Fernandez-Espejo and colleagues suggested that the endocannabinoid system is altered in schizophrenia and that dysregulation of this system, perhaps induced by exogenous cannabis, can interact with neurotransmitter systems in a way so that a "cannabinoid hypothesis" can be integrated with other neurobiologic hypotheses (eg, those involving dopamine and glutamate).
Evidence Accumulates for Links Between Marijuana and Psychosis
Michael T. Compton, MD, MPH
Introduction
A number of studies in recent years have revealed complex links between marijuana use and psychotic symptoms and diagnosable psychotic disorders like schizophrenia. Although a thorough review of this broad literature is beyond the purview of this brief communication, two avenues of research will be succinctly summarized, pertaining to (1) associations between cannabis use and clinical manifestations of psychosis, and (2) the biologic plausibility of the observed links.
Cannabis and Psychosis
Diverse studies suggest that cannabis use is associated with psychotic phenomenology. First, in addition to being the most abused illicit substance in the general US population, cannabis is clearly the most abused illegal drug among individuals with schizophrenia.[1,2] Furthermore, the initiation of cannabis use among those with psychotic disorders often precedes the onset of psychosis by several years.[1,3,4]
Second, cannabis use in adolescence is increasingly recognized as an independent risk factor for psychosis and schizophrenia.[5-7] That is, several epidemiologic studies suggest that cannabis use is a component cause of schizophrenia.[8,9]
Very recently, McGrath and colleagues[10] reported that early cannabis use is associated with psychosis-related outcomes (having a nonaffective psychotic disorder, scoring in the highest quartile of the Peters Delusions Inventory,[11] and reporting hallucinations) in a cohort of 3801 individuals assessed at age 18-23 years. Findings among 228 sibling pairs in that study reduce the likelihood that unmeasured confounding variables account for the results.[10]
Third, cannabis use may interact with genetic factors to elevate risk for psychotic disorders. One sentinel study demonstrated that the catechol-O-methyltransferase Val158Met functional polymorphism moderates the effects of adolescent-onset cannabis use on the later development of psychosis.[12]
Fourth, preliminary research suggests that cannabis use before the manifestation of psychiatric symptoms may be associated with an earlier age at onset of psychotic symptoms,[13] and perhaps even an earlier onset of prodromal symptoms.[14] We found that simply classifying first-episode psychosis patients according to their maximum frequency of use before onset of psychotic symptoms (ie, categorizing into none, ever, weekly, or daily use) revealed no significant effects of cannabis use on risk for onset, but analyzing the change in frequency of use before onset (using time-dependent covariates), revealed that progression to daily cannabis use was associated with age at onset.[14]
Fifth, aside from studies linking cannabis use and psychotic disorders, an increasing body of research suggests a potential association between cannabis use and schizotypal symptoms, or psychosis-proneness, in the general population.[15,16]
Several lines of evidence support the potential biologic plausibility of these links between cannabis use and psychosis.
First, exogenous (eg, Δ-9-tetrahydrocannabinol) and endogenous cannabinoids (eg, anandamide) exert their effects (such as modulating the release of neurotransmitters including dopamine and glutamate) by interactions with specific cannabinoid (CB1) receptors that are distributed in brain regions implicated in schizophrenia.
Second, several studies have shown an increased CB1 receptor density in brain regions of interest in schizophrenia, including the dorsolateral prefrontal cortex and the anterior cingulate cortex.[17,18]
Third, other studies report elevated levels of endogenous cannabinoids in the blood and cerebrospinal fluid of patients with schizophrenia.[19-21]
Fourth, acute, controlled administration of Δ-9-tetrahydrocannabinol causes both patients and controls to experience transient increases in cognitive impairments and schizophrenia-like positive and negative symptoms.[22]
In summarizing these and many other findings, Fernandez-Espejo and colleagues[23] have suggested that the endocannabinoid system is altered in schizophrenia and that dysregulation of this system, perhaps induced by exogenous cannabis, can interact with neurotransmitter systems in a way so that a "cannabinoid hypothesis" can be integrated with other neurobiologic hypotheses (eg, those involving dopamine and glutamate).
Conclusion
In sum, a growing body of clinical and epidemiologic research suggests significant but complex links between cannabis use and psychosis. Concurrently, ongoing neurobiologic research is revealing findings in the endocannabinoid system that appear to support the biologic plausibility of such links. It should be noted that much of the research conducted to date does not allow for causal determinations. Ongoing research of varying designs will undoubtedly enlighten the field.
