Hallucinogen-related disorders encompass intoxication, , hallucinogen use disorder, and other hallucinogen-induced syndromes across two pharmacologic families: classic serotonergic hallucinogens (LSD, psilocybin, mescaline, DMT) and dissociative agents grouped separately in as phencyclidine-type substances. Classic hallucinogens act primarily as agonists and rarely produce a withdrawal , distinguishing them from most other drugs of abuse. DSM-5-TR retains separate diagnostic categories for phencyclidine use disorder and other hallucinogen use disorder, reflecting their divergent pharmacology and clinical risk profiles. Acute intoxication is usually self-limited and managed with supportive care and for agitation, while HPPD and persistent psychosis are rare but disabling complications. Renewed interest in psilocybin and MDMA-assisted therapy has reshaped the regulatory and research landscape, but recreational and high-dose unsupervised use continues to drive most clinical presentations. The bottom line: most cases resolve with supportive management, but clinicians must recognize the small subset who develop persistent perceptual, psychotic, or use-disorder sequelae.
Hallucinogen use is common in adolescents and young adults but use disorder is comparatively rare. Patterns vary widely across regions and cohort years.
Prevalence
- Past-year hallucinogen use among U.S. adults is in the range of 2-3% per recent NSDUH data, with lifetime use considerably higher.[1]
- 12-month prevalence of other hallucinogen use disorder is approximately 0.5% in U.S. adults; phencyclidine use disorder is substantially lower.[1-2]
- Past-year use is highest among adults aged 18-25, with recent national survey data showing rising trends in this age group.[1]
Demographics and risk factors
- Male sex predominates in both use and use disorder, with male-to-female ratios of roughly 1.5-2:1.[1-2]
- Polysubstance use is the norm; concurrent cannabis, MDMA, alcohol, and stimulant use is common.[2]
- Comorbid mood, anxiety, post-traumatic, and personality disorders are over-represented among individuals with hallucinogen use disorder.[2]
- Family history of substance use disorder and early age of first use are consistent risk factors.[2]
Suicide and overdose
- Classic serotonergic hallucinogens carry low lethality from direct pharmacologic toxicity; deaths are typically secondary to behavioral disturbance, trauma, or co-ingestion.[2-3]
- Phencyclidine and ketamine carry higher risk of medical emergencies including hypertensive crisis, rhabdomyolysis, and excited-delirium-like presentations.[3]
Classic and dissociative hallucinogens act on distinct receptor systems, which explains their divergent clinical pictures and addiction liability.
Receptor pharmacology
- Classic hallucinogens (LSD, psilocybin, mescaline, N,N-dimethyltryptamine) are partial agonists at 5-HT2A Receptor, with downstream effects on cortical pyramidal neurons in layer V.[3-4]
- 5-HT2A activation drives increased glutamatergic transmission in prefrontal and thalamocortical circuits, producing altered perception and ego dissolution.[4]
- Phencyclidine and ketamine are non-competitive antagonists, producing dissociation, analgesia, and sympathomimetic effects.[3-4]
- MDMA, classified separately under other stimulant/hallucinogen categories depending on framework, acts predominantly as a releaser with secondary dopamine and norepinephrine effects.[4]
Neurocircuitry and imaging
- Functional imaging during psilocybin shows reduced activity in the and increased between-network connectivity, correlating with ego-dissolution experiences.[5]
- Repeated dosing produces rapid 5-HT2A receptor downregulation, the proposed basis for tolerance.[4]
- Classic hallucinogens do not robustly activate mesolimbic dopamine, consistent with their low reinforcement and limited addiction liability.[3-4]
Genetics and environment
- Heritability of hallucinogen use disorder is less well characterized than for alcohol or opioid use disorders; shared liability across substance use disorders predominates.[2]
- Set (psychological state) and setting (environment) substantially modify the acute experience and the probability of distressing reactions.[3]
DSM-5-TR separates phencyclidine-related disorders from other hallucinogen-related disorders, reflecting differences in pharmacology and clinical course.[6] Both categories use the standard 11-criterion substance use disorder template.
