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Hwang ZA, Li CW, Hsu AL, Wu CW, Chan WP, Huang MC. Assessment of resting cerebral perfusion between methamphetamine-associated psychosis and schizophrenia through arterial spin labeling MRI. Eur Arch Psychiatry Clin Neurosci 2025; 275:873-883. [PMID: 38970667 DOI: 10.1007/s00406-024-01857-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/24/2023] [Accepted: 06/20/2024] [Indexed: 07/08/2024]
Abstract
OBJECTIVE The clinical manifestations of methamphetamine (METH)-associated psychosis (MAP) and acute paranoid schizophrenia (SCZ) are similar. This study aims to assess regional cerebral blood flow (rCBF) in individuals who use METH and in those with SCZ using the MRI arterial spin labeling (ASL) technique. METHODS We prospectively recruited 68 participants and divided them into four groups: MAP (N = 15), SCZ (N = 13), METH users with no psychosis (MNP; N = 22), and normal healthy controls (CRL; N = 18). We measured rCBF using an MRI three-dimensional pseudo-continuous ASL sequence. Clinical variables were assessed using the Positive and Negative Syndrome Scale (PANSS) and Brief Assessment of Cognition in Schizophrenia (BACS). Group-level rCBF differences were analyzed using a two-sample t-test. RESULTS Decreased rCBF was found in the precuneus, premotor cortex, caudate nucleus, dorsolateral prefrontal cortex, and thalamus in the MNP group compared with the CRL group. The MAP group had significantly decreased rCBF in the precuneus, hippocampus, anterior insula, inferior temporal gyrus, inferior orbitofrontal gyrus, and superior occipital gyrus compared with the MNP group. Increased rCBF in the precuneus and premotor cortex was seen in the MAP group compared with the SCZ group. rCBF in the precuneus and premotor cortex significantly correlated negatively with the PANSS but correlated positively with BACS scores in the MAP and SCZ groups. CONCLUSION METH exposure was associated with decreased rCBF in the precuneus and premotor cortex. Patients with MAP exhibited higher rCBF than those with SCZ, implying preserved insight and favorable outcomes. rCBF can therefore potentially serve as a diagnostic approach to differentiate patients with MAP from those with SCZ.
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Affiliation(s)
- Zhen-An Hwang
- Department of Radiology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
- Department of Radiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
| | - Chia-Wei Li
- Department of Radiology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
- GE Healthcare, Taipei, Taiwan
| | - Ai-Ling Hsu
- Bachelor Program in Artificial Intelligence, Chang Gung University, Taoyuan, Taiwan
- Department of Psychiatry, Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan
| | - Changwei W Wu
- Graduate Institute of Mind, Brain and Consciousness (GIMBC), Taipei Medical University, Taipei, Taiwan
| | - Wing P Chan
- Department of Radiology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
- Department of Radiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
| | - Ming-Chyi Huang
- Department of Addiction Sciences, Taipei City Psychiatric Center, Taipei City Hospital, Taipei, Taiwan
- Department of Psychiatry, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
- Psychiatric Research Center, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
- Psychiatric Research Center, Taipei Medical University Hospital, Taipei, Taiwan
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Ogyu K, Matsushita K, Honda S, Wada M, Tamura S, Takenouchi K, Tobari Y, Kusudo K, Kato H, Koizumi T, Arai N, Koreki A, Matsui M, Uchida H, Fujii S, Onaya M, Hirano Y, Mimura M, Nakajima S, Noda Y. Decrease in gamma-band auditory steady-state response in patients with treatment-resistant schizophrenia. Schizophr Res 2023; 252:129-137. [PMID: 36641960 DOI: 10.1016/j.schres.2023.01.011] [Citation(s) in RCA: 11] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/24/2022] [Revised: 09/26/2022] [Accepted: 01/05/2023] [Indexed: 01/15/2023]
Abstract
BACKGROUND Thirty percent of patients with schizophrenia do not respond to non-clozapine antipsychotics and are termed treatment-resistant schizophrenia (TRS). The 40-Hz auditory steady-state response (ASSR) is a well-known to be reduced in patients with schizophrenia compared to healthy controls (HCs), suggesting impaired gamma oscillation in schizophrenia. Given no ASSR study on TRS, we aimed to examine the neurophysiological basis of TRS employing 40-Hz ASSR paradigm. METHOD We compared ASSR measures among HCs, patients with non-TRS, and patients with TRS. TRS criteria were defined by a score of 4 or higher on two items of the Positive and Negative Syndrome Scale (PANSS) positive symptoms despite standard antipsychotic treatment. Participants were examined for ASSR with 40-Hz click-train stimulus, and then time-frequency analysis was performed to calculate evoked power and phase-locking factor (PLF) of 40-Hz ASSR. RESULTS A total of 79 participants were included: 27 patients with TRS (PANSS = 92.6 ± 15.8); 27 patients with non-TRS (PANSS = 63.3 ± 14.7); and 25 HCs. Evoked power in 40-Hz ASSR was lower in the TRS group than in the HC group (F2,79 = 8.37, p = 0.015; TRS vs. HCs: p = 0.012, d = 1.1) while no differences in PLF were found between the groups. CONCLUSION These results suggest that glutamatergic and GABAergic neurophysiological dysfunctions are involved in the pathophysiology of TRS. Our findings warrant more comprehensive and longitudinal studies for deep phenotyping of TRS.
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Affiliation(s)
- Kamiyu Ogyu
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan; Department of Psychiatry, National Hospital Organization Shimofusa Psychiatric Medical Center, Chiba 266-0007, Japan
| | - Karin Matsushita
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan
| | - Shiori Honda
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan
| | - Masataka Wada
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan
| | - Shunsuke Tamura
- Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan
| | - Kazumasa Takenouchi
- Department of Clinical Laboratory Medicine, National Hospital Organization Shimofusa Psychiatric Medical Center, Chiba 266-0007, Japan
| | - Yui Tobari
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan; Faculty of Environment and Information Studies, Keio University, Kanagawa, Kanagawa 252-0882, Japan
| | - Keisuke Kusudo
- Department of Psychiatry, National Hospital Organization Chiba Medical Center, Chiba 260-8606, Japan
| | - Hideo Kato
- Department of Epileptology, National Center of Neurology and Psychiatry Hospital, 4-1-1 Ogawa-Higashi, Kodaira, Tokyo 187-8551, Japan
| | - Teruki Koizumi
- Department of Psychiatry, National Hospital Organization Shimofusa Psychiatric Medical Center, Chiba 266-0007, Japan
| | - Naohiro Arai
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan
| | - Akihiro Koreki
- Department of Psychiatry, National Hospital Organization Shimofusa Psychiatric Medical Center, Chiba 266-0007, Japan
| | - Mie Matsui
- Department of Clinical Cognitive Neuroscience, Institute of Liberal Arts and Science, Kanazawa University, Kanazawa 920-1164, Japan
| | - Hiroyuki Uchida
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan
| | - Shinya Fujii
- Faculty of Environment and Information Studies, Keio University, Kanagawa, Kanagawa 252-0882, Japan
| | - Mitsumoto Onaya
- Department of Psychiatry, National Hospital Organization Shimofusa Psychiatric Medical Center, Chiba 266-0007, Japan
| | - Yoji Hirano
- Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; Department of Psychiatry, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, Japan
| | - Masaru Mimura
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan
| | - Shinichiro Nakajima
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan; Multimodal Imaging Group, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, ON M6J 1H4, Canada.
| | - Yoshihiro Noda
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo 160-8582, Japan.
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3
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Rungnirundorn T, Krusong K, Kalayasiri R, Maes M. Leukocyte telomere length is not shortened in methamphetamine dependence or methamphetamine-induced psychosis but is increased following traumatic events. World J Biol Psychiatry 2022; 23:613-621. [PMID: 34895035 PMCID: PMC9991870 DOI: 10.1080/15622975.2021.2016957] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/23/2021] [Revised: 12/06/2021] [Accepted: 12/07/2021] [Indexed: 01/25/2023]
Abstract
OBJECTIVE This study aims to examine the effects of methamphetamine (MA) use and dependence and MA withdrawal symptoms on the telomere length and whether shortening of the latter is associated with MA-induced psychosis (MIP). METHODS This study included 185 MA-abuse, 118 MA-dependent, and 67 MIP patients, diagnosed using DSM-IV criteria. The Semi-structured Assessment for Drug Dependence and Alcoholism (SSADDA) questionnaire was employed to collect MA-related data. MIP was confirmed using the Methamphetamine Experience Questionnaire (MEQ). The leukocyte telomere length was measured using real-time polymerase chain reaction measuring the Telomere/Single gene ratio (T/S ratio). Data were analysed using multivariate statistical analyses. RESULTS There were no significant associations between the T/S ratio and severity of MA-use, MIP, and MA withdrawal symptoms. MIP was significantly predicted by alcohol dependence, antisocial personality disorder, and MA-use severity. There were significantly positive associations between the T/S ratio and previous traumatic and life-threatening events. The T/S ratio was not affected by alcohol and nicotine dependence. Alcohol and nicotine dependence, antisocial personality disorder, and severity of MA use increased risk of MA withdrawal symptoms. CONCLUSION MIP and MA-use severity are not associated with leukocyte telomere length, but previous traumatic and life-threatening events are associated with increased telomere length.
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Affiliation(s)
| | - Kuakarun Krusong
- Structural and Computational Biology Research Unit, Department of Biochemistry, Faculty of Science, Chulalongkorn University, Bangkok, Thailand
| | - Rasmon Kalayasiri
- Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand
| | - Michael Maes
- Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand
- Department of Psychiatry, Medical University of Plovdiv, Plovdiv, Bulgaria
- IMPACT Strategic Research Centre, Deakin University, PO Box 281, Geelong, VIC, 3220, Australia
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Fiorentini A, Cantù F, Crisanti C, Cereda G, Oldani L, Brambilla P. Substance-Induced Psychoses: An Updated Literature Review. Front Psychiatry 2021; 12:694863. [PMID: 35002789 PMCID: PMC8732862 DOI: 10.3389/fpsyt.2021.694863] [Citation(s) in RCA: 46] [Impact Index Per Article: 11.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/13/2021] [Accepted: 11/17/2021] [Indexed: 01/22/2023] Open
Abstract
Background: On the current psychopharmacological panorama, the variety of substances able to provoke an episode of acute psychosis is rapidly increasing. Such psychotic episodes are classified according to the major category of symptoms: positive, negative, or cognitive psychotic episodes. On one hand, the abuse of methamphetamines, cannabis, and cocaine plays a big role in increasing the incidence of episodes resembling a psychotic disorder. On the other hand, the progress in terms of pharmacodynamics knowledge has led to the synthesis of new drugs, such as cannabinoids and cathinone's, which have rapidly entered into the common pool of abusers' habits. Regarding these newly synthesized substances of abuse, further clinical studies are needed to understand their psychogenic properties. The topic of this review is complicated due to the frequent abuse of psychotomimetic drugs by patients affected by psychotic disorders, a fact that makes it extremely difficult to distinguish between an induced psychosis and a re-exacerbation of a previously diagnosed disorder. Methods: The present narrative review summarizes results from clinical studies, thus investigating the psychotogenic properties of abused substances and the psychotic symptoms they can give rise to. It also discusses the association between substance abuse and psychosis, especially with regards to the differential diagnosis between a primary vs. a substance-induced psychotic disorder. Findings: Our findings support the theory that psychosis due to substance abuse is commonly observed in clinical practice. The propensity to develop psychosis seems to be a function of the severity of use and addiction. Of note, from a phenomenological point of view, it is possible to identify some elements that may help clinicians involved in differential diagnoses between primary and substance-induced psychoses. There remains a striking paucity of information on the outcomes, treatments, and best practices of substance-induced psychotic episodes.