References
1. Linszen DH, Dingemans PM, Lenior ME. Cannabis abuse and the course of recent onset schizophrenic disorders. Arch Gen Psychiatry. 1994;51:273-279. Abstract
2. Bersani G, Orlandi V, Kotzalidis GD, Pancheri P. Cannabis and schizophrenia: impact on onset, course, psychopathology and outcomes. Eur Arch Psychiatry Clin Neurosci. 2002;252:86-92. Abstract
3. Allebeck P, Adamsson C, Engstrom A, Rydberg U. Cannabis and schizophrenia: a longitudinal study of cases treated in Stockholm county. Acta Psychiatr Scand. 1993;88:21-24. Abstract
4. Stewart T, Goulding SM, Pringle M, Esterberg ML, Compton MT. A descriptive study of nicotine, alcohol, and cannabis use in urban, socially-disadvantaged, predominantly African-American patients with first-episode nonaffective psychosis. Clin Schizophr Relat Psychoses. 2010;3:217-225.
5. Smit F, Boiler L, Cuijpers P. Cannabis use and the risk of later schizophrenia: a review. Addiction. 2004;99:425-430. Abstract
6. Semple DM, McIntosh AM, Lawrie SM. Cannabis as a risk factor for psychosis: systematic review. J Psychopharmacol. 2005;19:187-194. Abstract
7. Weiser M, Noy S. Interpreting the association between cannabis use and increased risk for schizophrenia. Dialogues Clin Neurosci. 2005;7:81-85. Abstract
8. Andréasson S, Allebeck P, Rydberg U. Schizophrenia in users and nonusers of cannabis: a longitudinal study in Stockholm County. Acta Psychiatr Scand. 1989;79:505-510. Abstract
9. Zammit S, Allebeck P, Andréasson S, Lundberg I, Lewis G. Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study. BMJ. 2002;325:1199-1203. Abstract
10. McGrath J, Welham J, Scott J, et al. Association between cannabis use and psychosis-related outcomes using sibling pair analysis in a cohort of young adults. Arch Gen Psychiatry. 2010 Mar 1. [Epub ahead of print]
11. Peters ER, Joseph SA, Garety PA. Measurement of delusional ideation in the normal population: introducing the PDI (Peters et al. Delusions Inventory). Schizophr Bull. 1999;25:553-576. Abstract
12. Caspi A, Moffitt TE, Cannon M, et al. Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of a gene X environment interaction. Biol Psychiatry. 2005;57:1117-1127. Abstract
13. Compton MT, Ramsay CE. The impact of pre-onset cannabis use on age at onset of prodromal and psychotic symptoms. Primary Psychiatry. 2009;16:35-43.
14. Compton MT, Kelley ME, Ramsay CE, et al. Association of pre-onset cannabis, alcohol, and tobacco use with the age at onset of prodrome and age at onset of psychosis in first-episode patients. Am J Psychiatry. 2009;166:1251-1257. Abstract
15. Williams JH, Wellman NA, Rawlins JNP. Cannabis use correlates with schizotypy in healthy people. Addiction. 1996;91:869-877. Abstract
16. Compton MT, Goulding SM, Walker EF. Cannabis use, first-episode psychosis, and schizotypy: a summary and synthesis of recent literature. Curr Psychiatry Rev. 2007;3:161-171.
17. Dean B, Sundram S, Bradbury R, Scarr E, Copolov D. Studies on [3H]CP-55940 binding in the human central nervous system: regional specific changes in density of cannabinoid-1 receptors associated with schizophrenia and cannabis use. Neuroscience. 2001;103:9-15. Abstract
18. Zavitsanou K, Garrick T, Huang XF. Selective antagonist [3H]SR141716A binding to cannabinoid CB1 receptors is increased in the anterior cingulate cortex in schizophrenia. Progr Neuropsychopharmacol Biol Psychiatry. 2004;28:355-360.
19. Leweke FM, Giuffrida A, Wurster U, Emrich HM, Piomelli D. Elevated endogenous cannabinoids in schizophrenia. Neuroreport. 1999;10:1665-1669. Abstract
20. De Marchi N, De Petrocellis L, Orlando P, Daniele F, Fezza F, Di Marzo V. Endocannabinoid signaling in the blood of patients with schizophrenia. Lipids Health Dis. 2003;2:5-14. Abstract
21. Giuffrida A, Leweke FM, Gerth CW, et al. Cerebrospinal anandamide levels are elevated in acute schizophrenia and are inversely correlated with psychotic symptoms. Neuropsychopharmacology. 2004;29:2108-2114. Abstract
22. D’Souza DC, Abi-Saab WM, Madonick S, et al. Delta-9-tetrahydrocannabinol effects in schizophrenia: implications for cognition, psychosis, and addiction. Biol Psychiatry. 2005;57:594-608. Abstract
23. Fernandez-Espejo E, Viveros MP, Núñez L, Ellenbroek BA, Rodriguez de Fonseca F. Role of cannabis and endocannabinoids in the genesis of schizophrenia. Psychopharmacology. 2009;206:531-549.
