6.1 Substance-Related and Addictive Disorders

6.1 Substance-Related and Addictive Disorders

Quick Answer: The DSM-5-TR establishes a unified, single-continuum diagnosis of Substance Use Disorder (SUD), eliminating the previous DSM-IV distinction between substance abuse and substance dependence. SUD diagnosis relies on 11 distinct criteria organized into four functional groupings: impaired control (criteria 1–4), social impairment (criteria 5–7), risky use (criteria 8–9), and pharmacological indicators (criteria 10–11: tolerance and withdrawal). Severity is classified across a 12-month timeframe as mild (2–3 criteria), moderate (4–5 criteria), or severe (6 or more criteria). Importantly, tolerance and withdrawal do not count toward an SUD diagnosis when prescribed medications are taken strictly under legitimate medical supervision. Withdrawal from alcohol and sedative-hypnotics carries severe medical lethality (delirium tremens, tonic-clonic seizures), whereas opioid withdrawal, while excruciating, is rarely directly fatal in healthy adults. Gambling Disorder is the sole recognized non-substance behavioral addiction in the DSM-5-TR.

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DSM-5-TR Substance Use Disorder Diagnostic Framework

Historically, the Diagnostic and Statistical Manual of Mental Disorders divided addiction into two hierarchical categories: Substance Abuse (characterized primarily by psychosocial and legal consequences) and Substance Dependence (defined largely by physiological adaptation, tolerance, and compulsive use). The DSM-5 and DSM-5-TR discarded this dichotomous framework in favor of a single, dimensional diagnostic entity: Substance Use Disorder (SUD). This shift recognized that substance problems exist along an empirical severity gradient rather than across categorical boundaries.

The 11 Criteria Across Four Core Domains

To meet the diagnostic threshold for a Substance Use Disorder, a client must exhibit a problematic pattern of substance use leading to clinically significant impairment or distress, manifested by at least 2 of the following 11 criteria occurring within a 12-month period:

Domain 1: Impaired Control (Criteria 1–4)

1. Larger Amounts / Longer Duration: The substance is often taken in larger amounts or over a longer period than was initially intended (loss of behavioral control).
2. Unsuccessful Cut-Down Efforts: There is a persistent desire or unsuccessful efforts to cut down, regulate, or control substance use.
3. Excessive Time Spent: A great deal of time is spent in activities necessary to obtain the substance (e.g., visiting multiple doctors, driving long distances), use the substance, or recover from its physiological effects.
4. Craving: Craving, or a strong, overpowering desire or urge to use the substance. (Craving was introduced in DSM-5, replacing the DSM-IV recurrent legal problems criterion, reflecting neurobiological research on conditioned cue-reactivity in the ventral striatum and insular cortex).

Domain 2: Social Impairment (Criteria 5–7)

1. Role Failure: Recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences, poor academic performance, neglect of children).
2. Interpersonal Problems: Continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance (e.g., marital conflict, physical altercations).
3. Activities Given Up: Important social, occupational, or recreational activities are given up or substantially reduced because of substance use (e.g., abandoning hobbies, withdrawing from family gatherings to use).

Domain 3: Risky Use (Criteria 8–9)

1. Physically Hazardous Use: Recurrent substance use in situations in which it is physically hazardous (e.g., driving while intoxicated, operating machinery, swimming under the influence).
2. Use Despite Harm: Substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance (e.g., continued drinking despite a diagnosed bleeding peptic ulcer or alcohol-induced hepatic cirrhosis; continued cocaine use despite severe stimulant-induced depression).

Domain 4: Pharmacological Criteria (Criteria 10–11)

1. Tolerance: Defined by either of the following:
   • A need for markedly increased amounts of the substance to achieve intoxication or desired effect.
   • A markedly diminished effect with continued use of the same amount of the substance.
2. Withdrawal: Manifested by either of the following:
   • The characteristic physiological withdrawal syndrome for the specific substance.
   • The substance (or a closely related substance, such as a benzodiazepine for alcohol) is taken to relieve or avoid withdrawal symptoms.

The Medical Supervision Exception (High-Frequency Exam Trap)

[!IMPORTANT] A foundational rule tested repeatedly on the NCE: Tolerance and withdrawal criteria are NOT counted toward the diagnosis of a Substance Use Disorder when the medication is prescribed and taken strictly under appropriate medical supervision.