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Affiliation(s)
- Alessio Fiorentini
- Department of Neurosciences and Mental Health, Fondazione Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Ca' Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy
| | - Filippo Cantù
- Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy
| | - Camilla Crisanti
- Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy
| | - Guido Cereda
- Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy
| | - Lucio Oldani
- Department of Neurosciences and Mental Health, Fondazione Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Ca' Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy
| | - Paolo Brambilla
- Department of Neurosciences and Mental Health, Fondazione Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Ca' Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy
- Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy
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Abstract
Methamphetamine abuse leads to devastating consequences, including addiction, crime, and death. Despite decades of research, no medication has been approved by the U.S. Food and Drug Administration for the treatment of Methamphetamine Use Disorder. Thus, there is a need for new therapeutic approaches. Animal studies demonstrate that methamphetamine exposure dysregulates forebrain function involving the Group-I metabotropic glutamate receptor subtype 5 (mGlu5), which is predominantly localized to postsynaptic sites. Allosteric modulators of mGlu5 offer a unique opportunity to modulate glutamatergic neurotransmission selectively, thereby potentially ameliorating methamphetamine-induced disruptions. Negative allosteric modulators of mGlu5 attenuate the effects of methamphetamine, including rewarding/reinforcing properties of the drug across animal models, and have shown promising effects in clinical trials for Anxiety Disorder and Major Depressive Disorder. Preclinical studies have also sparked great interest in mGlu5 positive allosteric modulators, which exhibit antipsychotic and anxiolytic properties, and facilitate extinction learning when access to methamphetamine is removed, possibly via the amelioration of methamphetamine-induced cognitive deficits. Clinical research is now needed to elucidate the mechanisms underlying the mGlu5 receptor-related effects of methamphetamine and the contributions of these effects to addictive behaviors. The growing array of mGlu5 allosteric modulators provides excellent tools for this purpose and may offer the prospect of developing tailored and effective medications for Methamphetamine Use Disorder.
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McKetin R, Leung J, Stockings E, Huo Y, Foulds J, Lappin JM, Cumming C, Arunogiri S, Young JT, Sara G, Farrell M, Degenhardt L. Mental health outcomes associated with of the use of amphetamines: A systematic review and meta-analysis. EClinicalMedicine 2019; 16:81-97. [PMID: 31832623 PMCID: PMC6890973 DOI: 10.1016/j.eclinm.2019.09.014] [Citation(s) in RCA: 99] [Impact Index Per Article: 16.5] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/13/2019] [Revised: 09/20/2019] [Accepted: 09/20/2019] [Indexed: 01/25/2023] Open
Abstract
BACKGROUND The use of amphetamines is a global public health concern. We summarise global data on use of amphetamines and mental health outcomes. METHODS A systematic review and meta-analysis (CRD 42017081893). We searched Medline, EMBASE, PsycInfo for methamphetamine or amphetamine combined with psychosis, violence, suicidality, depression or anxiety. Included studies were human empirical cross-sectional surveys, case-control studies, cohort studies and randomised controlled trials that assessed the association between methamphetamine and one of the mental health outcomes. Random effects meta-analysis was used to pool results for any use of amphetamines and amphetamine use disorders. FINDINGS 149 studies were eligible and 59 were included in meta-analyses. There was significant heterogeneity in effects. Evidence came mostly from cross-sectional studies. Any use of amphetamines was associated with higher odds of psychosis (odds ratio [OR] = 2.0, 95%CI 1.3-3.3), violence (OR = 2.2, 95%CI 1.2-4.1; adjusted OR [AOR] = 1.4, 95%CI 0.8-2.4), suicidality OR = 4.4, 95%CI 2.4-8.2; AOR = 1.7, 95%CI 1.0-2.9) and depression (OR = 1.6, 95%CI 1.1-2.2; AOR = 1.3, 95%CI 1.2-1.4). Having an amphetamine use disorder was associated with higher odds of psychosis (OR = 3.0, 95%CI 1.9-4.8; AOR = 2.4, 95%CI 1.6-3.5), violence (OR = 6.2, 95%CI 3.1-12.3), and suicidality (OR = 2.3, 95%CI 1.8-2.9; AOR = 1.5, 95%CI 1.3-1.8). INTERPRETATION Methamphetamine use is an important risk factor for poor mental health. High quality population-level studies are needed to more accurately quantify this risk. Clinical responses to methamphetamine use need to address mental health harms.
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Affiliation(s)
- Rebecca McKetin
- National Drug and Alcohol Research Centre, University of New South Wales, Sydney, Australia
- Corresponding author.
| | - Janni Leung
- National Drug and Alcohol Research Centre, University of New South Wales, Sydney, Australia
- Faculty of Health and Behavioural Sciences, The University of Queensland, Australia
| | - Emily Stockings
- National Drug and Alcohol Research Centre, University of New South Wales, Sydney, Australia
| | - Yan Huo
- Faculty of Health and Behavioural Sciences, The University of Queensland, Australia
| | - James Foulds
- Department of Psychological Medicine, University of Otago, Christchurch, New Zealand
| | - Julia M. Lappin
- National Drug and Alcohol Research Centre, University of New South Wales, Sydney, Australia
- School of Psychiatry, University of NSW, Sydney, Australia
| | - Craig Cumming
- School of Population and Global Health, The University of Western Australia, Perth, Western Australia, Australia
| | - Shalini Arunogiri
- Turning Point, Eastern Health, Richmond, VIC, Australia
- Eastern Health Clinical School, Monash University, Box Hill, VIC, Australia
| | - Jesse T. Young
- School of Population and Global Health, The University of Western Australia, Perth, Western Australia, Australia
- National Drug Research Institute, Curtin University, Perth, Australia
- Justice Health Unit, Centre for Health Equity, Melbourne School of Population and Global Health, The University of Melbourne, Parkville, VIC, Australia
- Centre for Adolescent Health, Murdoch Children's Research Institute, Parkville, VIC, Australia
| | - Grant Sara
- Northern Clinical School, Sydney Medical School, University of Sydney, Australia
- InforMH, System Information and Analytics Branch, NSW Ministry of Health, Australia
| | - Michael Farrell
- National Drug and Alcohol Research Centre, University of New South Wales, Sydney, Australia
| | - Louisa Degenhardt
- National Drug and Alcohol Research Centre, University of New South Wales, Sydney, Australia
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Abstract
BACKGROUND AND AIMS To review early case reports and experimental inductions of amphetamine and methamphetamine psychosis, prior to the prohibition of these drugs, to gain a better understanding of the nature and aetiology of methamphetamine psychosis. METHODS Papers considered were historical case reports and case series of psychosis relating to the use and misuse of prescription amphetamine, focusing upon papers by Young & Scoville (1938), Connell (1958), and three subsequent experimental studies published in the early 1970s (Griffith 1972, Angrist & Gershon 1970 and Bell 1973), where psychosis was induced in volunteers using high-dose amphetamine and methamphetamine. RESULTS High-dose methamphetamine and amphetamine can result in a paranoid psychosis which remits rapidly (within days) of discontinuing use. The central feature is paranoia occurring in a clear state of consciousness. This may be accompanied by other psychotic symptoms (e.g. hallucinations). Pre-existing schizophrenia is not necessary, and the syndrome is not due to sleep deprivation. CONCLUSIONS Research findings from the 1930s to the 1970s suggest that paranoid psychosis should be considered a probable consequence of high-dose methamphetamine use. Individuals who experience psychotic symptoms for any substantive period after intoxication has ended should be suspected of having a functional non-organic psychosis, or a latent vulnerability thereto.
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Affiliation(s)
- Rebecca McKetin
- National Drug Research Institute, Curtin University, Perth, Australia.,National Drug and Alcohol Research Centre, University of New South Wales, Sydney, Australia
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Kawano T, Oshibuchi H, Kawano M, Muraoka H, Tsutsumi T, Yamada M, Ishigooka J, Nishimura K, Inada K. Diazepam suppresses the stress-induced dopaminergic release in the amygdala of methamphetamine-sensitized rat. Eur J Pharmacol 2018; 833:247-254. [PMID: 29885289 DOI: 10.1016/j.ejphar.2018.05.048] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/14/2017] [Revised: 05/31/2018] [Accepted: 05/31/2018] [Indexed: 10/14/2022]
Abstract
Although the benzodiazepine class of drugs has proven useful in treating anxiety symptoms, recent studies yield no consistent empirical support for their use in treating psychiatric disorders. However, animal studies using a fear conditioning paradigm have suggested that benzodiazepines facilitate fear memory extinction, dependent on treatment timing and subject conditions. However, we have no data on the effect of subject conditions. The purpose of this study was to investigate whether the effect of benzodiazepines depends on hypersensitivity to fear-memory processing. We examined the effect of diazepam, a benzodiazepine, on the extracellular dopamine level in the left amygdala of methamphetamine-sensitized, fear-conditioned model rats, using microdialysis and high-performance liquid chromatography. In this model, the dopamine level in the amygdala excessively increases in response to a fear-conditioned stimulus; the phenomenon has been proposed as a biological marker for hypersensitivity to fear-memory processing. Diazepam inhibited this excessive increase. The extent of the inhibitory effect was greater in the sensitized condition. Diazepam alone increased amygdalar dopamine levels under physiological conditions but not under sensitized conditions. Diazepam did not shorten freezing time in any group. These results suggest that diazepam modulates amygdala dopamine with state dependence and that amygdalar dopamine fine-tuning accounts for part of the therapeutic effect of benzodiazepines on fear memory processing. Further investigation is required to identify patients suitable for treatment with benzodiazepines. This is the first report on the pharmacodynamic effects of benzodiazepine on the amygdalar dopamine basal level and on fear memory processing.
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Affiliation(s)
- Takaaki Kawano
- Department of Psychiatry, Tokyo Women's Medical University, Kawada-cho 8-1, Shinjuku-ku, Tokyo 162-8666, Japan.
| | - Hidehiro Oshibuchi
- Department of Psychiatry, Tokyo Women's Medical University, Kawada-cho 8-1, Shinjuku-ku, Tokyo 162-8666, Japan.
| | - Masahiko Kawano
- Department of Psychiatry, Tokyo Women's Medical University, Kawada-cho 8-1, Shinjuku-ku, Tokyo 162-8666, Japan.
| | - Hiroyuki Muraoka
- Department of Psychiatry, Tokyo Women's Medical University, Kawada-cho 8-1, Shinjuku-ku, Tokyo 162-8666, Japan.
| | - Takahiro Tsutsumi
- Department of Psychiatry, Tokyo Women's Medical University, Kawada-cho 8-1, Shinjuku-ku, Tokyo 162-8666, Japan.
| | - Makiko Yamada
- Department of Psychiatry, Tokyo Women's Medical University, Kawada-cho 8-1, Shinjuku-ku, Tokyo 162-8666, Japan.
| | - Jun Ishigooka
- CNS Pharmacological Research Institute, 4-26-11, Sendagaya, Shibuya-ku, Tokyo 151-0051, Japan.
| | - Katsuji Nishimura
- Department of Psychiatry, Tokyo Women's Medical University, Kawada-cho 8-1, Shinjuku-ku, Tokyo 162-8666, Japan.
| | - Ken Inada
- Department of Psychiatry, Tokyo Women's Medical University, Kawada-cho 8-1, Shinjuku-ku, Tokyo 162-8666, Japan.
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Arunogiri S, McKetin R, Verdejo-Garcia A, Lubman DI. The Methamphetamine-Associated Psychosis Spectrum: a Clinically Focused Review. Int J Ment Health Addict 2018. [DOI: 10.1007/s11469-018-9934-4] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/16/2022] Open
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Gan H, Zhao Y, Jiang H, Zhu Y, Chen T, Tan H, Zhong N, Du J, Zhao M. A Research of Methamphetamine Induced Psychosis in 1,430 Individuals With Methamphetamine Use Disorder: Clinical Features and Possible Risk Factors. Front Psychiatry 2018; 9:551. [PMID: 30459651 PMCID: PMC6232294 DOI: 10.3389/fpsyt.2018.00551] [Citation(s) in RCA: 15] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/30/2018] [Accepted: 10/15/2018] [Indexed: 12/22/2022] Open
Abstract
Background and Aims: Methamphetamine (MA) abuse is commonly associated with the development of psychotic symptoms. The predictors and related risk factors of MA induced psychosis (MIP) are poorly understood. We investigated the occurrence of MIP, and analyzed the clinical features and possible risk factors among individuals with MA use disorder Method: One thousand four hundred and thirty participants with MA use disorder were recruited from compulsory rehabilitation centers in Shanghai. A structured questionnaire including demographic characteristics, drug use history, visual analog scales, Beck Depression Inventory-13 (BDI-13), and Hamilton anxiety scale-14 (HAMA-14) were used to collect clinical related information. Fifty-six participants had accomplished the test of CogState Battery. Results: Among the 1430 individuals with MA use disorder, 37.1% were diagnosed as MIP according DSM-IV. There were significant differences in age, marital status, age of drug use onset, MA use years, Average MA use dose, interval of MA use, maximum dose, concurrent use of alcohol, and other drugs, VAS score, MA dependence, BDI-13 scores, HAMA-14 scores, verbal learning memory, and visual learning memory between the MIP group and the none MIP group (P < 0.05). The age of drug use onset (OR = 0.978, p = 0.011), average drug use dose (OR = 1.800, p = 0.015), craving score (OR = 1.069, p = 0.031), MA dependence (OR = 2.214, p < 0.001), and HAMA scores (OR = 1.028, p < 0.001) were associated to MIP. Conclusion: Individuals with MIP had more severe drug use problems, emotional symptoms and cognitive impairment. Earlier onset of drug use, higher quantity of drug use, higher craving, middle or severe drug use disorder and more anxiety symptoms may be related risk factors of MIP.
