmacotherapy for aggressive and violent behavior.

A substantial body of research with both animals and humans demonstrates that pharmacologic modulation of three neurotransmitter systems (the GABAergic, the noradrenergic, and the serotonergic) and electrical stimulation of regions of the brain produce marked alterations in aggressive and violent behavior. The author reviews this research and uses case reports to illustrate how it has been applied in the development of a rational pharmacotherapy for violent patients. Four basic principles of clinical application that can enhance trials of pharmacologic treatment of the violent patient are identified. Evidence suggests that behavioral and social learning approaches to the treatment of violence can be more effective when administered after the patient has been stabilized through pharmacologic interventions.

Aggression↗
PubMed1984

Regional changes in monoamines and metabolites following defensive aggression in the rat.

Pharmacological studies have demonstrated that shock-induced defensive fighting is modulated by manipulations of the serotonergic, noradrenergic and dopaminergic neurotransmitter systems. In the present study, regional changes in 5- hydroxytryptamine , norepinephrine, dopamine and their metabolites 5-hydroxyindoleacetic acid, 3-methoxy-4-hydroxyphenylethylene glycol and 3,4-dihydroxyphenylacetic acid were measured following shock-induced fighting using high performance liquid chromatography coupled with electrochemical detection. Fighting produced reductions in the serotonergic, noradrenergic and dopaminergic systems and elevations in the noradrenergic and dopaminergic systems within the brain stem, hypothalamus, hippocampus, caudate and amygdala relative to shocked or non-shocked controls. These data demonstrate that the activities of these neurotransmitters are involved in defensive aggression in rats. The changes in catecholamines may indicate adaptive responses to stress, while the changes in serotonin may indicate a permissive function for serotonin depletion in defensive fighting.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Ethics and psychiatric research: problems and justification.

The discussion of ethics in psychiatry continues to increase. Research in psychiatry, like all medical research, is of ethical concern because it often involves risks to subjects so that others may benefit. It also involves the allocation of monetary and human resources. In recent years these concerns have been brought to the forefront of professional and public attention. The authors consider the problem of justifying resource allocations and the risks involved in psychiatry research, survey some of the special problems faced by researchers in this field, and give a brief account of present government regulations that pertain to research ethics in psychiatry.

Behavioral Research↗
PubMed1983

Increased shock-induced fighting with supersensitive beta-adrenergic receptors.

Adult male rats were treated chronically with haloperidol (1 mg/kg) daily or propranolol (10 mg/kg bid) and evaluated for changes in shock-induced fighting. Haloperidol suppressed fighting. Chronic propranolol facilitated fighting when rats were tested eight hours after injection. Acutely, either 5 or 10 mg/kg of d,1-propranolol suppressed shock-induced fighting. Chronic pindolol (10 mg/kg bid) and chronic 1-propranolol (5 mg/kg bid) administration increased fighting. Chronic d,1-propranolol, 1-propranolol or pindolol administration was associated with an increase in Bmax for beta-adrenergic receptors. No change in fighting or Bmax was observed with the chronic administration of d-propranolol (5 mg/kg bid) or metoprolol (10 mg/kg bid). This increase in shock-induced fighting appears to be a behavioral response developing as a consequence of increased beta-adrenergic receptors responding to endogenously released norepinephrine.

Aggression↗
PubMed1983

The limbic system and aggression in humans.

This paper reviews the clinical literature relevant to the association between aggressive behavior and the limbic system in humans. Specific areas of review include aggressive behavior related to: (1) naturally occurring and iatrogenic brain lesions; (2) electrical disturbances; (3) pharmacologic intervention; and (4) central neurochemical concentrations which may implicate limbic lobe involvement.

Aggression↗