Cocaine-Related Psychiatric Disorders

Updated: Nov 18, 2021
Author: Christopher P Holstege, MD; Chief Editor: David Bienenfeld, MD 



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:

  • Stimulant use disorder
  • Stimulant intoxication
  • Stimulant withdrawal
  • Other stimulant-induced disorders
  • Unspecified stimulant-related disorder 


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.


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]




Diagnostic Criteria (DSM-5)

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) classifies cocaine use under the category of stimulant-related disorders. The five disorders now recognized are as follows:[1]

  • Stimulant use disorder
  • Stimulant intoxication
  • Stimulant withdrawal
  • Other stimulant-induced disorders
  • Unspecified stimulant-related disorder 

Stimulant use disorder

Symptoms of stimulant use disorders include craving for stimulants, failure to control use when attempted, continued use despite interference with major obligations or social functioning, use of larger amounts over time, development of tolerance, spending a great deal of time to obtain and use stimulants, and withdrawal symptoms that occur after stopping or reducing use, including fatigue, vivid and unpleasant dreams, sleep problems, increased appetite, or irregular problems in controlling movement.[1]

Stimulant intoxication

Criteria for stimulant intoxication are as follows:[1]

  • Recent use of an amphetamine-type substance, cocaine, or other stimulant.
  • Clinically significant problematic behavioral or psychological changes that developed during, or shortly after, use of stimulant.
  • Two or more of the following signs or symptoms:
    • Tachycardia or bradycardia
    • Pupillary dilation
    • Elevated or lowered blood pressure
    • Perspiration or chills
    • Nausea or vomiting
    • Evidence of weight loss
    • Psychomotor agitation or retardation
    • Muscular weakness, respiratory depression, chest pain, or cardiac arrhythmias
    • Confusion, seizure, dyskinesias, dystonias, or coma

Stimulant withdrawal

Withdrawal manifests after cessation or reduction of prolonged use of cocaine and results in a dysphoric mood and two (or more) of the following changes:[1]

  • Fatigue
  • Vivid, unpleasant dreams
  • Insomnia or hypersomnia
  • Increased appetite
  • Psychomotor retardation or agitation

These signs usually cause clinically significant distress or impairment and are not attributable to another medical condition or disorder.


Cocaine affects multiple organ systems. A thorough physical examination must be performed on patients suspected of cocaine abuse.

Vital signs

Acute cocaine intoxication is most commonly associated with tachycardia and hypertension due to an induced sympathomimetic syndrome.

Any patient presenting with a history of cocaine abuse and altered mental status must have an adequate temperature taken, preferably a core temperature, such as rectal. Hyperthermia associated with acute cocaine toxicity must be closely monitored.

Tachypnea may be simply a result of cocaine's stimulant effects. However, other etiologies of tachypnea include pulmonary edema, pneumothorax, pulmonary embolism, acute coronary syndrome, panic attacks, and withdrawal syndromes.

Skin and extremities

Acute cocaine toxicity is typically associated with diaphoresis.

The skin may be cool as a result of the vasoconstrictive effects of cocaine, despite an elevated core temperature.

Examine the skin for evidence of intravenous (track marks) or subcutaneous (skin popping) drug abuse.

Head, ears, eyes, nose, and throat

Close inspection of the head for signs such as edema, ecchymosis, or bony deformity is necessary to help exclude the possibility of head trauma.

Examine the eyes for pupil size (mydriasis with acute cocaine abuse), presence of nystagmus, and extraocular muscle function.

Individuals who chronically abuse cocaine who insufflate cocaine may have nasal septa perforations as a result of necrosis from repetitive cocaine-induced vasoconstriction and subsequent ischemia.


Heart sounds may reveal murmurs (endocarditis and/or valvular damage), rubs (pericarditis), or dysrhythmias.


Rales due to pulmonary edema (cardiac and noncardiac etiologies associated with cocaine), pneumonia (infectious or aspiration), or atelectasis (pulmonary embolism) may be present.

Decreased breath sounds may be noted as a result of a pneumothorax.

