Purposes of the Guidelines
The purposes of these Guidelines are to (1) optimize pain control, recognizing that a pain-free state may not be attainable; (2) enhance functional abilities and physical and psychologic well-being; (3) enhance the quality of life of patients; and (4) minimize adverse outcomes.
Focus
These Guidelines focus on the knowledge base, skills, and range of interventions that are the essential elements of effective management of chronic pain and pain-related problems. The Guidelines recognize that the management of chronic pain occurs within the broader context of health care, including psychosocial function and quality of life. These Guidelines apply to patients with chronic noncancer neuropathic, somatic (e.g., myofascial), or visceral pain syndromes. The Guidelines do not apply to patients with acute pain from an injury or postoperative recovery, cancer pain, degenerative major joint disease pain, headache syndromes (e.g., migraine and cluster), temporomandibular joint syndrome, or trigeminal or other neuralgias of the head or face. In addition, the Guidelines do not apply to pediatric patients and do not address the administration of intravenous drugs or surgical interventions other than implanted intrathecal drug delivery systems and nerve stimulators.
Application
These Guidelines are intended for use by anesthesiologists and other physicians serving as pain medicine specialists. The Guidelines recognize that all anesthesiologists or other physicians may not have access to the same knowledge base, skills, or range of modalities. However, aspects of the Guidelines may be helpful to anesthesiologists or other physicians who manage patients with chronic pain in a variety of practice settings. They may also serve as a resource for other physicians, nurses, and healthcare providers (e.g., rehabilitation therapists, psychologists, and counselors) engaged in the care of patients with chronic pain. They are not intended to provide treatment algorithms for specific pain syndromes.
Summary of Recommendations
I. Patient Evaluation
* All patients presenting with chronic pain should have a documented history and physical examination and an assessment that ultimately supports a chosen treatment strategy.
○History:
▪ A pain history should include a general medical history with emphasis on the chronology and symptomatology of the presenting complaints.
▪ A history of current illness should include information about the onset, quality, intensity, distribution, duration, course, and sensory and affective components of the pain and details about exacerbating and relieving factors.
▪ Additional symptoms (e.g., motor, sensory, and autonomic changes) should be noted.
▪ Information regarding previous diagnostic tests, results of previous therapies, and current therapies should be reviewed by the physician.
▪ In addition to a history of current illness, the history should include (1) a review of available records, (2) medical history, (3) surgical history, (4) social history including substance use or misuse, (5) family history, (6) history of allergies, (7) current medications including use or misuse, and (8) review of systems.
▪ The causes as well as the effects of pain (e.g., physical deconditioning, change in occupational status, and psychosocial dysfunction) and the impacts of previous treatment(s) should be evaluated and documented.
○ Physical examination: The physical examination should include an appropriately directed neurologic and musculoskeletal evaluation, with attention to other systems as indicated.
○ Psychosocial evaluation: The psychosocial evaluation should include information about the presence of psychologic symptoms (e.g., anxiety, depression, or anger), psychiatric disorders, personality traits or states, and coping mechanisms.
▪ An assessment should be made of the impact of chronic pain on a patient's ability to perform activities of daily living.
▪ An evaluation of the influence of pain and treatment on mood, ability to sleep, addictive or aberrant behavior, and interpersonal relationships should be performed.
▪ Evidence of family, vocational, or legal issues and involvement of rehabilitation agencies should be noted.
▪ The expectations of the patient, significant others, employer, attorney, and other agencies may also be considered.
○ Interventional diagnostic procedures: Appropriate diagnostic procedures may be conducted as part of a patient's evaluation, based on a patient's clinical presentation.
▪ The choice of an interventional diagnostic procedure (e.g., selective nerve root blocks, medial branch blocks, facet joint injections, sacroiliac joint injections, and provocative discography) should be based on the patient's specific history and physical examination and anticipated course of treatment.
▪ Interventional diagnostic procedures should be performed with appropriate image guidance.
▪ Diagnostic medial branch blocks or facet joint injections may be considered for patients with suspected facet-mediated pain to screen for subsequent therapeutic procedures.
