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Clinical Case Conference   |    
Remission of Persistent Methamphetamine-Induced Psychosis After Electroconvulsive Therapy: Presentation of a Case and Review of the Literature
David J. Grelotti, M.D.; Gen Kanayama, M.D., Ph.D.; Harrison G. Pope, Jr., M.D., M.P.H.
Am J Psychiatry 2010;167:17-23. doi:10.1176/appi.ajp.2009.08111695
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All authors report no financial relationships with commercial interests.

Supported in part by an American Psychiatric Institute for Research and Education/Janssen Resident Psychiatric Research Scholarship to Dr. Grelotti.

Received Nov. 17, 2008; revision received March 20, 2009; accepted April 13, 2009. From the Department of Psychiatry, Massachusetts General Hospital, Boston; the Department of Psychiatry, Harvard Medical School, Boston; McLean Hospital, Belmont, Mass.; and the Biological Psychiatry Laboratory, McLean Hospital. Address correspondence and reprint requests to Dr. Pope at McLean Hospital, Belmont, MA 02178; hpope@mclean.harvard.edu (e-mail).

Received November 17, 2008; Accepted April 13, 2009.

Copyright © American Psychiatric Association

Abstract

Abstract  Illicit methamphetamine abuse represents a major problem in many countries worldwide, including the United States. Prolonged regular smoking or injection of methamphetamine can cause a psychosis, typically characterized by paranoid delusions and auditory hallucinations and often associated with disturbances in mood. These symptoms may persist long after methamphetamine is discontinued and may prove refractory to antipsychotic medications. The authors describe a patient who developed a typical methamphetamine psychosis that persisted despite months of abstinence from methamphetamine and weeks of treatment with antipsychotic medication but that responded promptly to electroconvulsive therapy (ECT) on two separate occasions: on initial presentation and again a year later when the patient relapsed into methamphetamine abuse and developed psychosis again. The authors review the large international literature on methamphetamine psychosis, much of which is from Japan and has not previously been summarized in English. Persistent methamphetamine psychosis has been widely reported in Japan for more than 50 years but is rarely discussed in the American literature, possibly because some such cases are misdiagnosed in the United States as primary psychotic disorders. Given the growing public health problem of methamphetamine abuse in the United States, the distinction between persistent methamphetamine psychosis and a primary psychotic disorder has grown increasingly important. Thus, American clinicians should be alert to the possibility of methamphetamine psychosis and may wish to consider ECT in refractory cases.

Abstract Teaser
Figures in this Article

Illicit methamphetamine use is a global problem, and the United States is one of the world's biggest markets (1). In 2007, an estimated 13 million Americans over age 12 had used illicit methamphetamine in their lifetime, 1.3 million of them in the previous year and 529,000 of them in the previous month (2). Moreover, the public health burden of American methamphetamine abuse has increased in the past decade. Once geographically confined largely to Hawaii and the West Coast, methamphetamine has now spread nationally (3), supplied by small-scale ("kitchen") and industrial-scale clandestine laboratories, where it is often manufactured using legally purchased ingredients (1). Increasing federal restrictions on the sale of methamphetamine precursors enacted from 1989 through 1997 appear to have temporarily reduced methamphetamine-related rates of arrests and treatment admissions, but the rates rebounded after a few years (4). Among all individuals admitted for substance abuse treatment in the United States, the proportion of primary methamphetamine users increased from 0.9% in 1992 to 8.3% in 2006 (from 14,570 to 149,415 admissions) (5, 6). Data from the Drug Abuse Warning Network, which monitors drug-related emergency department utilization statistics, indicate that among emergency department visits in 2006 for treatment involving illicit drug use, 11.2% involved amphetamines (7). In one Oregon hospital, methamphetamine use accounted for 2.4% of emergency room visits for any purpose in 2006 (8); at a San Diego trauma center, the number of individuals testing positive for methamphetamine rose by more than 70% from 2003 to 2005, causing methamphetamine to surpass marijuana as the most commonly detected drug of abuse (9). Thus, it appears likely that American clinicians will continue to encounter growing numbers of patients with methamphetamine-related syndromes.

Illicit methamphetamine use—which typically involves supratherapeutic doses administered by nonoral routes, such as smoking or injection—can produce a variety of adverse effects, both medical (e.g., arrhythmia, myocardial infarction, seizures, pulmonary edema) and psychiatric (anxiety, depression, skin-picking, psychosis) (10, 11). Methamphetamine psychosis is one of the most serious of these syndromes and has been recognized for decades (12, 13). Methamphetamine-induced psychotic symptoms may include persecutory delusions, ideas of reference, other delusions, and hallucinations (auditory, visual, and tactile) and are often associated with disorders of mood (11). Although psychotic symptoms usually remit after acute intoxication, some patients exhibit prolonged psychosis for weeks or months after stopping methamphetamine (11, 14). Few U.S. studies have described patients with prolonged methamphetamine psychosis, but a substantial literature on this topic has accumulated from other countries, especially Japan (1327); many of these studies are not in English, however. Given the recent evidence of rising methamphetamine-related morbidity in the United States, this international literature may become increasingly relevant to American clinicians. We describe a patient admitted with apparent methamphetamine-induced auditory hallucinations and paranoid delusions, accompanied by depression, who appeared to respond on two separate occasions to ECT. To our knowledge, this is the first report of treatment of methamphetamine psychosis with ECT. We then discuss the available literature on methamphetamine-induced psychotic disorders, including the many articles published in Japanese.

Mr. A, a 37-year-old openly homosexual software engineer, had a graduate education, stable employment, a comfortable suburban house, and supportive parents. He reported no family history of psychiatric disorder in any first-degree relative, although he had one second-degree relative, a paternal uncle, with bipolar disorder. His own past psychiatric history had been benign except for a mild depressive episode in college for which he received 6 weeks of counseling. However, by his late 20s, Mr. A became frustrated by loneliness and what he called social and sexual "inhibition," which kept him from pursuing both romantic and sexual partnerships. In an effort to remedy these self-perceived deficits, he turned to drugs. In 2003, at age 32, he began infrequently smoking methamphetamine, but he quickly increased his frequency of smoking and the amount of methamphetamine that he smoked because he felt that the drug enhanced his sex life. During the same period, about three times a month, he drank as many as five alcoholic drinks per occasion. He also reported occasional use of 3,4-methylenedioxyamphetamine (MDMA; "Ecstasy"), gamma-hydroxybutyrate (GHB), marijuana, and alkyl nitrites. Methamphetamine was his drug of choice, however, and he reported that by 2005 he was smoking it daily.

