Cocaine-Related Psychiatric Disorders

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Cocaine is a naturally occurring alkaloid found within the leaves of a shrub, Erythroxylon coca. The earliest reported use of cocaine dates back to times when the ancient inhabitants of Peru used the leaves for religious ceremonies. Cocaine was first isolated from the coca leaf in 1859. Its first use as a local anesthetic was reported in 1884. In the late 19th century, Sigmund Freud proposed cocaine for the treatment of depression, cachexia, and asthma. It later became prescribed for almost any illness and could be found in numerous tonics. In 1885, John Styth Pemberton registered a cocaine-containing drink in the United States. This drink was later named Coca-Cola. In 1914, the Harrison Narcotics Act banned all nonprescription use of cocaine. Finally, in 1970, the Controlled Substances Act prohibited the possession of cocaine in the United States, except for limited medical uses.

Cocaine may be abused through a number of different routes. The most widespread routes of administration include inhaling (snorting), subcutaneous injection (skin popping), intravenous injection (shooting-up), and smoking (freebasing or smoking crack). Because of poor absorption and significant first-pass metabolism, cocaine is rarely ingested.

Cocaine abuse is associated with numerous detrimental health effects. All organ systems can be adversely affected by its use. Cocaine-related psychiatric disorders have been well-documented in the literature.

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) recognizes substance related disorders resulting from the use of ten separate classes of drugs: alcohol, caffeine, cannabis, hallucinogens (phencyclidine or similarly acting arylcyclohexylamines), other hallucinogens such as LSD, inhalants, opioids, sedatives, hypnotics, anxiolytics, stimulants (including amphetamine-type substances, cocaine, and other stimulants), tobacco, and other or unknown substances.^[1]

There are 5 categories of stimulant-related disorders according to DSM-5.^[1]They are as follows:

The time to peak effects of cocaine depends on the dose and route of administration. When cocaine is injected intravenously or crack is smoked, the onset of action is within seconds and peak effects occur within 5 minutes. When snorted, the onset of action of cocaine is within the first 5 minutes and its effects typically peak within 30 minutes. Cocaine can be absorbed across any mucosal surface, including the respiratory, gastrointestinal, and genitourinary tracts.

Two major routes account for cocaine’s metabolism: (1) enzymatic metabolism by both liver esterases and plasma cholinesterase to ecgonine methyl ester and (2) nonenzymatic degradation to benzoylecgonine. The half-life of cocaine is 30-90 minutes. The metabolites ecgonine methyl ester and benzoylecgonine are excreted in the urine. Drug screens detect the presence of benzoylecgonine, which may be present in the urine for 2-3 days, depending on the dose and chronicity of usage. Rare cases of benzoylecgonine detection in the urine for 22 days following cocaine use have been reported.

Cocaine has a number of pharmacologic effects on the human body. Neuronal fast sodium channel blockade produces a local anesthetic effect that continues to be used in medicine today. During myocardial fast sodium channel blockade, cocaine blocks fast cardiac sodium channels, which results in type I antidysrhythmic activity. This may lead to prolongation of the QRS complex and contribute to the induction of the dysrhythmias associated with cocaine use.

Blockade of catecholamine reuptake (ie, norepinephrine, dopamine, and serotonin reuptake blockade) occurs in both the central and peripheral nervous systems. Blockade of reuptake of norepinephrine leads to the sympathomimetic syndrome associated with cocaine use. This syndrome consists of tachycardia, hypertension, tachypnea, mydriasis, diaphoresis, and agitation. Inhibition of dopamine reuptake in the CNS synapses, such as in the nucleus accumbens, contributes to the euphoria associated with cocaine. Norepinephrine release augments norepinephrine reuptake blockade effects.

United States

The following statistics are from the 2014 National Survey on Drug Use & Health (NSDUH) for the age group 12 years and older.^[2]

In 2014, there were 1.5 million current cocaine users aged 12 or older, or 0.6 percent of the population. About 913,000 people aged 12 or older in 2014 had a cocaine use disorder, which represents 0.3 percent of the people aged 12 or older.

The incidence of cocaine use generally rose throughout the 1970s to a peak in 1980 (1.7 million new users) and subsequently declined until 1991 (0.7 million new users). Cocaine initiation steadily increased during the 1990s, reaching 1.2 million in 2001.

The National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) study suggests the transition from use to dependence was highest for nicotine users, followed by cocaine, alcohol, and cannabis users.^[3]An increased risk of transition to dependence among minorities and those with psychiatric or dependence comorbidity highlights the importance of promoting outreach and treatment of these populations.

International

Cocaine continues to be a major drug of abuse internationally. In Mexico, for example, patients in drug abuse treatment programs in 16 cities report cocaine as the primary drug of choice.

Regarding emergency department (ED) visits in 2011, the Drug Abuse Warning Network (DAWN) reports that cocaine and marijuana were the most commonly involved drugs, with 505,224 ED visits (40.3%) and 455,668 ED visits (36.4%), respectively.^[4]

The etiologies of some deaths associated with cocaine abuse include cardiac dysrhythmias, myocardial infarctions, intractable seizures, strokes, and aortic dissection.

In the 2013 Youth Risk Behavior Survey, the prevalence of having ever used cocaine was higher among Hispanic (9.5%) than white (4.8%) and black (2.1%) students.^[5]

The 2011 Drug Abuse Warning Network (DAWN) data reported 185,748 whites, 236,089 African Americans, and 49,810 Hispanics presented to the ED for cocaine use.^[4]

In the 2013 National Youth Risk Behavior Survey, the prevalence of having ever used cocaine was higher among male (6.6%) than female (4.5%) students.^[5]

According to DAWN, males are disproportionately represented among deaths related to drug misuse or abuse. After adjusting for population size, the rate of drug misuse deaths per 1,000,000 population for males was 2.4 that for females.

According to the 2013 National Youth Risk Behavior Survey, the prevalence of having ever used cocaine was higher among 11th-grade (6.8%) and 12th-grade (7.1%) than 9th-grade (4.4%) and 10th-grade (4.0%) students, higher among 11th-grade female (5.8%) than 10th-grade female (3.1%) students, and higher among 11th-grade male (7.9%) and 12th-grade male (9.5%) than 9th-grade male (4.6%) and 10th-grade male (5.0%) students.^[5]

Data from the 2014 Monitoring the Future study show that among students surveyed as part of the the last fifteen years, cocaine use has declined in all three grades; annual 12th grade use stands at a historical low of just 2.6% in 2014, with use by 8th and 10th graders still lower.^[6]

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Christopher P Holstege, MD Professor of Emergency Medicine and Pediatrics, University of Virginia School of Medicine; Chief, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Center

Christopher P Holstege, MD is a member of the following medical societies: American Academy of Clinical Toxicology, Medical Society of Virginia, Society of Toxicology, Wilderness Medical Society, European Association of Poisons Centres and Clinical Toxicologists, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine