ICD-116C45

DISORDERS DUE TO USE OF COCAINE

Disorders due to use of cocaine
ICD-10F14Mental and behavioural disorders due to use of cocaine
DSM-5-TRF14.20Stimulant Use Disorder, Cocaine, Moderate or Severe

1. Definition and nosology

Cocaine use disorders (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

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

3. Epidemiology

  • Annual global users 21 mln (UNODC).
  • Sex: 2 times higher in males.
  • Comorbidity: alcohol, opioids, MDD, BPD, psychosis, cardiovascular mortality.

4. Aetiology and pathogenesis

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

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 the single DSM-5-TR 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 Source-specific clarifications

  • SAMHSA TIP 33 — stimulant use.

6.3 Diagnostic algorithm

  1. Clinical interview + toxicology.
  2. EKG, troponin (especially if chest pain).
  3. HIV, HCV, syphilis.
  4. Comorbidity and suicide risk (high during withdrawal).

6.4 Differential diagnosis

ConditionDistinguishing feature
Amphetamine/stimulant (6C46)Toxicology differential.
Manic episodeSubstance history and temporal relationship.
Psychosis (cocaine-induced and primary)Remission after substance elimination.
Hyperthyroidism, pheochromocytomaEndocrine tests.

7. Examination and assessment

  • Toxicology.
  • EKG, troponin, cardiac assessment.
  • HIV, HCV.
  • C-SSRS.

8. Treatment

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

Source-specific specifications

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

Treatment methods

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

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 first-line.

Myth 3: “Cocaine ‘crash’ is safe, 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; socio-economic factors have a stronger impact (Frank D.A. JAMA 2001 review).

11. Sources

  1. WHO. ICD-11. 6C45 Disorders due to use of cocaine. 2024.
  2. APA. DSM-5-TR. 2022.
  3. SAMHSA. TIP 33: Treatment for Stimulant Use Disorders. 2021 update.
  4. NIDA. Research Report: Cocaine. 2016.
  5. Petry N.M., Alessi S.M., Olmstead T.A. Contingency management treatment for substance use disorders. Psychol Addict Behav 2017;31(8):897–906.
  6. Frank D.A. et al. Growth, development, and behavior in early childhood following prenatal cocaine exposure. JAMA 2001;285(12):1613–1625.
  7. 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.

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