In August 2006, Mr. A first developed auditory hallucinations, which he attributed to conversation among his neighbors. In November 2006, a single voice emerged and became nearly constant. He identified it as the voice of his former roommate; it told him that he was a "terrible person" who had "had sex with over 300 men" and spread to them syphilis and HIV. The voice told him to jump out of an eighth-floor window of a hotel; he went to the window but did not jump. At about the same time that he began to hear hallucinations, Mr. A developed paranoid delusions, believing, for example, that a tan sport utility vehicle was the police or that the FBI was following him. Also starting in November 2006, he began to experience depression with erratic sleep, ruminative thoughts, difficulty concentrating, poor appetite with weight loss, and suicidal ideation.

Alarmed by these experiences, Mr. A stopped all illicit drug use in February 2007, although he still occasionally used alcohol in the same amount and frequency described above. Nevertheless, the auditory hallucinations and persecutory delusions persisted, and his depression worsened. He rarely left his apartment, and when he did leave his apartment for work, he "sat around all day unable to function." Fearing the loss of his job in June 2007, he first sought mental health treatment at a local clinic, where he was evaluated and immediately referred for admission to McLean Hospital. Although the extent of his psychosis was not immediately apparent on admission, he was soon transferred to a psychotic disorders unit after disclosing that he was experiencing command auditory hallucinations.

Results of initial medical evaluations, including physical examination, routine laboratory studies, serology for syphilis and HIV, neurological evaluation, and noncontrast brain MRI, were normal. Mr. A was not taking any medications at the time of admission, and he reported that his last alcoholic drink was 10 days earlier. His only medical problems, ulcerative colitis and genital herpes, were not active. He was started on olanzapine, which was titrated up to a dose of 20 mg/day by hospital day 3, but no improvement was seen in his mood or psychotic symptoms after 2 weeks. On hospital day 17, Mr. A's case was presented at a departmental case conference; the discussant (H.G.P.) noted that from a purely phenomenological standpoint, the clinical picture was one of agitated psychotic depression, and he therefore recommended ECT as a treatment likely to be effective. Mr. A was started on right unilateral ECT on hospital day 18. He showed some improvement even after the first ECT treatment, and by the sixth treatment, on hospital day 30, he was euthymic and completely free of psychotic symptoms. He was discharged on hospital day 32 on olanzapine, at 20 mg/day, and planned maintenance ECT. However, Mr. A attended only one additional session of ECT, and because of sedation with olanzapine, he was switched by his outpatient psychiatrist to bupropion, 150 mg/day, and aripiprazole, 15 mg/day.

As an outpatient, Mr. A continued to be essentially asymptomatic. Whereas before admission he had been unable to fulfill most of his obligations at work because of cognitive impairments, after ECT he returned to his full baseline level of social and occupational functioning. He adopted a "sober lifestyle," did not drink or use drugs, and attended 12-step groups, although he had no sponsor. Five months later, in December 2007, he resumed smoking methamphetamine "sporadically" in the setting of the same perceived social isolation and dissatisfaction with his sex life. He spent hours viewing pornography on his computer and smoked methamphetamine to facilitate meeting sexual partners and to enhance sexual experience. Although he also occasionally used alkyl nitrites and GHB at that time, he denied use of alcohol, marijuana, and Ecstasy. Over the next 2 months, his methamphetamine smoking steadily increased, and during that time his auditory hallucinations returned, although he did not initially find them problematic. He curtailed his use of methamphetamine in February 2008. By May 2008, however, he was feeling "lonely" and "disconnected" from the majority of his friends who were actively smoking methamphetamine; he reverted to smoking methamphetamine daily for a period of 3 weeks and during that time developed florid auditory hallucinations and persecutory delusions nearly identical to those that he had at the time of his first admission. He was readmitted to McLean Hospital in June 2008.

Mr. A was started on quetiapine, 200 mg/day, at admission, and he started a second course of right unilateral ECT on hospital day 3. After only four treatments, his symptoms resolved entirely, and both the patient and his parents reported that he was back to his baseline of functioning. On hospital day 11, he was discharged after his fifth ECT session with instructions to take quetiapine, 200 mg/day, and with a complement of aftercare supports, including continued psychopharmacological management, psychotherapy, referral to substance abuse group for homosexual men with methamphetamine addiction, referral to a 12-step program, and five maintenance ECT treatments over the next 3 weeks.

Three months after discharge, Mr. A continued to be free of psychotic symptoms, maintaining his baseline level of social and occupational functioning and remaining abstinent from methamphetamine.

Mr. A, a man with no premorbid history of schizophrenia or other psychotic disorders, developed auditory hallucinations and paranoid delusions starting 2—3 years after he began regularly smoking illicit methamphetamine. The latency from his first methamphetamine smoking to the onset of psychosis is comparable to the mean latency of 1.7 years (SD=2.0) from first use to onset of psychosis recently reported for 42 methamphetamine smokers in Japan (18). Mr. A's psychotic symptoms persisted for approximately 5 months even after stopping methamphetamine use—a phenomenon often reported in previous studies of illicit methamphetamine users, as described below (11, 1315, 19, 28, 29). An initial trial of an atypical antipsychotic showed little benefit—a problem also previously reported in the treatment of methamphetamine psychosis (14, 15). However, Mr. A's psychotic and affective symptoms appeared to respond quickly to ECT and remained in remission until he resumed smoking methamphetamine. Reexposure to methamphetamine produced a rapid recurrence of the psychotic symptoms—an observation also consistent with the prior literature (2931). These symptoms again appeared to respond to a brief course of ECT.

