Cocaine abuse as precipitating factor of tumoral bleeding in an oligoastrocitoma

Cocaine abuse has been associated with a variety of intracranial haemorrhagic disorders, such as intracerebral, subdural or subarachnoidal haemorrhage. Frequently, these patients harbour underlying vascular malformations, like cerebral aneurysms or arteriovenous malformations (AVM). To the best of our knowledge only two cases of tumoral haemorrhage induced by cocaine abuse have been previously reported. We describe a new case of intracerebral haemorrhage after cocaine inhalation, in which both the preoperative imaging studies and the pathological examination showed a brain tumour as the origin of the haemorrhage. We think that cocaine abuse may be considered as a new precipitating factor in intratumoral haemorrhage.     

Cerebral atrophy in habitual cocaine abusers: a planimetric CT study

We compared cranial CTs of 35 habitual cocaine abusers, 16 self-reported 1st-time users, and 54 headache patients using linear planimetric measures. All patients met the following criteria: age 20 to 40 years, no polydrug abuse (including alcohol), HIV seronegativity, normal albumin level, and no history of any other neurologic disease. The sex ratios and ages were not significantly different in the 3 groups. The planimetric measurements and calculated indices of cerebral atrophy were significantly different in the habitual cocaine abusers compared with the 2 other groups of patients. There were no differences between 1st-time cocaine users and controls. Among the habitual cocaine abusers there was a positive correlation between the approximate duration of cocaine abuse and the calculated atrophy indices. The findings suggest that cerebral atrophy develops in chronic cocaine abusers, and the severity correlates with the duration of abuse.     

Antecedents and consequences of cocaine abuse among opioid addicts. A 2.5-year follow-up

During a 2.5-year follow-up of opioid addicts, we examined psychosocial antecedents and consequences of the onset and remission of cocaine abuse. Patients who never used cocaine were compared with those whose use increased or decreased along several dimensions of treatment outcome including drug abuse, legal, employment, family, social, psychological, and medical problems. Cocaine abuse had a marked impact on almost every outcome area except medical problems. Patients whose cocaine use increased during follow-up had more severe problems than either those whose use decreased or those who never used cocaine. Furthermore, the attainment of cocaine abstinence among abusers was associated with improved psychosocial functioning, whereas the onset of cocaine abuse was associated with increased problem severity. Compared with drug-free and detoxification alone treatments, methadone maintenance may minimize legal complications of cocaine abuse, but otherwise it did not significantly reduce psychosocial morbidity from increasing cocaine abuse. These findings suggest that treatment-seeking opioid addicts are vulnerable to wide-ranging deterioration when they become increasingly involved with cocaine but that with the attainment of abstinence many problem areas improve.     

A 2.5-year follow-up of cocaine use among treated opioid addicts. Have our treatments helped?

During a 2.5-year follow-up study of opioid addicts, we found that cocaine abuse had become an increasing and major problem through 1983. Cocaine abuse had only minimally declined during the follow-up period despite treatment, and the number of opioid addicts with at least weekly cocaine abuse had doubled. The clear effect of methadone maintenance treatment in reducing opioid abuse was not evident for cocaine abuse. During the follow-up period, more cocaine use was reported by the methadone-treated subjects than by those undergoing detoxification only. Prognostically, cocaine users were more likely to be nonwhites and men. Subjects who increased their cocaine use during the follow-up period were more likely to have depressive disorders and more likely to be found among methadone- and "drug-free"-treated subjects than among detoxification subjects. Thus, among methadone- and drug-free-treated subjects, depression appeared to be a risk factor for escalating cocaine abuse; this risk factor may benefit from specific interventions.     

Cocaine addiction: relationship to seasonal affective disorder.

We report a 25 year-old patient with seasonal affective disorder (SAD) and cocaine abuse who experienced cyclical fluctuations in cocaine craving which were concomitant with seasonal alterations in mood. The temporal association of both disorders in this patient suggests that they may share a common underlying pathophysiology. Since disturbances in circadian rhythms and pineal melatonin functions may in part underlie the pathophysiology of SAD and the psychomimetic effects of cocaine are mediated in part through the pineal gland, we propose that dysfunction of circadian rhythms and pineal melatonin functions may partly mediate the association of SAD with cocaine abuse. This hypothesis may have potential clinical and therapeutic implications for a subgroup of cocaine abusers with SAD since light therapy, which is efficacious in the therapy of SAD, may also prove to be beneficial in reducing cocaine addiction. Furthermore, the report illustrates the need for investigations of environmental cues for cocaine abuse with specific attention given to the effects of light on circadian mood changes.     