For example, a cancer patient receiving high-dose oral morphine under palliative oncological care, or a client with generalized anxiety disorder taking clonazepam exactly as directed by a psychiatrist, will naturally develop physiological tolerance and will experience acute withdrawal if the medication is abruptly stopped. These physiological neuroadaptations represent normal, expected pharmacological responses—not addiction. If such patients exhibit no signs of impaired control, cravings, risky use, or social dysfunction, they do not meet criteria for an Opioid Use Disorder or Sedative Use Disorder. The clinician must explicitly exclude tolerance and withdrawal from the symptom tally when medical supervision is intact.

Severity Continuum and Course Specifiers

The DSM-5-TR stratifies Substance Use Disorder into three distinct levels of clinical acuity based on the cumulative count of criteria met within the preceding 12 months:

• Mild: 2 to 3 criteria present.
• Moderate: 4 to 5 criteria present.
• Severe: 6 or more criteria present.

Additionally, clinicians apply specific diagnostic specifiers to describe the longitudinal trajectory of recovery:

• In Early Remission: Applied when none of the criteria for Substance Use Disorder have been met for at least 3 months but for less than 12 months (with the sole exception that Criterion 4, Craving, may still be present).
• In Sustained Remission: Applied when none of the criteria have been met at any time during a period of 12 months or longer (again, Craving may persist without breaking sustained remission).
• On Maintenance Therapy: Applied if the individual is taking an approved agonist, partial agonist, or antagonist medication (e.g., methadone or buprenorphine for opioid use disorder; nicotine replacement therapy) and meets no other criteria for that substance class.
• In a Controlled Environment: Applied when the individual is living in an environment where access to the substance is strictly restricted or prohibited (e.g., locked inpatient rehabilitation facility, psychiatric hospital, therapeutic community, correctional facility).

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Diagnostic Framework Comparison Table

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Clinical Profiles of Major Substance Classes

Professional counselors must master the specific intoxication signs, withdrawal presentations, neurobiological mechanisms, and medical emergencies associated with each major substance class.

1. Alcohol (Central Nervous System Depressant)

Alcohol (ethanol) enhances inhibitory gamma-aminobutyric acid (GABA-A) receptor neurotransmission while simultaneously inhibiting excitatory N-methyl-D-aspartate (NMDA) glutamate receptors, leading to widespread central nervous system depression.

Intoxication Presentation

Clinically significant maladaptive behavioral or psychological changes (e.g., inappropriate sexual or aggressive behavior, mood lability, impaired judgment) accompanied by: slurred speech, incoordination, unsteady gait, nystagmus (involuntary rhythmic oscillation of the eyes), impairment in attention or memory, and stupor or coma.

Withdrawal Syndrome and Medical Lethality

Alcohol withdrawal begins within 6 to 24 hours following cessation or marked reduction in heavy, prolonged intake. Symptoms include:

• Autonomic hyperactivity (sweating, resting pulse > 100 bpm, hypertension)
• Coarse hand tremor ("the shakes")
• Insomnia and vivid psychomotor nightmares
• Nausea, retching, and vomiting
• Transient visual, tactile, or auditory hallucinations or illusions
• Psychomotor agitation and rebound anxiety
• Generalized tonic-clonic seizures (typically occurring within 12 to 48 hours post-cessation)

[!CAUTION] Delirium Tremens (DTs): DTs is an acute, life-threatening medical emergency occurring in approximately 5% of individuals experiencing severe alcohol withdrawal, typically developing 48 to 96 hours after the last drink. DTs is characterized by profound clouding of consciousness, disorientation, severe autonomic storm (fever, diaphoresis, tachycardia, severe hypertension), and terrifying visual or tactile hallucinations (e.g., insects or small animals crawling on the skin). Without immediate medical intervention (intravenous benzodiazepines, supportive hydration, hemodynamic stabilization), the mortality rate of DTs can reach 15% to 20%.