How common are psychotic symptoms with methamphetamine use? Such symptoms are almost certainly rare with ordinary therapeutic doses; methamphetamine is pharmacologically similar to other amphetamines (32, 33), and amphetamines are widely prescribed for conditions such as attention deficit hyperactivity disorder, with very little risk of psychosis (34, 35). By contrast, illicit use of methamphetamine, especially in supratherapeutic doses taken by nonoral routes of administration, may produce psychotic symptoms more frequently. For example, a recent Australian study of 277 non-treatment-seeking illicit methamphetamine users with no prior diagnosis of schizophrenia or other psychotic disorders found that 51 (18%) had "clinically significant" psychotic symptoms (36). Similarly, a recent U.S. study of 42 cocaine-dependent and 43 methamphetamine-dependent individuals, screened to exclude patients with other axis I disorders, reported psychotic symptoms of at least some type in at least 60% of both groups (37).

How often do methamphetamine-induced psychotic symptoms persist long after methamphetamine is discontinued, as appeared to be the case in our patient? The available literature on this topic, much of which is in Japanese, suggests that persistent methamphetamine psychosis is not uncommon. In Japan, methamphetamine has been by far the most widely abused illicit drug for more than 50 years; until recently, Japanese substance abusers rarely consumed drugs other than methamphetamine, thus allowing investigators to assess the effects of methamphetamine without the confounding effects of other substances (29). One early Japanese study (13) described 74 patients with methamphetamine psychosis observed prior to the era of neuroleptics. About two-thirds remitted within 20 days after stopping methamphetamine, but about 10% displayed psychosis lasting more than 6 months and in some cases even a few years. In another early study, Teraoka (28) reported "schizophrenia-like symptoms" in 32 (28%) of 114 former methamphetamine users followed up after 8—12 years. A more recent study (19) described 132 consecutive patients with methamphetamine psychosis admitted to a Tokyo hospital from 1978 to 1987; about 28% required more than 61 days of hospitalization. A subsequent report from the same group (15) described 104 additional patients with methamphetamine psychosis admitted to the same hospital from 1988 to 1991; despite abstinence from methamphetamine and administration of antipsychotic drugs, 16 (15%) required more than 3 months of hospitalization. A more recent Japanese study at another center found that 28% of inpatients with methamphetamine psychosis had symptoms that persisted for longer than 6 months of abstinence (29). Similarly, Akiyama (14) described 32 female prisoners treated with standard antipsychotic medications for methamphetamine psychosis; none of these women was reported to have displayed psychosis or a diagnosis of schizophrenia prior to methamphetamine use. As prisoners, the women had no access to further methamphetamine. Although the exact numbers of those who did and did not respond to treatment cannot be calculated from the article, it appears that a majority of patients, especially those with more severe symptoms, were still symptomatic even after many months of antipsychotic treatment.

An additional literature, much of it also in Japanese (23, 30, 3842), has noted that methamphetamine users may display a rapid recurrence of psychotic symptoms on reexposure to the drug—as appeared to be the case with our patient. This phenomenon of long-lasting "sensitization" or "reverse tolerance" to methamphetamine and other dopamine agonists has been demonstrated in animals (21, 22, 43) and is believed to reflect noradrenergic hyperactivity and increased dopamine release (44).

Japanese investigators generally concur that methamphetamine can produce prolonged psychotic syndromes even in individuals who had no premorbid psychiatric symptoms or evidence of a psychotic diathesis (17, 20). By contrast, Western observers seem to have been more hesitant to adopt this view; for example, Connell's classic 1958 monograph (12) implies that prolonged cases of amphetamine psychosis must reflect some "latent paranoia." Similarly, as recently as 1996, a U.S. review noted that "it is widely taught that if psychotic symptoms persist beyond 6 weeks of sobriety, such symptoms can no longer be linked to drug abuse, no matter how severe the abuse or how long the drugs were used" (45, p. 263). Although DSM-IV-TR does not place a specific time limit on "substance-induced psychotic disorder," it implies that persistence of psychotic symptoms for "a substantial period of time (i.e., a month or more)" after stopping the drug would tend to suggest a primary psychotic illness (p. 339). However, the patient described here showed no evidence of a primary psychotic illness or predisposition to a psychotic disorder in either his personal history or that of his immediate family, yet he developed apparent methamphetamine-associated psychotic symptoms that persisted for months after stopping the drug—an observation consistent with the Japanese consensus that methamphetamine alone can cause such persistent syndromes. If the Japanese view is correct, it would follow that the prevalence of methamphetamine psychosis may currently be underestimated in the United States, because patients like Mr. A might be misclassified as having primary psychotic disorders.

Even in individuals with no obvious premorbid disposition, there may nevertheless be specific risk factors for methamphetamine-induced psychotic or mood disorders, such as a history of head injury (46), personality factors (47), familial loading for schizophrenia (48), or a history of attention deficit hyperactivity disorder (31). However, it may well be that with a sufficient cumulative lifetime dose of methamphetamine, even fully intact individuals may develop methamphetamine-induced psychosis as a result of damage to dopaminergic, serotonergic, and noradrenergic circuits. For example, methamphetamine-induced accumulation of intracellular dopamine is thought to engender the creation of free radicals that damage dopa­minergic neurons (49). Also, unlike many other stimulants, methamphetamine affects serotonergic neurons as well. The mechanism of this serotonergic neurotoxicity is less well understood but again may be attributable to free radical formation (49).

Antipsychotic medications may have limited efficacy in methamphetamine psychosis, as seemed to be the case in our patient. The paucity of research in this area is highlighted by a 2008 Cochrane Review (50) that found only one randomized controlled trial of treatment of amphetamine psychosis in all of the published literature. That study (51) compared olanzapine and haloperidol in 58 patients with amphetamine psychosis (presumably most or all methamphetamine) in Thailand; 27 (93%) of 29 patients on olanzapine and 23 (79%) of 29 patients on haloperidol showed at least 40% improvement on the Brief Psychiatric Rating Scale after 4 weeks, but it is not clear how many patients still exhibited psychotic symptoms at endpoint. Also, because the study lacked a placebo arm, it is difficult to judge whether the improvement observed was significantly superior to the natural course of amphetamine psychosis alone. Two recent case reports found risperidone (52) and olanzapine (53) effective for methamphetamine psychosis, but each described only a single patient. By contrast, as noted above, Japanese studies have frequently reported discouraging results with standard antipsychotic drugs, with many patients remaining clinically psychotic even after many months of treatment (14, 24).