Cocaine abuse among schizophrenic patients

Initial studies have indicated that stimulant abuse is prevalent among schizophrenic persons. To assess the phenomenon of cocaine abuse by patients with schizophrenia, 17 male cocaine-abusing schizophrenic patients were compared with 22 male schizophrenic patients who did not use cocaine. The cocaine-abusing subjects had been hospitalized more frequently, were more likely to be of the paranoid subtype, and were more likely to be depressed at the time of interview. It appears that cocaine abuse may influence both the psychopathologic presentation of schizophrenic patients and the intensity of care that they require.     

Desipramine facilitation of initial cocaine abstinence

We conducted a double-blind, random assignment, six-week comparison of desipramine hydrochloride (n = 24), lithium carbonate (n = 24), and placebo (n = 24) treatments for cocaine dependence. Subjects were 72 outpatient cocaine abusers who met DSM-III-R dependence criteria for cocaine but not for other substance abuse. Subjects in each treatment group were similar in history of cocaine and other substance abuse, cocaine craving, sociodemographics, and other psychiatric comorbidity. Desipramine, compared with both other treatments, substantially decreased cocaine use. Lithium treatment outcome did not differ from that of placebo. Desipramine-treated subjects attained contiguous periods of abstinence substantially more frequently than subjects receiving lithium or placebo. Fifty-nine percent of the desipramine-treated subjects were abstinent for at least three to four consecutive weeks during the six-week study period, compared with 17% for placebo and 25% for lithium. Cocaine craving reductions were also substantially greater in the desipramine-treated subjects. Establishment of initial abstinence is the first stage in recovery from cocaine dependence. Our findings indicate that desipramine is an effective general treatment, for this first treatment stage, in actively cocaine-dependent outpatients.     

Bromocriptine treatment for cocaine abuse: the dopamine depletion hypothesis

The authors review the evidence that cocaine exerts its rewarding effects through the acute activation of dopamine (DA) pathways in the brain. Chronic cocaine administration is hypothesized to lead to DA depletion, which results in cocaine craving and cocaine abstinence states. Treatment of these states with bromocriptine, a DA/antagonist, appears to have efficacy with acute and maintenance trials, and may represent a new adjunctive treatment for cocaine abuse. DA antagonists appear to exacerbate cocaine craving, which is consistent with the DA depletion hypothesis of chronic cocaine abuse. Theoretical issues relating to drug addiction and endogenous reward centers are discussed.     

Individual differences in cocaine conditioned taste aversion are developmentally stable and independent of locomotor effects of cocaine

Drugs of abuse induce complex motivational states in their users which have been shown to vary developmentally. In addition to developmental variation, interindividual variation in the rewarding and aversive effects of drugs of abuse is an important consideration. A rat model was used to assess whether the conditioned rewarding/aversive effects of cocaine were maintained as individuals matured from adolescence into adulthood. We tested rats in the cocaine conditioned taste aversion task as adolescents and again in adulthood. We observed a wide range of approach/avoidance behaviors in this task, and also observed that the relative interindividual differences in approach/avoidance are remarkably stable across the two developmental stages. Furthermore, we observed that these interindividual differences are not attributable to individual differences in cocaine-induced locomotor effects or individual differences in blood or brain cocaine levels. Taken together, these findings indicate that sensitivity to cocaine's motivational effects is stable across development and part of a unique neurological process.     

Dopaminergic sensitivity and cocaine abuse: response to apomorphine

Ten male patients with chronic cocaine abuse received a single dose of the dopamine agonist apomorphine. Self-ratings of cocaine craving, depression, and anxiety decreased in response to apomorphine. Neuroendocrine response was consistent with central dopaminergic stimulation. Patients in the "craving" phase of the cocaine abuse cycle differed in behavioral but not neuroendocrine response to apomorphine from patients in the "crash" phase. Decrease in cocaine craving correlated with decrease in plasma homovanillic acid (pHVA). Total cocaine consumption correlated negatively with baseline prolactin and pHVA levels and inversely with peak change in prolactin following apomorphine. Patients had blunted neuroendocrine response to apomorphine in comparison to historical normal controls. Implications for the "dopamine" hypothesis of cocaine abuse are discussed.     

