Authors: Sadock, Benjamin James; Sadock, Virginia Alcott
Title: Kaplan & Sadock's Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry, 10th Edition
Copyright ©2007 Lippincott Williams & Wilkins
> Table of Contents > 12 - Substance-Related Disorders > 12.3 - Amphetamine (or Amphetamine-like)-Related Disorders
Amphetamine (or Amphetamine-like)-Related Disorders
Amphetamines and amphetamine-like drugs are the most widely used illicit substances, second only to cannabis, in the United States, Asia, Great Britain, Australia, and several other western European countries. Methamphetamine, a congener of amphetamine, has become even more popular in recent years.
The racemate amphetamine sulfate (Benzedrine) was first synthesized in 1887 and was introduced to clinical practice in 1932 as an over-the-counter inhaler for the treatment of nasal congestion and asthma. In 1937, amphetamine sulfate tablets were introduced for the treatment of narcolepsy, postencephalitic parkinsonism, depression, and lethargy. In the 1970s, a variety of social and regulatory factors began to curb widespread amphetamine distribution. The current US Food and Drug Administration (FDA)-approved indications for amphetamine are limited to attention-deficit/hyperactivity disorder (ADHD) and narcolepsy; however, amphetamines are also used in the treatment of obesity, depression, dysthymia, chronic fatigue syndrome, acquired immune deficiency syndrome (AIDS), dementia, and neurasthenia.
The major amphetamines currently available and used in the United States are dextroamphetamine (Dexedrine), methamphetamine (Desoxyn), a mixed dextroamphetamine-amphetamine salt (Adderall), and the amphetamine-like compound methylphenidate (Ritalin). These drugs go by such street names as ice, crystal, crystal meth, and speed. As a general class,
the amphetamines are referred to as analeptics, sympathomimetics, stimulants, and psychostimulants. The typical amphetamines are used to increase performance and to induce a euphoric feeling, for example, by students studying for examinations, by long-distance truck drivers on trips, by business people with important deadlines, by athletes in competition, and by soldiers during wartime. Although not as addictive as cocaine, amphetamines are nonetheless addictive drugs.
Other amphetamine-like substances are ephedrine, pseudoephedrine, and phenylpropanolamine (PPA). These drugs, PPA in particular, can dangerously exacerbate hypertension, precipitate a toxic psychosis, cause intestinal infarction, or result in death. The safety margin for PPA is particularly narrow, and three to four times the normal dose can result in life-threatening hypertension. In 2005, medications containing PPA were recalled by the FDA, and in 2006, the FDA prohibited the sale of over-the-counter medications containing ephedrine and regulated the sale of over-the-counter medications containing pseudoephedrine, which was being used illegally to make methamphetamine.
Amphetamine-type drugs with abuse potential also include phendimetrazine (Preludin), which is included in Schedule II of the Controlled Substance Act (CSA), and diethylpropion (Tenuate), benzphetamine (Didrex), and phentermine (Ionamin), which are included in Schedules III or IV of the CSA. It is presumed that all of these drugs are capable of producing all of the listed amphetamine-induced disorders. Modafinil (Provigil), used in the treatment of narcolepsy, also has stimulant and euphorigenic effects in humans but its toxicity and likelihood of producing amphetamine-induced disorders are unknown.
Methamphetamine is a potent form of amphetamine that abusers of the substance inhale, smoke, or inject intravenously (IV). Its psychological effects last for hours and are described as particularly powerful. Unlike cocaine (see Section 12.6), which must be imported, methamphetamine is a synthetic drug that can be manufactured domestically in illicit laboratories.
Other agents called substituted or designer amphetamines are discussed separately later in this section.
The National Household Survey on Drug Abuse (NHSDA) conducted in 2001 found that 7.1 percent of persons (12 years of age and older) reported lifetime nonmedical use of stimulants, a significant increase since the 4.5 percent found in the 1997 survey. The highest rates of use in the past year (1.5 percent) were among 18- to 25-year-olds, followed by 12- to 17-year-olds. The treatment admission rate for primary amphetamine abuse in the United States is about 30 per 100,000 people 12 years of age or older. Thirteen states had amphetamine admission rates of at least 55 per 100,000, and eight of these had rates of 100 per 100,000 or more. A strong association of methamphetamine abuse and crime exists.