Neurocognitive Complications: Wernicke-Korsakoff Syndrome

Chronic alcohol dependence frequently results in severe nutritional malnutrition, specifically malabsorption and depletion of thiamine (Vitamin B1). Thiamine deficiency impairs cerebral glucose metabolism, leading to focal neurodegeneration in the mammillary bodies, thalamus, and periaqueductal gray matter:

• Wernicke's Encephalopathy: The acute, reversible neuro-psychiatric phase characterized by a classic clinical triad: (1) acute mental confusion/encephalopathy, (2) ataxia (gait instability), and (3) ophthalmoplegia/nystagmus (abnormal eye movements and cranial nerve VI palsies). It is an acute medical emergency requiring immediate high-potency parenteral thiamine administration. Clinical Rule: Always administer thiamine before intravenous glucose; infusing glucose into a thiamine-deficient client precipitates acute, fatal Wernicke's encephalopathy.
• Korsakoff's Psychosis (Amnestic Syndrome): The chronic, largely irreversible neurocognitive condition that develops when Wernicke's encephalopathy goes untreated. Korsakoff's syndrome is characterized by dense anterograde amnesia (inability to form new memories), retrograde amnesia, and confabulation—the spontaneous fabrication of elaborate, plausible memories without conscious intent to deceive, generated to compensate for cognitive memory voids. Clients remain alert and maintain basic social conversation but have zero retention of recent events.

2. Opioids (Heroin, Fentanyl, Morphine, Oxycodone, Hydrocodone, Methadone)

Opioids bind to endogenous mu-opioid receptors in the brain, spinal cord, and gastrointestinal tract, producing profound analgesia, euphoria, and sedation.

Intoxication and the Overdose Triad

Intoxication features initial euphoria followed by apathy, dysphoria, psychomotor retardation, drowsiness ("on the nod"), slurred speech, and impaired attention. The pathognomonic physical sign is pupillary constriction (miosis / "pinpoint pupils"); however, severe pupillary dilation (mydriasis) can occur secondary to profound terminal anoxia in end-stage overdose.

[!IMPORTANT] The Opioid Overdose Triad:

1. Pinpoint Pupils (Miosis)
2. Respiratory Depression (shallow, irregular breathing, cyanosis, respiratory rate < 8–10 breaths per minute)
3. Unconsciousness / Stupor / Coma Severe respiratory depression is the definitive cause of death in opioid overdose.

Emergency Reversal: Naloxone (Narcan)

Naloxone is a pure, high-affinity competitive mu-opioid receptor antagonist. When administered intravenously, intramuscularly, or intranasally, it rapidly displaces opioid molecules from receptor sites, completely reversing respiratory depression and restoring consciousness within 2 to 3 minutes. Because synthetic opioids like fentanyl have extreme lipid solubility and long-acting opioids like methadone have prolonged elimination half-lives, naloxone's short half-life (30–90 minutes) means that the client may relapse into lethal respiratory depression once naloxone clears. Continuous monitoring and repeated naloxone doses are frequently mandatory.

Opioid Withdrawal Presentation

Opioid withdrawal begins within 6 to 12 hours for short-acting agents (heroin, oxycodone) or 24 to 48 hours for long-acting agents (methadone). Symptoms include dysphoric mood, intense nausea and vomiting, muscle cramping, bone aches, lacrimation (tearing eyes), rhinorrhea (runny nose), pupillary dilation (mydriasis), piloerection (goosebumps—the linguistic origin of the phrase "cold turkey"), sweating, diarrhea, yawning, fever, and severe insomnia. Involuntary muscle twitching and leg spasms give rise to the colloquial phrase "kicking the habit." While intensely agonizing and emotionally traumatic, opioid withdrawal in otherwise healthy adults does not cause hyperthermic autonomic storm or status epilepticus, making it rarely directly fatal (unlike alcohol and benzodiazepine withdrawal).

Medication-Assisted Treatment (MAT) for Opioid Use Disorder

MAT combines pharmacotherapy with behavioral counseling, representing the evidence-based gold standard for opioid treatment:

