CNS EFFECTS OF “RECREATIONAL” COCAINE USE
Psychiatric Effects of Cocaine
Acute euphoria. The acute psychiatric effects of cocaine include a brief “rush,” excitability, hyper-vigilance and anxiety. Cocaine euphoria can positively reinforce drug-taking behavior. In “recreational” cocaine use, psychiatric status and safety depends on the degree of emotional instability, physical exhaustion, behavioral agitation, sleep alterations and suicidal behavior.
Cocaine can induce psychotic symptoms that have included delusions, hallucinations or both. Brady and coworkers examined 55 patients who were consecutively admitted for cocaine treatment and found that approximately 50% reported that they had experienced a short-lived psychosis. In the study, the risk factors for cocaine psychosis included male gender, a greater duration of use and a greater use in the 12 months before admission. However, it is important to note that studies conducted with treatment samples may embody a bias.
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Among cocaine’s most feared complications are suicidal, parasuicidal and homicidal behaviors. Studies worldwide have linked cocaine to intentional and unintentional injuries. Cocaine exacerbates suicidal and omnipotent fantasies, making the prevention of self-harm an important treatment focus. Suicidal intent is a common psychiatric complaint related to cocaine presentation in the emergency department. Roy compared the characteristics of 124 cocaine-dependent patients who had never attempted suicide with the characteristics of 84 patients who were admitted with cocaine dependence and suicide attempt. The study found a 33% risk of suicide attempt among patients with recent cocaine use. Compared to cocaine users who had never attempted suicide, cocaine users who had attempted suicide reported more suicide risk factors across lifespan. Autopsy studies that were conducted in New York also implicated recent cocaine use in suicide deaths and motor vehicle fatalities.
Cocaine abstinence. Cocaine withdrawal is associated with negative affect states, such as apathy, anxiety, irritability, depression and suicidal thoughts. Among cocaine-withdrawn patients, severe depression and/or suicidality appeared to cor relate with prior depression or long-term. In some studies, severe abstinence symptoms significantly increased premature drop-out from cocaine treatment and enhanced the subjective response to cocaine. Interestingly, Kampman and colleagues used cocaine withdrawal assessment and intake urine toxicology results to predict treatment attrition, suggesting a potential strategy in selecting patients for focused treatment intervention.
Neurologic Complications of Cocaine
In the past two decades, abundant preclinical and clinical data on the neurologic side effects of cocaine have appeared.
Gestational effects of cocaine. From preliminary studies, the fetal effects of cocaine have included autonomic hyperarousal, delayed CNS development and attentional deficits after birth. However, caution must be used to attribute in utero effects to cocaine alone because of the prevalence of cigarette smoking, anemia, malnutrition and infectious diseases among cocaine-using pregnant women. Indeed, the occurrence of cocaine-induced teratogenicity and “crack babies” has been questioned. Excellent reviews on prenatal cocaine exposure are available, and this subject is beyond the scope of this paper.
Effects in adult cocaine users.
a) Neurovascular effects of cocaine. Neurologic complications of cocaine among adults include headaches, fainting attacks, cerebrovascular accidents, CNS vasculitis and encephalopathies. Ischemic or hemorrhagic strokes can occur within three hours of cocaine use. Peterson and colleagues completed a three-year prospective study of 31,081 admissions in an inner-city trauma unit. Neurovascular events were approximately 3% of 979 admissions related to cocaine and the incident population was aged <45 years.
b) Delirium and seizures. Delirium and seizures are significant contributors to cocaine’s morbidity and mortality. Cocaine-associated delirium is a medical emergency. Hospitalization may be required for close monitoring and to exclude infection, trauma and CNS bleeding. Similarly, cocaine-induced seizures should be diagnosed only after excluding common causes of seizures. Cocaine provokes seizures (partial or generalized) independent of the route of drug administration. cheap levitra professional
c) Movement disorders. Movement disorders in long-term cocaine users include resting tremors, stereotypy, dystonia and chorea. Cocaine-induced hand tremors differ from physiologic tremors of 9 Hz found in normal individuals at rest. Physiologic tremors are worsened during sympathoadrenergic arousal but not during action or intention. Cocaine is associated with low-frequency (4-6Hz) tremors that are not present during movement or intention. Unlike alcohol tremors, cocaine tremors are not associated with cerebellar signs.
Cocaine tremors are not visible to the naked eye. Bauer used an accelerometer to study chronic cocaine users at 100 days of monitored abstinence and found evidence of rest tremors. Generally, cocaine can worsen preexisting movement disorders, including antipsychotic-induced movement disorders.