Amphetamine use occurs in all socioeconomic groups, and is increasing among white professionals. Because amphetamines are available by prescription for specific indications, prescribing physicians must be aware of the risk of amphetamine abuse by others, including friends and family members of the patient receiving the amphetamine. No reliable data are available on the epidemiology of designer amphetamine use, but they are greatly abused. According to the text revision of the 4th edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), the lifetime prevalence of amphetamine dependence and abuse is 1.5 percent, and the male to female ratio is 1.
According to NHSDA, methamphetamine abuse continues to spread geographically and to different populations. In addition to the “super labs” in California and trafficking from Mexico, a proliferation of small “mom and pop” laboratories has occurred throughout the country, especially in rural areas. Methamphetamine abuse and production levels are high in Hawaii, West Coast areas, and some Southwestern areas, and abuse and manufacture continue to move eastward. New populations of methamphetamine uses include Hispanics, young people in Denver, club goers in Boston, and African-Americans in Texas. One half of women arrested in Honolulu tested positive in 2002, as did nearly 42 percent in Phoenix and 37 percent in San Diego. Not only methamphetamine users, but also children exposed to methamphetamine laboratories are also in danger of serious health consequences.
All the amphetamines are rapidly absorbed orally and have a rapid onset of action, usually within 1 hour when taken orally. The classic amphetamines are also taken IV and have an almost immediate effect by this route. Nonprescribed amphetamines and designer amphetamines are also inhaled (“snorting”). Tolerance develops with both classic and designer amphetamines, although amphetamine users often overcome the tolerance by taking more of the drug. Amphetamine is less addictive than cocaine, as evidenced by experiments on rats in which not all animals spontaneously self-administered low doses of amphetamine.
The classic amphetamines (i.e., dextroamphetamine, methamphetamine, and methylphenidate) produce their primary effects by causing the release of catecholamines, particularly dopamine, from presynaptic terminals (see Fig. 3.3-7). The effects are particularly potent for the dopaminergic neurons projecting from the ventral tegmental area to the cerebral cortex and the limbic areas. This pathway has been termed the reward circuit pathway, and its activation is probably the major addicting mechanism for the amphetamines. The designer amphetamines cause the release of catecholamines (dopamine and norepinephrine) and of serotonin, the neurotransmitter implicated as the major neurochemical pathway for hallucinogens. Therefore, the clinical effects of designer amphetamines are a blend of the effects of classic amphetamines and those of hallucinogens.
The DSM-IV-TR lists many amphetamine (or amphetamine-like)-related disorders (Table 12.3-1), but specifies diagnostic criteria only for amphetamine intoxication (Table 12.3-2), amphetamine withdrawal (Table 12.3-3), and amphetamine-related disorder not otherwise specified (Table 12.3-4) in the section on amphetamine (or amphetamine-like)-related disorders. The diagnostic criteria for the other amphetamine (or amphetamine-like)-related disorders are contained in the DSM-IV-TR sections dealing with the primary phenomenological symptom (e.g., psychosis).
Table 12.3-1 DSM-IV-TR Amphetamine (or Amphetamine-like)-Related Disorders
Amphetamine Dependence and Amphetamine Abuse
The DSM-IV-TR criteria for dependence and abuse are applied to amphetamine and its related substances (see Tables 12.1-3, 12.1-4, and 12.1-5 in Section 12.1). Amphetamine dependence can result in a rapid downward spiral of a person's abilities to cope with work- and family-related obligations and stresses. A person who abuses amphetamines requires increasingly high doses of amphetamine to obtain the usual high, and physical signs of amphetamine abuse (e.g., decreased weight and paranoid ideas) almost always develop with continued abuse.
The intoxication syndromes of cocaine (which blocks dopamine reuptake) and amphetamines (which cause the release of dopamine) are similar. Because more rigorous, in-depth research has been done on cocaine abuse and intoxication than on amphetamines, the clinical literature on amphetamines has been strongly influenced by the clinical findings of cocaine abuse. In DSM-IV-TR, the diagnostic criteria for amphetamine intoxication (Table 12.3-2) and cocaine intoxication (see Table 12.6-2) are separated, but are virtually the same. DSM-IV-TR specifies perceptual disturbances as a symptom of amphetamine intoxication. If intact reality testing is absent, a diagnosis of amphetamine-induced psychotic disorder with onset during intoxication is indicated. The symptoms of amphetamine intoxication are mostly resolved after 24 hours and are generally completely resolved after 48 hours.