• Methadone: A synthetic, long-acting full mu-opioid agonist with an elimination half-life of 24–36 hours. It suppresses withdrawal symptoms and drug craving while blocking the euphoric effects of other opioids through cross-tolerance. Under federal law (42 CFR Part 8), methadone for addiction can only be dispensed through accredited Opioid Treatment Programs (OTPs / methadone clinics).
• Buprenorphine: A high-affinity partial mu-opioid agonist and kappa-opioid antagonist with a plateau ("ceiling effect") on respiratory depression, substantially reducing overdose mortality risk compared to full agonists. Buprenorphine can be prescribed in general office-based clinical practices. It is commonly formulated with naloxone (Suboxone, 4:1 ratio). When taken sublingually as prescribed, the naloxone is unabsorbed due to poor bioavailability; however, if the tablet or film is crushed and injected intravenously, the naloxone immediately blocks receptors and precipitates agonizing acute withdrawal, acting as an abuse deterrent.
• Naltrexone: A pure opioid receptor antagonist that completely blocks the subjective and physiological effects of exogenous opioids. Available as a daily oral tablet or a monthly extended-release intramuscular injection (Vivitrol). Crucially, a client must be entirely opioid-free for at least 7 to 10 days prior to initiating naltrexone; administering naltrexone while opioids are active in the body triggers violent, precipitated withdrawal.

3. Sedatives, Hypnotics, and Anxiolytics (Benzodiazepines & Barbiturates)

This class includes benzodiazepines (alprazolam, diazepam, lorazepam, clonazepam) and barbiturates (phenobarbital, secobarbital). Like alcohol, these agents bind to the GABA-A receptor complex, potentiating inhibitory neurotransmission.

Intoxication

Slurred speech, incoordination, ataxia, impaired cognition, anterograde amnesia, emotional disinhibition, and stupor. Combining benzodiazepines with alcohol or opioids produces synergistic respiratory depression, representing a leading cause of accidental polysubstance overdose fatalities.

Withdrawal and Medical Risks

Sedative-hypnotic withdrawal resembles alcohol withdrawal: severe rebound anxiety, autonomic instability (tachycardia, hypertension, diaphoresis), fine tremors, sensory hypersensitivity, photophobia, delirium, and life-threatening grand mal seizures. Abrupt cessation of high-dose benzodiazepines can be fatal. Detoxification mandates a gradual, medically monitored taper utilizing a long-acting substitute (e.g., diazepam or chlordiazepoxide) titrated downward over weeks or months.

4. Stimulants (Cocaine & Amphetamines)

Stimulants—including cocaine, crack, methamphetamine, prescription amphetamines (Adderall, Dexedrine), and methylphenidate (Ritalin)—block the reuptake and stimulate the massive release of monoamine neurotransmitters (dopamine, norepinephrine, serotonin) in the central and sympathetic nervous systems.

Intoxication Signs

Tachycardia or bradycardia, pupillary dilation (mydriasis), elevated blood pressure, perspiration or chills, nausea or vomiting, evidence of weight loss, psychomotor agitation, muscular weakness, cardiac arrhythmias, chest pain, and confusion. Psychological signs include euphoria, hypervigilance, grandiosity, extreme talkativeness, and paranoia.

• Stimulant-Induced Psychotic Disorder: High-dose or chronic stimulant use frequently precipitates transient paranoia, persecutory delusions, and auditory hallucinations. Clients may experience formication (tactile hallucinations of bugs or insects crawling under or on their skin, colloquially called "coke bugs" or "meth mites"), leading to compulsive skin-picking, severe excoriations, and chronic ulcerations.

Withdrawal Presentation ("The Crash")

Stimulant withdrawal is primarily psychological and affective rather than somatic. When stimulants are discontinued, depleted dopamine reserves result in "the crash": profound dysphoric mood, extreme physical exhaustion and fatigue, vivid and terrifying nightmares, insomnia or hypersomnia, increased appetite (hyperphagia), and marked psychomotor retardation. Intense psychological cravings and severe, acute depressive episodes with elevated suicide risk represent the primary clinical danger during acute stimulant withdrawal.

5. Cannabis

Cannabis acts on cannabinoid (CB1 and CB2) receptors throughout the central nervous system and immune system.

Intoxication

Marked by behavioral changes (impaired motor coordination, euphoria, anxiety, sensation of slowed time, impaired judgment, social withdrawal) and objective physical signs:

• Conjunctival injection (prominent scleral vascular dilation / bloodshot eyes)
• Increased appetite (colloquially termed "the munchies")
• Dry mouth (xerostomia)
• Tachycardia (mild resting elevation in heart rate)

Cannabis Withdrawal Syndrome (Added in DSM-5)

Withdrawal occurs upon cessation of heavy, daily use, manifested by at least 3 symptoms developing within one week: irritability/anger/aggression, nervousness/anxiety, sleep difficulty (insomnia, vivid disturbing dreams), decreased appetite or weight loss, restlessness, depressed mood, and at least one physical symptom causing significant discomfort (abdominal pain, shakiness/tremors, sweating, fever, chills, or headache).

