Disorders due to use of cocaine

ICD-10F14	Mental and behavioral disorders due to use of cocaine
DSM-5-TRF14.20	Stimulant Use Disorder, Cocaine, Moderate or Severe

1. Definition and nosology

Disorders due to use of cocaine (ICD-11: 6C45; DSM-5-TR: F14.20) — impaired control over cocaine use or harmful use. Includes intoxication, withdrawal, harmful pattern of use, dependence, induced psychotic and mood disorders.

2. History

1. Coca leaves have been used in the Andes for thousands of years.
2. Niemann A. (1860) — cocaine isolation.
3. Freud (1884) — “Über Coca” — later criticized the clinical effect.
4. 1970s–1980s — ‘crack’ epidemic in the US.

3. Epidemiology

• Approximately 25 million people use cocaine annually worldwide (UNODC 2025).
• Sex: twice as common in males.
• Comorbidity: alcohol, opioids, MDD, BPD, psychosis, cardiovascular mortality.

4. Etiology and pathogenesis

• Heritability 40–50%.
• Neurobiological — blockade of dopamine reuptake → increased mesolimbic reward; tolerance and down-regulation.
• Social-cultural — peer, accessibility, socioeconomic.

5. Clinical features

• Dependence syndrome (DSM-5-TR criteria).
• Intoxication — euphoria, hypervigilance, mydriasis, tachycardia, hypertension, hyperthermia; in severe cases, paranoid delusions, hallucinations, agitation, myocardial infarction, stroke, seizures.
• Withdrawal — “crash” — depressive mood, anhedonia, fatigue, hypersomnia, increased appetite, intense cravings; high suicide risk.

6. Diagnosis

6.1 Unified diagnostic criteria

DSM-5-TR 11 criteria (AUD structure). Unlike DSM-5-TR, which uses a single severity scale, ICD-11 uses three separate categories: episode of harmful use, harmful pattern of use, and dependence. ICD-11 duration requirement: harmful pattern of use — at least 12 months if use is episodic, at least 1 month if continuous; dependence — at least 12 months, or at least 3 months if use is continuous (daily or almost daily).

6.2 Differences between sources

• SAMHSA TIP 33 — stimulant use.

6.3 Diagnostic algorithm

• Clinical interview + toxicology.
• ECG, troponin (especially if chest pain).
• HIV, HCV, syphilis.
• Comorbidity and suicide risk (high during withdrawal).

6.4 Differential diagnosis

7. Examination and assessment

1. Toxicology.
2. ECG, troponin, cardiac assessment.
3. HIV, HCV.
4. C-SSRS.

8. Treatment

• Psychosocial — first-line:
  1. Contingency management — strongest evidence base (Petry N.M. reviews).
  2. CBT;
  3. MI;
  4. Community Reinforcement Approach (CRA).
• Pharmacotherapy — No medication is approved by the FDA for this indication. Off-label studies — disulfiram, modafinil, topiramate — mixed results.
• Comorbidity treatment.
• Acute intoxication — benzodiazepine (lorazepam); cardiac monitoring; antipsychotic in psychosis.

8.1 Treatment methods

• Contingency Management — Petry (Petry N.M.), Higgins (Higgins S.) — Voucher/reward for negative toxicology tests; evidence base strongest for cocaine.
• CBT and Community Reinforcement Approach (CRA) — Trigger management, alternative rewarding activities.
• MI — Motivation for behavior change.

8.2 Differences between sources

1. SAMHSA TIP 33 — contingency management gold standard.
2. NIDA — no specific pharmacotherapy for cocaine.

9. Prognosis

• Significant improvement with contingency management.
• Comorbid substance use and psychiatric disorder — poor prognosis.

10. Myths and misconceptions

Myth 1: “Cocaine is a ‘recreational’ substance, not addictive”

Evidence: Cocaine has high addiction potential; cardiovascular mortality, psychosis, social impairment.

Myth 2: “FDA-approved treatment for cocaine exists”

Evidence: none yet; psychosocial intervention is first-line.

Myth 3: “Cocaine ‘crash’ is safe and requires no treatment”

Evidence: Suicide risk is high during the withdrawal period; active monitoring is required.

Myth 4: “Crack and cocaine powder are different disorders”

Evidence: Same substance (cocaine); route of administration (smoked vs intranasal) alters pharmacokinetics and addiction speed.

Myth 5: “The ‘crack baby’ concept in pregnancy — lasting harm in children”

Evidence: latest reviews — long-term effects of prenatal cocaine exposure are less than initially thought; socioeconomic factors have a stronger impact (Frank D.A. JAMA 2001 review).

11. Sources

• WHO. ICD-11. 6C45 Disorders due to use of cocaine. 2024.
• APA. DSM-5-TR. 2022.
• SAMHSA. TIP 33: Treatment for Stimulant Use Disorders. 2021 update.
• NIDA. Research Report: Cocaine. 2016.
• Petry N.M., Alessi S.M., Olmstead T.A. Contingency management treatment for substance use disorders. Psychol Addict Behav 2017;31(8):897–906.
• Frank D.A. et al. Growth, development, and behavior in early childhood following prenatal cocaine exposure. JAMA 2001;285(12):1613–1625.
• Higgins S.T., Budney A.J., Bickel W.K. et al. Incentives improve outcome in outpatient behavioral treatment of cocaine dependence. Arch Gen Psychiatry 1994;51(7):568–576.