Table 12.3-2 DSM-IV-TR Diagnostic Criteria for Amphetamine Intoxication
An 18-year-old high school senior was brought to the emergency room by police after being picked up wandering in traffic on the Triborough Bridge. He was angry, agitated, and aggressive and talked of various people who were deliberately trying to “confuse” him by giving him misleading directions. His story was rambling and disjointed, but he admitted to the police officer that he had been using “speed.” In the emergency room he had difficulty focusing his attention and had to ask that questions be repeated. He was disoriented as to time and place and was unable to repeat the names of three objects after five minutes. The family gave a history of the patient's regular use of “pep pills” over the past two years, during which time he was frequently “high” and did very poorly in school. (From DSM-III-R Casebook.)
Table 12.3-3 DSM-IV-TR Diagnostic Criteria for Amphetamine Withdrawal
Table 12.3-4 DSM-IV-TR Diagnostic Criteria for Amphetamine- Related Disorder Not Otherwise Specified
After amphetamine intoxication, a crash occurs with symptoms of anxiety, tremulousness, dysphoric mood, lethargy, fatigue, nightmares (accompanied by rebound rapid eye movement [REM] sleep), headache, profuse sweating, muscle cramps, stomach cramps, and insatiable hunger. The withdrawal symptoms generally peak in 2 to 4 days and are resolved in 1 week. The most serious withdrawal symptom is depression, which can be particularly severe after the sustained use of high doses of amphetamine and which can be associated with suicidal ideation or behavior. The DSM-IV-TR diagnostic criteria for amphetamine withdrawal (Table 12.3-3) specify that a dysphoric mood and physiological changes are necessary for the diagnosis.
Amphetamine Intoxication Delirium
Under substance-related disorder, DSM-IV-TR includes a diagnosis of amphetamine intoxication delirium (see Table 10.2-6). Delirium associated with amphetamine use generally results from high doses of amphetamine or from sustained use, and so sleep deprivation affects the clinical presentation. The combination of amphetamines with other substances and the use of amphetamines by a person with preexisting brain damage can also cause development of delirium. It is not uncommon for university students using amphetamines to cram for examinations to exhibit this type of delirium.
Amphetamine-Induced Psychotic Disorder
The clinical similarity of amphetamine-induced psychosis to paranoid schizophrenia has prompted extensive study of the neurochemistry of amphetamine-induced psychosis to elucidate the pathophysiology of paranoid schizophrenia. The hallmark of amphetamine-induced psychotic disorder is the presence of paranoia. Amphetamine-induced psychotic disorder can be distinguished from paranoid schizophrenia by several differentiating characteristics associated with the former, including a predominance of visual hallucinations, generally appropriate affects, hyperactivity, hypersexuality, confusion and incoherence, and little evidence of disordered thinking (e.g., looseness of associations). In several studies, investigators also noted that, although the positive symptoms of amphetamine-induced psychotic disorder and schizophrenia are similar, amphetamine-induced psychotic disorder generally lacks the affective flattening and alogia of schizophrenia. Clinically, however, acute amphetamine-induced psychotic disorder can be completely indistinguishable from schizophrenia, and only the resolution of the symptoms in a few days or a positive finding in a urine drug screen test eventually reveals the correct diagnosis.
The treatment of choice for amphetamine-induced psychotic disorder is the short-term use of an antipsychotic medication such as haloperidol (Haldol). DSM-IV-TR lists the diagnostic criteria for amphetamine-induced psychotic disorder with the other psychotic disorders (see Table 14.4-7) and allows clinicians to specify whether delusions or hallucinations are the predominant symptoms.
Amphetamine-Induced Mood Disorder
According to DSM-IV-TR, the onset of amphetamine-induced mood disorder can occur during intoxication or withdrawal (see Table 15.3-10). In general, intoxication is associated with manic or mixed mood features, whereas withdrawal is associated with depressive mood features.
Amphetamine-Induced Anxiety Disorder
In DSM-IV-TR, the onset of amphetamine-induced anxiety disorder can also occur during intoxication or withdrawal (see Table 16.7-3). Amphetamine, as with cocaine, can induce symptoms similar to those seen in obsessive-compulsive disorder, panic disorder, and phobic disorders, in particular.