6. Hallucinogens and Phencyclidine (PCP)

Phencyclidine (PCP) and Dissociative Anesthetics

PCP (and ketamine) acts as an antagonist at NMDA glutamate receptors. Intoxication presents with a unique, dangerous clinical picture: belligerence, impulsivity, unpredictability, psychomotor agitation, and profound analgesia (loss of pain sensitivity), leading individuals to fight through restraint or sustain catastrophic injuries without distress. The classic, pathognomonic physical sign of PCP intoxication is nystagmus (specifically vertical or rotary nystagmus), accompanied by hypertension, tachycardia, numbness, ataxia, dysarthria, and muscle rigidity.

Classic Hallucinogens (LSD, Psilocybin, Mescaline, MDMA)

These substances act primarily as agonists at 5-HT2A serotonin receptors. Intoxication induces marked perceptual alterations (depersonalization, derealization, illusions, perceptual intensification), synesthesia (the blending of sensory modalities, such as "seeing sounds" or "hearing colors"), pupillary dilation, tachycardia, sweating, palpitations, and tremors. Acute adverse reactions ("bad trips") involve terrifying panic, paranoid delusions, and fears of going permanently insane.

Hallucinogen Persisting Perception Disorder (HPPD)

Following cessation of hallucinogen use, the individual re-experiences one or more of the perceptual symptoms that were experienced while intoxicated with the hallucinogen (e.g., geometric hallucinations, false perceptions of movement in the peripheral fields, flashes of color, intensified colors, trails of images behind moving objects, macropsia, micropsia). These "flashbacks" cause clinically significant distress and can persist intermittently for months or years.

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Summary of Substance Classes and Clinical Characteristics

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Non-Substance-Related Behavioral Addictions: Gambling Disorder

In the DSM-5 and DSM-5-TR, Gambling Disorder was officially relocated from the Impulse-Control Disorders Not Elsewhere Classified chapter to the Substance-Related and Addictive Disorders chapter. Empirical neuroimaging research revealed that pathological gambling activates the exact same dopaminergic reward pathways (ventral tegmental area and nucleus accumbens) and exhibits the identical behavioral phenomena of tolerance, withdrawal-like irritability, craving, and impaired executive prefrontal inhibition as substance use disorders.

Diagnostic Criteria for Gambling Disorder

A client must display persistent and recurrent problematic gambling behavior leading to clinically significant impairment or distress, exhibiting at least 4 of the following 9 criteria in a 12-month period:

1. Needs to gamble with increasing amounts of money in order to achieve the desired excitement (equivalent to pharmacological tolerance).
2. Is restless or irritable when attempting to cut down or stop gambling (equivalent to pharmacological withdrawal).
3. Has made repeated unsuccessful efforts to control, cut back, or stop gambling (impaired control).
4. Is often preoccupied with gambling (e.g., having persistent thoughts of reliving past gambling experiences, handicapping or planning the next venture, thinking of ways to get money with which to gamble).
5. Often gambles when feeling distressed (e.g., helpless, guilty, anxious, depressed; negative reinforcement / self-medication).
6. After losing money gambling, often returns another day to get even ("chasing" one's losses). This is the hallmark, quintessential cognitive feature of disordered gambling.
7. Lies to conceal the extent of involvement with gambling (deception of family, therapists, or employers).
8. Has jeopardized or lost a significant relationship, job, or educational/career opportunity because of gambling (severe psychosocial role impairment).
9. Relies on others to provide money to relieve desperate financial situations caused by gambling (a "bailout").

Differential Diagnosis and Exclusions

• Manic Episode: The gambling behavior must not be better explained by a Manic Episode. During mania or hypomania, an individual may engage in reckless, grandiose financial spending and high-stakes gambling; if the gambling occurs exclusively during manic mood episodes, the correct diagnosis is Bipolar I Disorder, not Gambling Disorder.
• Social / Recreational Gambling: Involves gambling with friends, setting strict personal spending limits, accepting losses as the acceptable cost of entertainment, and stopping when losses reach pre-set thresholds. There is no compulsive "chasing" of losses, loss of control, or deceptive concealment.
• Professional Gambling: Characterized by calculated, discipline-bound risk assessment, emotional detachment, and systematic financial management. Losses are absorbed as normal business overhead rather than pursued through impulsive chasing.