Hallucinogen use disorder (other hallucinogen)
- Diagnosed when a problematic pattern of hallucinogen use produces clinically significant impairment or distress, with at least 2 of 11 criteria in a 12-month period.[6]
- Criteria mirror the standard set: impaired control (larger amounts, persistent desire, time spent, craving), social impairment (role failure, interpersonal problems, activities given up), risky use (hazardous use, continued use despite physical or psychological problems), and pharmacologic criteria (tolerance).[6]
- A withdrawal criterion is NOT included for other hallucinogens, because clinically significant withdrawal has not been established.[6]
- Severity is coded as mild (2-3 criteria), moderate (4-5), or severe (6 or more).[6]
Phencyclidine use disorder
- Uses the same 11-criterion template, again without a withdrawal criterion.[6]
- Includes ketamine and other arylcyclohexylamines within its scope.[6]
Hallucinogen intoxication
- Recent use with clinically significant behavioral or psychological changes (marked anxiety, depression, paranoid ideation, ideas of reference, impaired judgment) developing during or shortly after use.[6]
- Perceptual changes occurring in a state of full wakefulness and alertness (intensified perceptions, , , illusions, , synesthesias).[6]
- At least two physical signs: pupillary dilation, tachycardia, sweating, palpitations, blurring of vision, tremors, incoordination.[6]
- Symptoms not attributable to another medical condition or better explained by another mental disorder.[6]
Hallucinogen Persisting Perception Disorder
- Re-experiencing of perceptual symptoms experienced during prior hallucinogen intoxication, following cessation of use.[6]
- Common phenomena include geometric hallucinations, false perceptions of movement in peripheral vision, flashes of color, intensified colors, trails of images, positive afterimages, halos around objects, macropsia, and micropsia.[6-7]
- Symptoms cause clinically significant distress or impairment; reality testing remains intact, distinguishing HPPD from psychosis.[6-7]
Other syndromes
- Phencyclidine intoxication features vertical or horizontal nystagmus, hypertension or tachycardia, numbness or diminished pain response, ataxia, dysarthria, muscle rigidity, seizures or coma, and hyperacusis.[6]
- Hallucinogen-induced psychotic, mood, anxiety, and related disorders are coded when the syndrome dominates the clinical picture and exceeds expected intoxication effects.[6]
ICD-11 differences
- organizes hallucinogen-related disorders under disorders due to use of hallucinogens within chapter 06, with separate categories for dissociative drugs including ketamine and PCP.[8]
- ICD-11 includes a single episode of harmful use as a distinct diagnostic entity, which has no DSM-5-TR equivalent.[8]
DSM-5-TR retains the term hallucinogen use disorder despite renewed interest in classifying classic psychedelics separately based on receptor pharmacology and low addiction liability.[6]
The acute syndrome varies by agent, dose, and setting, but core perceptual disturbances with preserved consciousness are characteristic of classic hallucinogens.[3]
Classic hallucinogen intoxication
- Onset within 30-60 minutes after oral psilocybin or LSD; peak effects at 2-4 hours; duration 4-12 hours for psilocybin and 8-12 hours for LSD.[3-4]
- DMT produces an intense but brief experience lasting 15-30 minutes when smoked or vaporized.[4]
- Visual phenomena dominate: intensification of colors, geometric patterns, trails, and synesthesia (cross-modal perception, such as seeing sounds).[3]
- Ego dissolution, mystical-type experiences, and altered time perception are common at moderate-to-high doses.[3,5]
- Autonomic features include mydriasis, tachycardia, hypertension, hyperthermia, and tremor.[3]
Classic hallucinogens cause mydriasis; phencyclidine causes nystagmus.[3]
Phencyclidine and ketamine intoxication
- Dissociation, depersonalization, and analgesia with relative preservation of cardiorespiratory function at moderate doses.[3]
- Vertical or rotary nystagmus is a near-pathognomonic finding for PCP intoxication.[3]
- Severe intoxication can produce agitation, violent behavior, hyperthermia, rhabdomyolysis, seizures, and excited-delirium-like presentations.[3]
- Ketamine-specific findings include urinary symptoms with chronic use (ketamine cystitis) and dissociative emergence phenomena.[4]
Bad trips and challenging experiences