Acute bronchospasm (wheezing) may be noted secondary to smoking crack cocaine or cocaine insufflation abuse.

Gastrointestinal: Vomiting, diarrhea, and hyperactive bowel sounds may be noted with acute cocaine abuse.


People who abuse cocaine may present with seizures, agitation, tremor, and hyperreflexia.

Focal muscular weakness or sensory changes may occur secondary to cerebral vascular accident.


The American Psychiatric Association recognizes a number of cocaine-induced psychiatric conditions.

Patients may present with delirium, psychosis, delusions, hallucinations, depression, mania, and anxiety (see History).


Numerous potential causes and risks factors have been cited as associated with cocaine abuse.

  • The US National Institute on Drug Abuse estimates that approximately 10% of people who begin to use cocaine progress to heavy, chronic abuse.

  • A family history of substance abuse directly correlates both with the development of cocaine abuse and with earlier age of onset of cocaine abuse.

  • Approximately 50% of those who abuse illicit drugs also have a co-occurring mental disorder.

  • For example, individuals who abuse cocaine have higher rates of antisocial personality disorder, depression, anxiety, and attention-deficit/hyperactivity disorder.

  • Low levels of family bonding and high levels of peer antisocial activity were consistently associated with higher prevalence of illicit drug initiation among youths aged 12-21.





Laboratory Studies

When caring for patients with suspected cocaine-induced psychiatric disorders, a number of laboratory studies may be considered. For example, a patient with marked agitation with or without psychotic features may have complications from cocaine intoxication, such as rhabdomyolysis, myocardial infarction, or renal failure. The need for specific laboratory and ancillary tests noted below will vary depending on the clinical scenario.


Typically, hypokalemia occurs in acute cocaine intoxication from intracellular shifts of potassium ions. This corrects as the intoxication resolves. In severe cocaine toxicity, hyperkalemia may develop and lead to cardiac dysrhythmias. The exact etiology of this is unclear, but rhabdomyolysis may be a contributing factor.

Metabolic acidosis (a decreased serum bicarbonate level) also may be observed in acute cocaine intoxication. This also corrects as the toxicity resolves. A progressively worsening metabolic acidosis associated with progressive altered mental status is a poor prognostic sign. Closely monitor these patients.


Toxicology tests include the following:

  • Urine drug screens: Benzoylecgonine, a metabolite of cocaine, may be present in the urine for 60 hours after a single use of cocaine. In heavy cocaine use, it has been found in the urine as much as 22 days after cessation of cocaine use. Positive screen results are typically verified with gas chromatography with mass spectrometry.
  • Plasma cocaine levels: Because cocaine has a short half-life of 30-45 minutes and the metabolites are present in the urine for a much longer period, plasma cocaine levels typically are not as helpful as the tests that analyze for cocaine metabolites in the urine.

  • Cardiac enzymes: Because of the significant prevalence of myocardial infarction associated with cocaine use, patients presenting with chest pain and cocaine abuse should be considered candidates for cardiac enzyme monitoring.

Other lab tests include the following:

  • Glucose:In any patient presenting with altered mental status, obtain a rapid glucose determination to rule out hypoglycemia.
  • Renal function tests:Renal failure due to rhabdomyolysis and renal artery thrombosis has been reported with cocaine abuse.
  • Creatine kinase: This test may help diagnose rhabdomyolysis.
  • Urinalysis: If an agitated patient shows a urine-dip test result that is positive for blood but microscopic analysis reveals no red blood cells, consider urine myoglobin and rhabdomyolysis as the cause.
  • Pregnancy test: All women of childbearing age should receive a pregnancy test.
  • Liver function tests: Hepatic damage may occur in the acutely intoxicated patient. In addition, patients who use cocaine are at risk for infectious hepatitis, which also may result in acute mental status changes.
  • Complete blood cell count: Anemia, leukocytosis, and leukopenia all may lead the clinician to consider other disease entities.

Imaging Studies

Chest radiographs

Chest radiographs should be obtained in patients exhibiting pulmonary signs or symptoms after cocaine use. Pneumomediastinum, pneumothorax, pneumonia, pulmonary embolism, atelectasis, and other air-space diseases have been reported with cocaine use.