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Affiliation(s)
- Hong Gan
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Yan Zhao
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Haifeng Jiang
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Youwei Zhu
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Tianzhen Chen
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Haoye Tan
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Na Zhong
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Jiang Du
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Min Zhao
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.,Shanghai Key Laboratory of Psychotic Disorders, Shanghai, China
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Wearne TA, Parker LM, Franklin JL, Goodchild AK, Cornish JL. Behavioral sensitization to methamphetamine induces specific interneuronal mRNA pathology across the prelimbic and orbitofrontal cortices. Prog Neuropsychopharmacol Biol Psychiatry 2017; 77:42-48. [PMID: 28351548 DOI: 10.1016/j.pnpbp.2017.03.018] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/16/2017] [Revised: 03/15/2017] [Accepted: 03/23/2017] [Indexed: 12/31/2022]
Abstract
Schizophrenia is associated with significant pathophysiological changes to interneurons within the prefrontal cortex (PFC), with mRNA and protein changes associated with the GABA network localized to specific interneuron subtypes. Methamphetamine is a commonly abused psychostimulant that can induce chronic psychosis and symptoms that are similar to schizophrenia, suggesting that chronic METH induced psychosis may be associated with similar brain pathology to schizophrenia in the PFC. The aim of this study, therefore, was to examine mRNA expression of interneuron markers across two regions of the PFC (prelimbic (PRL) and orbitofrontal cortices (OFC)) following METH sensitization, an animal model of METH psychosis. We also studied the association between GABA mRNA expression and interneuronal mRNA expression to identify whether particular changes to the GABA network could be localized to a specific inhibitory cellular phenotype. METH sensitization increased the transcriptional expression of calbindin, calretinin, somatostatin, cholecyctokinin and vasoactive intestinal peptide in the PRL while parvalbumin, calbindin, cholectokinin and vasoactive intestinal peptide were upregulated in the OFC. Based on our previous findings, we also found significant correlations between GAD67, GAT1 and parvalbumin while GAD67, GAD65 and GAT1 were positively correlated with cholecystokinin in the PRL of METH sensitized rats. Within the OFC, the expression of GABAAα1 was positively correlated with somatostatin while GABAAα5 was negatively associated with somatostatin and calbindin. These findings suggest that METH sensitization differentially changes the expression of mRNAs encoding for multiple peptides and calcium binding proteins across the PRL and the OFC. Furthermore, these findings support that changes to the GABA network may also occur within specific cell types. These results, therefore, provide the first evidence that METH sensitization mediates differential interneuronal pathology across the PRL and OFC and such changes could have profound consequences on behavior and cognitive output.
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Affiliation(s)
- Travis A Wearne
- Department of Psychology, Faculty of Human Sciences, Centre for Emotional Health, Macquarie University, Sydney, NSW, Australia
| | - Lindsay M Parker
- Department of Biomedical Science, Faculty of Medicine and Health Science, Macquarie University, Sydney, NSW, Australia; ARC Center of Excellence for Nanoscale BioPhotonics, Macquarie University, Sydney, NSW, Australia
| | - Jane L Franklin
- Department of Psychology, Faculty of Human Sciences, Centre for Emotional Health, Macquarie University, Sydney, NSW, Australia
| | - Ann K Goodchild
- Department of Biomedical Science, Faculty of Medicine and Health Science, Macquarie University, Sydney, NSW, Australia
| | - Jennifer L Cornish
- Department of Psychology, Faculty of Human Sciences, Centre for Emotional Health, Macquarie University, Sydney, NSW, Australia; ARC Center of Excellence for Nanoscale BioPhotonics, Macquarie University, Sydney, NSW, Australia.
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12
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Willi TS, Barr AM, Gicas K, Lang DJ, Vila-Rodriguez F, Su W, Thornton AE, Leonova O, Giesbrecht CJ, Procyshyn RM, Rauscher A, MacEwan WG, Honer WG, Panenka WJ. Characterization of white matter integrity deficits in cocaine-dependent individuals with substance-induced psychosis compared with non-psychotic cocaine users. Addict Biol 2017; 22:873-881. [PMID: 26833821 DOI: 10.1111/adb.12363] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/02/2015] [Revised: 11/10/2015] [Accepted: 12/11/2015] [Indexed: 01/19/2023]
Abstract
With sufficient drug exposure, some individuals develop transient psychotic symptoms referred to as 'substance-induced psychosis' (SIP), which closely resemble the symptoms observed in schizophrenia spectrum disorders. The comparability in psychotic presentation between SIP and the schizophrenias suggests that similar underlying neural deficits may contribute to the emergence of psychosis across these disorders. Only a small number of studies have investigated structural alterations in SIP, and all have been limited to volumetric imaging methods, with none controlling for the effects of chronic drug exposure. To investigate white matter abnormalities associated with SIP, diffusion tensor imaging was employed in a group of individuals with cocaine-associated psychosis (CAP; n = 24) and a cocaine-dependent non-psychotic (CDN) group (n = 43). Tract-based spatial statistics was used to investigate group differences in white matter diffusion parameters. The CAP group showed significantly lower fractional anisotropy values than the CDN group (p < 0.05) in voxels within white matter tracts of fronto-temporal, fronto-thalamic and interhemispheric pathways. The greatest differences in white matter integrity were present in the corpus callosum, corona radiata, bilateral superior longitudinal fasciculi and bilateral inferior longitudinal fasciculi. Additionally, the CAP group had voxels of significantly higher radial diffusivity in a subset of the previously mentioned pathways. These results are the first description of white matter integrity abnormalities in a SIP sample and indicate that differences in these pathways may be a shared factor in the expression of different forms of psychosis.
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Affiliation(s)
- Taylor S. Willi
- Department of Psychiatry; University of British Columbia; Vancouver Canada
| | - Alasdair M. Barr
- Department of Pharmacology; University of British Columbia; Vancouver Canada
| | - Kristina Gicas
- Department of Psychology; Simon Fraser University; Burnaby Canada
| | - Donna J. Lang
- Department of Radiology; University of British Columbia; Vancouver Canada
| | | | - Wayne Su
- Department of Psychiatry; University of British Columbia; Vancouver Canada
| | | | - Olga Leonova
- Department of Psychiatry; University of British Columbia; Vancouver Canada
| | | | - Ric M. Procyshyn
- Department of Psychiatry; University of British Columbia; Vancouver Canada
| | - Alexander Rauscher
- Department of Radiology; University of British Columbia; Vancouver Canada
| | - William G. MacEwan
- Department of Psychiatry; University of British Columbia; Vancouver Canada
| | - William G. Honer
- Department of Psychiatry; University of British Columbia; Vancouver Canada
| | - William J. Panenka
- Department of Psychiatry; University of British Columbia; Vancouver Canada
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13
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T Bakare A. Psychoactive Substances Use among In-patients in a Nigerian Neuropsychiatric Hospital: Prevalence, Pattern and Presentation. ACTA ACUST UNITED AC 2016. [DOI: 10.15406/mojamt.2016.02.00016] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/06/2022]
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14
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Willi TS, Lang DJ, Honer WG, Smith GN, Thornton AE, Panenka WJ, Procyshyn RM, Vila-Rodriguez F, Su W, Vertinsky AT, Leonova O, Rauscher A, MacEwan GW, Barr AM. Subcortical grey matter alterations in cocaine dependent individuals with substance-induced psychosis compared to non-psychotic cocaine users. Schizophr Res 2016; 176:158-163. [PMID: 27499362 DOI: 10.1016/j.schres.2016.08.001] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/05/2016] [Revised: 07/29/2016] [Accepted: 08/02/2016] [Indexed: 11/28/2022]
Abstract
After prolonged psychostimulant abuse, transient psychotic symptoms referred to as "substance-induced psychosis" (SIP) can develop - closely resembling symptoms observed in schizophrenia spectrum disorders. The comparability in psychotic presentation between SIP and schizophrenias suggests that similar underlying neural deficits may contribute to the expression of psychosis across these disorders. To date, neuroanatomical characterization of grey matter structural alterations in SIP has been limited to methamphetamine associated psychosis, with no studies controlling for potential neurotoxic effects of the psychostimulant that precipitates psychosis. To investigate grey matter subcortical alterations in SIP, a voxel-based analysis of magnetic resonance images (MRI) was performed between a group of 74 cocaine dependent nonpsychotic individuals and a group of 29 individuals with cocaine-associated psychosis. The cocaine-associated psychosis group had significantly smaller volumes of the thalamus and left hippocampus, controlling for age, total brain volume, current methamphetamine dependence, and current marijuana dependence. No differences were present in bilateral caudate structures. The findings of reduced thalamic and hippocampal volumes agree with previous reports in the schizophrenia literature, suggesting alterations of these structures are not specific to schizophrenia, but may be common to multiple forms of psychosis.
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Affiliation(s)
- Taylor S Willi
- Department of Psychiatry, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada
| | - Donna J Lang
- Department of Radiology, University of British Columbia, Vancouver V5Z 1M9, Canada
| | - William G Honer
- Department of Psychiatry, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada
| | - Geoff N Smith
- Department of Psychiatry, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada
| | - Allen E Thornton
- Department of Psychology, Simon Fraser University, Burnaby B.C. V5A 1S6, Canada
| | - William J Panenka
- Department of Psychiatry, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada
| | - Ric M Procyshyn
- Department of Psychiatry, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada
| | - Fidel Vila-Rodriguez
- Department of Psychiatry, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada
| | - Wayne Su
- Department of Psychiatry, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada
| | - A Talia Vertinsky
- Department of Psychiatry, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada
| | - Olga Leonova
- Department of Psychiatry, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada
| | - Alexander Rauscher
- Department of Radiology, University of British Columbia, Vancouver V5Z 1M9, Canada
| | - G William MacEwan
- Department of Psychiatry, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada
| | - Alasdair M Barr
- Department of Pharmacology, 2176 Health Sciences Mall, University of British Columbia, Vancouver B.C. V6T 1Z3, Canada.
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15
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Thomas E, Lategan H, Verster C, Kidd M, Weich L. Methamphetamine-induced psychosis: Clinical features, treatment modalities and outcomes. S Afr J Psychiatr 2016; 22:980. [PMID: 30263171 PMCID: PMC6138095 DOI: 10.4102/sajpsychiatry.v22i1.980] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/26/2016] [Accepted: 07/12/2016] [Indexed: 11/10/2022] Open
Abstract
OBJECTIVE To investigate the clinical features, prescribing patterns and outcomes of psychiatric inpatients admitted with methamphetamine-induced psychosis. METHOD A cross-sectional, descriptive pilot study was conducted between March 2014 and August 2014 at three South African Mental Health Care Act designated hospitals prior to admission to a psychiatric hospital. Patients with methamphetamine-related psychotic symptoms according to the DSM-5 criteria were eligible. Structured face-to-face interviews were conducted and the Brief Psychiatric Rating Scale was employed as a measure of current psychopathology. RESULTS Fifty-six participants were included. Positive psychotic symptoms (e.g. hallucinations) were more prominent than negative symptoms (e.g. affective blunting). Almost half the participants (43%) had previous episodes of methamphetamine-induced psychosis. Within this group, all had defaulted on the prescribed treatment prior to admission. Only 29% of the participants had received prior formal substance-use rehabilitation as treatment for their disorder. High rates of comorbid cannabis and alcohol use (51%) were recorded. Most of the participants required transfer to specialist psychiatric hospitals. The amounts of methamphetamine used were not a predictor of the persistence of psychosis; however, the pattern of use was. CONCLUSION Clinical features correspond with other international findings. The currently employed model of sequential, non-integrated psychiatric and substance use treatment in this setting appears ineffective.
