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Biomedical subjects

R B Lacoursiere

Publications and source records attributed to R B Lacoursiere.

At least 19 recordsLinked to original sources
PubMed2001

"Burnout" and substance user treatment: the phenomenon and the administrator-clinician's experience.

"Burnout" began to be identified in the mid-1970s in the substance user treatment field with the meaning being that one's "fuel" to continue such work was essentially exhausted. "Burnout" is mostly manifest by emotional exhaustion and sometimes by various physical and psychiatric symptoms. In substance user treatment staff there is more "burnout" with more work pressure, unclear work policies, and decreased coping ability, with some "burnout" protection from peer and supervisor support. "Burnout" adversely effects substance user treatment and other human service interventions, with increased absenteeism and job turnover, and it appears to be helped with a variety of methods, including diversity of supports and interests. A case study of the author's substance user treatment and administrative work from the perspective of "burnout" considerations is included.

Burnout, Professional↗
PubMed1995

A double-blind, placebo-controlled study of nortriptyline and bromocriptine in male alcoholics subtyped by comorbid psychiatric disorders.

This double-blind, placebo-controlled, 6-month follow-up treatment study investigated the efficacy of bromocriptine and nortriptyline in attenuating drinking behavior and psychiatric symptoms in 216 male alcoholic patients subtyped by comorbid psychiatric disorder(s). Three well-defined subtypes were examined: alcoholism only, alcoholism + affective/anxiety disorder, and alcoholism + antisocial personality disorder. It was hypothesized that both medications would relieve negative affective symptoms associated with alcohol use and would be particularly effective for the affective/anxiety subgroup. Contrary to our predictions, the only significant effects found were with the antisocial personality disorder patients who were receiving nortriptyline. One interpretation of the results was that nortriptyline may have reduced impulsive drinking in the antisocial personality disorder subgroup by actions on serotonergic neurotransmission.

Adult↗
PubMed1989

Excluding a psychoactive substance use disorder in forensic psychiatric evaluations.

The forensic psychiatrist is sometimes asked to exclude that a person has a psychoactive substance use disorder, for example, in a security worker who has access to weapons, in a health care professional who may be alcohol/drug impaired, or in a parent, in a deprived child or custody hearing matter. After examining the data that are leading to the evaluation, these evaluations require corroborated background information to look for developmental and genetic antecedents that might be consistent with substance abuse and dependence; inquiry into the history of substance use; and an examination of areas, in which problems from substance use can occur, namely in family and other social relationships, at work, in legal settings, in physical health, and in personal and psychiatric reactions, for example, in suicidal behavior. Then a physical exam and laboratory evaluation are conducted to look for medical evidence of substance use and complications therefrom, and a mental status exam is performed and psychological testing is obtained as required, for example, a Minnesota Multiphasic Personality Inventory (MMPI) or neuropsychological testing. When such an evaluation is essentially negative, the examiner can say, within the limits of the evaluation, that a psychoactive substance use disorder does not exist.

Adult↗
PubMed1986

Disulfiram treatment of alcoholism. A Veterans Administration cooperative study.

We conducted a controlled, blinded, multicenter study of disulfiram treatment of alcoholism in 605 men randomly assigned to 250 mg of disulfiram (202 men); 1 mg of disulfiram (204 men), a control for the threat of the disulfiram-ethanol reaction; or no disulfiram (199 men), a control for the counseling that all received. Bimonthly treatment assessments were done for one year. Relative/friend interviews and blood and urine ethanol analyses were used to corroborate patients' reports. There were no significant differences among the groups in total abstinence, time to first drink, employment, or social stability. Among the patients who drank and had a complete set of assessment interviews, those in the 250-mg disulfiram group reported significantly fewer drinking days (49.0 +/- 8.4) than those in the 1-mg (75.4 +/- 11.9) or the no-disulfiram (86.5 +/- 13.6) groups. There was a significant relationship between adherence to drug regimen and complete abstinence in all groups. We conclude that disulfiram may help reduce drinking frequency after relapse, but does not enhance counseling in aiding alcoholic patients to sustain continuous abstinence or delay the resumption of drinking.

Actuarial Analysis↗
PubMed1984

Elimination kinetics of disulfiram in alcoholics after single and repeated doses.

Elimination kinetics of disulfiram were determined in 15 male alcoholics after 250 mg disulfiram taken by mouth as a single dose and again after 12 days of dosing. Apparent t 1/2s were calculated for disulfiram, diethyldithiocarbamate (DDTC), diethyldithiocarbamate-methyl ester (DDTC-Me), diethylamine (DEA), and carbon disulfide (CS2) and were found to be 7.3, 15.5, 22.1, 13.9, and 8.9 hr. Elimination t 1/2 for CS2 in breath was 13.3 hr. Average time to reach maximal plasma concentration after either single or repeated doses was 8 to 10 hr for disulfiram, DDTC, DDTC-Me, DEA, and CS2 in breath, while plasma CS2 concentration peaked 5 to 6 hr after disulfiram. In these studies, 22.4% and 31.3% of the disulfiram after single and repeated dosing was eliminated in the breath during one dosing interval. In urine, 1.7% and 8.3% of the disulfiram dose was eliminated as DDTC-glucuronide after single and repeated dosing, while DEA accounted for 1.6% and 5.7% of the dose. There was marked intersubject variability in plasma levels of disulfiram and its metabolites. This variability may be the result of the lipid solubility of disulfiram, differences in plasma protein binding, or the effect of enterohepatic cycling.