Head CT scan

Patients exhibiting acute mental status changes or focal neurological signs and symptoms may require a head CT scan. Cocaine use has been associated with intracranial bleeding and embolic and thrombotic strokes.

Positron emission tomography (PET) imaging

PET imaging studies have shown that cocaine dependence is associated with the dysregulation of striatal dopamine signaling, which is linked to cocaine-seeking behavior. A study by Martinez et al suggests low dopamine transmission is associated with treatment failure. These data suggest that the combination of behavioral treatment with methods that increase striatal dopamine signaling might serve as a therapeutic strategy for cocaine dependence.[7]

Other Tests

Arterial blood gas determination

This test may be useful in patients with either marked tachypnea or a decreased serum bicarbonate level to further delineate the etiology.


An ECG should be obtained if an individual who abuses cocaine reports chest pain, shortness of breath, syncope, or palpitations. Cocaine-induced myocardial ischemia, infarction, and dysrhythmias have been reported.

Cocaine is a known fast sodium channel blocker of cardiac myocytes. This can lead to a delay in the upstroke of phase 1 of depolarization and subsequent widening of the QRS duration.

Cocaine can cause either myocardial ischemia or infarction. This can subsequently lead to ST depression or elevation depending on the ischemia/infarct region. However, many young patients who abuse cocaine have a baseline J-point elevation that may be difficult to differentiate from an infarct pattern. In addition, normal ECG findings do not rule out the possibility of myocardial injury in a patient who abuses cocaine who has chest pain.

Acute cocaine toxicity also may result in hyperkalemia. This can lead to a diffuse peaking of T waves, widening of the QRS, loss of P waves, or, in the most severe cases, a sinusoidal wave pattern.



Medical Care

People who abuse cocaine present with many different medical symptoms. At times, clinicians may have difficulty determining which signs and symptoms are significant and which are not. For example, cocaine-induced chest pain is usually benign. However, these patients may have an acute coronary syndrome, pneumothorax, pulmonary embolism, pulmonary edema, or aortic dissection. Before these patients are discharged home or admitted to a psychiatric ward, the clinicians involved must evaluate the patient for other nonpsychiatric medical problems.

Cocaine intoxication

Acute cocaine intoxication is usually self limited and can be managed with supportive care.

Benzodiazepines are the first-line therapy in treating patients who are intoxicated from cocaine and are extremely agitated. Typically, benzodiazepines can be titrated until the patient is calm and the pulse and blood pressure have stabilized.

Use neuroleptics with caution in acute intoxication. Acute hyperthermia syndromes associated with acute cocaine intoxication have been reported, and the use of neuroleptics with the risk of neuroleptic malignant syndrome may confuse this situation.

Specific laboratory tests can be ordered as necessary.

Cocaine-induced chest pain

Chest pain associated with cocaine use may be from musculoskeletal, cardiovascular, or pulmonary etiologies.

Obtain a chest radiograph to exclude localized infiltrates, pneumothorax, pneumomediastinum, and pulmonary edema. An ECG and serial cardiac enzyme evaluation assist in excluding acute myocardial infarction and acute coronary syndromes.

If an acute coronary syndrome is suggested, then oxygen, aspirin, benzodiazepines, and nitroglycerin can be administered. Nonselective beta-blockers are best avoided in all patients who are intoxicated with cocaine.


Cocaine-induced hypertension is treated first with benzodiazepines. Benzodiazepines decrease the cocaine-induced sympathomimetic drive from the CNS.

If this fails, phentolamine may be considered. Phentolamine is an alpha-antagonist and counteracts cocaine's vasoconstrictive effects.

Nitroprusside and nitroglycerin also may be considered.


Cocaine-induced seizures may be either generalized or partial and result from cocaine toxicity itself or from a cocaine-induced process, such as a cerebral vascular accident.

The first-line therapy is benzodiazepines, followed by barbiturates.

Consider a head CT scan for seizures associated with the use of cocaine.