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Affiliation(s)
- Eileen Thomas
- Department of Psychiatry, Stellenbosch University, South Africa
| | - Helena Lategan
- Department of Psychiatry, Stellenbosch University, South Africa
| | - Chris Verster
- Department of Psychiatry, Stellenbosch University, South Africa
| | - Martin Kidd
- Centre for Statistical Consultation, Stellenbosch University, South Africa
| | - Lize Weich
- Department of Psychiatry, Stellenbosch University, South Africa
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16
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Asor E, Ben-Shachar D. Gene environment interaction in periphery and brain converge to modulate behavioral outcomes: Insights from the SP1 transient early in life interference rat model. World J Psychiatry 2016; 6:294-302. [PMID: 27679768 PMCID: PMC5031929 DOI: 10.5498/wjp.v6.i3.294] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/23/2016] [Revised: 07/21/2016] [Accepted: 08/08/2016] [Indexed: 02/05/2023] Open
Abstract
It is generally assumed that behavior results from an interaction between susceptible genes and environmental stimuli during critical life stages. The present article reviews the main theoretical and practical concepts in the research of gene environment interaction, emphasizing the need for models simulating real life complexity. We review a novel approach to study gene environment interaction in which a brief post-natal interference with the expression of multiple genes, by hindering the activity of the ubiquitous transcription factor specificity protein 1 (Sp1) is followed by later-in-life exposure of rats to stress. Finally, this review discusses the role of peripheral processes in behavioral responses, with the Sp1 model as one example demonstrating how specific behavioral patterns are linked to modulations in both peripheral and central physiological processes. We suggest that models, which take into account the tripartite reciprocal interaction between the central nervous system, peripheral systems and environmental stimuli will advance our understanding of the complexity of behavior.
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17
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Samiei M, Vahidi M, Rezaee O, Yaraghchi A, Daneshmand R. Methamphetamine-Associated Psychosis and Treatment With Haloperidol and Risperidone: A Pilot Study. IRANIAN JOURNAL OF PSYCHIATRY AND BEHAVIORAL SCIENCES 2016; 10:e7988. [PMID: 27822286 PMCID: PMC5097836 DOI: 10.17795/ijpbs-7988] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Received: 11/15/2015] [Revised: 04/11/2015] [Accepted: 08/05/2016] [Indexed: 11/25/2022]
Abstract
BACKGROUND Different studies have suggested that antipsychotic medications of the first generation have better effectiveness for the treatment of psychotic symptoms compared with antipsychotic medications of the second generation. OBJECTIVES The current study was the first pilot study in Iran that compared Haloperidol with Risperidone in the treatment of positive symptoms of psychosis among a group of methamphetamine-dependent patients. MATERIALS AND METHODS This randomized clinical trial was designed and conducted in 2012. Overall, 44 patients who met the diagnostic and statistical manual of mental disorders, fourth edition-text revised (DSM.IV-TR) criteria for methamphetamine-associated psychosis (MAP) and were hospitalized at Razi psychiatric hospital in Tehran were selected. Patients (1: 1) were randomly divided to two groups. Overall, 22 subjects received Haloperidol (5 - 20 mg) and 22 subjects received Risperidone (2 - 8 mg). All subjects were assessed at baseline, during three consecutive weeks of treatment and one week after treatment (i.e., follow-up). Scale of assessment of positive symptoms (SAPS) was completed for each subject. RESULTS The study findings indicated that both Haloperidol (< 0.05) and Risperidone (< 0.05) were similarly applicable in the treatment of MAP but no differential effectiveness was found between the two medications. The treatment effects of both medications increased in the first two weeks of treatment and remained stable in the second two weeks. CONCLUSIONS Risperidone and Haloperidol are two effective antipsychotic medications for the treatment of positive symptoms of MAP but other aspects of these two neuroleptic medications such as the long-term treatment effects should be studied. Further studies with more samples and longer follow-ups are suggested.
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Affiliation(s)
- Mercede Samiei
- Department of Psychiatry, University of Social Welfare and Rehabilitation Sciences, Tehran, IR Iran
| | - Mohammad Vahidi
- Department of Psychiatry, University of Social Welfare and Rehabilitation Sciences, Tehran, IR Iran
| | - Omid Rezaee
- Department of Psychiatry, University of Social Welfare and Rehabilitation Sciences, Tehran, IR Iran
| | - Azadeh Yaraghchi
- Faculty of Psychology, Science and Research Branch, Islamic Azad University, Tehran, IR Iran
| | - Reza Daneshmand
- Substance Abuse and Dependence Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, IR Iran
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18
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Ma J, Leung LS. Dual Effects of Limbic Seizures on Psychosis-Relevant Behaviors Shown by Nucleus Accumbens Kindling in Rats. Brain Stimul 2016; 9:762-769. [PMID: 27267861 PMCID: PMC4980124 DOI: 10.1016/j.brs.2016.05.006] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/04/2016] [Revised: 05/11/2016] [Accepted: 05/16/2016] [Indexed: 10/21/2022] Open
Abstract
BACKGROUND A paradox in epilepsy and psychiatry is that temporal lobe epilepsy is often predisposed to schizophrenic-like psychosis, whereas convulsive therapy can relieve schizophrenic symptoms. We have previously demonstrated that the nucleus accumbens is a key structure in mediating postictal psychosis induced by a hippocampal electrographic seizure. OBJECTIVE/HYPOTHESIS The purpose of this study is to test a hypothesis that accumbens kindling cumulating in a single (1-time) or repeated (5-times) convulsive seizures have different effects on animal models of psychosis. METHODS Electrical stimulation at 60 Hz was applied to nucleus accumbens to evoke afterdischarges until one, or five, convulsive seizures that involved the hind limbs (stage 5 seizures) were attained. Behavioral tests, performed at 3 days after the last seizure, included gating of hippocampal auditory evoked potentials (AEP) and prepulse inhibition to an acoustic startle response (PPI), tested without drug injection or after ketamine (3 mg/kg s.c.) injection, as well as locomotion induced by ketamine or methamphetamine (1 mg/kg i.p.). RESULTS Compared to non-kindled control rats, 1-time, but not 5-times, convulsive seizures induced PPI deficit and decreased gating of hippocampal AEP, without drug injection. Compared to non-kindled rats, 5-times, but not 1-time, convulsive seizures antagonized ketamine-induced hyperlocomotion, ketamine-induced PPI deficit and AEP gating decrease. However, both 1- and 5-times convulsive seizures significantly enhanced methamphetamine-induced locomotion as compared to non-kindled rats. CONCLUSIONS Accumbens kindling ending with 1 convulsive seizure may induce schizophrenic-like behaviors, while repeated (≥5) convulsive seizures induced by accumbens kindling may have therapeutic effects on dopamine independent psychosis.
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Affiliation(s)
- Jingyi Ma
- Department of Physiology and Pharmacology, The University of Western Ontario, Medical Sciences Building, London, ON, Canada N6A 5C1.
| | - L Stan Leung
- Department of Physiology and Pharmacology, The University of Western Ontario, Medical Sciences Building, London, ON, Canada N6A 5C1; Graduate Program of Neuroscience, The University of Western Ontario, Medical Sciences Building, London, ON, Canada N6A 5C1
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19
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Fabian JM. Methamphetamine Motivated Murder: Forensic Psychological/Psychiatric & Legal Applications in Criminal Contexts. ACTA ACUST UNITED AC 2016. [DOI: 10.1177/009318530703500403] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/17/2022]
Abstract
This article examines the clinical and forensic (psycho-legal) aspects of methamphetamine use. The author will describe the clinical and psychiatric effects of the drug on an individual's functioning. Forensic psychological/psychiatric issues including substance-induced psychosis relevant to a not guilty by reason of insanity defense, diminished capacity, and mitigation at capital sentencing will be addressed. Case law pursuant to forensic aspects of methamphetamine use will also be thoroughly explored.
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20
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Okada N, Takahashi K, Nishimura Y, Koike S, Ishii-Takahashi A, Sakakibara E, Satomura Y, Kinoshita A, Takizawa R, Kawasaki S, Nakakita M, Ohtani T, Okazaki Y, Kasai K. Characterizing prefrontal cortical activity during inhibition task in methamphetamine-associated psychosis versus schizophrenia: a multi-channel near-infrared spectroscopy study. Addict Biol 2016; 21:489-503. [PMID: 25619621 DOI: 10.1111/adb.12224] [Citation(s) in RCA: 30] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/28/2022]
Abstract
Methamphetamine abuse and dependence, frequently accompanied by schizophrenia-like psychotic symptoms [methamphetamine-associated psychosis (MAP)], is a serious public health problem worldwide. Few studies, however, have characterized brain dysfunction associated with MAP, nor investigated similarities and differences in brain dysfunction between MAP and schizophrenia. We compared prefrontal cortical activity associated with stop-signal inhibitory task in 21 patients with MAP, 14 patients with schizophrenia and 21 age- and gender-matched healthy controls using a 52-channel near-infrared spectroscopy (NIRS) system. Both the MAP and the schizophrenia groups showed significantly reduced activation in the bilateral ventrolateral prefrontal cortex compared with controls; however, only the MAP group showed reduced activation in the frontopolar prefrontal cortex. The MAP group demonstrated significant positive correlations between task performance and hemodynamic responses in the bilateral ventrolateral, polar and left dorsolateral regions of the prefrontal cortex. The MAP and schizophrenia groups demonstrated a significant difference in the relationship of impulsivity to hemodynamic changes in the bilateral premotor cortex. These findings characterize similarities and differences in prefrontal cortical dysfunction between psychosis associated with methamphetamine and schizophrenia. The reduced hemodynamic changes in the bilateral ventrolateral prefrontal cortex suggest a common underlying pathophysiology of MAP and schizophrenia, whereas those in the frontopolar prefrontal cortex point to an impaired state that is either inherent or caused specifically by methamphetamine use.
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Affiliation(s)
- Naohiro Okada
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
- Department of Psychiatry; Tokyo Metropolitan Matsuzawa Hospital; Japan
| | | | - Yukika Nishimura
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
- Department of Psychiatry; Tokyo Metropolitan Matsuzawa Hospital; Japan
| | - Shinsuke Koike
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
- Office for Mental Health Support; Division for Counseling and Support; The University of Tokyo; Japan
| | - Ayaka Ishii-Takahashi
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
| | - Eisuke Sakakibara
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
| | - Yoshihiro Satomura
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
| | - Akihide Kinoshita
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
| | - Ryu Takizawa
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
| | - Shingo Kawasaki
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
- Application Development Office; Hitachi Medical Corporation; Japan
| | - Mayumi Nakakita
- Department of Psychiatry; Tokyo Metropolitan Matsuzawa Hospital; Japan
- Department of Psychiatry; Sawa Hospital; Japan
| | - Toshiyuki Ohtani
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
- Department of Psychiatry; Tokyo Metropolitan Matsuzawa Hospital; Japan
- Safety and Health Organization; Chiba University; Japan
| | - Yuji Okazaki
- Department of Psychiatry; Tokyo Metropolitan Matsuzawa Hospital; Japan
- Department of Psychiatry; Michinoo Hospital; Japan
| | - Kiyoto Kasai
- Department of Neuropsychiatry; Graduate School of Medicine; The University of Tokyo; Japan
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Okazaki K, Makinodan M, Yamamuro K, Takata T, Kishimoto T. Blonanserin treatment in patients with methamphetamine-induced psychosis comorbid with intellectual disabilities. Neuropsychiatr Dis Treat 2016; 12:3195-3198. [PMID: 28008256 PMCID: PMC5167479 DOI: 10.2147/ndt.s120374] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/16/2022] Open
Abstract
OBJECTIVE Methamphetamine (MA) use has recently been associated with high levels of psychiatric hospitalization and serious social dysfunction. MA use causes frequent psychotic symptoms, which can be treated with antipsychotics. However, people with intellectual disabilities (ID) are vulnerable to adverse effects resulting from treatment with antipsychotic medications. METHOD We report two cases of MA-induced psychosis (MAP) in patients with ID who were treated with the antipsychotic blonanserin. RESULTS In both the cases presented, symptoms of psychosis were improved by switching medications from other antipsychotic drugs to blonanserin. Despite the presence of ID in these patients, no significant adverse effects, such as sedation, were detected after treatment with blonanserin. CONCLUSION Blonanserin may be an effective and well-tolerated pharmacotherapeutical treatment for patients with MAP comorbid with ID. However, further work is necessary to validate this claim.