Given the limited evidence for the efficacy of antipsychotic drugs, the apparent response of our patient to ECT is encouraging. The mechanism whereby ECT might benefit methamphetamine psychosis remains speculative, however. Notably, striatal dopamine is reduced in rhesus monkeys (54) and rodents (55, 56) exposed to methamphetamine and is also reduced in postmortem tissue from persons with methamphetamine addiction (57). Conversely, chronic electroconvulsive shock (ECS) increases striatal dopamine in healthy rats (58, 59). Neuroimaging findings in chronic methamphetamine users show a decrease in dopamine transporters that recovers only gradually after prolonged abstinence, suggesting dopamine terminal damage that is very slow to repair (60). Recent animal data suggest that chronic methamphetamine exposure leads to decreased immediate early gene (e.g., c-fos) expression (61). By contrast, ECS is associated with increased brain-derived neurotrophic factor, nerve growth factor, and immediate early gene (e.g., c-fos) expression, and therefore ECT may confer neuroprotection and neuroplasticity (59). Thus, one might speculate that ECT counteracts the effects of methamphetamine at least partially through normalization of the neural environment or by stimulating the proliferation of nerve terminals. However, one must be very cautious in extrapolating from animal studies, given that such studies may use larger amphetamine doses than used by humans and may not mimic the gradual escalation of dosage typical in human abusers, a pattern that may attenuate amphetamine-associated neurotoxic effects (56).

To our knowledge, there are no other published reports of ECT in methamphetamine-induced mood or psychotic disorders. Given the extensive Japanese experience with methamphetamine psychosis, one might at first expect to find such a report from Japan, but because ECT was not widely used in Japanese psychiatry until recently (62), it is not surprising to find that the Japanese literature lacks trials of ECT in methamphetamine psychosis. We are aware of one case from Germany somewhat analogous to ours, describing an individual with extensive use of Ecstasy who displayed depression refractory to pharmacological treatment but was responsive to bilateral ECT (63). The authors hypothesized that Ecstasy use was associated with a disruption of serotonergic neurons, which rendered ineffective the antidepressants that the patient had tried.

Like other case reports, ours describes observations of a single individual. Thus, several limitations of our report should be considered. First, although the nature and timing of Mr. A's symptoms appear to be typical of those described in the literature on methamphetamine psychosis, we cannot exclude the possibility that his symptoms were at least partially attributable to the use of other drugs, such as cannabis and Ecstasy. Unfortunately, toxicological screening was not performed during the patient's admissions, and thus the history is based on his self-report. However, the patient's self-report remained consistent with several different observers during two hospital admissions and was corroborated by his outpatient therapist.

Second, we must consider the possibility that some of the patient's symptoms might have been attributable to an underlying primary axis I disorder. However, the patient showed good academic and occupational functioning prior to regular methamphetamine smoking. The latency from his first methamphetamine smoking to the onset of psychosis was in the same range as that reported in previous studies of methamphetamine psychosis, as noted earlier (18). After the patient was discharged from his first hospitalization, he exhibited no psychotic symptoms or major mood disorder during the time that he remained abstinent from methamphetamine. However, when he resumed regular methamphetamine smoking, he rapidly developed a recurrence of psychotic symptoms similar to those of the previous episode, precipitating his second admission. Given this chronology, illicit methamphetamine smoking appears to be the most parsimonious explanation for the etiology of his symptoms.

Third, we lack formal assessments of the patient's cognitive status. Cognitive difficulties, such as deficits in verbal memory, are reported in methamphetamine-dependent individuals (64, 65), and indeed neurocognitive testing was ordered during the patient's second admission. However, the testing was not performed because the patient started ECT, which could confound the test results. The patient's cognition appeared to improve markedly after ECT on both occasions. However, when considering the possibility of ECT in other methamphetamine-dependent patients, some element of caution might need to be exercised in light of the fact that such patients may have existing cognitive deficits that might be compounded, at least temporarily, by ECT. Cognitive testing would likely be of value in such cases.

Fourth, the patient's improvement following ECT is confounded with time, and in the absence of a placebo condition, it cannot be stated with certainty that the improvement was attributable to ECT. However, given the chronicity of symptoms prior to initiation of ECT and the rapid remission of symptoms on two separate occasions following the initiation of ECT, it seems likely that ECT was responsible for the patient's improvement.

Further experience with other patients will be required to support our impressions from this case. Given the public health problem posed by illicit methamphetamine use, it would seem warranted to pursue further investigation of patients with apparent methamphetamine-induced syndromes.

The authors thank Drs. Dost Öngür and Elizabeth Liebson for their comments on a draft of the manuscript.

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McKetin  R;  McLaren  J;  Lubman  DI;  Hides  L:  The prevalence of psychotic symptoms among methamphetamine users.  Addiction 2006; 101:1473—1478
[CrossRef] | [PubMed]
 
Mahoney  JJ  3rd;  Kalechstein  AD;  De La Garza  R  2nd;  Newton  TF:  Presence and persistence of psychotic symptoms in cocaine- versus methamphetamine-dependent participants.  Am J Addict 2008; 17:83—98
[CrossRef] | [PubMed]
 
Sato  M:  Acute exacerbation of methamphetamine psychosis and lasting dopaminergic supersensitivity: a clinical survey.  Psychopharmacol Bull 1986; 22:751—756
[PubMed]
 
Sato  M:  A lasting vulnerability to psychosis in patients with previous methamphetamine psychosis.  Ann NY Acad Sci 1992; 654:160—170
[CrossRef] | [PubMed]
 
Sato  M;  Chen  CC;  Akiyama  K;  Otsuki  S:  Acute exacerbation of paranoid psychotic state after long-term abstinence in patients with previous methamphetamine psychosis.  Biol Psychiatry 1983; 18:429—440
[PubMed]
 
