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Biomedical subjects

I Maltzman

Publications and source records attributed to I Maltzman.

42 records · Page 3Linked to original sources

Aversive conditioning in the sociopath.

Results of two experiments on differential conditioning of the skin conductance (SCR) in sociopaths and normal control subjects are described. In the first experiment it was found that an equal number of sociopaths and control subjects were aware of the conditioning contingency. However, only the normal subjects displayed reliable differential SCR conditioning. Sociopaths showed a dissociation between verbal learning and conditioning of a physiological change. The second experiment examined the differential conditioning of normal subjects and sociopaths in partial remission. The number of aware subjects in the two groups did not differ. Aware subjects in both groups showed differential SCR conditioning. Differential conditioning in sociopaths did not persist over trials as it did in control subjects. A deficiency in ACTH 4--10 as well as neurological dysfunctions were considered possible factors in the etiology of sociopathy. Further research on the relation of neuropeptides to the etiology and treatment of sociopathy is suggested.

Adrenocorticotropic Hormone↗

Heart rate deceleration is not an orienting reflex; heart rate acceleration is not a defensive reflex.

Graham and Clifton (1966) proposed an integration of Sokolov's theory of orienting and defensive reflexes with the stimulus intake/rejection dichotomy of the Laceys. This integration consisted of hypothesizing that heart rate deceleration is a measure of the orienting reflex, and that cardiac acceleration is a measure of the defensive reflex. This article demonstrates that Graham and Clifton failed to establish a valid integration of these two theories. This failure is a consequence of 1) their misconstruing Sokolov's theory, and 2) an inaccurate and selective review of the research literature then available. Consideration of more recent research would seem to rule out the possibility that their thesis was correct in spite of these flaws in its derivation. Cardiac responding in the OR context thus remains open to further investigation and interpretation.

Acoustic Stimulation↗

Why alcoholism is a disease.

Arguments of proponents and critics of a disease concept of alcoholism are reviewed. It is concluded that the disease concept of alcoholism is in accord with modern usage of the concept of disease in the philosophy of science and the practice of biomedical science. Ascription of the term "disease" involves a value judgment by experts that observed lawfully recurring signs and symptoms are a significant deviation from a norm or standard of health. Value judgments of this and other kinds are inherent in biobehavioral science and its application. Criticisms of the traditional conception of the disease concept fail to distinguish empirical questions of etiology, treatment, and the characteristic features of alcoholism from the conventional and evaluative nature of the classification "disease." A critical review of the empirical research purporting to question the signs and symptoms of loss of control in alcoholics is also provided.

Alcoholism↗

Reply to Lilienfeld: why alcoholism is a disease.

Lilienfeld's attack on my conceptual examination of the disease concept of alcoholism suffers from erroneous interpretations, fallacious reasoning, and a lack of familiarity with relevant alcoholism research. He offers an alternative nominalist interpretation of the disease concept of alcoholism based on a fuzzy boundary between disease and wellness. He fails to recognize that the basic issue between nominalist and realist accounts of a lower-order concept such as alcoholism is the presence or absence of general principles that may account for the observed signs and symptoms characterizing a specific disease entity, not fuzzy boundaries between higher-order categories. Extensive evidence (which Lilienfeld ignores) of biological bases for the pathognomic signs and symptoms of alcoholism, particularly loss of control, demonstrates that the disease concept of alcoholism refers to a disease entity that has a biological basis. It is not a "mental construct."

Alcohol Drinking↗

Arousal-related P3a to novel auditory stimuli is abolished by a moderately low alcohol dose.

Concurrent measures of event-related potentials (ERPs) and skin conductance responses were obtained in an auditory oddball task consisting of rare target, rare non-signal unique novel and frequent standard tones. Twelve right-handed male social drinkers participated in all four cells of the balanced placebo design in which effects of beverage and instructions as to the beverage content (expectancy) were independently manipulated. The beverage contained either juice only, or vodka mixed with juice in the ratio that successfully disguised the taste of alcohol and raised average peak blood-alcohol level to 0.045% (45 mg/dl). ERPs were sensitive to adverse effects of mild inebriation, whereas behavioural measures were not affected. Alcohol ingestion reliably increased N2 amplitude and reduced the late positive complex (LPC). A large, fronto-central P3a (280 ms latency) was recorded to novel sounds in the placebo condition, but only on the trials that also evoked electrodermal-orienting responses. Both novel and target stimuli evoked a posterior P3b (340 ms), which was independent of orienting. Alcohol selectively attenuated the P3a to novel sounds on trials with autonomic arousal. This evidence confirms the previously suggested distinction between the subcomponents of the LPC: P3a may be a central index of orienting to novel, task-irrelevant but potentially significant stimuli and is an important component of the arousal system. P3b does not have a clear relationship with arousal and may embody voluntary cognitive processing of rare task-related stimuli. Overall, these results indicate that alcohol affects multiple brain systems concerned with arousal, attentional processes and cognitive-autonomic integration.

Adult↗