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Affiliation(s)
- Kosuke Okazaki
- Department of Psychiatry, Nara Medical University School of Medicine, Kashihara, Japan
| | - Manabu Makinodan
- Department of Psychiatry, Nara Medical University School of Medicine, Kashihara, Japan
| | - Kazuhiko Yamamuro
- Department of Psychiatry, Nara Medical University School of Medicine, Kashihara, Japan
| | - Tomoyo Takata
- Department of Psychiatry, Nara Medical University School of Medicine, Kashihara, Japan
| | - Toshifumi Kishimoto
- Department of Psychiatry, Nara Medical University School of Medicine, Kashihara, Japan
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22
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Moran LV, Masters GA, Pingali S, Cohen BM, Liebson E, Rajarethinam R, Ongur D. Prescription stimulant use is associated with earlier onset of psychosis. J Psychiatr Res 2015; 71:41-7. [PMID: 26522870 PMCID: PMC4630672 DOI: 10.1016/j.jpsychires.2015.09.012] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/08/2015] [Revised: 08/14/2015] [Accepted: 09/17/2015] [Indexed: 10/23/2022]
Abstract
A childhood history of attention deficit hyperactivity disorder (ADHD) is common in psychotic disorders, yet prescription stimulants may interact adversely with the physiology of these disorders. Specifically, exposure to stimulants leads to long-term increases in dopamine release. We therefore hypothesized that individuals with psychotic disorders previously exposed to prescription stimulants will have an earlier onset of psychosis. Age of onset of psychosis (AOP) was compared in individuals with and without prior exposure to prescription stimulants while controlling for potential confounding factors. In a sample of 205 patients recruited from an inpatient psychiatric unit, 40% (n = 82) reported use of stimulants prior to the onset of psychosis. Most participants were prescribed stimulants during childhood or adolescence for a diagnosis of ADHD. AOP was significantly earlier in those exposed to stimulants (20.5 vs. 24.6 years stimulants vs. no stimulants, p < 0.001). After controlling for gender, IQ, educational attainment, lifetime history of a cannabis use disorder or other drugs of abuse, and family history of a first-degree relative with psychosis, the association between stimulant exposure and earlier AOP remained significant. There was a significant gender × stimulant interaction with a greater reduction in AOP for females, whereas the smaller effect of stimulant use on AOP in males did not reach statistical significance. In conclusion, individuals with psychotic disorders exposed to prescription stimulants had an earlier onset of psychosis, and this relationship did not appear to be mediated by IQ or cannabis.
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Affiliation(s)
- Lauren V. Moran
- McLean Hospital, Psychotic Disorders Division, Belmont, Massachusetts; Harvard Medical School,Correspondence to Dr. Lauren Moran, McLean Hospital, Admissions Building, 115 Mill Street, Belmont, MA 02478, Office: (617) 855-3395,
| | - Grace A. Masters
- McLean Hospital, Psychotic Disorders Division, Belmont, Massachusetts; Harvard Medical School
| | - Samira Pingali
- McLean Hospital, Psychotic Disorders Division, Belmont, Massachusetts; Harvard Medical School
| | - Bruce M. Cohen
- McLean Hospital, Psychotic Disorders Division, Belmont, Massachusetts; Harvard Medical School
| | - Elizabeth Liebson
- McLean Hospital, Psychotic Disorders Division, Belmont, Massachusetts; Harvard Medical School
| | - R.P. Rajarethinam
- McLean Hospital, Psychotic Disorders Division, Belmont, Massachusetts; Harvard Medical School
| | - Dost Ongur
- McLean Hospital, Psychotic Disorders Division, Belmont, Massachusetts; Harvard Medical School
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Differential patterns of blood oxygenation in the prefrontal cortex between patients with methamphetamine-induced psychosis and schizophrenia. Sci Rep 2015; 5:12107. [PMID: 26178613 PMCID: PMC4503985 DOI: 10.1038/srep12107] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/07/2015] [Accepted: 05/07/2015] [Indexed: 11/09/2022] Open
Abstract
Despite some slight differences in symptomatology, differential diagnosis of methamphetamine-induced psychosis (MAP) versus schizophrenia can be challenging because both disorders present a large overlap in their clinical symptoms. However, a recent study has shown that near-infrared spectroscopy (NIRS) performed during a cognitive task can be a powerful tool to differentiate between these two disorders. Here, we evaluated verbal fluency task performance during NIRS in 15 patients diagnosed with MAP and 19 with schizophrenia matched for age and sex. We used prefrontal probes and a 24-channel NIRS machine to measure the relative concentrations of oxyhaemoglobin every 0.1 s during the task. For each patient, the neurocognitive function and clinical psychopathology were evaluated using the Positive and Negative Symptom Scale (PANSS), and the Brief Assessment of Cognition in Schizophrenia (BACS). Oxyhaemoglobin changes in the prefrontal cortex were significantly higher in the MAP group compared to those in the schizophrenia group, particularly in the right dorsolateral prefrontal cortex. In contrast, we found no significant difference in PANSS and BACS scores. Our findings suggest that NIRS measurement could be applied to differentiate patients with MAP from those with schizophrenia, even in cases where clinical symptoms are similar.
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Nakajima S, Takeuchi H, Plitman E, Fervaha G, Gerretsen P, Caravaggio F, Chung JK, Iwata Y, Remington G, Graff-Guerrero A. Neuroimaging findings in treatment-resistant schizophrenia: A systematic review: Lack of neuroimaging correlates of treatment-resistant schizophrenia. Schizophr Res 2015; 164:164-75. [PMID: 25684554 PMCID: PMC4409508 DOI: 10.1016/j.schres.2015.01.043] [Citation(s) in RCA: 65] [Impact Index Per Article: 6.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/15/2014] [Revised: 01/28/2015] [Accepted: 01/30/2015] [Indexed: 12/21/2022]
Abstract
BACKGROUND Recent developments in neuroimaging have advanced the understanding of biological mechanisms underlying schizophrenia. However, neuroimaging correlates of treatment-resistant schizophrenia (TRS) and superior effects of clozapine on TRS remain unclear. METHODS Systematic search was performed to identify neuroimaging characteristics unique to TRS and ultra-resistant schizophrenia (i.e. clozapine-resistant [URS]), and clozapine's efficacy in TRS using Embase, Medline, and PsychInfo. Search terms included (schizophreni*) and (resistan* OR refractory OR clozapine) and (ASL OR CT OR DTI OR FMRI OR MRI OR MRS OR NIRS OR PET OR SPECT). RESULTS 25 neuroimaging studies have investigated TRS and effects of clozapine. Only 5 studies have compared TRS and non-TRS, collectively providing no replicated neuroimaging finding specific to TRS. Studies comparing TRS and healthy controls suggest that hypometabolism in the prefrontal cortex, hypermetabolism in the basal ganglia, and structural anomalies in the corpus callosum contribute to TRS. Clozapine may increase prefrontal hypoactivation in TRS although this was not related to clinical improvement; in contrast, evidence has suggested a link between clozapine efficacy and decreased metabolism in the basal ganglia and thalamus. CONCLUSION Existing literature does not elucidate neuroimaging correlates specific to TRS or URS, which, if present, might also shed light on clozapine's efficacy in TRS. This said, leads from other lines of investigation, including the glutamatergic system can prove useful in guiding future neuroimaging studies focused on, in particular, the frontocortical-basal ganglia-thalamic circuits. Critical to the success of this work will be precise subtyping of study subjects based on treatment response/nonresponse and the use of multimodal neuroimaging.
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Affiliation(s)
- Shinichiro Nakajima
- Multimodal Imaging Group - Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Canada; Geriatric Mental Health Division, Centre for Addiction and Mental Health, Toronto, Canada; Department of Psychiatry, University of Toronto, Toronto, Canada; Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan.
| | - Hiroyoshi Takeuchi
- Department of Psychiatry, University of Toronto, Toronto, Canada; Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan; Schizophrenia Division, Complex Mental Illness Program, Centre for Addiction and Mental Health, Toronto, Canada.
| | - Eric Plitman
- Multimodal Imaging Group - Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Canada; Institute of Medical Science, University of Toronto, Toronto, Canada.
| | - Gagan Fervaha
- Schizophrenia Division, Complex Mental Illness Program, Centre for Addiction and Mental Health, Toronto, Canada; Institute of Medical Science, University of Toronto, Toronto, Canada.
| | - Philip Gerretsen
- Multimodal Imaging Group - Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Canada; Geriatric Mental Health Division, Centre for Addiction and Mental Health, Toronto, Canada; Department of Psychiatry, University of Toronto, Toronto, Canada; Institute of Medical Science, University of Toronto, Toronto, Canada.
| | - Fernando Caravaggio
- Multimodal Imaging Group - Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Canada; Institute of Medical Science, University of Toronto, Toronto, Canada.
| | - Jun Ku Chung
- Multimodal Imaging Group - Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Canada; Institute of Medical Science, University of Toronto, Toronto, Canada.
| | - Yusuke Iwata
- Multimodal Imaging Group - Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Canada; Department of Psychiatry, University of Toronto, Toronto, Canada; Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan.
| | - Gary Remington
- Department of Psychiatry, University of Toronto, Toronto, Canada; Schizophrenia Division, Complex Mental Illness Program, Centre for Addiction and Mental Health, Toronto, Canada; Campbell Research Institute, Centre for Addiction and Mental Health, Toronto, Canada.
| | - Ariel Graff-Guerrero
- Multimodal Imaging Group - Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Canada; Geriatric Mental Health Division, Centre for Addiction and Mental Health, Toronto, Canada; Department of Psychiatry, University of Toronto, Toronto, Canada; Campbell Research Institute, Centre for Addiction and Mental Health, Toronto, Canada.
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Bountouni I, Zis P, Chaudhuri KR, Schrag A. Psychosis in Parkinson’s Disease. NEUROPSYCHIATRIC SYMPTOMS OF MOVEMENT DISORDERS 2015. [DOI: 10.1007/978-3-319-09537-0_6] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
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Sepehrmanesh Z, Ahmadvand A, Moraveji A. Comorbidity and pattern of substance use in hospitalized psychiatric patients. IRANIAN RED CRESCENT MEDICAL JOURNAL 2014; 16:e19282. [PMID: 25389488 PMCID: PMC4222014 DOI: 10.5812/ircmj.19282] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 04/05/2014] [Revised: 05/15/2014] [Accepted: 06/09/2014] [Indexed: 11/16/2022]
Abstract
BACKGROUND Substance use in patients with psychiatric disorder is an every-day seen. Detection of this comorbidity can significantly affect the treatment of these disorders, as well as substance use. OBJECTIVES This study has been conducted to determine the prevalence and pattern of substance use in hospitalized psychiatric patients. PATIENTS AND METHODS In this cross-sectional study, 210 hospitalized psychiatric patients were selected by simple randomization from all records of hospitalized patients. The instrument of gathering data was a demographic checklist including age, gender, marital status, education, type of disorder and substance abuse and duration of psychiatric disorder. Data were analyzed by SPSS version 16 using Fisher exact and Chi square tests. RESULTS The mean age of patients was 37.9 years. Most of the patients were male, married and unemployed. The Prevalence of substance use was 36.7%. The most prevalent pattern of substance use was opium, opioid, methamphetamines and other substances (poly substance). The prevalence of substance use in patients with mood disorders was more than the other disorders and the most prevalent substance use in these patients was opium and opioid. Poly substance use was the most prevalent pattern of use (80 %) in psychotic and mood disorders due to substance. Significant difference was seen between genders, marital status, occupation, duration of illness and frequency of substance use (P < 0.05 ), however no significant difference was seen between educational levels, age and substance use. CONCLUSIONS The patients with mood disorders had the highest comorbidity with substance use and concurrent use of poly substance was the most prevalent pattern of use in these patients. Therefore, successful treatment of psychiatric disorders and substance use needs multimodal and more serious interventions. Regarding to the pattern of poly substance use in these patients, careful screening should be performed at admission.