- Acute panic, paranoia, and dysphoric depersonalization can develop in any user, but are more likely with high dose, polysubstance use, pre-existing psychopathology, and unfavorable setting.[3]
- Most resolve with reassurance and a calm environment; benzodiazepines are reserved for marked agitation.[3]
Persistent sequelae
Differential diagnosis turns on identifying the agent, the duration of symptoms, and whether reality testing is preserved.[3]
Substance-induced and related
- Stimulant intoxication (amphetamines, cocaine, synthetic cathinones): tachycardia, hypertension, paranoia, but typically without classic hallucinogen visual phenomena.[3]
- Cannabis intoxication: conjunctival injection, increased appetite, less prominent autonomic activation; high-potency cannabinoids can produce psychotic features.[3]
- intoxication: severe agitation, seizures, acute kidney injury; clinical picture often more dangerous than expected from cannabis-like exposure.[3]
- delirium (Datura, Jimson weed, antihistamines): tachycardia, mydriasis, dry mucous membranes, urinary retention, flushed skin, hyperthermia; the classic toxidrome is distinguishable on examination.[3]
- from MDMA or polysubstance use: hyperreflexia, clonus, autonomic instability, hyperthermia.[3]
Primary psychiatric
- Brief psychotic disorder and : persistent delusions and thought disorder with less prominent visual hallucinations; auditory hallucinations more typical.[6]
- Panic disorder: paroxysmal anxiety with autonomic features but no perceptual distortions in the absence of intoxication.[6]
- Dissociative disorders: depersonalization or derealization without an acute toxic exposure.[6]
Medical mimics
- Complex partial seizures with visual phenomena: stereotyped, brief, often with postictal confusion.[3]
- Migraine with aura: scintillating scotoma, gradual march, often unilateral, followed by headache.[3]
- CNS infection or autoimmune encephalitis: fever, focal signs, altered consciousness; can mimic both PCP intoxication and primary psychosis and merits consideration in atypical presentations.[3]
- Delirium from any cause: fluctuating attention and consciousness, distinguishable from the alert, oriented state of classic hallucinogen intoxication.[3]
| Feature | Classic hallucinogen intoxication | Phencyclidine intoxication | Anticholinergic delirium |
|---|---|---|---|
| Pupils | Mydriasis | Variable, often normal | Marked mydriasis |
| Eye signs | None specific | Vertical/rotary nystagmus | None specific |
| Skin/mucosa | Sweaty, flushed | Diaphoresis | Dry, flushed |
| Consciousness | Alert, oriented | Variable; can be agitated/comatose | Delirious, fluctuating |
| Duration | 4-12 hours | Hours to days | Hours to days |
| First-line management | Supportive; benzodiazepines for agitation | Supportive; benzodiazepines; manage hyperthermia | Supportive; physostigmine in selected cases |
Assessment prioritizes ruling out medical emergencies, identifying co-ingestants, and establishing the timeline of use.[3]
History
- Substance identity (street name, source), dose, route, time of last use, and pattern of prior use.[3]
- Co-ingestants including alcohol, cannabis, stimulants, and opioids; novel psychoactive substances are frequently mislabeled.[3]
- Pre-existing psychiatric history, family history of psychosis, prior bad trips, and current psychosocial stressors.[3]
- Setting of use and time elapsed since ingestion.[3]
Physical examination
- Vital signs, pupillary size and reactivity, eye movements (nystagmus), skin (diaphoresis, flushing, dryness), reflexes (clonus, hyperreflexia), and neurologic examination.[3]
- Mental status with attention to consciousness, orientation, perception, and reality testing.[3]
Laboratory and imaging
- Standard urine drug screens do not detect LSD, psilocybin, DMT, mescaline, or most novel psychedelics; phencyclidine is detected on most panels and ketamine on some.[3]
- Targeted toxicology (gas chromatography-mass spectrometry) is required when identification matters clinically.[3]
- Basic metabolic panel, creatine kinase (for rhabdomyolysis), and EKG when hyperthermia, agitation, or sympathomimetic features are prominent.[3]
- Neuroimaging when focal neurologic findings, head trauma, or atypical course raise concern for an alternative cause.[3]
Rating scales
- The Mystical Experience Questionnaire and Challenging Experience Questionnaire are used in research settings to characterize psychedelic experiences but have limited clinical utility in acute care.[5]