HUBUNGKAIT ANTARA GANJA DAN PENYAKIT MENTAL
JOM TANGANI GEJALA SOSIAL
KENYATAAN MEDIA
MAC 23, 2009 (SELASA)
MENANGANI GEJALA SOSIAL SECARA TUNTAS
Selaku Pengerusi Jawatankuasa Induk Menangani Gejala Sosial Negeri Selangor saya menyeru kepada semua pihak daripada jabatan dan agensi kerajaan, syarikat swasta, ahli akademik, ahli korporat, NGO, persatuan belia dan wanita, aktivis masyarakat, kaunselor, pesara, remaja dan belia, PIBG, Majlis Permuafakatan Tadika Selangor (MPTS), Majlis Permuafakatan Mahasiswa Selangor (MPMS), Majlis Permuafakatan Institusi Pendidikan Islam Selangor (MAPPIS), sekolah-sekolah, Universiti/kolej, institusi keagamaan, JKKK, Kelab remaja dll.
Semua boleh menerima kenyataan bahawa untuk mengatasi gejala social yang semakin meruncing memerlukan tindakan menyeluruh, sepadu dan dirancang teliti. Ia memerlukan pendekatan inklusif yang mampu mensinergi sumber kepakaran, masa, tenaga, wang ringgit dan segala sistem sokongan.
Saya menyeru kepada semua pihak yang terlibat dan berpengalaman serta mereka yang benar-benar mahu Selangor bebas daripada gejala sosial tampil ke depan untuk membantu kerajaan Negeri Selangor yang berikhtiar sedaya upaya untuk membanteras perkara negatif ini.
Sila hubungi Pegawai Penyelaras Jawatankuasa Menangani Gejala Sosial
EN AZREEN Tel : 0355447215
Dr Hjh Halimah Ali
Exco Pendidikan, Pendidikan Tinggi Dan
Pembangunan Modal Insan Negeri Selangor
Merangkap Adun Selat Klang. Read More “JOM TANGANI GEJALA SOSIAL” »»
SIAKAP SENOHONG GELAMA IKAN DURI CAKAP BOHONG AKAN JADI MENTERI
MP yang disebut Zahrain akan "melompat" jika Peristiwa 16 September 2008 benar-benar berlaku selain Ghapur (kiri), ialah Datuk Seri Anifah Aman (BN-Kimanis), Datuk Bung Moktar Radin (BN-Kinabatangan), Datuk Chua Soon Bui (Bebas-Tawau) dan Datuk Eric Majimbun (Bebas-Sepanggar).
Nama lain yang disebut ialah Dr Mohd Puad Zarkashi (BN-Batu Pahat), Datuk Seri Tengku Azlan Sultan Abu Bakar (BN-Jerantut) dan Tengku Razaleigh Hamzah (BN-Gua Musang).
Zahrain juga mendakwa seorang timbalan speaker dikatakan akan menyertai PKR
Ghapur: Zahrain penipu besar
Ahli parlimen Kalabakan, Datuk Abdul Ghapur Salleh, yang dinamakan sebagai satu daripada lapan MP yang akan berpaling tadah kepada pembangkang pada 16 Sept membidas Datuk Seri Zahrain Hashim yang didakwa menipu di Dewan Rakyat.
Bekas MP PKR yang mengisytiharkan dirinya sebagai ahli bebas itu, minggu lalu mendedahkan bahawa Abdul Ghapur yang mewakili Umno Sabah dinamakan antara kumpulan berkenaan.
Menurut Ghapur, Zahrain telah melakukan satu penipuan besar.
Sehubungan itu, beliau mahu ahli parlimen dari Bayan Baru itu segera menarik semula kenyataannya dan menyenaraikan mereka yang dikatakan akan berpaling tadah itu.
Abdul Ghapur juga mencabar Zahrain mendedahkan nama 30 MP yang dikatakan akan menyertai ketua umum PKR, Datuk Seri Anwar Ibrahim dalam rancangan Pakatan Rakyat untuk menumbangkan kerajaan Barisan Nasional, jika apa yang didakwanya sebelum ini adalah benar.