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Affiliation(s)
- Zahra Sepehrmanesh
- Department of Psychiatry, Kashan University of Medical Sciences, Kashan, IR Iran
| | - Afshin Ahmadvand
- Department of Psychiatry, Kashan University of Medical Sciences, Kashan, IR Iran
- Corresponding Author: Afshin Ahmadvand, Department of Psychiatry, Kashan University of Medical Sciences, Kashan, IR Iran. Tel: +98-9131625987, E-mail:
| | - Alireza Moraveji
- Department of Epidemiology, Kashan University of Medical Sciences, Kashan, IR Iran
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Hsieh JH, Stein DJ, Howells FM. The neurobiology of methamphetamine induced psychosis. Front Hum Neurosci 2014; 8:537. [PMID: 25100979 PMCID: PMC4105632 DOI: 10.3389/fnhum.2014.00537] [Citation(s) in RCA: 115] [Impact Index Per Article: 10.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/03/2014] [Accepted: 07/01/2014] [Indexed: 11/18/2022] Open
Abstract
Chronic methamphetamine abuse commonly leads to psychosis, with positive and cognitive symptoms that are similar to those of schizophrenia. Methamphetamine induced psychosis (MAP) can persist and diagnoses of MAP often change to a diagnosis of schizophrenia over time. Studies in schizophrenia have found much evidence of cortical GABAergic dysfunction. Methamphetamine psychosis is a well studied model for schizophrenia, however there is little research on the effects of methamphetamine on cortical GABAergic function in the model, and the neurobiology of MAP is unknown. This paper reviews the effects of methamphetamine on dopaminergic pathways, with focus on its ability to increase glutamate release in the cortex. Excess cortical glutamate would likely damage GABAergic interneurons, and evidence of this disturbance as a result of methamphetamine treatment will be discussed. We propose that cortical GABAergic interneurons are particularly vulnerable to glutamate overflow as a result of subcellular location of NMDA receptors on interneurons in the cortex. Damage to cortical GABAergic function would lead to dysregulation of cortical signals, resulting in psychosis, and further support MAP as a model for schizophrenia.
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Affiliation(s)
- Jennifer H. Hsieh
- Department of Psychiatry and Mental Health, University of Cape TownWestern Cape, South Africa
| | | | - Fleur M. Howells
- Department of Psychiatry and Mental Health, University of Cape TownWestern Cape, South Africa
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Kalayasiri R, Verachai V, Gelernter J, Mutirangura A, Malison RT. Clinical features of methamphetamine-induced paranoia and preliminary genetic association with DBH-1021C→T in a Thai treatment cohort. Addiction 2014; 109:965-76. [PMID: 24521142 PMCID: PMC4018411 DOI: 10.1111/add.12512] [Citation(s) in RCA: 31] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/01/2013] [Revised: 10/28/2013] [Accepted: 02/03/2014] [Indexed: 12/31/2022]
Abstract
AIMS To explore the clinical features of methamphetamine-induced paranoia (MIP) and associations between MIP and a genetic polymorphism in dopamine β-hydroxylase (DBH-1021C→T). DESIGN Retrospective analysis of clinical presentation and genetic association by χ(2) test and logistic regression analysis. SETTING A Thai substance abuse treatment center. PARTICIPANTS A total of 727 methamphetamine-dependent (MD) individuals. MEASUREMENTS Clinical: Semi-Structured Assessment for Drug Dependence and Alcoholism (SSADDA) and the Methamphetamine Experience Questionnaire (MEQ). Genetic: DBH-1021C→T. FINDINGS Forty per cent of individuals (289 of 727; 39.8%) with MD had MIP. Within-binge latency to MIP onset occurred more rapidly in the most recent compared with initial MIP episode (P = 0.02), despite unchanging intake (P = 0.89). Individuals with MIP were significantly less likely to carry lower (TT/CT) compared with higher (CC) activity genotypes (34.3 versus 43.3%; χ(2) 1 = 5, P = 0.03). DBH effects were confirmed [odds ratio (OR) = 0.7, P = 0.04] after controlling for associated clinical variables (MD severity, OR = 3.4, P < 0.001; antisocial personality disorder, OR = 2.2, P < 0.001; alcohol dependence, OR = 1.4, P = 0.05; and nicotine dependence, OR = 1.4, P = 0.06). TT/CT carriers were more likely to initiate cigarette smoking (OR = 3.9, P = 0.003) and probably less likely to be dependent on alcohol (OR = 0.6, P = 0.05). CONCLUSIONS Among methamphetamine-dependent individuals, paranoia appears to occur increasingly rapidly in the course of a session of methamphetamine use. Severity of methamphetamine dependence and antisocial personality disorder predicts methamphetamine-induced paranoia. The genetic polymorphism in dopamine β-hydroxylase is associated with methamphetamine-induced paranoia and influences smoking initiation.
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Affiliation(s)
- Rasmon Kalayasiri
- Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand,Corresponding Author: Rasmon Kalayasiri, M.D. Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, 1873 Rama 4 Road, Pathumwan, Bangkok 10330, Thailand. Telephone number: + 66 2 256 4298; Fax: +66 2 256 4298;
| | - Viroj Verachai
- Thanyarak Institute on Drug Abuse, Department of Medical Service, Ministry of Public Health, Pathumtani, Thailand
| | - Joel Gelernter
- Department of Psychiatry, Yale School of Medicine, New Haven, CT 06511, USA
| | - Apiwat Mutirangura
- Center of Excellence in Molecular Genetics of Cancer and Human Diseases, Department of Anatomy, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
| | - Robert T. Malison
- Department of Psychiatry, Yale School of Medicine, New Haven, CT 06511, USA
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Leyton M, Vezina P. Striatal ups and downs: their roles in vulnerability to addictions in humans. Neurosci Biobehav Rev 2013; 37:1999-2014. [PMID: 23333263 PMCID: PMC3743927 DOI: 10.1016/j.neubiorev.2013.01.018] [Citation(s) in RCA: 87] [Impact Index Per Article: 7.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/02/2012] [Revised: 01/03/2013] [Accepted: 01/07/2013] [Indexed: 01/05/2023]
Abstract
Susceptibility to addictive behaviors has been related to both increases and decreases in striatal function. Both profiles have been reported in humans as well as in animal models. Yet, the mechanisms underlying these opposing effects and the manner in which they relate to the behavioral development and expression of addiction remain unclear. In the present review of human studies, we describe a number of factors that could influence whether striatal hyper- or hypo-function is observed and propose a model that integrates the influence of these opposite responses on the expression of addiction related behaviors. Central to this model is the role played by the presence versus absence of addiction related cues and their ability to regulate responding to abused drugs and other rewards. Striatal function and incentive motivational states are increased in the presence of these cues and decreased in their absence. Alternations between these states might account for the progressive narrowing of interests as addictions develop and point to relevant processes to target in treatment.
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Affiliation(s)
- Marco Leyton
- Department of Psychiatry, McGill University, 1033 Pine Avenue West, Montreal, Quebec, H3A 1A1 Canada.
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31
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Signorelli MS, Battaglia E, Costanzo MC, Cannavò D. Pramipexole induced psychosis in a patient with restless legs syndrome. BMJ Case Rep 2013; 2013:bcr-2013-009716. [PMID: 24049088 DOI: 10.1136/bcr-2013-009716] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022] Open
Abstract
In the last few years, dopamine agonists (DA) have been used as first-line treatment for restless legs syndrome (RLS), a disabling sensorimotor disorder. Only recently have they reported some possible iatrogenic side effects, as shown below. The following case presents a RLS patient who developed hallucinatory and delusional symptoms with paranoid ideation after pramipexole assumption; these symptoms gradually decreased after pramipexole suspension and treatment by an oral antipsychotic therapy (quetiapine XR). Correlation between DAs assumption and psychotic symptoms is still not clear. The development of these side effects might be related to many risk factors such as genetic susceptibility, premorbid personality and psychosocial stressor; in order to minimise the risk of iatrogenic psychosis it could be useful to assess patients' vulnerability factors selecting an alternative medication regime.
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32
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Aoki Y, Orikabe L, Takayanagi Y, Yahata N, Mozue Y, Sudo Y, Ishii T, Itokawa M, Suzuki M, Kurachi M, Okazaki Y, Kasai K, Yamasue H. Volume reductions in frontopolar and left perisylvian cortices in methamphetamine induced psychosis. Schizophr Res 2013; 147:355-61. [PMID: 23688384 DOI: 10.1016/j.schres.2013.04.029] [Citation(s) in RCA: 30] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/28/2012] [Revised: 04/21/2013] [Accepted: 04/22/2013] [Indexed: 11/18/2022]
Abstract
Consumption of methamphetamine disturbs dopaminergic transmission and sometimes provokes schizophrenia-like-psychosis, named methamphetamine-associated psychosis (MAP). While previous studies have repeatedly reported regional volume reductions in the frontal and temporal areas as neuroanatomical substrates for psychotic symptoms, no study has examined whether such neuroanatomical substrates exist or not in patients with MAP. Magnetic resonance images obtained from twenty patients with MAP and 20 demographically-matched healthy controls (HC) were processed for voxel-based morphometry (VBM) using Diffeomorphic Anatomical Registration using Exponentiated Lie Algebra. An analysis of covariance model was adopted to identify volume differences between subjects with MAP and HC, treating intracranial volume as a confounding covariate. The VBM analyses showed significant gray matter volume reductions in the left perisylvian structures, such as the posterior inferior frontal gyrus and the anterior superior temporal gyrus, and the frontopolar cortices, including its dorsomedial, ventromedial, dorsolateral, and ventrolateral portions, and white matter volume reduction in the orbitofrontal area in the patients with MAP compared with the HC subjects. The smaller regional gray matter volume in the medial portion of the frontopolar cortex was significantly correlated with the severe positive symptoms in the individuals with MAP. The volume reductions in the left perisylvian structure suggest that patients with MAP have a similar pathophysiology to schizophrenia, whereas those in the frontopolar cortices and orbitofrontal area suggest an association with antisocial traits or vulnerability to substance dependence.
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Affiliation(s)
- Yuta Aoki
- Department of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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Manning EE, van den Buuse M. BDNF deficiency and young-adult methamphetamine induce sex-specific effects on prepulse inhibition regulation. Front Cell Neurosci 2013; 7:92. [PMID: 23781174 PMCID: PMC3679473 DOI: 10.3389/fncel.2013.00092] [Citation(s) in RCA: 42] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/12/2012] [Accepted: 05/26/2013] [Indexed: 12/30/2022] Open
Abstract
Brain-derived neurotrophic factor (BDNF) has been implicated in the pathophysiology of schizophrenia, yet its role in the development of specific symptoms is unclear. Methamphetamine (METH) users have an increased risk of psychosis and schizophrenia, and METH-treated animals have been used extensively as a model to study the positive symptoms of schizophrenia. We investigated whether METH treatment in BDNF heterozygous (HET) mutant mice has cumulative effects on sensorimotor gating, including the disruptive effects of psychotropic drugs. BDNF HETs and wildtype (WT) littermates were treated during young adulthood with METH and, following a 2-week break, prepulse inhibition (PPI) was examined. At baseline, BDNF HETs showed reduced PPI compared to WT mice irrespective of METH pre-treatment. An acute challenge with amphetamine (AMPH) disrupted PPI but male BDNF HETs were more sensitive to this effect, irrespective of METH pre-treatment. In contrast, female mice treated with METH were less sensitive to the disruptive effects of AMPH, and there were no effects of BDNF genotype. Similar changes were not observed in the response to an acute apomorphine (APO) or MK-801 challenge. These results show that genetically-induced reduction of BDNF caused changes in a behavioral endophenotype relevant to the positive symptoms of schizophrenia. However, major sex differences were observed in the effects of a psychotropic drug challenge on this behavior. These findings suggest sex differences in the effects of BDNF depletion and METH treatment on the monoamine signaling pathways that regulate PPI. Given that these same pathways are thought to contribute to the expression of positive symptoms in schizophrenia, this work suggests that there may be significant sex differences in the pathophysiology underlying these symptoms. Elucidating these sex differences may be important for our understanding of the neurobiology of schizophrenia and developing better treatments strategies for the disorder.