Yui  K;  Goto  K;  Ikemoto  S;  Nishijima  K;  Yoshino  T;  Ishiguro  T:  Susceptibility to subsequent episodes of spontaneous recurrence of methamphetamine psychosis.  Drug Alcohol Depend 2001; 64:133—142
[CrossRef] | [PubMed]
 
Takezaki  H;  Inotani  T;  Ikeda  T;  Yasuoka  T:  A case of acute recurrent methamphetamine psychosis characterized by fancy delusions of grandeur.  Seishin Shinkeigaku Zasshi 1984; 86:621—630 (Japanese)
[PubMed]
 
Sato  M:  An experimental study of onset and relapse mechanisms of chronic methamphetamine psychosis.  Seishin Shinkeigaku Zasshi 1979; 81:21—32 (Japanese)
[PubMed]
 
Yui  K;  Ikemoto  U;  Goto  K:  Spontaneous recrudescence of psychotic diseases caused by methamphetamine (a stimulant): the stress type and the role of noradrenaline and dopamine systems.  Nihon Shinkei Seishin Yakurigaku Zasshi 2004; 24:319—320 (Japanese)
[PubMed]
 
Boutros  NN;  Bowers  MB  Jr:  Chronic substance-induced psychotic disorders: state of the literature.  J Neuropsychiatry Clin Neurosci 1996; 8:262—269
[PubMed]
 
Fujii  D:  Risk factors for treatment-resistive methamphetamine psychosis.  J Neuropsychiatry Clin Neurosci 2002; 14:239—240
[CrossRef] | [PubMed]
 
Chen  CK;  Lin  SK;  Sham  PC;  Ball  D;  Loh  EW;  Hsiao  CC;  Chiang  YL;  Ree  SC;  Lee  CH;  Murray  RM:  Pre-morbid characteristics and co-morbidity of methamphetamine users with and without psychosis.  Psychol Med 2003; 33:1407—1414
[CrossRef] | [PubMed]
 
Chen  CK;  Lin  SK;  Sham  PC;  Ball  D;  Loh  el-W;  Murray  RM:  Morbid risk for psychiatric disorder among the relatives of methamphetamine users with and without psychosis.  Am J Med Genet B Neuropsychiatr Genet 2005; 136B:87—91
[CrossRef] | [PubMed]
 
Hanson  GR;  Rau  KS;  Fleckenstein  AE:  The methamphetamine experience: a NIDA partnership.  Neuropharmacology 2004; 47(suppl 1):92—100
[CrossRef] | [PubMed]
 
Shoptaw  SJ;  Kao  U;  Ling  WW:  Treatment for amphetamine psychosis.  Cochrane Database Syst Rev 2008(4):CD003026
[PubMed]
 
Leelahanaj  T;  Kongsakon  R;  Netrakom  P:  A 4-week, double-blind comparison of olanzapine with haloperidol in the treatment of amphetamine psychosis.  J Med Assoc Thai 2005; 88(suppl 3):S43—S52
[PubMed]
 
Misra  L;  Kofoed  L:  Risperidone treatment of methamphetamine psychosis (letter).  Am J Psychiatry 1997; 154:1170
[PubMed]
 
Misra  LK;  Kofoed  L;  Oesterheld  JR;  Richards  GA:  Olanzapine treatment of methamphetamine psychosis.  J Clin Psychopharmacol 2000; 20:393—394
[CrossRef] | [PubMed]
 
Seiden  LS;  Fischman  MW;  Schuster  CR:  Long-term methamphetamine induced changes in brain catecholamines in tolerant rhesus monkeys.  Drug Alcohol Depend 1976; 1:215—219
[CrossRef] | [PubMed]
 
Wagner  GC;  Seiden  LS;  Schuster  CR:  Methamphetamine-induced changes in brain catecholamines in rats and guinea pigs.  Drug Alcohol Depend 1979; 4:435—438
[CrossRef] | [PubMed]
 
Segal  DS;  Kuczenski  R;  O'Neil  ML;  Melega  WP;  Cho  AK:  Escalating dose methamphetamine pretreatment alters the behavioral and neurochemical profiles associated with exposure to a high-dose methamphetamine binge.  Neuropsychopharmacology 2003; 28:1730—1740
[CrossRef] | [PubMed]
 
Wilson  JM;  Kalasinsky  KS;  Levey  AI;  Bergeron  C;  Reiber  G;  Anthony  RM;  Schmunk  GA;  Shannak  K;  Haycock  JW;  Kish  SJ: Striatal dopamine nerve terminal markers in human, chronic methamphetamine users. Nat Med 1996; 2:699—703
 
Glue  P;  Costello  MJ;  Pert  A;  Mele  A;  Nutt  DJ:  Regional neurotransmitter responses after acute and chronic electroconvulsive shock.  Psychopharmacology  (Berl) 1990; 100:60—65
[CrossRef] | [PubMed]
 
Lisanby  SH;  Belmaker  RH:  Animal models of the mechanisms of action of repetitive transcranial magnetic stimulation (RTMS): comparisons with electroconvulsive shock (ECS).  Depress Anxiety 2000; 12:178—187
[CrossRef] | [PubMed]
 
Volkow  ND;  Chang  L;  Wang  GJ;  Fowler  JS;  Franceschi  D;  Sedler  M;  Gatley  SJ;  Miller  E;  Hitzemann  R;  Ding  YS;  Logan  J:  Loss of dopamine transporters in methamphetamine abusers recovers with protracted abstinence.  J Neurosci 2001; 21:9414—9418
[PubMed]
 
Marshall  JF;  Belcher  AM;  Feinstein  EM;  O'Dell  SJ:  Methamphetamine-induced neural and cognitive changes in rodents.  Addiction 2007; 102(suppl 1):61—69
[CrossRef] | [PubMed]
 
Nakajima  K;  Yamazaki  K;  Moriya  H:  Current problems with attitudes and informed consent on ECT: a questionnaire survey of psychiatrists.  Seishin Shinkeigaku Zasshi 1993; 95:537—554 (Japanese)
[PubMed]
 