Amphetamine-Induced Sexual Dysfunction
Amphetamines may be prescribed as an antidote to the sexual side effects of serotonergic agents such as fluoxetine (Prozac), but they are often misused by persons to enhance sexual experiences. High doses and long-term use are associated with erectile disorder and other sexual dysfunctions. These dysfunctions are classified in DSM-IV-TR as amphetamine-induced sexual dysfunction with onset during intoxication (see Table 21.2-17).
Amphetamine-Induced Sleep Disorder
The diagnostic criteria for amphetamine-induced sleep disorder with onset during intoxication or withdrawal are found in the DSM-IV-TR section on sleep disorders (see Table 24.2-21). Amphetamine intoxication can produce insomnia and sleep deprivation, whereas persons undergoing amphetamine withdrawal can experience hypersomnolence and nightmares.
Disorder Not Otherwise Specified
If an amphetamine (or amphetamine-like)-related disorder does not meet the criteria of one or more of the categories discussed above, it can be diagnosed as an amphetamine-related disorder not otherwise specified (Table 12.3-4).
In persons who have not previously used amphetamines, a single 5-mg dose increases the sense of well-being and induces elation, euphoria, and friendliness. Small doses generally improve attention and increase performance on written, oral, and performance tasks. An associated decrease in fatigue, induction of anorexia, and heightening of the pain threshold are also seen. Undesirable effects result from the use of high doses for long periods.
Amphetamine abuse can produce adverse effects, the most serious of which include cerebrovascular, cardiac, and gastrointestinal effects. Among the specific life-threatening conditions are myocardial infarction, severe hypertension, cerebrovascular disease, and ischemic colitis. A continuum of neurological symptoms, from twitching to tetany to seizures to coma and death, is associated with increasingly high amphetamine doses. Intravenous use of amphetamines can transmit human immunodeficiency virus (HIV) and hepatitis and further the development of lung abscesses, endocarditis, and necrotizing angiitis. Several studies have shown that abusers of amphetamines knew little—or did not care—about safe-sex practices and the use of condoms. The non–life-threatening adverse effects of amphetamine abuse include flushing, pallor, cyanosis, fever, headache, tachycardia, palpitations, nausea, vomiting, bruxism (teeth grinding), shortness of breath, tremor, and ataxia. Pregnant women who use amphetamines often have babies with low birthweight, small head circumference, early gestational age, and growth retardation.
The adverse psychological effects associated with amphetamine use include restlessness, dysphoria, insomnia, irritability, hostility, and confusion. Amphetamine use can also induce symptoms of anxiety disorders, such as generalized anxiety disorder and panic disorder, as well as ideas of reference, paranoid delusions, and hallucinations.
MDMA (3,4-methylene-dioxymethamphetamine) is one of a series of substituted amphetamines that also includes MDEA, MDA (3,4-methylene-dioxyamphetamine), DOB (2,5-dimethoxy-4-bromoamphetamine), PMA (paramethoxyamphetamine), and others. These drugs produce subjective effects resembling those of amphetamine and LSD (lysergic acid diethylamide), and in that sense, MDMA and similar analogues may represent a distinct category of drugs.
A methamphetamine derivative that came into use in the 1980s, MDMA was not technically subject to legal regulation at the time. Although it has been labeled a “designer drug” in the belief that it was deliberately synthesized to evade legal regulation, it was actually synthesized and patented in 1914. Several psychiatrists used it as an adjunct to psychotherapy and concluded that it had value. At one time, it was advertised as legal and was used in psychotherapy for its subjective effects. It was never approved by the FDA, however. Its use raised questions of both safety and legality, because the related amphetamine derivatives MDA, DOB, and PMA had caused a number of overdose deaths, and MDA was known to cause extensive destruction of serotonergic nerve terminals in the central nervous system (CNS). Using emergency scheduling authority, the Drug Enforcement Agency made MDMA a Schedule I drug under the CSA, along with LSD, heroin, and marijuana. Despite its illegal status, MDMA continues to be manufactured, distributed, and used in the United States, Europe, and Australia. Its use is common in Australia and Great Britain at extended dances (“raves”) popular with adolescents and young adults.
Mechanisms of Action
The unusual properties of the drugs may be a consequence of the different actions of the optical isomers: the R(-) isomers produce LSD-like effects and the amphetamine-like properties are linked to S(+) isomers. The LSD-like actions, in turn, may be linked to the capacity to release serotonin. The various derivatives may exhibit significant differences in subjective effects and toxicity. Animals in laboratory experiments will self-administer the drugs, suggesting prominent amphetamine-like effects.