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Affiliation(s)
- Elizabeth E Manning
- Behavioural Neuroscience Laboratory, The Florey Institute of Neuroscience and Mental Health Melbourne, VIC, Australia
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Ren Q, Zhang JC, Fujita Y, Ma M, Wu J, Hashimoto K. Effects of TrkB agonist 7,8-dihydroxyflavone on sensory gating deficits in mice after administration of methamphetamine. Pharmacol Biochem Behav 2013; 106:124-7. [PMID: 23567202 DOI: 10.1016/j.pbb.2013.03.016] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/27/2012] [Revised: 03/21/2013] [Accepted: 03/29/2013] [Indexed: 12/31/2022]
Abstract
Several lines of evidence suggest that the brain-derived neurotrophic factor (BDNF)-tropomyosin-related kinase B (TrkB) signaling pathway plays a role in behavioral abnormalities observed after administration of psychostimulants, such as methamphetamine (METH). This study was undertaken to examine whether the potent TrkB agonist, 7,8-dihydroxyflavone (7,8-DHF) could improve prepulse inhibition (PPI) deficits in mice seen after a single dose of METH. Treatment with 7,8-DHF (3.0, 10 or 30 mg/kg) improved PPI deficits in mice associated with exposure to METH (3.0 mg/kg), in a dose dependent manner. Furthermore, co-administration of ANA-12 (0.5 mg/kg), a TrkB antagonist, significantly blocked the effects of 7,8-DHF (30 mg/kg) on METH-induced PPI deficits. In contrast, administration of 5,7-dihydroxyflavone (5,7-DHF: 30 mg/kg), an inactive TrkB ligand, did not affect METH-induced PPI deficits in mice. An in vivo microdialysis study in conscious mice showed that 7,8-DHF (30 mg/kg) significantly attenuated increased dopamine release in the striatum, after METH administration (3 mg/kg). This study suggests that 7,8-DHF can improve PPI deficits in these mice, through the inhibition of METH-induced dopamine release. Therefore, it is likely that TrkB agonists, such as 7,8-DHF, may constitute a novel class of therapeutic drugs for neuropsychiatric diseases such as METH-use disorder and schizophrenia.
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Affiliation(s)
- Qian Ren
- Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba, Japan
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Salo R, Fassbender C, Buonocore MH, Ursu S. Behavioral regulation in methamphetamine abusers: an fMRI study. Psychiatry Res 2013; 211:234-8. [PMID: 23149023 PMCID: PMC3594424 DOI: 10.1016/j.pscychresns.2012.10.003] [Citation(s) in RCA: 35] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/11/2012] [Revised: 10/16/2012] [Accepted: 10/18/2012] [Indexed: 10/27/2022]
Abstract
The goal of this study was to extend our previous findings of abnormal prefrontal function in methamphetamine (MA) abusers and controls and to link the imaging data to behavioral, demographic and drug use variables. We used a fast event-related functional magnetic resonance imaging (fMRI) design to examine trial-to-trial reaction time (RT) adjustments in 30 MA abusers and 30 controls. A variant of the Stroop task was employed to measure influence of response conflict on RT, including the level of trial-to-trial RT adjustments seen after conflict trials. Compared to control subjects, MA abusers exhibited reduced RT adjustments and reduced activation in the prefrontal cortex (PFC) after conflict trials. RT adjustment correlated negatively with PFC brain activity in the MA group, while a trend for a positive correlation was observed in controls. No correlations were observed between task performance or brain activity and age, education or drug use variables. These data support our previous findings that the ability to adapt a behavioral response based on prior experience is compromised in MA abusers. Interestingly, these impairments do not appear to be linked to drug use patterns or to educational levels.
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Affiliation(s)
- Ruth Salo
- Deparment of Psychiatry and Behavioral Sciences, University of California, Davis, CA, USA.
| | - Catherine Fassbender
- Dept. of Psychiatry and Behavioral Sciences, University of California, Davis, CA,Imaging Research Center, University of California, Davis, CA
| | - Michael H. Buonocore
- Imaging Research Center, University of California, Davis, CA,Department of Radiology, University of California, Davis
| | - Stefan Ursu
- Dept. of Psychiatry and Behavioral Sciences, University of California, Davis, CA,Imaging Research Center, University of California, Davis, CA
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Gururajan A, Manning EE, Klug M, van den Buuse M. Drugs of abuse and increased risk of psychosis development. Aust N Z J Psychiatry 2012; 46:1120-35. [PMID: 22833579 DOI: 10.1177/0004867412455232] [Citation(s) in RCA: 37] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/15/2023]
Abstract
OBJECTIVE There is considerable evidence to suggest that the abuse of illicit drugs, particularly cannabis and methamphetamine, has aetiological roles in the pathogenesis of psychosis and schizophrenia. Factors that may increase susceptibility to the propsychotic effects of these drugs include the age at which the abuse starts as well as family history of genetic polymorphisms relevant to the pathophysiology of this disorder. However, the neurobiological mechanisms involved in drug abuse-associated psychosis remain largely unclear. METHODS AND RESULTS This paper presents an overview of the available evidence, including clinical, animal model, and molecular studies, with a focus on brain regions and neurotransmitters systems, such as dopamine and glutamate, previously implicated in psychosis. CONCLUSION It is clear that further studies are urgently needed to provide a greater insight into the mechanisms that mediate the long-term and neurodevelopmental effects of cannabis and methamphetamine. A dialogue between basic science and clinical research may help to identify at-risk individuals and novel pathways for treatment and prevention.
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Affiliation(s)
- Anand Gururajan
- Mental Health Research Institute, University of Melbourne, Melbourne, Australia
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Schmidt-Hansen M, Le Pelley M. The positive symptoms of acute schizophrenia and latent inhibition in humans and animals: underpinned by the same process(es)? Cogn Neuropsychiatry 2012; 17:473-505. [PMID: 22443090 DOI: 10.1080/13546805.2012.667202] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/28/2022]
Abstract
INTRODUCTION It has been suggested that the positive symptoms of acute schizophrenia are a consequence of a disruption of the process that produces latent inhibition (slower acquisition of conditioned responding after preexposure to the conditioned stimulus) and that this effect can be modelled by pro- and antipsychotic compounds in healthy participants and in nonhuman animals. This idea assumes that latent inhibition in humans and animals is underpinned by the same process(es). METHOD First, we question the equivalence of human and animal latent inhibition. Second, we review the studies that have examined latent inhibition in populations with schizophrenia and in healthy populations after administration of amphetamine or haloperidol. RESULTS Theoretical analysis of the similarities and differences in latent inhibition effects, and the procedures used to generate them, in humans and animals renders the suggested equivalence between them unconvincing. The studies examining latent inhibition in populations with schizophrenia and in healthy populations after administration of amphetamine or haloperidol are marked by a number of methodological shortcomings and reveal discrepant results. CONCLUSIONS The theoretical and empirical analyses provide little support for a common process underlying deficits of latent inhibition in patients exhibiting positive symptoms of acute schizophrenia, and such deficits in experimental models in healthy humans and infrahumans.
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Abstract
Schizophrenia is a debilitating neurodevelopmental disorder affecting approximately 1% of the population and imposing a significant burden on society. One of the most replicated and well-established postmortem findings is a deficit in the expression of the gene encoding the 67-kDa isoform of glutamic acid decarboxylase (GAD67), the primary GABA-producing enzyme in the brain. GAD67 is expressed in various classes of interneurons, with vastly different morphological, molecular, and physiological properties. Importantly, GABA system deficits in schizophrenia encompass multiple interneuronal subtypes, raising several important questions. First, do different classes of interneurons regulate different aspects of behavior? Second, can we model cell-type-specific GABAergic deficits in mice, and will the rodent findings translate to human physiology? Finally, will this knowledge open the door to knowledge-based approaches to treat schizophrenia?
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Affiliation(s)
- Martin J Schmidt
- Department of Psychiatry, Vanderbilt Kennedy Center, Vanderbilt University, Nashville, Tenn., USA.
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Shariat SV, Elahi A. Symptoms and course of psychosis after methamphetamine abuse: one-year follow-up of a case. PRIMARY CARE COMPANION TO THE JOURNAL OF CLINICAL PSYCHIATRY 2011; 12. [PMID: 21274351 DOI: 10.4088/pcc.10l00959gry] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 10/18/2022]
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Orikabe L, Yamasue H, Inoue H, Takayanagi Y, Mozue Y, Sudo Y, Ishii T, Itokawa M, Suzuki M, Kurachi M, Okazaki Y, Kasai K. Reduced amygdala and hippocampal volumes in patients with methamphetamine psychosis. Schizophr Res 2011; 132:183-9. [PMID: 21784619 DOI: 10.1016/j.schres.2011.07.006] [Citation(s) in RCA: 51] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/03/2011] [Revised: 06/30/2011] [Accepted: 07/05/2011] [Indexed: 01/08/2023]
Abstract
The similarity between psychotic symptoms in patients with schizophrenia such as hallucinations and delusions and those caused by administration of methamphetamine has been accepted. While the etiology of schizophrenia remains unclear, methamphetamine induced psychosis, which is obviously occurred by methamphetamine administration, had been widely considered as a human pharmaceutical model of exogenous psychosis. Although volume reductions in medial temporal lobe structure in patients with schizophrenia have repeatedly been reported, those in patients with methamphetamine psychosis have not yet been clarified. Magnetic resonance images (MRI) were obtained from 20 patients with methamphetamine psychosis and 20 age, sex, parental socio-economic background, and IQ matched healthy controls. A reliable manual tracing methodology was employed to measure the gray matter volume of the amygdala and the hippocampus from MRIs. Significant gray matter volume reductions of both the amygdala and hippocampus were found bilaterally in the subjects with methamphetamine psychosis compared with the controls. The degree of volume reduction was significantly greater in the amygdala than in hippocampus. While the total gray, white matter and intracranial volumes were also significantly smaller-than-normal in the patients; the regional gray matter volume reductions in these medial temporal structures remained statistically significant even after these global brain volumes being controlled. The prominent volume reduction in amygdala rather than that in hippocampus could be relatively specific characteristics of methamphetamine psychosis, since previous studies have shown significant volume reductions less frequently in amygdala than in hippocampus of the other psychosis such as schizophrenia.
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Affiliation(s)
- Lina Orikabe
- Department of Neuropsychiatry, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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Kishi T, Fukuo Y, Okochi T, Kitajima T, Ujike H, Inada T, Yamada M, Uchimura N, Sora I, Iyo M, Ozaki N, Correll CU, Iwata N. No significant association between SIRT1 gene and methamphetamine-induced psychosis in the Japanese population. Hum Psychopharmacol 2011; 26:445-50. [PMID: 21882241 DOI: 10.1002/hup.1223] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/17/2011] [Accepted: 06/19/2011] [Indexed: 11/09/2022]
Abstract
OBJECTIVES We previously showed that the sirtuin 1 gene (SIRT1 gene), one of the clock genes, was associated with schizophrenia in a Japanese patient population. Because the symptoms of methamphetamine (METH)-induced psychosis are similar to those of paranoid type schizophrenia and because not every METH user develops psychosis, it is conceivable that METH-induced psychosis and schizophrenia have common susceptibility genes. Therefore, we conducted an analysis of the association of SIRT1 gene with METH-induced psychosis, hypothesizing a significant relationship. METHODS This paper presents a case-control study of the SIRT1 gene in 515 Japanese individuals (197 with METH-induced psychosis and 318 age-matched and sex-matched controls) with four tagging single nucleotide polymorphisms (rs12778366, rs2273773, rs4746720, and rs10997875), selected a priori using the HapMap database. RESULTS rs10997875 (located in the 3' flanking region) was associated with METH-induced psychosis (unadjusted p(genotype) = 0.0203). However, these results became non-significant after Bonferroni correction (corrected p(genotype) = 0.0812). In the all-marker haplotype analysis, the SIRT1 gene was not associated with METH-induced psychosis (p = 0.146). CONCLUSION Our findings suggest that SIRT1 gene does not contribute to the development of METH-induced psychosis in the Japanese population. However, a replication study using larger samples should be conducted to obtain conclusive results.
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Affiliation(s)
- Taro Kishi
- Department of Psychiatry Research, The Zucker Hillside Hospital, Glen Oaks, New York 11004, USA.