Beliau juga memberi amaran kepada Umno agar tidak menerima Zahrain sebagai ahlinya kerana jika bekas ketua PKR Pulau Pinang itu sanggup berpaling tadah terhadap Anwar, dia juga, katanya, suatu hari nanti akan menikam pemimpin BN juga.
Selain Ghapur (kiri), MP dari Sabah yang dinamakan oleh Zahrain ialah Datuk Seri Anifah Aman (BN-Kimanis), Datuk Bung Moktar Radin (BN-Kinabatangan), Datuk Chua Soon Bui (Bebas-Tawau) dan Datuk Eric Majimbun (Bebas-Sepanggar).
Nama lain yang disebut ialah Dr Mohd Puad Zarkashi (BN-Batu Pahat), Datuk Seri Tengku Azlan Sultan Abu Bakar (BN-Jerantut) dan Tengku Razaleigh Hamzah (BN-Gua Musang).
Zahrain juga mendakwa seorang timbalan speaker juga dikatakan akan menyertai PKR.
Hazlan Zakaria/malaysiakini
===============================================================
Pengundi Bayan Baru desak Zahrain kosong kerusi
Ahli parlimen Bayan Lepas yang keluar PKR baru-baru ini dan menjadi calon Bebas, Datuk Zahrain Mohd Hashim menerima kejutan hari ini apabila menerima petisyen yang mengandungi 2,108 tandatangan, mendesaknya mengosongkan kerusinya sebelum Dewan Rakyat bersidang mulai esok.
ADUN Pantai Jerejak, Sim Tze Tsin berkata, tandatangan itu dikutip dalam tempoh dua hari dari kalangan pengundi di sekitar pasar Bayan Baru dan Tapak Pesta di Sungai Nibong, Pulau Pinang.
DUN Pantai Jerejak terletak di bawah Parlimen Bayan Baru.
"Ramai yang merasa tertipu dengan tindakan Zahrain keluar parti, jadi kita terpaksa menghantarr mesej ini kepadanya," kata Sim yang juga timbalan ketua Angkatan Muda PKR Pulau Pinang.
"Saya diberitahu yang Zahrain terperanjat dan pucat sewaktu menerima petisyen tersebut, tetapi beliau tetap menerimanya," katanya.
Zahrain keluar PKR pada 12 Februari lalu selepas mengecam Ketua Menteri Pulau Pinang yang juga setiausaha agung DAP, Lim Guan Eng sebagai "seorang diktator dan perkauman.
Susan Loone/Malaysiakini
ADAKAH ANDA MENGALAMI GANGGUAN MOOD?
Quick Screen Test Valid, Efficient in Detecting Psychiatric Illness in Primary Care
March 16, 2010 (Updated March 18, 2010) — The My Mood Monitor (M-3) checklist is a valid, efficient, and feasible tool for screening patients for multiple common psychiatric illnesses in primary care and has a diagnostic accuracy that equals that of currently used single-disorder screens. It can also be filled out by patients in the waiting room in less than 5 minutes, and the majority of practitioners are able to review the checklist in 30 seconds or less.
Bradley Gaynes, MD, MPH, from the University of North Carolina School of Medicine, Chapel Hill, and colleagues found that compared with the Mini International Neuropsychiatric Interview, the reference standard, the M-3 checklist had a sensitivity of 0.84 for depression and a specificity of 0.80.
"This means that the M-3 checklist will successfully identify 84% of patients who have major depressive disorder, which is its sensitivity, and successfully identify 80% of those who do not have major depressive disorder, which is its specificity," Dr. Gaynes told Medscape Psychiatry. For bipolar spectrum disorder, the M-3 checklist had a sensitivity of 0.88 and a specificity of 0.70.
The anxiety module had a sensitivity of 0.82 and a specificity of 0.76, whereas sensitivity for posttraumatic stress disorder (PTSD) was 0.88 and specificity was 0.76. As a screen for any psychiatric disorder, the sensitivity of the M-3 was 0.83, and the specificity was 0.76.
According to investigators, 83% of clinicians reviewed the checklist in 30 or fewer seconds, and 80% thought it was helpful in reviewing patients' emotional health.
The study was published in the March/April issue of the Annals of Family Medicine.
Designed Specifically for General Practitioners
The questions asked on the M-3 checklist were developed by a group of experienced mental health clinicians and were specifically designed for use in primary care settings. The completed tool consists of a 23-item self-report symptom checklist that asks patients whether they have experienced symptoms of major depressive disorder, generalized anxiety disorder, panic disorder, social anxiety disorder, PTSD, or obsessive-compulsive disorder during the last 2 weeks.
The checklist also asks patients about a lifetime history of symptoms of bipolar spectrum disorder, as well as additional functional impairment questions. The wording and grammar of the M-3 checklist are at a sixth-grade reading level.