After taking usual doses (100 to 150 mg), MDMA users experience elevated mood and, according to various reports, increased self-confidence and sensory sensitivity; peaceful feelings coupled with insight, empathy, and closeness to persons; and decreased appetite. Difficulty concentrating and an increased capacity to focus have both been reported. Dysphoric reactions, psychotomimetic effects, and psychosis have also been reported. Higher doses seem more likely to produce psychotomimetic effects. Sympathomimetic effects of tachycardia, palpitation, increased blood pressure, sweating, and bruxism are common. The subjective effects are reported to be prominent for about 4 to 8 hours, but they may not last as long or may last longer, depending on the dose and route of administration. The drug is usually taken orally but is also snorted and injected. Both tachyphylaxis and some tolerance are reported by users.
Although it is not as toxic as MDA, various somatic toxicities have been attributed to MDMA use as well as fatal overdoses. It does not appear to be neurotoxic when injected into the brains of animals, but it is metabolized to MDA in both animals and humans. In animals, MDMA produces selective, long-lasting damage to serotonergic nerve terminals. It is not certain if the levels of the MDA metabolite reached in humans after the usual doses of MDMA suffice to produce lasting damage. Users of MDMA show differences in neuroendocrine responses to serotonergic probes, and studies of former MDMA users show global and regional decreases in serotonin transporter binding, as measured by positron emission tomography.
Currently, no established clinical uses exist for MDMA, although before its regulation, there were several reports of its beneficial effects as an adjunct to psychotherapy.
The fresh leaves of Catha edulis, a bush native to East Africa, have been used as a stimulant in the Middle East, Africa, and the Arabian Peninsula for at least 1,000 years. Khat is still widely used in Ethiopia, Kenya, Somalia, and Yemen. The amphetamine-like effects of khat have long been recognized, and although efforts to isolate the active ingredient were first undertaken in the 19th century, only since the 1970s has
cathinone (S[-] α-aminopropiophenone or S[-]2-amino-1-phenyl-1-propanone) been identified as the substance responsible. Cathinone is a precursor moiety that is normally enzymatically converted in the plant to the less-active entities norephedrine and cathine (norpseudoephedrine), which explains why only the fresh leaves of the plant are valued for their stimulant effects. Cathinone has most of the CNS and peripheral actions of amphetamine and appears to have the same mechanism of action. In humans, it elevates mood, decreases hunger, and alleviates fatigue. At high doses, it can induce an amphetamine-like psychosis in humans. Because it is typically absorbed buccally after chewing the leaf and because the alkaloid is metabolized relatively rapidly, high toxic blood levels are rarely reached. Concern about khat use is linked to its dependence-producing properties rather than to its acute toxicity. It is estimated that five million doses are consumed each day, despite prohibition of its use in a number of African and Arab countries.
In the 1990s, several clandestine laboratories began synthesizing methcathinone, a drug with actions similar to those of cathinone. Known by a number of street names (e.g., “CAT,” “goob,” and “crank”), its popularity is primarily owing to its ease of synthesis from ephedrine or pseudoephedrine, which were readily available until placed under special controls. Methcathinone has been moved to Schedule I of the CSA. The patterns of use, adverse effects, and complications closely resemble those reported for amphetamine.
The use of a certain group of substances popularly called club drugs is often associated with dance clubs, bars, and all-night dance parties (raves). The group includes LSD, γ-hydroxybutyrate (GHB), ketamine, methamphetamine, MDMA (ecstasy), and Rohypnol or “roofies” (flunitrazepam). These substances are not all in the same drug class, nor do they produce the same physical or subjective effects. GHB, ketamine, and Rohypnol have been called date rape drugs because they produce disorienting and sedating effects, and often users cannot recall what occurred during all or part of an episode under the influence of the drug. Hence, it is alleged that these drugs might be surreptitiously placed in a beverage, or a person might be convinced to take the drug and then not recall clearly what occurred after ingestion.
Emergency department mentions of GHB, ketamine, and Rohypnol are relatively few. Of the club drugs, methamphetamine is the substance that accounts for the largest share of treatment admissions.