Freudenmann  RW;  Schonfeldt-Lecuona  C;  Spitzer  M;  Hermle  L;  Gron  G:  Electroconvulsive therapy in the treatment of depression in a former Ecstasy user.  J Psychopharmacol 2006; 20:860—862
[CrossRef] | [PubMed]
 
Jaffe  C;  Bush  KR;  Straits-Troster  K;  Meredith  C;  Romwall  L;  Rosenbaum  G;  Cherrier  M;  Saxon  AJ:  A comparison of methamphetamine-dependent inpatients childhood attention deficit hyperactivity disorder symptomatology.  J Addict Dis 2005; 24:133—152
[CrossRef] | [PubMed]
 
McCann  UD;  Kuwabara  H;  Kumar  A;  Palermo  M;  Abbey  R;  Brasic  J;  Ye  W;  Alexander  M;  Dannals  RF;  Wong  DF;  Ricaurte  GA:  Persistent cognitive and dopamine transporter deficits in abstinent methamphetamine users.  Synapse 2008; 62:91—100
[CrossRef] | [PubMed]
 
References Container
+

References

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Kraman  P:  Drug abuse in America: rural meth, in TrendsAlert: Critical Information for State Decision-Makers .  Lexington, Ky,  Council of State Governments, 2004 (http://www.csg.org/pubs/Documents/TA0403RuralMeth.pdf)
 
Cunningham  JK;  Liu  LM:  Impact of methamphetamine precursor chemical legislation, a suppression policy, on the demand for drug treatment.  Soc Sci Med 2008; 66:1463—1473
[CrossRef] | [PubMed]
 
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 Substance Abuse and Mental Health Services Administration Office of Applied Studies: Treatment Episode Data Set (TEDS): Highlights, 2006: National Admissions to Substance Abuse Treatment Services, DASIS Series S-40. DHHS Publication No. SMA 08—4313 .  Rockville, Md,  Substance Abuse and Mental Health Services Administration,  Jan2008 (http://www.oas.samhsa.gov/teds2k6highlights/teds2k6highWeb.pdf)
 
 Substance Abuse and Mental Health Services Administration Office of Applied Studies: Drug Abuse Warning Network, 2005: National Estimates of Drug-Related Emergency Department Visits. DAWN Series D-9, DHHS Publication No. SMA 07—4256 .  Rockville, Md,  Substance Abuse and Mental Health Services Administration,  Aug2008 (http://dawninfo.samhsa.gov/files/ED2006/DAWN2k6ED.pdf)
 
Hendrickson  RG;  Cloutier  R;  McConnell  KJ:  Methamphetamine-related emergency department utilization and cost.  Acad Emerg Med 2008; 15:23—31
[CrossRef] | [PubMed]
 
Swanson  SM;  Sise  CB;  Sise  MJ;  Sack  DI;  Holbrook  TL;  Paci  GM:  The scourge of methamphetamine: impact on a level I trauma center.  J Trauma 2007; 63:531—537
[CrossRef] | [PubMed]
 
Meredith  CW;  Jaffe  C;  Ang-Lee  K;  Saxon  AJ:  Implications of chronic methamphetamine use: a literature review.  Harv Rev Psychiatry 2005; 13:141—154
[CrossRef] | [PubMed]
 
Rawson  RA;  Ling  W:  Clinical management: methamphetamine, in Textbook of Substance Abuse Treatment, 4th ed . Edited by Galanter  M;  Kleber  HD.  Washington, DC,  American Psychiatric Publishing, 2008, pp 169—179
 
Connell  PH:  Amphetamine Psychosis .  London,  Chapman & Hall, 1958
 
Hayashi  S:  Chronic methamphetamine addiction.  Sogo-Igaku 1955; 12:656—661 (Japanese)
 
Akiyama  K:  Longitudinal clinical course following pharmacological treatment of methamphetamine psychosis which persists after long-term abstinence.  Ann NY Acad Sci 2006; 1074:125—134
[CrossRef] | [PubMed]
 
Iwanami  A;  Sugiyama  A;  Kuroki  N;  Toda  S;  Kato  N;  Nakatani  Y;  Horita  N;  Kaneko  T:  Patients with methamphetamine psychosis admitted to a psychiatric hospital in Japan: a preliminary report.  Acta Psychiatr Scand 1994; 89:428—432
[CrossRef] | [PubMed]
 
Konuma  K:  Multiphasic clinical types of methamphetamine psychosis and its dependence.  Seishin Shinkeigaku Zasshi 1984; 86:315—339 (Japanese)
[PubMed]
 
Matsumoto  T:  Clinical features of recent methamphetamine abusers: comparison between smoking abusers and injection abusers.  Seishin Shinkeigaku Zasshi 2000; 102:498—513 (Japanese)
[PubMed]
 
Matsumoto  T;  Kamijo  A;  Miyakawa  T;  Endo  K;  Yabana  T;  Kishimoto  H;  Okudaira  K;  Iseki  E;  Sakai  T;  Kosaka  K:  Methamphetamine in Japan: the consequences of methamphetamine abuse as a function of route of administration.  Addiction 2002; 97:809—817
[CrossRef] | [PubMed]
 
Nakatani  Y;  Yoshizawa  F;  Yamada  H;  Iwanami  A;  Sakaguchi  M;  Katoh  N:  Methamphetamine psychosis in Japan: a survey.  Br J Addict 1989; 84:1548—1549
[CrossRef] | [PubMed]
 
Ozaki  S:  Current situation of substance abuse/dependence in psychiatric hospital settings.  Nihon Arukoru Yakubutsu Igakkai Zasshi  [Japanese Journal of Alcohol Studies and Drug Dependence] 2004; 39:35—40 (Japanese)
[PubMed]
 
Sato  M:  Basic and clinical studies on methamphetamine-related psychosis.  Seishin Shinkeigaku Zasshi  [Psychiatria et Neurologia Japonica] 2002; 104:179—209 (Japanese)
[PubMed]
 