▪ Diagnostic sacroiliac joint injections or lateral branch blocks may be considered for the evaluation of patients with suspected sacroiliac joint pain.
▪ Diagnostic selective nerve root blocks may be considered to further evaluate the anatomic level of radicular pain.
▪ The use of sympathetic blocks may be considered to support the diagnosis of sympathetically maintained pain.
▪ They should not be used to predict the outcome of surgical, chemical, or radiofrequency sympathectomy.
▪ Peripheral blocks may be considered to assist in the diagnosis of pain in a specific peripheral nerve distribution.
▪ Provocative discography may be considered for the evaluation of selected patients with suspected discogenic pain.
▪ Provocative discography should not be used for the routine evaluation of the patient with chronic nonspecific back pain.
* Findings from the patient history, physical examination, and diagnostic evaluation should be combined to provide the foundation for an individualized treatment plan focused on the optimization of the risk–benefit ratio with an appropriate progression of treatment from a lesser to greater degree of invasiveness.
* Whenever possible, direct and ongoing contact should be made and maintained with the other physicians caring for the patient to ensure optimal care management.
Multimodal or Multidisciplinary Interventions
* Multimodal interventions should be part of a treatment strategy for patients with chronic pain.
* A long-term approach that includes periodic follow-up evaluations should be developed and implemented as part of the overall treatment strategy.
* When available, multidisciplinary programs may be used.
Single Modality Interventions
* Ablative techniques (other treatment modalities should be attempted before consideration of the use of ablative techniques):
○ Chemical denervation (e.g., alcohol, phenol, or high concentration local anesthetics) should not be used in the routine care of patients with chronic noncancer pain.
○ Cryoablation may be used in the care of selected patients (e.g., postthoracotomy pain syndrome, low back pain [medial branch], and peripheral nerve pain).
○ Thermal intradiscal procedures: IDET may be considered for young, active patients with early single-level degenerative disc disease with well-maintained disc height.
○ Radiofrequency ablation:
▪ Conventional (e.g., 80°C) or thermal (e.g., 67°C) radiofrequency ablation of the medial branch nerves to the facet joint should be performed for low back (medial branch) pain when previous diagnostic or therapeutic injections of the joint or medial branch nerve have provided temporary relief.
▪ Conventional radiofrequency ablation may be performed for neck pain.
▪ Water-cooled radiofrequency ablation may be used for chronic sacroiliac joint pain.
▪ Conventional or other thermal radiofrequency ablation of the dorsal root ganglion should not be routinely used for the treatment of lumbar radicular pain.
* Acupuncture: Acupuncture may be considered as an adjuvant to conventional therapy (e.g., drugs, physical therapy, and exercise) in the treatment of nonspecific, noninflammatory low back pain.
* Blocks:
○ Joint blocks:
▪ Intraarticular facet joint injections may be used for the symptomatic relief of facet-mediated pain.
▪ Sacroiliac joint injections may be considered for the symptomatic relief of sacroiliac joint pain.
○ Nerve and nerve root blocks:
▪ Celiac plexus blocks using local anesthetics with or without steroids may be used for the treatment of pain secondary to chronic pancreatitis.
▪ Lumbar sympathetic blocks or stellate ganglion blocks may be used as components of the multimodal treatment of CRPS if used in the presence of consistent improvement and increasing duration of pain relief.
▪ Sympathetic nerve blocks should not be used for the long-term treatment of non-CRPS neuropathic pain.
▪ Medial branch blocks may be used for the treatment of facet-mediated spine pain.
▪ Peripheral somatic nerve blocks should not be used for long-term treatment of chronic pain.
* Botulinum toxin:
○ Botulinum toxin should not be used in the routine care of patients with myofascial pain.
○ Botulinum toxin may be used as an adjunct for the treatment of piriformis syndrome.