- Standard substance use disorder instruments (Addiction Severity Index, DSM-5 Self-Rated Level 1 Cross-Cutting Symptom Measure) apply when use disorder is suspected.[6]
Do not assume a negative urine drug screen excludes hallucinogen use; most classic hallucinogens are not detected on routine panels.[3]
Most acute presentations resolve with supportive care. Persistent perceptual or psychotic sequelae, and use disorder, require longer-term management. Evidence for specific pharmacotherapy of HPPD and hallucinogen use disorder remains limited.[7,9]
Pharmacotherapy
- For acute agitation or marked anxiety during intoxication, evidence suggests lorazepam 1-2 mg PO or IM q4-6h PRN or diazepam 5-10 mg PO or IV q4-6h PRN.[3,9]
- For severe agitation unresponsive to benzodiazepines, particularly in phencyclidine intoxication, limited evidence suggests adjunctive antipsychotics such as haloperidol 2-5 mg IM q4-6h PRN, with caution regarding QTc prolongation and lowered seizure threshold.[3,9]
- Antipsychotics are generally avoided in pure classic-hallucinogen intoxication because they may worsen dysphoria and have limited efficacy compared with benzodiazepines.[3]
- For HPPD, it is uncertain whether any pharmacotherapy is reliably effective; limited evidence and case series describe variable response to benzodiazepines (clonazepam), lamotrigine, and selected antiepileptics; and antipsychotics have produced mixed results and may worsen symptoms in some patients.[7]
- For hallucinogen use disorder, no medication has FDA approval; treatment is symptom-directed and focused on comorbid conditions.[9]
Psychotherapy
- Strong evidence supports and as foundational interventions across substance use disorders, with extrapolation to hallucinogen use disorder.[9]
- Limited evidence suggests psychoeducation, harm reduction counseling, and supportive psychotherapy reduce risky use patterns in hallucinogen users.[9]
- Trauma-focused therapy is recommended when post-traumatic stress disorder co-occurs.[9]
Neuromodulation
- It is uncertain whether neuromodulation has a role in hallucinogen-related disorders; high-quality evidence is lacking.[9]
Adjunctive
- Treatment of comorbid mood, anxiety, and post-traumatic disorders follows standard guidelines.[9]
- Mutual-help groups oriented toward broader substance use recovery may be useful, although tailored hallucinogen-specific programs are uncommon.[9]
- Harm reduction counseling addressing set, setting, dose, and avoidance of co-ingestants is recommended for individuals who continue to use.[9]
PUPIL
Classic hallucinogens dilate Pupils, Phencyclidine causes nystagmUs, anticholinergics dry mucosa, stimulants raise Pressure, opioids constrIct, sedatives cause Lethargy.
Reassurance and a quiet environment ("talking down") resolves most distressing classic hallucinogen experiences without medication.[3]
| Intervention | Evidence base/Comparator | Benefits | Harms | Certainty | Notes |
|---|---|---|---|---|---|
| Benzodiazepines for acute agitation | Expert consensus, observational data, extrapolation from other intoxications[3,9] | Reduces anxiety, agitation, autonomic activation | Sedation, respiratory depression with co-ingestants | moderate | First-line for distressing intoxication |
| Antipsychotics for severe agitation | Case series and expert opinion[3,9] | Useful adjunct in phencyclidine-related agitation | QTc prolongation, dystonia, lowered seizure threshold | low | Avoid as first-line in classic hallucinogen intoxication |
| Supportive care and reassurance | Expert consensus[3] | Resolves most challenging experiences | None significant | moderate | Calm setting, hydration, monitoring |
| Pharmacotherapy for HPPD (clonazepam, lamotrigine) | Small case series[7] | Variable symptom reduction | Sedation, drug-specific adverse effects | very_low | No FDA-approved agent |
| Psychotherapy for use disorder (MI, CBT) | Extrapolation from other substance use disorders[9] | Reduced use, improved engagement | Minimal | low | No hallucinogen-specific RCT base |
| Harm reduction counseling | Observational and program-level data[9] | Reduces high-risk patterns | None significant | low | Set, setting, dose, co-ingestant guidance |
Direct pharmacologic toxicity from classic hallucinogens is low, but behavioral and persistent psychiatric harms warrant emphasis. The evidence base for specific pharmacotherapy of HPPD and hallucinogen use disorder is small.