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Co-Occurring Disorders (Dual Diagnosis) & Integrated Treatment Models

A co-occurring disorder (historically termed dual diagnosis or comorbidity) refers to the concurrent presence of at least one independent Substance Use Disorder and at least one independent psychiatric disorder (e.g., Major Depressive Disorder, Bipolar Disorder, Schizophrenia, Borderline Personality Disorder, PTSD). Epidemiological data consistently reveal that over 50% of individuals with severe mental illness experience a co-occurring substance disorder during their lifetime, and over 40% of individuals seeking addiction treatment meet criteria for a co-occurring affective or anxiety disorder.

Historical vs. Modern Service Delivery Models

1. Sequential Treatment Model (Historical / Ineffective): The client is required to receive treatment for one disorder before receiving care for the other. Typically, addiction agencies demanded "clean time" (e.g., 30–90 days of sobriety) before initiating psychiatric care, while psychiatric clinics refused psychotherapy until the substance problem was resolved. This resulted in extreme client drop-out, circular blame, untreated suffering, and high mortality.
2. Parallel Treatment Model (Fragmented): The client receives mental health treatment from one clinician/agency and substance abuse treatment from a separate clinician/agency simultaneously. The two systems frequently operated under conflicting treatment philosophies (e.g., an abstinence-focused 12-step counselor telling a client that psychotropic antidepressant medication is a "chemical crutch," while a psychiatrist ignored ongoing substance use), placing the burden of integration entirely on the client.
3. Integrated Treatment Model (Evidence-Based Gold Standard): Both the psychiatric condition and the substance use disorder are treated simultaneously by the same clinician or the same multidisciplinary clinical team within a single, unified treatment plan. Integrated treatment provides a shared conceptual framework, continuous cross-training, harmonized treatment goals, and coordinated psychopharmacological and psychosocial interventions.

The SAMHSA Four Quadrants of Care

The Substance Abuse and Mental Health Services Administration (SAMHSA) conceptualizes co-occurring disorders across four quadrants based on illness severity, guiding appropriate service allocation:

• Quadrant I (Low MH / Low SUD): Served primarily in primary care settings and general outpatient behavioral health clinics.
• Quadrant II (High MH / Low SUD): Served primarily within the mental health delivery system, with embedded addiction consultation.
• Quadrant III (Low MH / High SUD): Served primarily within the substance abuse treatment system, with embedded psychiatric consultation.
• Quadrant IV (High MH / High SUD): Requires specialized, highly intensive integrated dual diagnosis treatment programs, such as Assertive Community Treatment (ACT) teams, dual-diagnosis residential units, or combined psychiatric-addiction intensive outpatient programs (IOP).

Core Principles of Integrated Treatment

• Staged Interventions: Clinical strategies are tailored to the client's specific stage of readiness for change for each disorder independently (e.g., a client may be in the Action stage for depression but in Precontemplation for alcohol use).
• Assertive Outreach and Engagement: Proactive case management, motivational interviewing, and community-based support to sustain treatment engagement.
• Harm Reduction: Acknowledging incremental behavioral gains, risk reduction, and safety enhancement rather than requiring rigid, absolute sobriety as a condition for receiving mental health care.
• Longitudinal Perspective: Recognizing that co-occurring disorders are chronic, relapsing conditions requiring long-term, continuous, phase-based supportive care.

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On the NCE Exam: Key Tips and Traps

• The Prescribed Medication Exception: If a vignette describes a client with chronic spinal pain taking prescribed oxycodone who experiences withdrawal when missing a dose and requires escalating doses due to tolerance, but takes the medication exactly as directed without cravings, social impairment, or risky behaviors, the correct answer is No Substance Use Disorder.
• Withdrawal Lethality: If asked which substance withdrawal presentations carry direct medical mortality risks, select alcohol and sedatives/hypnotics/benzodiazepines (due to status epilepticus and DTs). Do not select opioids, cannabis, or stimulants.
• Overdose Triad Identification: Respiratory depression + pinpoint pupils (miosis) + unresponsiveness = opioid toxicity requiring naloxone.
• Gambling Hallmark: The single most distinctive cognitive hallmark of Gambling Disorder tested on the NCE is "chasing losses" (returning another day to recoup lost funds).