Treatment and Rehabilitation
The treatment of amphetamine (or amphetamine-like)-related disorders shares with cocaine-related disorders the difficulty of helping patients remain abstinent from the drug, which is powerfully reinforcing and induces craving. An inpatient setting and the use of multiple therapeutic methods (individual, family, and group psychotherapy) are usually necessary to achieve lasting abstinence. The treatment of specific amphetamine-induced disorders (e.g., amphetamine-induced psychotic disorder and amphetamine-induced anxiety disorder) with specific drugs (e.g., antipsychotic and anxiolytics) may be necessary on a short-term basis. Antipsychotics may be prescribed for the first few days. In the absence of psychosis, diazepam (Valium) is useful to treat patients' agitation and hyperactivity.
Physicians should establish a therapeutic alliance with patients to deal with the underlying depression, personality disorder, or both. Because many patients are heavily dependent on the drug, however, psychotherapy may be especially difficult.
Comorbid conditions, such as depression, may respond to antidepressant medication. Bupropion (Wellbutrin) may be of use after patients have withdrawn from amphetamine. It has the effect of producing feelings of well-being as these patients cope with the dysphoria that may accompany abstinence.
Ellis RJ, Childers ME, Cherner M, Lazzaretto D, Letendre S, Grant I. The HIV Neurobehavioral Research Center Group. Increased human immunodeficiency virus loads in active methamphetamine users are explained by reduced effectiveness of antiretroviral therapy. J Infect Dis. 2003;188:1820.
Gorelick DA. Pharmacologic interventions for cocaine, crack, and other stimulant addiction. In: Graham AW, Schultz TK, Mayo-Smith FM, Ries RK, Wilford BB, eds. Principles of Addiction Medicine. 3rd ed. Chevy Chase, MD: American Society of Addiction Medication, Inc.; 2003.
Gorelick DA, Cornish JL. The pharmacology of cocaine, amphetamines, and other stimulants. In: Graham AW, Schultz TK, Mayo-Smith FM, Ries RK, Wilford BB, eds. Principles of Addiction Medicine. 3rd ed. Chevy Chase, MD: American Society of Addiction Medication, Inc.; 2003.
Green AR, Mechan AO, Elliott JM, O'Shea E, Colado MI. The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, “Ecstasy”). Pharmacol Rev. 2003;55:463.
Jaffe JH. Amphetamine (or amphetamine-like)-related disorders. In: Sadock BJ, Sadock VA, eds. Kaplan & Sadock's Comprehensive Textbook of Psychiatry. 7th ed. Vol. 1. Baltimore: Lippincott Williams & Wilkins; 2000:924.
Jaffe JH, Ling W, Rawson RA. Amphetamine (or amphetamine-like)-related disorders. In: Sadock BJ, Sadock VA, eds. Kaplan & Sadock's Comprehensive Textbook of Psychiatry. 8th ed. Vol. 1. Baltimore: Lippincott Williams & Wilkins; 2005:1188.
Jaworski JN, Kozel MA, Philpot KB, Kuhar MJ. Intra-accumbal injection of CART (cocaine-amphetamine regulated transcript) peptide reduces cocaine-induced locomotor activity. J Pharmacol Exp Ther. 2003;307:1038.
Kendler KS, Prescott CA, Myers J, Neale MC. The structure of genetic and environmental risk factors for common psychiatric and substance use disorders in men and women. Arch Gen Psychiatry. 2003;60:929.
London ED, Simon SL, Berman SM, Mandelkern MA, Lichtman AM, Bramen J, Shinn AK, Miotto K, Learn J, Dong Y, Matochik JA, Kurian V, Newton T, Woods R, Rawson R, Ling R. Regional cerebral dysfunction associated with mood disturbances in abstinent methamphetamine abusers. Arch Gen Psychiatry. 2004;61:73.
Rodriguez N, Katz C, Webb VJ, Schaefer DR. Examining the impact of individual, community, and market factors on methamphetamine use: A tale of two cities. Journal of Drug Issues. 2005;35:665–694.
Suto N, Tanabe LM, Austin JD, Creekmore E, Vezina P. Previous exposure to VTA amphetamine enhances cocaine self-administration under a progressive ratio schedule in an NMDA, AMPA/Kainate, and metabotropic glutamate receptor-dependent manner. Neuropsychopharmacology. 2003;28:629.
Sweeting M, Farrell M. Methamphetamine psychosis: How is it related to schizophrenia? A review of the literature. Current Psychiatry Reviews. 2005;1:115–122.