No evidence exists that anticonvulsants prevent cocaine-induced seizures, and they are not recommended for this purpose.


Rhabdomyolysis may manifest in patients who are agitated and intoxicated with cocaine. This disorder must be recognized early to prevent secondary renal failure.

Obtain a creatine kinase measurement and test the urine for myoglobin. If the urinalysis reveals blood on the dipstick but no red blood cells upon microscopic examination, then myoglobinuria may be present.

Treatment of rhabdomyolysis focuses on ensuring adequate urine output and, possibly, alkalization of the urine.


Cocaine-induced dyspnea has multiple causes.

Obtain a chest radiograph to exclude pulmonary edema, focal infiltrate, pneumothorax, and pneumomediastinum

Sleep disturbance

In a study by Morgan et al, modafinil was evaluated for its ability to normalize sleep patterns in chronic cocaine users. Progressive cocaine abstinence is associated with disruptive sleep outcomes. In patients who received modafinil each morning, nocturnal sleep was promoted and daytime sleepiness decreased compared with those taking placebo.[8]


A number of consultations may be necessary when caring for a patient who abuses cocaine. Consultations to consider include medical toxicologists, regional poison control center personnel, cardiologists, neurologists, psychiatrists, substance abuse clinicians, and social services personnel, depending on the presenting signs and symptoms.



Recent work has suggested that a cocaine vaccine may induce the formation of sufficient antibodies to reduce cocaine use.

Martell et al conducted a phase IIb randomized, double-blind, placebo-controlled trial to evaluate the immunogenicity, safety, and efficacy of a cocaine vaccine in cocaine-dependent and opioid-dependent individuals. Of the 115 patients recruited, 94 (82%) completed the trial. Participants were administered 5 vaccinations with placebo or succinylnorcocaine over 12 weeks. Within the vaccine group, those with serum IgG anticocaine antibody levels ≥ 43 mcg/mL had significantly more cocaine-free urine samples than those with serum levels < 43 mcg/mL and those who received placebo. Reduction of cocaine use by 50% was significantly greater if a high IgG level was achieved (53% of participants) compared with a low IgG level (23% of participants) (P =0.048).[9]



Medication Summary

Benzodiazepines are the drugs of choice for acute cocaine intoxication with extreme agitation. Pharmacologic therapy depends on presenting signs and symptoms (eg, treat chest pain with oxygen, benzodiazepines, aspirin, and nitroglycerin). All possible pharmacotherapies for various cocaine-induced medical conditions are beyond the scope of this article. For a complete review of treating cocaine-induced nonpsychiatric effects, refer to Toxicity, Cocaine.

Avoid use of beta-blockers because of the unopposed alpha-agonist activity. The mood shifts, abnormal sleep and even delusions associated with acute cocaine intoxication or withdrawal often are transient and do not require medications. Persistent mood disorders with mania may be treated with lithium, whereas antidepressants are advocated for mood disorders with depressive features. Antipsychotics are advocated to treat persistent psychotic disorders.


Class Summary

Bind specific benzodiazepine receptor on GABA-receptor complex, thereby increasing GABA affinity for its receptor. Increase the frequency of chlorine channel opening in response to GABA binding. GABA receptors are chlorine channels that mediate postsynaptic inhibition, resulting in postsynaptic neuron hyperpolarization. The final result is a sedative-hypnotic effect that counteracts the stimulant effect of cocaine.

Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation) possibly by increasing activity of GABA. Individualize dose and increase cautiously to avoid adverse effects.

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. Increases action of GABA (ie, major inhibitory neurotransmitter in brain). May depress all levels of CNS, including limbic and reticular formation.

Midazolam (Versed)

Short-acting benzodiazepine used for acute or short-term sedation. Also exhibits amnestic effects.

Antipsychotic agents

Class Summary

High-potency antipsychotic agents in the butyrophenone class (eg, haloperidol, droperidol) are used for rapid sedation. Easily titrated and cause less sedation and orthostasis; however, they cause extrapyramidal symptoms more often than lower-potency agents. Used short term to rapidly control psychosis.