Neuropsychologic Complications of Cocaine
Bolla and colleagues have studied the neurocogni-tive effects of chronic cocaine abuse among 51 community-based adult volunteers (30 cocaine-using and 21 control subjects). The drug-using group reported using cocaine at least four times per month for at least one year, with an average dose of 2.3 g per week for about 6.7 years, and urine toxicology screening was positive for cocaine metabolites at the time of admission. The study compared the heavier cocaine users, intermittent users and control subjects with respect to their performances on neuropsychologic batteries. The result showed a correlation of heavier use of cocaine with greater impairment in visuomotor tracking, speed of information processing and other areas of neuropsychologic functioning (Table 1). buy cialis super active
Table 1. Summary of the results of studies evaluating neuropsychologic performances in cocaine abusers
|Authors||Cocaine Subjects Studied||Cognitive Domains with Significant Deficits among Cocaine Users||Cocaine Variable Correlating with the Observed Deficit(s)|
|Ardila et al., 199179||N=37||Verbal memory Attention||Lifetime cocaine use|
|O’Malley et al.,199280||N=20 (inpatients)||Concentration Verbal memory Nonverbal problem-solving||Dose of cocaine used; Recent use|
|Mittenberg et al.,199381 N=16||Verbal memory||Dose of cocaine used|
|Berry et al., 199382||N=16 (inpatients)||Memory|
|Recent use of cocaine|
|Hoff et al., 199683||N=38 (inpatients)||Spatial memory Perceptual motor speed Cognitive flexibilty||3-4 years of continuous use|
|Gillen et al., 199884||N=19 (outpatients and inpatients)||Visual memory Verbal generation Sequencing||None*|
|Smelson et al., 199985||N=35||WAIS arithmetic Grooved pegboard Trails В||None*|
|Bolla et al., 199978||N=30 (community sample) Visuomotor tracking|
Intormation processing Mental flexibility
|Dose of cocaine used|
|Rosselli et al., 200186 N=42 Attention|
* The study reported no cocaine variables correlating with the observed cognitive deficits
Other studies also found an association between chronic cocaine use and deficits in neurocognitive domains, such as visual, spatial memory, perceptual motor speed, mental flexibility, verbal generation, attention and concentration (Table 1). Because these studies were conducted following periods of abstinence of two weeks to six months, the observed deficits are unlikely to be due to acute effects of cocaine. Some of the studies suggested that cocaine use variables, including lifetime use, quantity used, peak dose, and frequent and recent use, were significant predictors of neurocognitive deficits.
Importantly, alcohol has well-documented neurocognitive effects. Concurrent use of alcohol and cocaine is common, suggesting the possibility of confounding in studies of the neurocognitive effects of cocaine. To address this question, investigators have compared the neuropsychologic performances of cocaine users versus cocaine-alcohol users although not all studies used a control group of non-drug-using individuals. Nevertheless, these studies were able to demonstrate some cognitive effects of cocaine even after accounting for the neurocognitive effects of alcohol (Table 2).
Table 2. Results of studies evaluating neuropsychologic performances in cocaine abusers vs. cocaine-alcohol abusers
|Authors||Number of Subjects||Duration of Abstinence Prior to Initial Testing (Days)||Comparison of Neurocognitive Deficits among the Drug Users||Cocaine Variables|
|Brown et al., 1994||Cocaine: N=64 Alcohol: N=64||28 days||Similar profiles among drug-abusing groups||None*|
|Robinson et al., 1999||Cocaine: N=30 Alcohol: N=30 Controls N=30||96 days||Profiles similar except for worse motor skills in the cocaine group||None*|
|Bolla et al., 2000||Cocaine: N=29 Alcohol: N=27 No controls||1-3 days||Differential neurocognitive effectst||Dose used|
|Di Sclafani et al., 2002 Cocaine: N=20 35 days Similar profiles Quantity used;|
Alcohol: N=37 among drug-using Duration of Controls N=29 groups peak dose
* The study reported no cocaine variables correlating with the observed cognitive deficits; t Cocaine affected performances on block design, Trails В and Stroop tests, whereas alcohol affected reaction time on go-no-go test and Ray Auditory Verbal Learning test, learning rate and total
For example, Robinson and coworkers found that the cognitive profiles of cocaine users and cocaine-alcohol users were similar. But Bolla and colleagues found that the cognitive effects of cocaine and the cognitive effects of alcohol were different. The study by Bolla et al. suggested that cocaine affected performances on block design, Trails В and Stroop, whereas alcohol affected reaction time on go-no-go test and Ray Auditory Verbal Learning Test, learning rate and total, indicating that alcohol use might worsen neurobehavioral function in patients with CUDs. Viagra Super Active