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Biomedical subjects

L L Judd

Publications and source records attributed to L L Judd.

At least 73 records · Page 4Linked to original sources
PubMed1985

The effect of antipsychotic drugs on driving and driving related psychomotor functions.

Despite the extremely widespread use of antipsychotic medications, there is little evidence from the surveys conducted to date, that this class of psychoactive medications is significantly implicated in vehicular crashes or deaths. In five major surveys of vehicular fatalities, in which drug and alcohol analyses were obtained, only two of over 800 victims studied involved detection of antipsychotic medications. It is clear that the acute administration of antipsychotics in normal individuals does induce sedation and performance decrements in visual-motor coordination and specific attentional behaviors, which have a deleterious effect on driving behavior. On the other hand, it should be emphasized that antipsychotics are rarely used on an acute basis and tolerance to the sedation and decreased alertness does occur during chronic treatment. Antipsychotic drugs have the capacity to potentiate the effects of alcohol, sedative hypnotics, narcotics and antihistamines; therefore, the combination of antipsychotics with these substances increases the impairment of driving behavior. There is an indication that the less sedating piperazine phenothiazines and the butyrophenones may have little or no effect on psychomotor performance, and antipsychotic drugs of these two subclasses may have a distinct advantage, at least in terms of driving performance, over the other more sedating drugs. Antipsychotic drugs are almost never used for recreational or abuse purposes; therefore, more central to the focus of this review is the effect that antipsychotics may have on the driving behavior of those seriously disordered mentally ill patients who require continued maintenance on these medications. There is good agreement in the literature which suggests that schizophrenic patients demonstrate improved psychomotor performance during chronic treatment with antipsychotic drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Antipsychotic Agents↗
PubMed1984

Lithium antagonizes ethanol intoxication in alcoholics.

Thirty-five detoxified alcoholics given lithium in a placebo-controlled, double-blind study reported less intoxication, a decrease in the desire to continue drinking, and less cognitive dysfunction when challenged by standardized doses of ethanol. Lithium also appeared to antagonize the ethanol-induced decrement in cognitive and perceptual motor performance. No differential lithium effect was noted when alcoholics were divided by diagnoses of affective disorder versus no affective disorder. The authors suggest that, in addition to mood normalization, lithium's capacity to directly affect ethanol intoxication may help explain its potential therapeutic efficacy in alcoholism, providing further confirmatory evidence that lithium may be useful in the treatment of alcoholism.

Adult↗
PubMed1982

Blunted prolactin response. A neuroendocrine abnormality manifested by depressed patients.

Prolactin concentrations of 30 unmedicated psychiatric inpatients and 11 normal controls were measured at baseline and at 30 and 60 minutes after the administration of 10 mg of intramuscular methadone hydrochloride. Methadone raised the prolactin level at 60 minutes to more than twice the mean baseline level for the full subject sample. Patients with depressive disorders had lower mean basal prolactin levels than did the other subjects, and also manifested attenuated prolactin responses to methadone. Eight of 16 depressives had markedly blunted prolactin responses, a finding consistent with other studies reporting deficient responses in depression. These data are consistent with the hypothesis that the pathophysiology of depressive disorders involves dysfunctions in the anterior pituitary itself or in the hypothalamic neurotransmitter and neuromodulator systems (eg, endorphins) that regulate the secretion of prolactin and other neurohormones.

Adult↗
PubMed1982

The effect of methadone on the behavioral and neuroendocrine responses of manic patients.

In a double-blind, crossover design, 10 mg of methadone or an inert placebo were administered intramuscularly to nine acutely manic patients in identical experimental sessions separated by 1 day. Standardized behavioral observations, self-ratings of mood and affect, and blood samples for prolactin and cortisol were obtained at baseline and 30, 60, and 120 minutes after the administration of methadone or placebo. Methadone decreased symptoms of euphoria, elation, and grandiosity in these manics. There was a significant rise in prolactin, peaking at 60 minutes, and a significant decrease in cortisol, maximal at 120 minutes following methadone administration. There appeared to be a correlational consistency between the subduing effects of methadone on behavior and its effect upon prolactin and cortisol secretion. These findings, together with data from previous studies of our own and others, suggest that a potentially important interrelationship may exist between the central endogenous opioid peptide systems, various neuroendocrine regulatory factors, and the pathophysiology of affective disorder.

Adult↗
PubMed1981

Effects of lithium carbonate on methylphenidate-induced mood, behavior, and cognitive processes.

Evidence is presented which suggests that lithium modifies the mood and behavioral alterations resulting from IV methylphenidate. Specifically, lithium significantly reduces the level of arousal-activation, euphoria-grandiosity, and the total score of manic-state ratings following a methylphenidate challenge. In addition, lithium appears to be capable of modifying the growth hormone response to methylphenidate.

Adult↗
PubMed1981

Effects of naloxone-HCl on cortisol levels in patients with affective disorder and normal controls.

Cortisol levels were measured before and after administration of naloxone-HCl in patients with affective disorder (n = 16) and normal control subjects (n = 8). On two consecutive days, 20 mg of naloxone-HCl or placebo was administered i.v. over 15 minutes in a double-blind crossover design. Blood samples were collected at 30, 15, and l minute(s) both before and after infusion. Cortisol rose from a mean baseline level of 14.8 microgram% to a mean peak level of 23.1 microgram% following the naloxone administration. Significant cortisol increases were found in both the 15- and 30-minute samples during the naloxone session. There were no differences between patient and normal subject samples or between diagnostic groups. A subgroup of manic patients who had responded to naloxone with a reduction of their manic behavior also had an attenuated cortisol response to naloxone. This proved to be an artifact secondary to variability in the cortisol response in these patients.

Adult↗
PubMed1980

Naloxone-induced behavioral and physiological effects in normal and manic subjects.

Intravenous naloxone hydrochloride (20 mg) was administered to eight normal control subjects and 12 affective disorder patients manifesting manic or hypomanic symptoms. On two consecutive days, in a counterbalanced order, naloxone and placebo were given in a double-blind crossover design. The overall effect of naloxone was to decrease pulse rate and to promote lethargy and inactivation. The normal controls manifested reduced feelings of well-being, and the manic patients noted a subjective sense of slowing. There was a variable response pattern to naloxone in the manic patients in which four of the 12 patients manifested an observable reduction in their manic symptoms and behavior after the naloxone administration. Naloxone seems to have had a nonspecific subduing effect in both normal subjects and patients and may also have had a selectively greater effect in a small subsample of the manics.

Adult↗
PubMed1980

The effects of naloxone on methylphenidate-induced mood and behavioral changes: a negative study.

The effects of naloxone on IV methylphenidate-induced mood, behavior, and neurohumoral changes were assessed in eight psychiatric inpatients. While methylphenidate alone produced anticipated changes, the indications for significant naloxone-methylphenidate interactions were minimal. It is speculated that larger doses of naloxone might be required to produce modification of the psychostimulant effects.

Behavior↗