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Biomedical subjects

C A Dackis

Publications and source records attributed to C A Dackis.

At least 19 recordsLinked to original sources
PubMed1990

Addictiveness of central stimulants.

Central stimulants have been abused since their inception and we are currently in the midst of a cocaine epidemic that challenges our resources and capabilities. Through their actions on powerful endogenous reward centers, central stimulants produce intense euphoria that reinforces subsequent usage and eventual dependence. Considerable evidence indicates that the activation of dopamine circuits mediates stimulant reward. With regard to cocaine, it has been hypothesized that depletion of central dopamine leads to craving. Euphoria and craving, the key dynamics of stimulant addiction, may therefore result largely from neurochemical alterations of dopamine systems in the brain's reward center. Progressive deterioration of the stimulant addict involving medical, psychiatric, and psychosocial impairment occurs rapidly, underscoring the addiction potential of these agents. Tolerance, sensitization and withdrawal phenomena are discussed from clinical and neurochemical perspectives.

Amphetamines↗
PubMed1987

Single-dose bromocriptine reverses cocaine craving.

Thirteen hospitalized cocaine addicts complaining of cocaine craving were given a single dose of bromocriptine, a dopamine agonist, in a randomized, double-blind, placebo-controlled study design. Compared to placebo, bromocriptine caused a significant reduction in craving ratings. These data suggest that bromocriptine may be effective as a new, nonaddictive pharmacological treatment for cocaine addicts and support the notion that functional dopamine depletion occurs with chronic cocaine use. Open trials indicate that low-dose bromocriptine may be useful in cocaine detoxification.

Adult↗
PubMed1987

The relationship of addiction, tolerance, and dependence to alcohol and drugs: a neurochemical approach.

Alcohol and drug addiction are defined in behavioral terms as the preoccupation with, compulsive use of, and relapse to drugs that are descriptive and confirmatory. The basis of addiction may involve neurochemical changes in the brain that distort and redirect the drive states (instincts). Tolerance and dependence may only be incidentally associated with addiction as a result of a nonspecific adaptation by the body to the presence of a drug. The cellular adaptation may be the same in all organs. Addiction to alcohol and drugs may have no specific relationship to tolerance and dependence. Addiction occurs in the absence of observable tolerance and dependence to alcohol and drugs. Alcohol and drug addiction is probably more complex than tolerance and dependence. Addiction is difficult to study because of the variability of behavioral phenomena and the underlying intricacies of the neurosubstrates. Tolerance and dependence are still useful as they are indicators of drug use. It is a misconception that long term chronic use is necessary for tolerance and dependence to develop. Some studies have shown that tolerance can develop within hours and days to a single dose of alcohol or other drugs. Anxiety, depression and insomnia can occur after a single dose of ethanol in humans. These symptoms of withdrawal from the alcohol or drug constitute dependence. Redefining the criteria for addiction tolerance and dependence to alcohol and other drugs may be in order. A neurochemical model may provide a more definitive and uniform basis for considering addiction, tolerance, and dependence to alcohol and drugs.

Brain Chemistry↗
PubMed1986

Evaluating depression in alcoholics.

The persistence of untreated depression was evaluated in 49 severely depressed alcoholics. After 2 weeks of sobriety, 80% of patients with initial major depression by Research Diagnostic Criteria were no longer depressed. These patients improved without antidepressant medications, suggesting the need for a 2-week period of sobriety before psychopharmacotherapy for depression is instituted. Many severe depressions in actively drinking or recently sober alcoholics may represent alcohol-induced organic affective syndromes which, unlike major depressive illness, remit spontaneously with sobriety.

Adult↗
PubMed1986

Central stimulant abuse: neurochemistry and pharmacotherapy.

This paper reviews certain clinical and neurochemical aspects of cocaine abuse. Once entrenched patterns of addiction have developed, cocaine addicts suffer progressive financial, medical, psychiatric and psychosocial deterioration that results, to some extent, from cocaine-induced neurochemical alterations in the brain. While cocaine produces euphoria through its stimulatory effect on dopamine neurons, several lines of evidence suggest that dopamine depletion occurs after chronic cocaine abuse. The dopamine neurotransmitter system is therefore a natural starting point for understanding the biology of cocaine addiction and selecting suitable adjunctive pharmacological agents. Furthermore, the dopamine depletion hypothesis implies that cocaine is "physically" addictive and provides a biological framework for understanding this disease and refining present therapeutic approaches.

Antipsychotic Agents↗
PubMed1986

Role of the laboratory in the evaluation of suspected drug abuse.

Despite the high incidence of substance abuse, it remains a common cause of misdiagnosis. In patients who have abused or who are currently abusing drugs, symptoms of a psychiatric illness may be mimicked by either the drug's presence or absence. The laboratory can aid in making a differential diagnosis and eliminating drugs from active consideration as a cause of psychosis, depression, mania, and personality changes. Treatment planning and prevention of serious medical consequences often rest on the accuracy of the admission drug screen. Testing is widely used to assess improvement in substance abuse in both inpatient and outpatient settings. In occupational settings, testing has been used as an early indicator that a problem exists and as a successful prevention tool. The appropriate use of analytic technology in drug abuse testing requires an understanding of available test methodologies. These include drug screens by thin-layer chromatography, comprehensive testing using enzyme immunoassay, and computer-assisted gas chromatography-mass spectrometry (GC-MS). Testing for specific drugs considered likely causes or precipitants of "psychiatric" complaints is available with enzyme assays, radioimmunoassay, or definitive forensic-quality testing using GC-MS.

Alcoholism↗
PubMed1986

Sexual dysfunction secondary to cocaine abuse in two patients.

Hyperprolactinemia and sexual dysfunction occurred in 7 of 10 chronic cocaine users. Two of these 7 patients who underwent rehabilitation for cocaine abuse and developed hyperprolactinemia and decreased libido are described. One patient developed galactorrhea. These adverse effects were reversed by bromocriptine. The pathophysiology of cocaine abuse and the central dopaminergic influence on sexual function are discussed.

Adult↗
PubMed1985

New concepts in cocaine addiction: the dopamine depletion hypothesis.

Euphoric properties of cocaine lead to the development of chronic abuse, and appear to involve the acute activation of central DA neuronal systems. This is based upon known effects of cocaine on DA neurons, and the role played by DA in reward states and self-stimulation behavior. With chronic cocaine use, neurotransmitter and neuroendocrine alterations occur. DA depletion is hypothesized to result from overstimulation of these neurons and excessive synaptic metabolism of the neurotransmitter. DA depletion may underlie dysphoric aspects of cocaine abstinence, and cocaine urges. Neurochemical disruptions caused by cocaine are consistent with the concept of "physical" rather than "psychological" addiction. Possible pharmacological interventions in cocaine addiction are outlined and the psychological approach to these patients is discussed.

Animals↗
PubMed1985

Pharmacological approaches to cocaine addiction.

The involvement of central dopamine (DA) neurons in the rewarding action of cocaine is well established. Cocaine euphoria depends on DA activation, and cocaine increases DA neurotransmission by blocking synaptic reuptake. Chronic cocaine use, however, appears to deplete brain DA, and perhaps leads to cocaine craving and withdrawal states. Bromocriptine, a specific DA receptor agonist, appears to ameliorate cocaine craving. Possible clinical roles for bromocriptine, and for DA receptor antagonists, are outlined.

Brain Chemistry↗
PubMedDate not supplied

Bromocriptine.

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Acromegaly↗