Subarachnoid hemorrhage precipitated by cocaine snorting

We studied two cases of subarachnoid hemorrhage that occurred within several minutes of "snorting" cocaine. In one case the bleeding was from an anterior communicating artery aneurysm, and in the other case from an arteriovenous malformation in the temporoparietal region. To our knowledge, this hazard of cocaine abuse has not been previously reported.     

Identification of patients with coexisting alcohol and cocaine disorders at a community mental health center

To measure the prevalence of cocaine abuse at a community mental health center's inpatient alcohol unit, a 20 item document was used to obtain information from the medical records of 162 patients admitted from January 1988 through July 1988. The data collected were analyzed to evaluate the assessment, diagnosis, treatment and referral of patients with coexisting alcohol and cocaine disorders. Of the 162 patients in the sample, 154 (95%) had a diagnosis of alcohol abuse/withdrawal and five (3%) had a diagnosis of cocaine abuse. Fifty-five patients had used cocaine for at least one year and 39 (24%) of the patients had a positive laboratory test for the drug upon admission. Eighty-six patients, over 53 percent of the sample, met the DSM III-R criteria for cocaine abuse, but only five (3%) of the patients were referred to substance abuse clinics or support groups upon discharge. These findings highlight the inadequate diagnosis, treatment and follow-up of patients with coexisting alcohol and cocaine disorders.     

Stroke in young adults who abuse amphetamines or cocaine: a population-based study of hospitalized patients

CONTEXT: The abuse of stimulant drugs is increasing in the western United States. Although numerous case reports and animal studies suggest a link with stroke, epidemiologic studies have yielded conflicting results. OBJECTIVE: To test the hypothesis that young adults who abuse amphetamines or cocaine are at a higher risk of stroke. Design, Setting, and PARTICIPANTS: Using a cross-sectional design and from a quality indicators' database of 3 148 165 discharges from Texas hospitals, we estimated the secular trends from January 1, 2000, to December 31, 2003, in the abuse of various drugs and of strokes. We developed separate logistic regression models of risk factors for hemorrhagic (n = 937) and ischemic (n = 998) stroke discharges of persons aged 18 to 44 years in 2003, and for mortality risk in patients with stroke. Main Outcome Measure Incidence of stroke using definitions from the Agency for Healthcare Research and Quality's stroke mortality Inpatient Quality Indicator. RESULTS: From 2000 to 2003, the rate of increase was greatest for abuse of amphetamines, followed by cannabis and cocaine. The rate of strokes also increased, particularly among amphetamine abusers. In 812 247 discharges in 2003, amphetamine abuse was associated with hemorrhagic stroke (adjusted odds ratio [OR], 4.95; 95% confidence interval [CI], 3.24-7.55), but not with ischemic stroke; cocaine abuse was associated with hemorrhagic (OR, 2.33; 95% CI, 1.74-3.11) and ischemic (OR, 2.03; 95% CI, 1.48-2.79) stroke. Amphetamine, but not cocaine, abuse was associated with a higher risk of death after hemorrhagic stroke (OR, 2.63; 95% CI, 1.07-6.50). CONCLUSION: Increases in stimulant drug abuse may increase the rate of hospital admissions for strokes and stroke-related mortality.     

Nonnarcotic drug use over an addiction career--a study of heroin addicts in Baltimore and New York City

Detailed interview data from 250 male narcotic addicts attending methadone maintenance treatment centers in Baltimore and New York City were used to confirm and extend previous findings regarding the frequency of nonnarcotic drug abuse among relevant addict subgroups. Consistent with earlier results, abuse of nonnarcotic drugs in general, and particularly cocaine, was higher during periods of addiction than during periods of nonaddiction. Overall, marijuana and cocaine were the two main drugs of abuse, but variations were present according to addiction status period, city, and ethnic group membership. Relationships between cocaine use and specific types of criminal activity were also examined. It was found that there were high associations between cocaine use and several different kinds of crime.     

Priapism Following Trazodone Overdose with Cocaine Use

Priapism is a urologic disorder and medical emergency with a variety of known etiologies including the use of psychotropic medications. The antidepressant trazodone is the agent most frequently implicated in the precipitation of priapism. Additionally, a number of drugs of abuse including marijuana, ethanol, and cocaine have been known to cause the disorder. It is unknown if drugs may act in an additive or a synergistic manner to cause priapism. We report a case of priapism which occurred following trazodone overdose in an individual actively using cocaine. This case suggests that combined trazodone and cocaine use may pose an additional risk of priapism. Since trazodone is commonly employed as a hypnotic and often chosen for polysubstance abusers due to its low abuse potential, clinicians should be aware of the possible additive risk of priapism in this patient population.     

