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Biomedical subjects

T Kosten

Publications and source records attributed to T Kosten.

At least 19 recordsLinked to original sources
PubMed2001

Buprenorphine for opiate addiction: potential economic impact.

This study evaluated the potential economic impact of the buprenorphine/naloxone combination in the context of practice in the United States of America. In comparison to treatment provided through methadone clinics, buprenorphine/naloxone therapy in office practice may be associated with increased medication, physician, and nursing costs, but reduced costs for dispensing, toxicology screens, counseling and administration. It may also result in markedly reduced costs for patients, especially travel costs, resulting in net savings for society as a whole. A review of controlled studies suggest that buprenorphine/naloxone is not likely to be any more or less effective than methadone, but since it will be less expensive in the long run, it may be more cost-effective than methadone when provided to comparable groups of patients. Because of the convenience of office-based treatment, buprenorphine/naloxone may increase access to opiate substitution for some addicts. To the extent that treatment is provided to additional high-cost patients who are involved in extensive criminal activity or who undergo multiple detoxifications each year, net cost savings could be substantial. To the extent that treatment is extended to better adjusted addicts who are employed, married and experience fewer adverse effects from their addiction, costs could increase. The total cost impact will depend on which addict sub-populations make greatest use of the treatment opportunity presented by buprenorphine/naloxone.

Buprenorphine↗
PubMed2001

Elevated motor threshold in drug-free, cocaine-dependent patients assessed with transcranial magnetic stimulation.

BACKGROUND: Transcranial magnetic stimulation (TMS) provides a noninvasive method of examining cortical inhibitory and excitatory processes and cortical excitability in awake subjects. There is evidence from clinical and electroencephalographic (EEG) data that cortical excitability may be abnormal in some psychiatric populations. Chronic cocaine abuse influences a number of neurotransmitters that are involved in the excitatory/inhibitory balance of the cerebral cortex. This pilot study was conducted to ascertain the possible utility of TMS in examining cortical excitability in a population of chronic cocaine abusers. METHODS: The right and left motor thresholds of ten cocaine-dependent subjects, according to DSM-IV, and ten normal control subjects were examined using single pulse TMS. RESULTS: The resting motor thresholds resulting from stimulation of the right or the left motor cortical regions were significantly elevated in cocaine-dependent subjects compared with matched control subjects. CONCLUSIONS: These pilot data suggest that chronic cocaine use significantly alters cortical excitability in the direction of increased inhibition or decreased excitability. We hypothesize that this observation reflects adaptation to those effects of cocaine intoxication that promote cortical excitability and seizures.

Adult↗
PubMed2000

Cocaine use and the mid-latency auditory evoked responses.

To examine the effects of chronic cocaine use on the mid-latency auditory evoked responses (MLAERs), we recorded the evoked responses of 15 cocaine-dependent subjects and 13 age-matched healthy control subjects. Two evoked response paradigms were used: a trains paradigm with four different inter-stimulus intervals (ISIs) and a paired-click paradigm. Our data suggest that cocaine-dependent subjects generate smaller P50 components when long ISIs are used with multiple repetitions (in the trains paradigm). In a single repetition paradigm (paired clicks), a significant decrease in the ability to attenuate the N100 component was seen in the cocaine-dependent subjects.

Acoustic Stimulation↗
PubMed1999

Pharmacotherapy of stimulant dependence: one of Japan's greatest public health challenges.

Stimulant dependence has become a major public health problem in the world over the last 15 years, and pharmacotherapies have been evolved based on our understanding of the neurobiological alterations induced by these drugs. Among the stimulants cocaine and amphetamine are the most common dependencies, and they share several common pathophysiologies in producing disease and in guiding medication approaches to treatment--neurotransmitter re-normalization, reversal of cerebral perfusion abnormalities and peripheral cocaine blockers. First is neurotransmitter re-normalization. A relative catecholamine deficiency occurs following prolonged abuse of cocaine and amphetamine due to transporter upregulation and receptor downregulation. This abnormality in dopamine and serotonin neurotransmission appears to be associated with depression and has supported antidepressant treatments to re-normalize neurotransmission. Dopaminergic and serotonergic agonists have also been given to re-normalize neurotransmission, but in contrast to substitution therapies such as methadone, LAAM or buprenorphine for opioids, these approaches have had limited success in unselected cocaine dependent patients. As a correlary approach to substitution, however, aspects of dopamine function can be augmented by dopamine beta hydroxylase inhibitors such as disulfiram to increase the aversive properties of stimulants and decrease their abuse. The second medication approach relates to cerebral perfusion defects and associated cognitive deficits due to vasoconstriction and abnormalities in platelets, which can respond to antiplatelet therapies as well as excitatory amino acid (EAA) antagonists. These EAA antagonists can prevent neuronal damage that is due to the release of EAA during cerebral ischemia induced by stimulant use. Finally, peripheral blockade treatment for cocaine may be possible using a newly developed active vaccine that blocks the uptake of cocaine from the bloodstream into the brain. Its potential efficacy has been shown in rodents that decrease their self-administration of cocaine when immunized with this vaccine, and preliminary human studies support its safety and immunogenicity. In summary, stimulant pharmacotherapy has made great progress in developing treatments based on understanding the neurobiology of these abused drugs, but these pharmacotherapies must be delivered in the context of appropriate behavioral and cognitive psychotherapies, which are also rapidly evolving.