Newer antipsychotics (eg, risperidone, olanzapine, quetiapine) are used for long-term management. Improvements over earlier antipsychotics include fewer anticholinergic effects and less dystonia, parkinsonism, and tardive dyskinesia. Affect dopamine and serotonin receptors.

Haloperidol (Haldol)

DOC for acute psychosis. Parenteral dosage form may be admixed in same syringe with 2 mg lorazepam for better anxiolytic effects.

Droperidol (Inapsine)

DOC for severely disturbed and/or violent patient. Faster acting and more sedating than haloperidol but more likely to cause hypotension. May exert antipsychotic activity through dopaminergic system. Evidence suggests it alters dopamine action in CNS.

Risperidone (Risperdal)

Binds to dopamine D2-receptor with 20-times lower affinity than for 5-HT2-receptor. Improves negative symptoms of psychoses and reduces prevalence of adverse extrapyramidal effects.

Olanzapine (Zyprexa)

May inhibit serotonin, muscarinic, and dopamine effects.

Quetiapine (Seroquel)

May act by antagonizing dopamine and serotonin effects.


Class Summary

While numerous antidepressants are currently available, selective serotonin reuptake inhibitors (SSRIs) provide many advantages over past antidepressants. MAOIs should be avoided in mood disorders with depressive features. MAOIs are lethal if patient relapses from abstinence and combines them with cocaine.

Citalopram (Celexa)

Enhances serotonin activity by selective reuptake inhibition at the neuronal membrane.

Fluoxetine (Prozac)

Selectively inhibits presynaptic serotonin reuptake with minimal or no effect on reuptake of norepinephrine or dopamine.

Fluvoxamine (Luvox)

Inhibits neuronal serotonin reuptake. Does not significantly bind to alpha-adrenergic, histamine, or cholinergic receptors, thus has fewer adverse effects than TCAs.

Paroxetine (Paxil)

Alternative DOC. Potent selective inhibitor of neuronal serotonin reuptake. Weak effect on norepinephrine and dopamine neuronal reuptake.

Sertraline (Zoloft)

Selectively inhibits presynaptic serotonin reuptake.

Venlafaxine (Effexor)

Inhibits neuronal serotonin and norepinephrine reuptake. Also causes beta-receptor down-regulation.



Further Outpatient Care

Outpatient treatment is effective for many patients with cocaine addiction. The goals of treatment for cocaine addiction are 3-fold: (1) achievement of abstinence, (2) prevention of relapse, and (3) rehabilitation. Treatment is available to assist individuals who are addicted to cocaine to achieve these goals.

Unlike the use of methadone therapy for the treatment of opiate addiction, no safe and effective cocaine replacement therapy is available as an alternative to abstinence. Currently, no FDA-approved pharmacological therapy is available for any stage of cocaine addiction treatment.

Numerous medications have been studied for the treatment of cocaine addiction, and many show promise. Topiramate, an anticonvulsant, shows some promise for cocaine-dependent patients. Baclofen and tiagabine, as well as modafinil have also shown promise in reducing cocaine use. Disulfiram may increase the aversive effects of cocaine and reduce its use.

Cognitive and behavioral therapies have been designed to prevent relapse in patients addicted to cocaine. These therapies help minimize exposure to drug cues and help modify patients' responses to cues they encounter. For example, a relapse prevention strategy may include minimizing the free cash the cocaine addict has available to buy drugs. Another example is behavioral therapy such as contingency management, in which vouchers are provided and are redeemable for goods or services contingent on performance of desired behaviors.

Tragically, access to existing outpatient treatments is often limited. In addition, if the addicted patient has insurance, many times the coverage for such therapy is limited, placing further stress on the patient.

Programs specifically structured for substance abuse should be arranged for patients who abuse cocaine. Twelve-step programs for cocaine addiction may be useful. These self-help groups are based on the principles of Alcoholics Anonymous and include a commitment to abstinence. Psychiatric follow-up at a minimum of within 2 weeks of the initial evaluation aids compliance.