The role of progestins in the behavioral effects of cocaine and other drugs of abuse: Human and animal research

This review summarizes findings from human and animal research investigating the influence of progesterone and its metabolites allopreganolone and pregnanolone (progestins) on the effects of cocaine and other drugs of abuse. Since a majority of these studies have used cocaine, this will be the primary focus; however, the influence of progestins on other drugs of abuse will also be discussed. Collectively, findings from these studies support a role for progestins in (1) attenuating the subjective and physiological effects of cocaine in humans, (2) blocking the reinforcing and other behavioral effects of cocaine in animal models of drug abuse, and (3) influencing behavioral responses to other drugs of abuse such as alcohol and nicotine in animals. Administration of several drugs of abuse in both human and nonhuman animals significantly increased progestin levels, and this is explained in terms of progestins acting as homeostatic regulators that decrease and normalize heightened stress and reward responses which lead to increased drug craving and relapse. The findings discussed here highlight the complexity of progestin–drug interactions, and they suggest a possible use for these agents in understanding the etiology of and developing treatments for drug abuse.     

A five-minute, but not a fifteen-minute, conditioning trial duration induces conditioned place preference for cocaine administration into the olfactory tubercle

The establishment of conditioned place preference (CPP) with intracranial injections requires specific injection sites, drug doses, and conditioning trial durations. We examined the role of conditioning trial duration in CPP with cocaine injections into the medial olfactory tubercle. Only those rats that had spent 5 min in the compartments showed CPP for cocaine, while rats that had been removed immediately or spent 15 min following cocaine injections did not show CPP. Effective conditioning trial durations for CPP induced by intracranial cocaine injections are apparently much shorter than those typically used for intracranial injections of other drugs of abuse.     

The role of progestins in the behavioral effects of cocaine and other drugs of abuse: Human and animal research

This review summarizes findings from human and animal research investigating the influence of progesterone and its metabolites allopreganolone and pregnanolone (progestins) on the effects of cocaine and other drugs of abuse. Since a majority of these studies have used cocaine, this will be the primary focus; however, the influence of progestins on other drugs of abuse will also be discussed. Collectively, findings from these studies support a role for progestins in (1) attenuating the subjective and physiological effects of cocaine in humans, (2) blocking the reinforcing and other behavioral effects of cocaine in animal models of drug abuse, and (3) influencing behavioral responses to other drugs of abuse such as alcohol and nicotine in animals. Administration of several drugs of abuse in both human and nonhuman animals significantly increased progestin levels, and this is explained in terms of progestins acting as homeostatic regulators that decrease and normalize heightened stress and reward responses which lead to increased drug craving and relapse. The findings discussed here highlight the complexity of progestin-drug interactions, and they suggest a possible use for these agents in understanding the etiology of and developing treatments for drug abuse.     

Subtle biobehavioral effects produced by paternal cocaine exposure

Despite the increased prevalence of cocaine use and abuse in males when compared with females, possible effects of paternal cocaine exposure on biobehavioral development have received little attention. We therefore exposed male mice to cocaine (20 mg/kg, i.p.) or vehicle for 10 weeks and then used those mice as sires. We then behaviorally phenotyped the F1 offspring to assess the consequences of paternal cocaine exposure on brain function. We report the presence of a subtle but significant increase in immobility in the tail suspension test, a measure of behavioral depression, following paternal cocaine. Body weight was also significantly decreased in paternal cocaine‐exposed offspring. Other aspects of neurobehavioral function, including locomotor activity, anxiety, and learning and memory, were not affected by paternal cocaine history. These data suggest alterations in brain systems and/or circuitry underlying mood regulation in the offspring of cocaine‐using fathers. Synapse 2012. © 2012 Wiley Periodicals, Inc.     

Freebase cocaine and memory

Despite the seriousness of acute medical and psychological consequences of cocaine abuse, little knowledge exists about the chronic effects of the drug. Investigation of a sample of abstinent freebase (crack) abusers in the Bahamas provides the first research evidence that prolonged cocaine abuse may result in persistent short-term memory disturbances.