Animals↗
PubMed1998

Fluoxetine treatment of depressive disorders in methadone-maintained opioid addicts.

This study tested the effectiveness of fluoxetine as a treatment for depression in a population of methadone-maintained opioid addicts. Methadone-maintained opioid addicts (44) with depression received fluoxetine or placebo in addition to their methadone, in a double-blind randomized trial, for 12 weeks. Depressive symptoms decreased significantly overall with no significant differences between the groups treated with fluoxetine versus placebo. In addition, drug use outcomes, including cocaine and heroin self-reported use and urine toxicology were measured. There was a significant decrease in heroin use in treatment, but no medication effect. Cocaine use, was unchanged from pre-treatment to endpoint. In separately analyzing data for the subsample of subjects with the most severe depression, there was a significant decrease in depression during treatment and a significant decrease in self-reported cocaine use, but no medication effect on either depressive symptoms or on cocaine use. This study suggests that fluoxetine is not an effective agent in treating depression or cocaine use in this population.

Adult↗
PubMed1994

Antisocial personality disorder as a prognostic factor for pharmacotherapy of cocaine dependence.

Pharmacotherapy response was compared in 94 cocaine-abusing methadone patients with (n = 75) and without (n = 19) antisocial personality disorder (ASP), in a 12-week, randomized, double-blind trial using desipramine 150 mg daily (n = 30), amantadine 300 mg daily (n = 33), and placebo (n = 31). Retention was lower for the ASP group (ASP 9.6 weeks vs. non-ASP 11.2 weeks). During the first 2 weeks, there was no significant difference in the percentage of cocaine-free urines between the ASP vs. non-ASP patients (9% vs. 18%), but during the last 2 weeks, the non-ASP patients showed a significantly greater percentage of cocaine-free urines (30% vs. 7%). Placebo-treated patients in both groups demonstrated no significant difference in their urine toxicologies comparing the first to the last two weeks of treatment. However, the percentage of cocaine-free urines increased from 15% to 32% in medicated non-ASP patients, but showed no change in medicated ASP patients. Thus, antisocial personality disorder was a poor prognostic factor for treatment retention and continued cocaine abuse, and medication did not improve treatment outcome for the ASP patients, but did for the non-ASP patients.

Adult↗
PubMed1992

Cocaine-associated panic attacks in methadone-maintained patients.

The incidence of panic attacks methadone-maintained patients has increased over a 10-year period from 1 to 6-13%. Cocaine use appears to be associated with this increase, although other environmental and constitutional factors may be contributory. Patients with cocaine-associated panic differ from other panic patients in rates of psychiatric hospitalization and medical illness, but not in depression, other drug use, or agoraphobia.

Adult↗
PubMed1992

Intravenous cocaine challenges during desipramine maintenance.

Intravenous challenges with placebo and cocaine doses ranging from 0.125 to 0.5 mg/kg were administered to five subjects using a within subjects design during placebo and active desipramine (DMI) maintenance at a fixed dose of 150 mg daily for at least 10 days. The "high" reported after cocaine infusion was not altered by DMI, but "desire for cocaine" after a single dose was attenuated. Together with the results of clinical trials of DMI for cocaine abuse, these laboratory results suggest that DMI may reduce cocaine craving both during and between cocaine binges. Physiologically, baseline heart rate was higher on DMI, but the incremental heart rate response to cocaine was attenuated.

Adult↗
PubMed1992

Adjunctive desipramine in the treatment of cocaine abusing schizophrenics.

Because schizophrenic patients have a lifetime prevalence rate for cocaine abuse between 15 and 50 percent, the use of adjunctive pharmacotherapy should be considered in cocaine-abuse treatment programs. This 12-week, open-label outpatient study compares 12 cocaine-abusing schizophrenic patients treated with desipramine (DMI) 100 to 150 mg and antipsychotic agents to 15 patients treated with only antipsychotic agents (no DMI). All 27 patients participated in a Dual Diagnosis Relapse Prevention (DDRP) program, which integrates traditional substance-abuse relapse prevention and psychiatric social skills training. The DMI group was more likely to complete the study (83% vs. 60%, odds ratio = 3.3, NS) and had fewer cocaine-positive urines during the last 6 weeks (20% vs. 50%, odds ratio = 4.0, p < .01). In the context of a specialized dual diagnosis treatment program, patients receiving DMI substantially decreased cocaine usage and had improved psychiatric symptoms.

Adult↗