* Electrical nerve stimulation:
○ Neuromodulation with electrical stimulus:
▪ Subcutaneous peripheral nerve stimulation: Subcutaneous peripheral nerve stimulation may be used in the multimodal treatment of patients with painful peripheral nerve injuries who have not responded to other therapies.
▪ Spinal cord stimulation: Spinal cord stimulation may be used in the multimodal treatment of persistent radicular pain in patients who have not responded to other therapies.
* Spinal cord stimulation may also be considered for other selected patients (e.g., CRPS, peripheral neuropathic pain, peripheral vascular disease, and postherpetic neuralgia).
* Shared decision making regarding spinal cord stimulation should include a specific discussion of potential complications associated with spinal cord stimulator placement.
* A spinal cord stimulation trial should be performed before considering permanent implantation of a stimulation device.
○ TENS:
▪ TENS should be used as part of a multimodal approach to pain management for patients with chronic back pain and may be used for other pain conditions (e.g., neck and phantom limb pain).
* Epidural steroids with or without local anesthetics:
○ Epidural steroid injections with or without local anesthetics may be used as part of a multimodal treatment regimen to provide pain relief in selected patients with radicular pain or radiculopathy.
▪ Shared decision making regarding epidural steroid injections should include a specific discussion of potential complications, particularly with regard to the transforaminal approach.
▪ Transforaminal epidural injections should be performed with appropriate image guidance to confirm correct needle position and spread of contrast before injecting a therapeutic substance
▪ Image guidance may be considered for interlaminar epidural injections to confirm correct needle position and spread of contrast before injecting a therapeutic substance
* Intrathecal drug therapies:
○ Neurolytic blocks: Intrathecal neurolytic blocks should not be performed in the routine management of patients with noncancer pain.
○ Intrathecal nonopioid injections:
▪ Intrathecal preservative-free steroid injections may be used for the relief of intractable postherpetic neuralgia nonresponsive to previous therapies.
▪ Ziconotide infusion may be used in the treatment of a select subset of patients with refractory chronic pain.
○ Intrathecal opioid injections: Intrathecal opioid injection or infusion may be used for neuropathic pain patients.
▪ Shared decision-making regarding intrathecal opioid injection or infusion should include a specific discussion of potential complications.
▪ Neuraxial opioid trials should be performed before considering permanent implantation of intrathecal drug delivery systems.
* Minimally invasive spinal procedures: Minimally invasive spinal procedures (e.g., vertebroplasty) may be used for the treatment of pain related to vertebral compression fractures.
* Pharmacologic management:
○ Anticonvulsants: Anticonvulsants (e.g.,α-2-delta calcium-channel antagonists, sodium-channel antagonists, and membrane-stabilizing drugs) should be used as part of a multimodal strategy for patients with neuropathic pain.
○ Antidepressants:
▪ Tricyclic antidepressants should be used as part of a multimodal strategy for patients with chronic pain.
▪ Serotonin–norepinephrine reuptake inhibitors should be used as part of a multimodal strategy for a variety of chronic pain patients.
▪ Selective serotonin reuptake inhibitors may be considered specifically for patients with diabetic neuropathy.
○ Other drugs:
▪ As part of a multimodal pain management strategy, extended-release oral opioids should be used for neuropathic or back pain patients, and transdermal, sublingual, and immediate-release oral opioids may be used.
▪ For selected patients, ionotropic NMDA receptor antagonists (e.g., neuropathic pain), NSAIDs (e.g., back pain), and topical agents (e.g., peripheral neuropathic pain) may be used, benzodiazepines and skeletal muscle relaxants may be considered.
○ A strategy for monitoring and managing side effects, adverse effects, and compliance should be considered for all patients undergoing any long-term pharmacologic therapy.
* Physical or restorative therapy:
○ Physical or restorative therapy may be used as part of a multimodal strategy for patients with low back pain.
○ Physical or restorative therapy may be considered for other chronic pain conditions.
* Psychological treatment:
○ Cognitive behavioral therapy, biofeedback, or relaxation training: These interventions may be used as part of a multimodal strategy for patients with low back pain, as well as for other chronic pain conditions.
