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KembaraXtra-Medicine – Amphetamine Use Disorder
Amphetamine use disorder is a pattern of amphetamine use marked by impairment in control of use or social obligations, risky use, or physical dependence within a 12-month period. Severity is categorized as mild, moderate, or severe based on the number of symptoms. Amphetamines are central nervous system stimulants that increase monoamine neurotransmitters (dopamine, norepinephrine, serotonin) and are defined by a phenylethylamine structure. Amphetamine and dextroamphetamine are FDA approved for AD/HD, narcolepsy, and obesity. Methamphetamine is a type of amphetamine that is FDA approved for AD/HD and obesity, but is more commonly illicitly produced and used recreationally. Synonyms include stimulant use disorder and methamphetamine use disorder. ICD-10CM codes include F15.10 (mild), F15.20 (moderate or severe), F15.11 (mild, in early or sustained remission), and F15.21 (moderate or severe, in early or sustained remission).
Epidemiologically, prevalence is described as rare: 0.6% among people ages ≥12 years (about 1.5 million) with methamphetamine use disorder, and 0.3% among people ≥12 years (about 758,000) with prescription stimulant use disorder. Among adults who used methamphetamine in the past year, 53% met criteria for methamphetamine use disorder. Methamphetamine use disorder is more common among those age 26 and older (0.6%) than under age 25, while prescription stimulant use disorder is more common between ages 12 and 25 compared with ≥26.
Risk increases in people with any substance use disorder. Among psychiatric comorbidities, bipolar disorder, schizophrenia, and antisocial personality disorder are associated with stimulant use disorder. Demographic risk factors for methamphetamine use include male sex, lower educational attainment, and non-Hispanic White ethnicity. Methamphetamine use is higher among men who have sex with men, including in “chemsex,” where methamphetamine and other stimulants are used to increase arousal and reduce inhibition during sexual sessions.
Clinically, amphetamine use disorder can develop as quickly as within 1 week of exposure, and most people experience physical dependence in the form of tolerance or withdrawal. Amphetamines may be used by oral ingestion, insufflation, injection, or smoking, and use is often described as chronic or episodic binges. During intoxication, patients may report euphoria and may present with hyperarousal, aggressive behavior, psychosis (paranoia and hallucinations), panic attacks, or suicidal and homicidal ideation. With toxicity, sympathomimetic signs such as hypertension, tachycardia, dilated pupils, and flushed skin can occur. Some intoxicated patients report chest pain, and amphetamine use increases risk of myocardial infarction, arrhythmias, and strokes. During withdrawal, patients commonly report depressive symptoms. Risk for psychosis increases with higher frequency and amount of use, and psychosis can occur within months to several years after starting amphetamine use.
The exact cause of amphetamine use disorder is not known, but amphetamine-type medications act on the dopamine and monoamine transporter (DAT and VMAT2), increasing dopamine transmission in the mesolimbic dopamine pathway (the reward pathway).
In diagnosis, amphetamine use disorder is different from amphetamine misuse, which refers to use inconsistent with prescription guidelines. Patients using PCP or novel psychoactive substances (such as cathinones/bath salts) may present similarly and can be distinguished with a toxicology test. Primary psychiatric disorders (e.g., schizophrenia) or depressive disorders (e.g., major depressive disorder) can be evaluated by establishing a timeline of symptoms relative to amphetamine use; psychosis that quickly improves is more consistent with amphetamine-induced psychosis.
Work-up may be difficult because detailed history can be hard to obtain during acute intoxication or withdrawal. An ECG should be performed in patients with tachycardia. A safety assessment is essential to determine whether the patient can safely care for themselves, especially when suicidal or homicidal ideation is reported. Recommended labs include basic testing such as Chem 7, serum lactate, creatine phosphokinase, thyroid function tests, and hepatic enzymes. A urine or serum toxicology test can confirm amphetamine presence. There are no radiographic tests for diagnosis of stimulant use disorder, but CT imaging may be considered for strokes or vasculopathies associated with amphetamine use.
Treatment is primarily nonpharmacologic, with behavioral interventions as the mainstay. Approaches such as contingency management, cognitive-behavioral therapy, behavioral activation, and exercise have shown mild effectiveness in reducing symptoms and sustaining abstinence. Contingency management, especially when combined with community reinforcement (reorganizing the environment so abstinence is more rewarding than drug use), has been particularly shown to be effective.
For acute general management, antipsychotics—especially olanzapine and haloperidol—have evidence for treating amphetamine-associated psychosis. No medication has been shown to be effective for amphetamine withdrawal. There is limited evidence that amineptine (a tricyclic antidepressant no longer available due to abuse potential) reduced discontinuation symptoms and improved clinical presentation, and there is mixed evidence that mirtazapine may reduce anxiety symptoms during withdrawal.
For chronic management, there is no evidence that pharmacologic treatment alone is sufficient. Randomized controlled trials show limited benefit from methylphenidate, bupropion, modafinil, and naltrexone in reducing amphetamine use.
Disposition-wise, methamphetamine use disorder often follows a course of intense use, sobriety, and relapse. Complications of amphetamine intoxication (including ecstasy) include hyponatremia due to SIADH (very rare; managed with water restriction), intracerebral hemorrhage (uncommon; CT/MRI if focal signs or reduced GCS), serotonin toxicity (uncommon; supportive care and cyproheptadine for serious cases), hypertension (uncommon; GTN infusion, benzodiazepines, labetalol; avoid beta-blockers), hyperthermia (common; cooling measures, diazepam, cyproheptadine), rhabdomyolysis (uncommon; IV fluids and cooling), supraventricular and ventricular tachycardia (uncommon; short-acting antiarrhythmics such as esmolol for SVT), and seizures (uncommon; IV diazepam).
Referral is typically to physicians and mental health professionals. Important pearls include that stimulant use disorders often co-occur with sedative substance use disorders (e.g., alcohol, marijuana, opioids) because these may relieve stimulant side effects such as insomnia and anxiety. Amphetamine use is also associated with an increased risk of death by suicide, so assessing suicidality is critical in any patient presenting with amphetamine use.
For prevention, community-based universal prevention programs that promote youth social-emotional skills and reduce risk factors have been shown to lead to sustained reductions in lifetime methamphetamine use.
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