Administration, Oral↗
PubMed1984

Comment on Roy's "Alcohol misuse and posttraumatic stress disorder (delayed): an alternative interpretation of the data".

The statistical methods used by Roy to compare veterans who served in Vietnam with Vietnam-era veterans who did not serve there are questionned. His method of pooling means is considered improper and his data are considered incomplete because they do not relate to alcohol use in veterans with posttraumatic stress disorder. Roy's argument that the military is not liable for problems caused by predispositions is questioned.

Alcoholism↗
PubMed1980

Traumatic neurosis in the etiology of alcoholism: Viet Nam combat and other trauma.

Traumatic neurosis from Viet Nam combat or other sources includes many symptoms that can be effectively self-medicated with alcohol, at least initially. These symptoms include chronic anxiety and restlessness, insomnia, and recurrent frightening dreams. Repeated self-medication with alcohol results in tolerance and a need to increase the amount consumed. Attempts to decrease consumption or to abstain can lead to alcohol withdrawal symptoms similar to and exacerbating the initial symptoms of traumatic neurosis. Continuing alcohol use, with the establishment of a vicious circle, can follow. The authors present three case examples. They note that treatment of alcoholism under the conditions described requires specific attention to the underlying traumatic neurosis.

Adult↗
PubMed1977

Phenothiazine effects on psychological and psychophysiological dysfunction in chronic schizophrenics.

This study examined the effects of phenothiazine treatment on attentional-perceptual, cognitive, and psychophysiological dysfunction in chronic schizophrenics. Under double-blind conditions, 20 patients receiving chlorpromazine and 20 receiving placebo for eight weeks were tested by performance measures, clinically rated, and monitored for skin resistance and heart rate on four occasions. Phenothiazine effects on measures of attention-perception and on psychophysiological response were demonstrable, but not on tests and ratings of cognitive dysfunction. The direction of effects was toward normalization of function. Drug treatment tended to improve ability to sustain set, to increase efficiency of selective attention, and to increase rate of information processing. Autonomic reactivity was reduced and a deactivation effect suggested. Clinical improvement was correlated with reduction in attentional dysfunction. The results are discussed in terms of their implications for hypothesized behavioral mechanisms of drug action, primary "behavioral site" of drug action, therapeutic response measurement, and functional theories of schizophrenic psychopathology.

Adolescent↗
PubMed1977

Mental health consultation in a law school clinic.

The author describes mental health consultation with legal interns in a law school legal clinic. Unique characteristics of this setting are described, including that it is not primarily a mental health area and that the consultees are trainees. Various types of consultee-centered consultation and direct and indirect client-centered consultation are discussed, as are problems that must be avoided, e.g., an excessive psychological focus on the part of the consultant or consultee.

Community Mental Health Services↗
PubMed1976

How long does chlorpromazine last?

How long does chlorpromazine last? This question regarding the persistence of chlorpromazine (CPZ) in chronically medicated schizophrenic patients after drug discontinuation led to wide ranging preliminary answers. These varied from a few to several days for blood studies up to many months for urinary and clinical studies. At least two implications of the question need to be considered: a) the pharmacological persistence of active drug and/or metabolites after drug discontinuation; and b) the persistence of the therapeutic effects regardless of whether or not active drug and/or metabolites are pharmacologically present. For example, a patient's behavior may improve while on CPZ and this improvement may persist after the active drug and/or metabolites cease to be present in the patient's body. These two areas of inquiry were examined by looking at blood, urinary, and clinical data. Although blood studies undoubtedly give the most definitive data, they are greatly complicated by the lack of definitive information regarding the active moiety (moieties) and crucial sites of action, the large number of metabolites (up to 150 or so), the minute quantities involved (ng/ml), the wide inter- and intrapatient variations, and the newness and lack of complete comparability of the quantitative methodologies. Within these limitations, there are a number of studies that are fairly consistent in showing a half-life of disappearance from the plasma of CPZ and/or metabolites in the range of a few to several hours. This would usually mean that most of the drug and metabolites are cleared from the plasma in a few days after drug discontinuation. Urinary studies are related less directly than blood studies to desired clinical effects. Under steady-state conditions in various studies, 43 to 63 per cent of a daily therapeutic dose of CPZ can be recovered in the urine in 24 hours. After drug discontinuation, urinary drug and/or metabolites in most studies last from about 3 to 18 days, with sometimes minimal or trace amounts after this. The clinical studies show a continuation of therapeutic benefits for up to 6 months and longer in some studies, but there are a number of studies showing placebo (withdrawn) groups deteriorating significantly more than continued drug groups much before this, even as early as 1 to 2 weeks off drug. This examination of the literature tends toward a duration of substantial pharmacological (therapeutic) action of CPZ of no more than a few days after drug discontinuation. For a small number of patients, clinical deterioration begins about the same time, whereas in many others, clinical improvement lasts weeks or months. Some of this latter continuation of improvement is likely not due to CPZ and/or metabolites currently active. There do remain many unanswered questions regarding the persistence of minute amounts of CPZ and/or metabolites in storage and possibly at active sites, and whether or not in some patients this makes a significant contribution.

Chlorpromazine↗