甲基苯丙胺可用在非醫療用途上，會被非法交易販售。甲基苯丙胺的非法使用在亞洲部分地區、大洋洲和美國最為普遍。在美國，消旋甲基苯丙胺、左旋及右旋甲基苯丙胺均為第二類管制藥品（英語：list of Schedule II drugs (US)）。左旋甲基苯丙胺的吸入型鼻塞緩解劑（英語：nasal decongestant）是美國的非處方藥，因此能直接在市面上購買[note 2]。在國際上，甲基安非他命名列《精神藥物公約》中的第二級分類表（schedule II），因此在從事甲基安非他命的生產、散播、銷售和加工等活動都被許多國家嚴格管制或禁止。右旋安非他命（Dextromethamphetamine）的藥效比甲基苯丙胺更加強烈，但因為甲基苯丙胺的化學合成難度較低，其前體較容易取得，因此比較容易非法製造生產甲基苯丙胺。
Synonyms and alternate spellings include: metamfetamine (International Nonproprietary Name (INN)), N-methylamphetamine, desoxyephedrine, Syndrox, Methedrine, and Desoxyn.[10][11][12] Common slang terms for methamphetamine include: speed, meth, crystal, crystal meth, glass, shards, ice, and tic[13] and, in New Zealand, "P".[14]
Lemke TL, Williams DA, Roche VF, Zito W. Foye's Principles of Medicinal Chemistry 7th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. 2013: 648. ISBN 1609133455. Alternatively, direct oxidation of amphetamine by DA β-hydroxylase can afford norephedrine. 引文格式1維護：冗餘文本 (link)
Code of Federal Regulations Title 21: Subchapter D – Drugs for human use. United States Food and Drug Administration. April 2015. （原始內容存檔於2015-09-18） 使用|archiveurl=需要含有|url= (幫助). Topical nasal decongestants --(i) For products containing levmetamfetamine identified in 341.20(b)(1) when used in an inhalant dosage form. The product delivers in each 800 milliliters of air 0.04 to 0.150 milligrams of levmetamfetamine.|section-url=被忽略 (幫助); |section=被忽略 (幫助); 使用|accessdate=需要含有|url= (幫助)
Malenka RC, Nestler EJ, Hyman SE. 15. Sydor A, Brown RY (編). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York: McGraw-Hill Medical. 2009: 370. ISBN 978-0-07-148127-4. Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons.
Krasnova IN, Cadet JL. Methamphetamine toxicity and messengers of death. Brain Res. Rev. May 2009, 60 (2): 379–407. PMC 2731235. PMID 19328213. doi:10.1016/j.brainresrev.2009.03.002. Neuroimaging studies have revealed that METH can indeed cause neurodegenerative changes in the brains of human addicts (Aron and Paulus, 2007; Chang et al., 2007). These abnormalities include persistent decreases in the levels of dopamine transporters (DAT) in the orbitofrontal cortex, dorsolateral prefrontal cortex, and the caudate-putamen (McCann et al., 1998, 2008; Sekine et al., 2003; Volkow et al., 2001a, 2001c). The density of serotonin transporters (5-HTT) is also decreased in the midbrain, caudate, putamen, hypothalamus, thalamus, the orbitofrontal, temporal, and cingulate cortices of METH-dependent individuals (Sekine et al., 2006) ... Neuropsychological studies have detected deficits in attention, working memory, and decision-making in chronic METH addicts ... There is compelling evidence that the negative neuropsychiatric consequences of METH abuse are due, at least in part, to drug-induced neuropathological changes in the brains of these METH-exposed individuals ... Structural magnetic resonance imaging (MRI) studies in METH addicts have revealed substantial morphological changes in their brains. These include loss of gray matter in the cingulate, limbic and paralimbic cortices, significant shrinkage of hippocampi, and hypertrophy of white matter (Thompson et al., 2004). In addition, the brains of METH abusers show evidence of hyperintensities in white matter (Bae et al., 2006; Ernst et al., 2000), decreases in the neuronal marker, N-acetylaspartate (Ernst et al., 2000; Sung et al., 2007), reductions in a marker of metabolic integrity, creatine (Sekine et al., 2002) and increases in a marker of glial activation, myoinositol (Chang et al., 2002; Ernst et al., 2000; Sung et al., 2007; Yen et al., 1994). Elevated choline levels, which are indicative of increased cellular membrane synthesis and turnover are also evident in the frontal gray matter of METH abusers (Ernst et al., 2000; Salo et al., 2007; Taylor et al., 2007).
Hussain F, Frare RW, Py Berrios KL. Drug abuse identification and pain management in dental patients: a case study and literature review. Gen. Dent. 2012, 60 (4): 334–345. PMID 22782046.