○ Supportive psychotherapy, group therapy, or counseling: These interventions may be considered as part of a multimodal strategy for chronic pain management.
* Trigger point injections: These injections may be considered for treatment of myofascial pain as part of a multimodal approach to pain management.
For these Guidelines, a literature review was used in combination with opinions obtained from expert consultants and other sources (e.g., ASA members, ASRA members, open forums, and Internet postings). Both the literature review and opinion data were based on evidence linkages or statements regarding potential relationships between clinical interventions and outcomes. The interventions listed below were examined to assess their impact on a variety of outcomes related to chronic noncancer pain.Cited Here...
I. Patient evaluation:
1. Medical records review or patient condition
2. Physical examination
3. Psychological and behavioral evaluation
4. Interventional diagnostic procedures
Diagnostic facet joint block
Diagnostic sacroiliac joint block
Diagnostic nerve block (e.g., peripheral or sympathetic, medial branch, celiac plexus, and hypogastric).
Provocative discography
II. Multimodal or multidisciplinary pain management programs (e.g., pain centers vs. single discipline care)
III. Single Modality Interventions
1. Ablative techniques:
Chemical denervation
Cryoneurolysis or cryoablation
Thermal intradiscal procedures (intervertebral disc annuloplasty [IDET], transdiscal biaculoplasty)
Conventional or thermal radiofrequency ablation (facet joint, sacroiliac joint, dorsal root ganglion)
2. Acupuncture
3. Blocks:
Joint blocks
Facet joint injections
Sacroiliac joint injections
Nerve or nerve root blocks
Celiac plexus blocks
Lumbar sympathetic blocks or lumbar paravertebral sympathectomy
Medial branch blocks
Peripheral nerve blocks
Stellate ganglion blocks or cervical paravertebral sympathectomy
4. Botox
5. Electrical nerve stimulation:
Peripheral nerve stimulation
Spinal cord or dorsal column stimulation
TENS
6. Epidural steroids:
Interlaminar steroids versus placebo
Interlaminar steroids with local anesthetics versus without local anesthetics
Transforaminal steroids versus placebo
Transforaminal steroids with local anesthetics versus without local anesthetics
7. Intrathecal drug therapies
Intrathecal neurolytic blocks
Intrathecal nonopioid injection (e.g., ziconotide, clonidine, or local anesthetics)
Intrathecal opioid injection
8. Minimally invasive spinal procedures
Kyphoplasty (percutaneous, glue, and balloon)
Vertebroplasty
Percutaneous disc decompression
9. Pharmacologic interventions
Anticonvulsants
Alpha-2-delta calcium channel antagonists
Sodium channel blockers
Membrane-stabilizing drugs
Antidepressants
Tricyclic antidepressants
Selective serotonin–norepinephrine reuptake inhibitors
Selective serotonin reuptake inhibitors
Benzodiazepines
NMDA receptor antagonists
NSAIDs
Opioid therapy
Sustained or controlled-release opioids
Tramadol
Skeletal muscle relaxants
Topical agents
Capsaicin
Lidocaine
Ketamine
10. Physical or restorative therapy
11. Psychologic treatment or counseling
Cognitive behavioral therapy, biofeedback, or relaxation training
Supportive psychotherapy or group therapy
CHRONIC PAIN MANAGEMENT BY the American Society of Anesthesiologists
ADAKAH ANDA MENGIMPIKAN GENERASI IDAMAN SELANGOR
Kerajaan Negeri Selangor serius merancang mahu menjadikan Selangor negeri idaman, maju, selamat, sejahtera dan berkebajikan. Diantara teras pembangunan lestari negeri ialah memacu pembangunan modal insan. Perancangan rapi yang mengambilkira input daripada pelbagai pakar pembangunan insan yang mempunyai pengalaman dan ahli akademik serta pakar motivasi dan telah dibentang kepada wakil warga pendidik, pimpinan masyarakat, siswa, belia dan NGO serta akitivis masyarakat. Maka, lahirlah satu model pambangunan modal insan sebagai satu dasar kerajaan baharu negeri Selangor iaitu S.P.I.E.S tm.