Investigators enrolled 647 consecutive adult patients who were seeking primary care at an academic family medicine clinic between July 2007 and February 2008. "We used a 2-step scoring procedure to make screening more efficient and within 30 days of the index visit, a research assistant administered the Mini International Neuropsychiatric Interview...to participating patients by telephone," the investigators write.
The Mini International Neuropsychiatric Interview is a reliable and valid diagnostic instrument serving as the reference standard to evaluate the performance of the M-3.
As the authors note, they used the functional impairment questions of the M-3 as a "first-stage" screen, and the remaining checklist symptoms were then scored for only those patients whose screen was positive for functional impairment. This so-called "gateway" method was felt to provide the best balance of increasing sensitivity and specificity of the M-3 checklist while permitting a quick, visually intuitive method for scoring by hand.
First-Step Screen
Investigators note that the "first-step" screen for functional impairment eliminated 349, or 53.9%, of the 647 participants from the checklist scoring process — 38 (10.9%) of whom nevertheless met Mini International Neuropsychiatric Interview criteria for a psychiatric diagnosis, the authors add. Of the remaining 298 patients who passed through the "gate" and who completed the symptom checklist, 186, or 62.4%, had a psychiatric diagnosis.
Indeed, those who passed through the "gate" were nearly 6 times more likely to have a psychiatric diagnosis than those who did not pass through the gate (P < .001). For the depression module, a positive screen was more than 4 times more likely to come from a patient with a depressive disorder than from a patient without one. "Further," investigators add, "given a 16% prevalence of depression in our population...a patient with a positive screen had a post-test odds for depression of approximately...40%." Overall, 287 patients, or 44% of the 647 enrolled in the study, were positive on the M-3 checklist, indicating that as a general screen, the M-3 had a positive predictive value of 0.65 and a negative predictive value of 0.89 for any mood or anxiety disorder. M-3 Psychometrics for Specific Diagnoses and for Any Diagnosis by Mini International Neuropsychiatric Interview Test Result Depression Bipolar Anxiety PTSD Any Diagnosis Sensitivity (95% confidence interval) 0.84 (0.77 - 0.89) 0.88 (0.77 - 0.95) 0.82 (0/75 - 0.87) 0.88 (0.74 - 0.96) 0.83 (0.77 - 0.88) Specificity (95% confidence interval) 0.80 (0.76 - 0.83) 0.70 (0.66 - 0.74) 0.78 (0.74 - 0.81) 0.76 (0.73 - 0.80) 0.76 (0.72 - 0.80) Positive M-3 screen 34% 35% 39% 28% 44% Diagnosed by Mini International Neuropsychiatric Interview 22% 9% 28% 6% 35% Having completed the M-3 checklist, approximately 70% of patients indicated that they subsequently talked to their physician about mood or feelings, and 63% of all participants said that the M-3 checklist had helped them to bring up the subject of mood or feelings with their physicians. "Many patients are reticent to initiate discussion of psychological distress with their primary care primary, so this tool helps allow patients initiate a discussion with their primary care provider," said Dr. Gaynes. "But it also helps the primary care physician to discuss the possibility of a psychiatric diagnosis with patients, and patients even have access to this tool online so that they could fill it out and then bring the form into their clinic as well." A Step Forward Michael Klinkman, MD, University of Michigan Depression Center, Ann Arbor, told Medscape Psychiatry that the M-3 checklist is a "good step forward" but that it still does not address all the screening needs in a primary care center. "It does a good job of taking and condensing the questions we use to try and identify patients with depressive disorder, but it does not confirm a diagnosis," he said. For example, if patients screen positive for bipolar disorder on the M-3 checklist, they still have less than a 1 in 4 chance of having that disorder because the symptoms used in the screening test are lifetime symptoms. and if patients answer yes, that doesn’t mean they are having symptoms now. "As long as physicians understand this and they have a place where they can refer patients to in order to get the rest of the screening done, it’s fine, but the checklist still leaves a lot of work for primary care physicians to do, and too many times, they do not have access to mental health experts to complete this process," Dr. Klinkman said. Data collection was supported by a grant from M-3 information. Dr. Gaynes has reported that he received grants and research support from the National Institute of Mental Health and the Agency for Healthcare Research and Quality. Dr. Klinkman has disclosed no relevant financial relationships. Ann Fam Med. 2010;8:160-169.
Sila layari di bawah untuk menjalani ujian MY METER (3M) dan mengenalpasti mood anda sekarang
http://www.mymoodmonitor.com/