Shoptaw SJ, Kao U, Ling W. Shoptaw SJ, Ali R , 編. Treatment for amphetamine psychosis. Cochrane Database Syst. Rev. 2009, (1): CD003026. PMID 19160215. doi:10.1002/14651858.CD003026.pub3. A minority of individuals who use amphetamines develop full-blown psychosis requiring care at emergency departments or psychiatric hospitals. In such cases, symptoms of amphetamine psychosis commonly include paranoid and persecutory delusions as well as auditory and visual hallucinations in the presence of extreme agitation. More common (about 18%) is for frequent amphetamine users to report psychotic symptoms that are sub-clinical and that do not require high-intensity intervention ... About 5–15% of the users who develop an amphetamine psychosis fail to recover completely (Hofmann 1983) ... Findings from one trial indicate use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis.
Richards JR, Albertson TE, Derlet RW, Lange RA, Olson KR, Horowitz BZ. Treatment of toxicity from amphetamines, related derivatives, and analogues: a systematic clinical review. Drug Alcohol Depend. May 2015, 150: 1–13. PMID 25724076. doi:10.1016/j.drugalcdep.2015.01.040.
Richards JR, Derlet RW, Duncan DR. Methamphetamine toxicity: treatment with a benzodiazepine versus a butyrophenone. Eur. J. Emerg. Med. September 1997, 4 (3): 130–135. PMID 9426992. doi:10.1097/00063110-199709000-00003.
Malenka RC, Nestler EJ, Hyman SE. Chapter 15: Reinforcement and Addictive Disorders. Sydor A, Brown RY (編). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York, USA: McGraw-Hill Medical. 2009: 386. ISBN 978-0-07-148127-4. Currently, cognitive–behavioral therapies are the most successful treatment available for preventing the relapse of psychostimulant use.
Perez-Mana C, Castells X, Torrens M, Capella D, Farre M. Efficacy of psychostimulant drugs for amphetamine abuse or dependence. Cochrane Database Syst. Rev. September 2013, 9: CD009695. PMID 23996457. doi:10.1002/14651858.CD009695.pub2. To date, no pharmacological treatment has been approved for [addiction], and psychotherapy remains the mainstay of treatment. ... Results of this review do not support the use of psychostimulant medications at the tested doses as a replacement therapy
Malenka RC, Nestler EJ, Hyman SE. Chapter 5: Excitatory and Inhibitory Amino Acids. Sydor A, Brown RY (編). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York, USA: McGraw-Hill Medical. 2009: 124–125. ISBN 978-0-07-148127-4. At membrane potentials more negative than approximately −50 mV, the Mg2+ in the extracellular fluid of the brain virtually abolishes ion flux through NMDA receptor channels, even in the presence of glutamate. ... The NMDA receptor is unique among all neurotransmitter receptors in that its activation requires the simultaneous binding of two different agonists. In addition to the binding of glutamate at the conventional agonist-binding site, the binding of glycine appears to be required for receptor activation. Because neither of these agonists alone can open this ion channel, glutamate and glycine are referred to as coagonists of the NMDA receptor. The physiologic significance of the glycine binding site is unclear because the normal extracellular concentration of glycine is believed to be saturating. However, recent evidence suggests that D-serine may be the endogenous agonist for this site.
Kanehisa Laboratories. Amphetamine – Homo sapiens (human). KEGG Pathway. 2014-10-10 [2014-10-31]. （原始內容存檔於2018-07-23）. Most addictive drugs increase extracellular concentrations of dopamine (DA) in nucleus accumbens (NAc) and medial prefrontal cortex (mPFC), projection areas of mesocorticolimbic DA neurons and key components of the "brain reward circuit". Amphetamine achieves this elevation in extracellular levels of DA by promoting efflux from synaptic terminals. ... Chronic exposure to amphetamine induces a unique transcription factor delta FosB, which plays an essential role in long-term adaptive changes in the brain.
Shoptaw SJ, Kao U, Heinzerling K, Ling W. Shoptaw SJ , 編. Treatment for amphetamine withdrawal. Cochrane Database Syst. Rev. 2009, (2): CD003021. PMID 19370579. doi:10.1002/14651858.CD003021.pub2. The prevalence of this withdrawal syndrome is extremely common (Cantwell 1998; Gossop 1982) with 87.6% of 647 individuals with amphetamine dependence reporting six or more signs of amphetamine withdrawal listed in the DSM when the drug is not available (Schuckit 1999) ... Withdrawal symptoms typically present within 24 hours of the last use of amphetamine, with a withdrawal syndrome involving two general phases that can last 3 weeks or more. The first phase of this syndrome is the initial "crash" that resolves within about a week (Gossop 1982;McGregor 2005)
Chomchai C, Na Manorom N, Watanarungsan P, Yossuck P, Chomchai S. Methamphetamine abuse during pregnancy and its health impact on neonates born at Siriraj Hospital, Bangkok, Thailand. The Southeast Asian Journal of Tropical Medicine and Public Health. 2004, 35 (1): 228–31. PMID 15272773.
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