Sato  M;  Nakajima  T;  Otsuki  S:  A clinical study of chronic methamphetamine psychoses.  Seishin Igaku 1982; 24:481—489 (Japanese)
 
Tatetsu  S;  Goto  A;  Fujiwara  T:  The Methamphetamine Psychosis.  Tokyo,  Igaku-Shoin, 1956 (Japanese)
 
Teraoka  A:  A study on methamphetamine psychosis in a psychiatric clinic: comparison of acute and chronic-type cases.  Seishin Shinkeigaku Zasshi 1998; 100:425—468 (Japanese)
[PubMed]
 
Tohhara  S;  Miyamoto  Y;  Nakajima  T:  Induced insanity occurring in hospitalized patients of chronic methamphetamine psychosis.  Arukoru Kenkyuto Yakubutsu Ison 1985; 20:350—358 (Japanese)
[PubMed]
 
Wada  K;  Fukui  S:  Relationship between years of methamphetamine use and symptoms of methamphetamine psychosis.  Arukoru Kenkyuto Yakubutsu Ison 1990; 25:143—158 (Japanese)
[PubMed]
 
Yukitake  A:  Amphetamine psychosis in Tokyo: its clinical features and social problems.  Folia Psychiatr Neurol Jpn 1983; 37:115—120
[PubMed]
 
Teraoka  A:  Prognostic and criminological studies on mental disorder caused by chronic methamphetamine intoxication.  Seishin Shinkeigaku Zasshi 1967; 69:597—619 (Japanese)
[PubMed]
 
Ujike  H;  Sato  M:  Clinical features of sensitization to methamphetamine observed in patients with methamphetamine dependence and psychosis.  Ann NY Acad Sci 2004; 1025:279—287
[CrossRef] | [PubMed]
 
Yui  K;  Ikemoto  S;  Goto  K;  Nishijima  K;  Yoshino  T;  Ishiguro  T:  Spontaneous recurrence of methamphetamine-induced paranoid-hallucinatory states in female subjects: susceptibility to psychotic states and implications for relapse of schizophrenia.  Pharmacopsychiatry 2002; 35:62—71
[CrossRef] | [PubMed]
 
Salo  R;  Nordahl  TE;  Leamon  MH;  Natsuaki  Y;  Moore  CD;  Waters  C;  Carter  CS:  Preliminary evidence of behavioral predictors of recurrent drug-induced psychosis in methamphetamine abuse.  Psychiatry Res 2008; 157:273—277
[CrossRef] | [PubMed]
 
Martin  WR;  Sloan  JW;  Sapira  JD;  Jasinski  DR:  Physiologic, subjective, and behavioral effects of amphetamine, methamphetamine, ephedrine, phenmetrazine, and methylphenidate in man.  Clin Pharmacol Ther 1971; 12:245—258
[PubMed]
 
Sevak  RJ;  Stoops  WW;  Hays  LR;  Rush  CR:  Discriminative stimulus and subject-rated effects of methamphetamine, d-amphetamine, methylphenidate, and triazolam in methamphetamine-trained humans.  J Pharmacol Exp Ther 2009; 328:1007—1018
[CrossRef] | [PubMed]
 
Poulton  A:  Long-term outcomes of stimulant medication in attention-deficit hyperactivity disorder.  Expert Rev Neurother 2006; 6:551—561
[CrossRef] | [PubMed]
 
Rappley  MD:  Clinical practice: attention deficit-hyperactivity disorder.  N Engl J Med 2005; 352:165—173
[CrossRef] | [PubMed]
 
McKetin  R;  McLaren  J;  Lubman  DI;  Hides  L:  The prevalence of psychotic symptoms among methamphetamine users.  Addiction 2006; 101:1473—1478
[CrossRef] | [PubMed]
 
Mahoney  JJ  3rd;  Kalechstein  AD;  De La Garza  R  2nd;  Newton  TF:  Presence and persistence of psychotic symptoms in cocaine- versus methamphetamine-dependent participants.  Am J Addict 2008; 17:83—98
[CrossRef] | [PubMed]
 
Sato  M:  Acute exacerbation of methamphetamine psychosis and lasting dopaminergic supersensitivity: a clinical survey.  Psychopharmacol Bull 1986; 22:751—756
[PubMed]
 
Sato  M:  A lasting vulnerability to psychosis in patients with previous methamphetamine psychosis.  Ann NY Acad Sci 1992; 654:160—170
[CrossRef] | [PubMed]
 
Sato  M;  Chen  CC;  Akiyama  K;  Otsuki  S:  Acute exacerbation of paranoid psychotic state after long-term abstinence in patients with previous methamphetamine psychosis.  Biol Psychiatry 1983; 18:429—440
[PubMed]
 
Yui  K;  Goto  K;  Ikemoto  S;  Nishijima  K;  Yoshino  T;  Ishiguro  T:  Susceptibility to subsequent episodes of spontaneous recurrence of methamphetamine psychosis.  Drug Alcohol Depend 2001; 64:133—142
[CrossRef] | [PubMed]
 
Takezaki  H;  Inotani  T;  Ikeda  T;  Yasuoka  T:  A case of acute recurrent methamphetamine psychosis characterized by fancy delusions of grandeur.  Seishin Shinkeigaku Zasshi 1984; 86:621—630 (Japanese)
[PubMed]
 
Sato  M:  An experimental study of onset and relapse mechanisms of chronic methamphetamine psychosis.  Seishin Shinkeigaku Zasshi 1979; 81:21—32 (Japanese)
[PubMed]
 
Yui  K;  Ikemoto  U;  Goto  K:  Spontaneous recrudescence of psychotic diseases caused by methamphetamine (a stimulant): the stress type and the role of noradrenaline and dopamine systems.  Nihon Shinkei Seishin Yakurigaku Zasshi 2004; 24:319—320 (Japanese)
[PubMed]
 
Boutros  NN;  Bowers  MB  Jr:  Chronic substance-induced psychotic disorders: state of the literature.  J Neuropsychiatry Clin Neurosci 1996; 8:262—269
[PubMed]
 