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Fuente-Sandoval CDL, León-Ortiz P, Favila R, Stephano S, Mamo D, Ramírez-Bermúdez J, Graff-Guerrero A. Higher levels of glutamate in the associative-striatum of subjects with prodromal symptoms of schizophrenia and patients with first-episode psychosis. Neuropsychopharmacology 2011; 36:1781-91. [PMID: 21508933 PMCID: PMC3154101 DOI: 10.1038/npp.2011.65] [Citation(s) in RCA: 187] [Impact Index Per Article: 13.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/09/2022]
Abstract
The glutamatergic and dopaminergic systems are thought to be involved in the pathophysiology of schizophrenia. Their interaction has been widely documented and may have a role in the neurobiological basis of the disease. The aim of this study was to compare, using proton magnetic resonance spectroscopy ((1)H-MRS), glutamate levels in the precommissural dorsal-caudate (a dopamine-rich region) and the cerebellar cortex (negligible for dopamine) in the following: (1) 18 antipsychotic-naïve subjects with prodromal symptoms and considered to be at ultra high-risk for schizophrenia (UHR), (2) 18 antipsychotic-naïve first- episode psychosis patients (FEP), and (3) 40 age- and sex- matched healthy controls. All subjects underwent a (1)H-MRS study using a 3Tesla scanner. Glutamate levels were quantified and corrected for the proportion of cerebrospinal fluid and percentage of gray matter in the voxel. The UHR and FEP groups showed higher levels of glutamate than controls, without differences between UHR and FEP. In the cerebellum, no differences were seen between the three groups. The higher glutamate level in the precommissural dorsal-caudate and not in the cerebellum of UHR and FEP suggests that a high glutamate level (a) precedes the onset of schizophrenia, and (b) is present in a dopamine-rich region previously implicated in the pathophysiology of schizophrenia.
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Affiliation(s)
- Camilo de la Fuente-Sandoval
- Experimental Psychiatry Laboratory, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico,Neuropsychiatry Department, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico
| | - Pablo León-Ortiz
- Neuropsychiatry Department, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico
| | - Rafael Favila
- MR Advanced Applications, GE Healthcare, Mexico City, Mexico
| | - Sylvana Stephano
- Neuropsychiatry Department, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico
| | - David Mamo
- Multimodal Neuroimaging Schizophrenia Group, PET Centre, Centre for Addiction and Mental Health & Department of Psychiatry, University of Toronto, Toronto, ON, Canada
| | - Jesús Ramírez-Bermúdez
- Neuropsychiatry Department, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico
| | - Ariel Graff-Guerrero
- Multimodal Neuroimaging Schizophrenia Group, PET Centre, Centre for Addiction and Mental Health & Department of Psychiatry, University of Toronto, Toronto, ON, Canada,Multimodal Neuroimaging Schizophrenia Group, PET Centre, Centre for Addiction and Mental Health, 250 College Street, Toronto, Ontario, Canada M5T 1R8. Tel: +1 416 535 8501 Ext 7376, Fax: +1 416 979 3855, E-mail:
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Yoshimura T, Usui H, Takahashi N, Yoshimi A, Saito S, Aleksic B, Ujike H, Inada T, Yamada M, Uchimura N, Iwata N, Sora I, Iyo M, Ozaki N. Association analysis of the GDNF gene with methamphetamine use disorder in a Japanese population. Prog Neuropsychopharmacol Biol Psychiatry 2011; 35:1268-72. [PMID: 21514351 DOI: 10.1016/j.pnpbp.2011.04.003] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/21/2010] [Revised: 03/07/2011] [Accepted: 04/02/2011] [Indexed: 11/28/2022]
Abstract
Methamphetamine (MAP) dependence is a highly heritable and aberrant dopaminergic signaling that has been implicated in the disease. Glial cell line-derived neurotrophic factor (GDNF), which plays an important role in the survival of dopaminergic neurons, may be involved in this disorder. In this study, we examined the association between GDNF and MAP dependence using a Japanese population-based sample. We selected eight single nucleotide polymorphisms (SNPs) in the GDNF locus for the association analysis. When patients with MAP dependence were divided into two subgroups consisting of multi-substance and MAP-only users, we detected a significant association between these two groups and the tagging SNP, rs2910704 (after Bonferroni's correction; allele P=0.034). Thus, GDNF is likely to be related to the severity of MAP use in the Japanese population.
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Affiliation(s)
- Tomoko Yoshimura
- Division of Clinical Science and Neuropsychopharmacology, Graduate School of Pharmacy, Meijo University, Aichi, Japan
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Abstract
PURPOSE OF REVIEW To review the role of brain-derived neurotrophic factor (BDNF) in neuroplasticity related to schizophrenia and the recent findings that have been reported on the status of BDNF in patients with schizophrenia and its association with the clinical measures. RECENT FINDINGS Peripheral BDNF levels have been found altered in first-episode patients with psychosis and also in chronic schizophrenia patients. A few studies have reported changes in peripheral BDNF levels following antipsychotic treatment. The role of Val66Met polymorphism in BDNF has been shown to play an important role in structural and functional plasticity in schizophrenia. SUMMARY Although peripheral BDNF levels hold promise for providing new perspectives for the development of novel therapeutic strategies for the treatment of schizophrenia, additional studies including efforts to prove its potential as a biomarker are warranted.
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Isolated delusional syndrome in Parkinson's Disease. Parkinsonism Relat Disord 2011; 16:550-2. [PMID: 20620094 DOI: 10.1016/j.parkreldis.2010.06.010] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/23/2010] [Revised: 06/13/2010] [Accepted: 06/14/2010] [Indexed: 11/20/2022]
Abstract
Psychotic features in patients with Parkinson's Disease usually present as visual hallucinations against a background of cognitive deterioration and dopaminomimetic therapy. Isolated delusions are rare. We report here 4 patients with Parkinson's Disease who developed a delusional syndrome resembling schizophreniform psychosis in the absence of changes in alertness, visual hallucinations or dementia. We suggest that this syndrome may be more common than previously recognized, and that it may be related to the use of dopaminergic medications and environmental triggers on a background of a susceptible individual. This syndrome suggests interesting parallels with the pathophysiology of amphetamine-induced psychosis and schizophrenia.
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Serotonin 6 receptor gene is associated with methamphetamine-induced psychosis in a Japanese population. Drug Alcohol Depend 2011; 113:1-7. [PMID: 20705401 DOI: 10.1016/j.drugalcdep.2010.06.021] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/16/2010] [Revised: 06/13/2010] [Accepted: 06/18/2010] [Indexed: 11/21/2022]
Abstract
BACKGROUND Altered serotonergic neural transmission is hypothesized to be a susceptibility factor for psychotic disorders such as schizophrenia. The serotonin 6 (5-HT6) receptor is therapeutically targeted by several second generation antipsychotics, such as clozapine and olanzapine, and d-amphetamine-induced hyperactivity in rats is corrected with the use of a selective 5-HT6 receptor antagonist. In addition, the disrupted prepulse inhibition induced by d-amphetamine or phencyclidine was restored by 5-HT6 receptor antagonist in an animal study using rats. These animal models were considered to reflect the positive symptoms of schizophrenia, and the above evidence suggests that altered 5-HT6 receptors are involved in the pathophysiology of psychotic disorders. The symptoms of methamphetamine (METH)-induced psychosis are similar to those of paranoid type schizophrenia. Therefore, we conducted an analysis of the association of the 5-HT6 gene (HTR6) with METH-induced psychosis. METHOD Using five tagging SNPs (rs6693503, rs1805054, rs4912138, rs3790757 and rs9659997), we conducted a genetic association analysis of case-control samples (197 METH-induced psychosis patients and 337 controls) in the Japanese population. The age and sex of the control subjects did not differ from those of the methamphetamine dependence patients. RESULTS rs6693503 was associated with METH-induced psychosis patients in the allele/genotype-wise analysis. Moreover, this association remained significant after Bonferroni correction. In the haplotype-wise analysis, we detected an association between two markers (rs6693503 and rs1805054) and three markers (rs6693503, rs1805054 and rs4912138) in HTR6 and METH-induced psychosis patients, respectively. CONCLUSION HTR6 may play an important role in the pathophysiology of METH-induced psychosis in the Japanese population.
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Futamura T, Akiyama S, Sugino H, Forbes A, McQuade RD, Kikuchi T. Aripiprazole attenuates established behavioral sensitization induced by methamphetamine. Prog Neuropsychopharmacol Biol Psychiatry 2010; 34:1115-9. [PMID: 20561555 DOI: 10.1016/j.pnpbp.2010.06.006] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/02/2010] [Revised: 06/08/2010] [Accepted: 06/08/2010] [Indexed: 11/25/2022]
Abstract
Psychostimulant-induced behavioral sensitization is an experimental model of the stimulant psychosis and the vulnerability to relapse in schizophrenia. This study investigated the effects of aripiprazole, an antipsychotic drug that has dopamine D2 receptor partial agonist activity, on established sensitization induced by methamphetamine (MAP) in mice. Repeated treatment with MAP (1.0mg/kg, s.c.) for 10 days progressively increased the ability of MAP to increase locomotor activity. The enhanced locomotion induced by a challenge dose of MAP (0.24 mg/kg, s.c.) also occurred after withdrawal from MAP pretreatment. Repeated treatment with aripiprazole from days 10 to 14 during withdrawal from MAP administration attenuated the effect of MAP pretreatment, enhancing the motor response to a challenge dose of stimulant 3 days after the aripiprazole preparation. In contrast, sulpiride, a dopamine D2 receptor specific antagonist, and risperidone, a serotonin 5-HT2 and dopamine D2 receptor antagonist, did not show effects similar to aripiprazole. The attenuation effect of aripiprazole was blocked by pretreatment with the specific serotonin 5-HT1A antagonist WAY100635. These results of aripiprazole suggest that the attenuation effect of aripiprazole was mediated by 5-HT1A receptors and imply that aripiprazole may have therapeutic value in treating drug-induced psychosis and schizophrenia.
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Affiliation(s)
- Takashi Futamura
- Q's Research Institute, Otsuka Pharmaceutical Co, Ltd, Tokushima 771-0192, Japan.
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Tsunoka T, Kishi T, Kitajima T, Okochi T, Okumura T, Yamanouchi Y, Kinoshita Y, Kawashima K, Naitoh H, Inada T, Ujike H, Yamada M, Uchimura N, Sora I, Iyo M, Ozaki N, Iwata N. Association analysis of GRM2 and HTR2A with methamphetamine-induced psychosis and schizophrenia in the Japanese population. Prog Neuropsychopharmacol Biol Psychiatry 2010; 34:639-44. [PMID: 20211215 DOI: 10.1016/j.pnpbp.2010.03.002] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/09/2009] [Revised: 02/24/2010] [Accepted: 03/02/2010] [Indexed: 12/20/2022]
Abstract
BACKGROUND Abnormalities in glutaminergic neural transmission have been suggested to be involved in the pathogenesis of schizophrenia. A recent study reported that alterations in the 5-HT2A-mGluR2 complex may be involved in neural transmission in the schizophrenic cortex. In addition, methamphetamine-induced psychosis is thought to be similar to schizophrenia. Therefore, we conducted a case-control study with Japanese samples (738 schizophrenia patients, 196 methamphetamine-induced psychosis patients, and 802 controls) to evaluate the association and interaction between GRM2, HTR2A and schizophrenia. METHODS We selected three 'tagging SNPs' in GRM2, and two biologically functional SNPs in HTR2A (T102C and A1438G), for the association analysis. RESULTS We detected a significant association between methamphetamine-induced psychosis and GRM2 in a haplotype-wise analysis, but not HTR2A. We did not detect an association between GRM2 or HTR2A and schizophrenia. In addition, no interactions of GRM2 and HTR2A were found in methamphetamine-induced psychosis or schizophrenia. We did not detect any novel polymorphisms in GRM2 when we performed a mutation search using methamphetamine-induced psychosis samples. CONCLUSION Our results suggested that GRM2 may play a role in the pathophysiology of methamphetamine-induced psychosis but not schizophrenia in the Japanese population. A replication study using larger samples or samples of other populations will be required for conclusive results.
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Affiliation(s)
- Tomoko Tsunoka
- Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi 470-1192, Japan
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Kishi T, Tsunoka T, Ikeda M, Kitajima T, Kawashima K, Okochi T, Okumura T, Yamanouchi Y, Kinoshita Y, Ujike H, Inada T, Yamada M, Uchimura N, Sora I, Iyo M, Ozaki N, Iwata N. Serotonin 1A receptor gene is associated with Japanese methamphetamine-induced psychosis patients. Neuropharmacology 2010; 58:452-6. [PMID: 19747927 DOI: 10.1016/j.neuropharm.2009.09.006] [Citation(s) in RCA: 27] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/24/2009] [Revised: 08/17/2009] [Accepted: 09/04/2009] [Indexed: 12/21/2022]
Affiliation(s)
- Taro Kishi
- Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi 470-1192, Japan.
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