Acute adverse effects
- Anxiety, panic, paranoia, and dysphoric depersonalization during intoxication.[3]
- Autonomic effects including hypertension, tachycardia, and hyperthermia, more pronounced with phencyclidine and high-dose MDMA.[3]
- Trauma and accidental injury due to impaired judgment and altered perception of the environment.[3]
Serious or rare adverse effects
- Persistent psychosis after classic hallucinogen use, particularly in individuals with predisposition to .[6-7]
- HPPD with disabling chronic visual disturbances.[6-7]
- Excited-delirium-like presentations with phencyclidine, with risk of hyperthermia, rhabdomyolysis, and cardiovascular complications.[3]
- Ketamine cystitis with chronic recreational use.[4]
- Serotonin syndrome with MDMA, especially with concurrent serotonergic medication.[3]
Monitoring and withdrawal
- Tolerance develops rapidly with classic hallucinogens and resolves within days of abstinence; clinically significant withdrawal is not characteristic.[6]
- Phencyclidine and ketamine produce some tolerance and craving, but a defined withdrawal syndrome is not recognized in DSM-5-TR.[6]
Evidence-base limitations
- Most pharmacologic recommendations for acute intoxication rest on expert consensus and small case series rather than randomized trials.[3,9]
- HPPD research is limited by small samples, retrospective designs, and ascertainment bias from self-selected clinical populations.[7]
- Polysubstance use in observational cohorts complicates attribution of harms to a single agent.[2]
- Renewed clinical-trial activity for psilocybin-assisted therapy is supervised and controlled; data do not generalize to unsupervised recreational use.[5]
Specific populations require tailored evaluation and harm reduction.
Adolescents
- Earlier first use is associated with higher rates of subsequent substance use disorder and psychopathology; assess academic, family, and developmental impact.[2]
- Confidentiality limits and parental involvement vary by jurisdiction; clarify at the start of evaluation.[9]
Geriatric
- Hallucinogen use is uncommon in older adults but rising in some cohorts; differential includes delirium, with visual hallucinations, and Parkinson disease psychosis.[3]
- Cardiovascular comorbidity raises the risk of acute autonomic complications.[3]
Perinatal
- Data on hallucinogen exposure in pregnancy are limited; advise abstinence and screen for polysubstance use.[9]
- Benzodiazepines for acute intoxication during pregnancy are used cautiously, weighing neonatal sedation and withdrawal risks.[9]
Comorbid psychiatric illness
- Pre-existing schizophrenia spectrum, bipolar, and severe personality disorders increase the risk of acute and persistent adverse psychiatric outcomes; counsel against use.[6-7]
- PTSD frequently co-occurs and influences treatment planning; trauma-focused therapy and standard pharmacotherapy are recommended.[9]
Cultural considerations
- Ceremonial and religious use of peyote (mescaline) and ayahuasca (DMT-containing brews) occurs in defined cultural contexts and should be assessed with cultural humility before pathologizing.[6]
Most hallucinogen exposures end without sequelae. A small subset develop persistent disorders.
Acute episode
- Resolution typically within 12-24 hours for classic hallucinogens; longer for phencyclidine, where symptoms can persist for several days.[3-4]
Persistent disorders
- HPPD prevalence is uncertain; survey data suggest that a minority of hallucinogen users report some persistent perceptual phenomena, though clinically significant cases are less common.[7]
- Hallucinogen-induced psychosis can persist for weeks to months and may unmask a primary psychotic disorder in vulnerable individuals.[6-7]
Use disorder trajectory
Acute hallucinogen presentations in the emergency setting require rapid medical stabilization and risk assessment.
Hospitalization criteria
- Severe agitation or violence not controlled with outpatient or emergency department measures.[3]
- Hyperthermia, rhabdomyolysis, or hemodynamic instability.[3]
- Persistent psychosis or suicidal ideation beyond resolution of acute intoxication.[3,9]
- Inability to maintain safety due to ongoing perceptual disturbance or impaired judgment.[3]
Acute management priorities
- Calm, low-stimulus environment, with continuous monitoring of vital signs.[3]
- Benzodiazepines first-line for agitation, with antipsychotic adjuncts reserved for unresponsive cases.[3,9]
- Aggressive cooling, hydration, and electrolyte management for hyperthermia and rhabdomyolysis.[3]
- Reassessment for co-ingestants and medical complications throughout the course.[3]
Do not rely on routine urine drug screens to exclude hallucinogen use; act on clinical assessment.[3]
Several clinical and regulatory questions remain unresolved.