Pembangunan insan secara menyeluruh dan sepadu ini digagaskan bagi melahirkan modal insan berkualiti sebagai agen yang akan menyokong dan mendokong pembangunan negeri Selangor hingga tercapai visi menjadi Selangor baldatun tayyibatun wa robbun ghafuur iaitu negeri yang baik dan diampuni serta dirahmati oleh Allah swt.
Namun, usaha pembangunan insan ini perlu diseimbangkan dengan program mitigasi insan liabiliti yakni meminimakan jumlah insan yang merugikan diri, keluarga, masyarakat dan negeri. Golongan yang dimaksudkan insan liabiliti ialah mereka yang terjebak dalam gejala sosial seperti penagihan dadah, penagihan arak, jenayah dan vandalisme.
Gejala social yang melanda masyarakat terutama yang melibatkan golongan remaja dan belia seperti buang bayi, sumbang mahram, video lucah,lumba haram dan sebagainya telah memporakperandakan institusi kekeluargaan dan mengancam keutuhan dan keharmonian masyarakat dan Negara. Fenomena ini dijangka akan bertambah teruk jika tiada tindakan yang drastik dan efektif dirangka dan dilaksanakan segera.
Kerajaan wajib melakukan dua perkara ini serentak bukan terasing atau terpisah-pisah seperti yang telah dilakukan oleh pihak berwajib dahulu. Inilah yang dimaksudkan dengan pendekatan amar ma’ruf nahi mungkar atau mengajak kepada perkara kebajikan dan mencegah kemungkaran.
Justeru, untuk mempastikan keberkesanan ikhtiar menangani gejala sosial maka kerajaan negeri Selangor melalui Jawatankuasa Tetap Pembangunan Modal Insan mewujudkan Jawatankuasa Induk Menangani Gejala Sosial di peringkat negeri yang melibat pelbagai jabatan dan agensi kerajaan seperti Jabatan Pelajaran, Jabatan Kesihatan, Jabatan Kebajikan, JAIS, PDRM, AADK, semua Pegawai Daerah, semua Datuk Bandar/YDP PIHAK BERKUASA TEMPATAN,NGO, pimpinan masyarakat, pertubuhan wanita dan belia, PIBG, Majlis Permuafakatan Tadika Selangor, pimpinan tertinggi IPT negeri dan aktivis masyarakat.
Jawatankuasa ini akan di wujudkan di daerah-daerah yang melibatkan komposisi ahli AJK yang sama dan juga penghulu. Segala program yang dirancang bagi membendung penularan gejala sosial dan jenayah akan di jalankan adalah diberi nama Program GeMS(Generasi Idaman Selangor).
Kaedah pelaksanaan GeMS menggunakan pendekatan 5P iaitu Pembangunan, Pencegahan, Pencelahan, Penguatkuasaan dan Pemulihan ke atas golongan sasaran secara bersepadu dan bersifat jangka panjang.
Ingin saya tekankan di sini, pendekatan yang diperlukan ialah pendekatan holistik dan inklusif. Strategi yang memungkinkan kejayaan mengatasi gejala social ialah kolaborasi sinergistik di antara pelbagai jabatan dan agensi kerajaaan serta badan-badan NGO, pimpinan setempat masyarakat serta keluarga dan rakan taulan. Sudah tentu polisi kerajaan dan pelaksanaan program berimpak tinggi yang sentiasa dipantau dan diberi penambahbaikan. Kajian & Penyelidikan perlu di utamakan.
Adalah harapan saya semua penduduk di Selangor memainkan peranan proaktif bagi melahirkan generasi idaman Selangor yang bersifat positif, berakhlak mulia dan mara ke depan melahirkan budaya bantu membantu, prihatin dan sentiasa peka kepada keadaan sekeliling dan kebajikan keluarga sekeliling.
HUBUNGKAIT ANTARA GANJA DAN PENYAKIT MENTAL
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.
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
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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
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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