Fujii  D:  Risk factors for treatment-resistive methamphetamine psychosis.  J Neuropsychiatry Clin Neurosci 2002; 14:239—240
[CrossRef] | [PubMed]
 
Chen  CK;  Lin  SK;  Sham  PC;  Ball  D;  Loh  EW;  Hsiao  CC;  Chiang  YL;  Ree  SC;  Lee  CH;  Murray  RM:  Pre-morbid characteristics and co-morbidity of methamphetamine users with and without psychosis.  Psychol Med 2003; 33:1407—1414
[CrossRef] | [PubMed]
 
Chen  CK;  Lin  SK;  Sham  PC;  Ball  D;  Loh  el-W;  Murray  RM:  Morbid risk for psychiatric disorder among the relatives of methamphetamine users with and without psychosis.  Am J Med Genet B Neuropsychiatr Genet 2005; 136B:87—91
[CrossRef] | [PubMed]
 
Hanson  GR;  Rau  KS;  Fleckenstein  AE:  The methamphetamine experience: a NIDA partnership.  Neuropharmacology 2004; 47(suppl 1):92—100
[CrossRef] | [PubMed]
 
Shoptaw  SJ;  Kao  U;  Ling  WW:  Treatment for amphetamine psychosis.  Cochrane Database Syst Rev 2008(4):CD003026
[PubMed]
 
Leelahanaj  T;  Kongsakon  R;  Netrakom  P:  A 4-week, double-blind comparison of olanzapine with haloperidol in the treatment of amphetamine psychosis.  J Med Assoc Thai 2005; 88(suppl 3):S43—S52
[PubMed]
 
Misra  L;  Kofoed  L:  Risperidone treatment of methamphetamine psychosis (letter).  Am J Psychiatry 1997; 154:1170
[PubMed]
 
Misra  LK;  Kofoed  L;  Oesterheld  JR;  Richards  GA:  Olanzapine treatment of methamphetamine psychosis.  J Clin Psychopharmacol 2000; 20:393—394
[CrossRef] | [PubMed]
 
Seiden  LS;  Fischman  MW;  Schuster  CR:  Long-term methamphetamine induced changes in brain catecholamines in tolerant rhesus monkeys.  Drug Alcohol Depend 1976; 1:215—219
[CrossRef] | [PubMed]
 
Wagner  GC;  Seiden  LS;  Schuster  CR:  Methamphetamine-induced changes in brain catecholamines in rats and guinea pigs.  Drug Alcohol Depend 1979; 4:435—438
[CrossRef] | [PubMed]
 
Segal  DS;  Kuczenski  R;  O'Neil  ML;  Melega  WP;  Cho  AK:  Escalating dose methamphetamine pretreatment alters the behavioral and neurochemical profiles associated with exposure to a high-dose methamphetamine binge.  Neuropsychopharmacology 2003; 28:1730—1740
[CrossRef] | [PubMed]
 
Wilson  JM;  Kalasinsky  KS;  Levey  AI;  Bergeron  C;  Reiber  G;  Anthony  RM;  Schmunk  GA;  Shannak  K;  Haycock  JW;  Kish  SJ: Striatal dopamine nerve terminal markers in human, chronic methamphetamine users. Nat Med 1996; 2:699—703
 
Glue  P;  Costello  MJ;  Pert  A;  Mele  A;  Nutt  DJ:  Regional neurotransmitter responses after acute and chronic electroconvulsive shock.  Psychopharmacology  (Berl) 1990; 100:60—65
[CrossRef] | [PubMed]
 
Lisanby  SH;  Belmaker  RH:  Animal models of the mechanisms of action of repetitive transcranial magnetic stimulation (RTMS): comparisons with electroconvulsive shock (ECS).  Depress Anxiety 2000; 12:178—187
[CrossRef] | [PubMed]
 
Volkow  ND;  Chang  L;  Wang  GJ;  Fowler  JS;  Franceschi  D;  Sedler  M;  Gatley  SJ;  Miller  E;  Hitzemann  R;  Ding  YS;  Logan  J:  Loss of dopamine transporters in methamphetamine abusers recovers with protracted abstinence.  J Neurosci 2001; 21:9414—9418
[PubMed]
 
Marshall  JF;  Belcher  AM;  Feinstein  EM;  O'Dell  SJ:  Methamphetamine-induced neural and cognitive changes in rodents.  Addiction 2007; 102(suppl 1):61—69
[CrossRef] | [PubMed]
 
Nakajima  K;  Yamazaki  K;  Moriya  H:  Current problems with attitudes and informed consent on ECT: a questionnaire survey of psychiatrists.  Seishin Shinkeigaku Zasshi 1993; 95:537—554 (Japanese)
[PubMed]
 
Freudenmann  RW;  Schonfeldt-Lecuona  C;  Spitzer  M;  Hermle  L;  Gron  G:  Electroconvulsive therapy in the treatment of depression in a former Ecstasy user.  J Psychopharmacol 2006; 20:860—862
[CrossRef] | [PubMed]
 
Jaffe  C;  Bush  KR;  Straits-Troster  K;  Meredith  C;  Romwall  L;  Rosenbaum  G;  Cherrier  M;  Saxon  AJ:  A comparison of methamphetamine-dependent inpatients childhood attention deficit hyperactivity disorder symptomatology.  J Addict Dis 2005; 24:133—152
[CrossRef] | [PubMed]
 
McCann  UD;  Kuwabara  H;  Kumar  A;  Palermo  M;  Abbey  R;  Brasic  J;  Ye  W;  Alexander  M;  Dannals  RF;  Wong  DF;  Ricaurte  GA:  Persistent cognitive and dopamine transporter deficits in abstinent methamphetamine users.  Synapse 2008; 62:91—100
[CrossRef] | [PubMed]
 
References Container
+
+

Self-Assessment Quiz - Expired

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1.
As a result of illicit methamphetamine use, a patient may present to the emergency room with psychosis as well as which of the following?
2.
Sensitization or reverse tolerance refers to which of the following?
3.
Which of the following statement represents the general concurrence of Japanese investigators based on their observations of methamphetamine abuse over 50 years?
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