- Whether classic psychedelics warrant a diagnostic category distinct from other hallucinogens, given their low addiction liability and emerging therapeutic indications, remains debated.[5-6]
- The boundary between persisting perceptual phenomena and HPPD as a discrete disorder is not well operationalized, contributing to wide prevalence estimates.[7]
- Evidence-based pharmacotherapy for HPPD remains undefined; common approaches rest on case series rather than controlled trials.[7]
- Psilocybin and MDMA have received expedited regulatory designations from the U.S. FDA for selected investigational indications, but supervised therapeutic use is distinct from recreational use; conflating the two risks confusing patients.[5]
- The risk of unmasking persistent psychosis in genetically vulnerable individuals is recognized but poorly quantified.[6-7]
- Regulatory status varies substantially across jurisdictions, with implications for clinical disclosure and harm reduction counseling.[5]
- Classic hallucinogens (LSD, psilocybin, mescaline, DMT) act primarily as 5-HT2A receptor partial agonists.[3-4]
- Phencyclidine and ketamine act as non-competitive NMDA receptor antagonists.[3-4]
- Vertical or rotary nystagmus is a near-pathognomonic finding for phencyclidine intoxication.[3]
- Mydriasis is characteristic of classic hallucinogen intoxication, in contrast to opioid-induced miosis.[3]
- DSM-5-TR does NOT include a withdrawal criterion for hallucinogen use disorder or phencyclidine use disorder.[6]
- HPPD requires re-experiencing perceptual symptoms after cessation, with preserved reality testing.[6-7]
- Routine urine drug screens do NOT detect LSD, psilocybin, DMT, or mescaline; phencyclidine is detected on most panels.[3]
- First-line management of severe agitation during hallucinogen intoxication is a benzodiazepine.[3,9]
- Classic hallucinogens have low mesolimbic dopamine activation, accounting for low addiction liability.[3-4]
- Psilocybin acutely reduces default mode network activity, correlating with ego-dissolution experiences.[5]
- Phencyclidine intoxication can produce hyperthermia, rhabdomyolysis, and an excited-delirium-like presentation.[3]
- Hallucinogen use disorder severity is graded as mild (2-3 criteria), moderate (4-5), or severe (6 or more), per DSM-5-TR.[6]
- Anti-NMDA receptor encephalitis can mimic both phencyclidine intoxication and primary psychosis and warrants consideration in atypical presentations.[3]
- Ceremonial peyote and ayahuasca use occurs in defined cultural contexts and is assessed with cultural humility before pathologizing.[6]
No external funding. No conflicts of interest declared. Peer-review status: pending.
- 1.Substance Abuse and Mental Health Services Administration. Key Substance Use and Mental Health Indicators in the United States: Results from the National Survey on Drug Use and Health. Rockville, MD: Center for Behavioral Health Statistics and Quality, SAMHSA; 2023.
- 2.Shalit N, Rehm J, Lev-Ran S. Epidemiology of hallucinogen use in the U.S. results from the National Epidemiologic Survey on Alcohol and Related Conditions III. Addict Behav. 2019;89:35-43.
- 3.TextbookSadock BJ, Sadock VA, Ruiz P. Kaplan & Sadock's Synopsis of Psychiatry. 12th ed. Philadelphia: Wolters Kluwer; 2022.
- 4.TextbookStahl SM. Stahl's Essential Psychopharmacology: Neuroscientific Basis and Practical Applications. 5th ed. Cambridge: Cambridge University Press; 2021.
- 5.Nichols DE. Psychedelics. Pharmacol Rev. 2016;68(2):264-355.
- 6.TextbookAmerican Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed, text rev. Washington, DC: American Psychiatric Association Publishing; 2022.
- 7.Halpern JH, Pope HG. Hallucinogen persisting perception disorder: what do we know after 50 years? Drug Alcohol Depend. 2003;69(2):109-119.
- 8.TextbookWorld Health Organization. International Classification of Diseases, Eleventh Revision (ICD-11). Geneva: WHO; 2019.
- 9.TextbookGalanter M, Kleber HD, Brady KT, editors. The American Psychiatric Association Publishing Textbook of Substance Use Disorder Treatment. 5th ed. Washington, DC: American Psychiatric Association Publishing; 2015.
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