A more intensive outpatient regimen of daily individual and group therapy and weekly family therapy typically is necessary for many patients. Close monitoring of patients for relapse should be part of treatment. When patients who are addicted relapse, many physicians are too ready to give up. An all-or-nothing attitude by physicians is unrealistic with addiction. Initial treatment may fail, and relapses may occur before a stable remission is achieved.

Patients with significant mental illness, such as major depressive disorder, bipolar disorder, posttraumatic stress disorder, and anxiety disorders, frequently require treatment specific to their illness (eg, medication, psychotherapy) in addition to a 12-step program. Programs that offer dual-diagnosis groups and 12-step programs are ideal if available. Inadequate treatment of either the mental illness or cocaine addiction increases the risk of relapse of both.

Multiple drug addictions can also occur, such as addiction to cocaine and alcohol. Treatment, to be successful and safe, requires careful assessment of intake of all possible drugs of addiction and a treatment plan designed to both detoxify from each drug and treat each addiction.

Further Inpatient Care

Patients with marked cognitive impairment, acute psychosis, severe depression, delirium, mania, and medical complications should be considered for admission to an inpatient facility. Achieving and maintaining stable abstinence depends on the specific treatment of addiction and on the detection of comorbid psychiatric and general medical disorders. These disorders may include conditions such as anxiety, depression, and bipolar disorder.

All patients should also be assessed for risk of harm to self or to others. This also may mandate further inpatient care. Careful assessment for suicidal ideation, plans, and level of intent to act on such ideation is crucial. If a plan and intent to act is present, psychiatric hospitalization is almost always warranted, even if requiring involuntary commitment. Also, assessing homicidal ideation, intent, and plan is critical. Not only may the patient require voluntary or involuntary psychiatric hospitalization, but one also may have a duty to warn an intended victim.

For patients with the more severe additive problems that have not been amenable to outpatient therapy, relatively long stays in residential programs are associated with better outcomes.

Inpatient & Outpatient Medications

See the list below:

  • Cocaine-induced mood disorder: Pharmacotherapy with antidepressant medications, such as SSRIs, may be necessary.

  • Cocaine-induced psychotic disorder: Pharmacotherapy with antipsychotic medications may be necessary.

  • Cocaine-induced anxiety disorder: Pharmacotherapy with anxiolytics, such as benzodiazepines, may be necessary. Several of the SSRIs and venlafaxine have been approved for generalized anxiety disorder, and, if anxiety or panic attacks persist, these medications may be helpful.


If adequate psychiatric inpatient services are not available, consider transfer to a facility with such services.

If the patient is critically ill due to cocaine intoxication, transfer to a facility with critical care services.


The key to deterrence and prevention is education.

Thoroughly review the complications of cocaine abuse with these patients at a level at which they can understand.

The earlier the intervention, the more likely the patient will succeed without long-term adverse health effects.


Complications may include the following:

  • Rhabdomyolysis

  • Acute coronary syndrome

  • Cerebral vascular accidents

  • Acute renal failure

  • Seizures

  • Hyperthermia

  • Pneumothorax

  • Pneumomediastinum

  • Pulmonary infarct

  • Pulmonary edema


Among subjects who present for cocaine dependence treatment, concurrent alcoholism predicts higher relapse risk and poorer outpatient therapy attendance.

Studies suggest that patients who have used cocaine as a primary drug of abuse for extended periods constitute a group with particularly high underlying psychopathology.

Patient Education

Education may be a challenge in patients who are addicted to cocaine if they have a limited educational background, have a low intelligence quotient, or are resistant to educational activities.

Complications associated with cocaine abuse may be difficult for people who are addicted to understand. An understanding of medical pathophysiology may be difficult for some patients to comprehend. They may be either resistant to the concept or lack insight into the cause-and-effect relationship of their disease process and cocaine abuse.

Intensive education is an important part of the success of any drug treatment program.

For excellent patient education resources, see eMedicineHealth's patient education articles Cocaine Abuse and Substance Abuse.

For further family and patient education, see the following Web sites:

  • Substance Abuse Treatment, Facility Locator


  • Free

  • Drugs of Abuse Information

  • Principles of Drug Addiction Treatment