اعتماد على مادة

من ويكيبيديا، الموسوعة الحرة
اذهب إلى التنقل اذهب إلى البحث
الاعتماد على مادة
من أنواع اضطراب تعاطي المخدرات،  وإدمان  تعديل قيمة خاصية صنف فرعي من (P279) في ويكي بيانات
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تصنيف وموارد خارجية
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ن.ف.م.ط.

الاعتماد على مادة المعروف أيضا باسم الاعتماد على المخدرات هي حالة تكيفية تنتج من تكرار تعاطي مادة أو دواء، مما يؤدي إلى أعراض انسحابية عند التوقف عن الاستخدام.[1][2] بينما الإدمان، وهو مفهوم خاص من الاعتماد على مواد، يعرف بأنه سلوك قهري وخارج عن السيطرة، على الرغم من العواقب السلبية. ΔFosB، عامل النسخ الجيني، من المعروف الآن أنه عنصر حاسم وعامل مشترك في تكوين تقريبا جميع أشكال الإدمان السلوكية والإدمان على المواد،[3][4][5] ولكن ليس الاعتماد.


في الطبعة الرابعة من الدليل التشخيصي والإحصائي للاضطرابات النفسية (DSM-IV)، الاعتماد على مادة يتم تعريفه على أنه إدمان للمخدرات، و يمكن تشخيصه دون حدوث متلازمة الانسحاب.[6] الآن يتم وصف الاعتماد على مادة كالتالي: "عندما يستمر الفرد في استخدام الكحول أو المخدرات الأخرى على الرغم من المشاكل المتعلقة باستخدام المادة، قد يمكن تشخيص الحالة بأنها اعتماد على مادة". الاستخدام القهري والمتكرر قد يؤدي إلى حدوث تحمل لتأثير المادة وأعراض الانسحاب عند انخفاض أو توقف الاستخدام. هذا الموضوع جنبا إلى جنب مع سوء استخدام المواد يعتبرا من اضطرابات تعاطي المواد."[7]

انظر أيضا[عدل]

فهرس الإدمان والاعتمادية[8][9][10][11]

مراجع وملاحظات[عدل]

  1. ^ "Chapter 15: Reinforcement and Addictive Disorders". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (الطبعة 2nd). McGraw-Hill Medical. 2009. صفحات 364–368. ISBN 9780071481274. The defining feature of addiction is compulsive, out-of-control drug use, despite negative consequences. ...
    Addictive drugs are both rewarding and reinforcing. ... Familiar pharmacologic terms such as tolerance, dependence, and sensitization are useful in describing some of the time-dependent processes that underlie addiction. ...
    Dependence is defined as an adaptive state that develops in response to repeated drug administration, and is unmasked during withdrawal, which occurs when drug taking stops. Dependence from long-term drug use may have both a somatic component, manifested by physical symptoms, and an emotional–motivation component, manifested by dysphoria. While physical dependence and withdrawal occur with some drugs of abuse (opiates, ethanol), these phenomena are not useful in the diagnosis of addiction because they do not occur with other drugs of abuse (cocaine, amphetamine) and can occur with many drugs that are not abused (propranolol, clonidine).

    The official diagnosis of drug addiction by the Diagnostic and Statistic Manual of Mental Disorders (2000), which makes distinctions between drug use, abuse, and substance dependence, is flawed. First, diagnosis of drug use versus abuse can be arbitrary and reflect cultural norms, not medical phenomena. Second, the term substance dependence implies that dependence is the primary pharmacologic phenomenon underlying addiction, which is likely not true, as tolerance, sensitization, and learning and memory also play central roles. It is ironic and unfortunate that the Manual avoids use of the term addiction, which provides the best description of the clinical syndrome.
     
  2. ^ "Substance use disorder". Pubmed Health. National Institutes of Health. تمت أرشفته من الأصل في 31 March 2014. اطلع عليه بتاريخ 12 سبتمبر 2014. Drug dependence means that a person needs a drug to function normally. Abruptly stopping the drug leads to withdrawal symptoms. Drug addiction is the compulsive use of a substance, despite its negative or dangerous effects 
  3. ^ "Transcriptional and epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11): 623–637. November 2011. PMID 21989194. doi:10.1038/nrn3111. ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states. 
  4. ^ "Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms". J. Psychoactive Drugs. 44 (1): 38–55. 2012. PMID 22641964. doi:10.1080/02791072.2012.662112. It has been found that deltaFosB gene in the NAc is critical for reinforcing effects of sexual reward. Pitchers and colleagues (2010) reported that sexual experience was shown to cause DeltaFosB accumulation in several limbic brain regions including the NAc, medial pre-frontal cortex, VTA, caudate, and putamen, but not the medial preoptic nucleus. Next, the induction of c-Fos, a downstream (repressed) target of DeltaFosB, was measured in sexually experienced and naive animals. The number of mating-induced c-Fos-IR cells was significantly decreased in sexually experienced animals compared to sexually naive controls. Finally, DeltaFosB levels and its activity in the NAc were manipulated using viral-mediated gene transfer to study its potential role in mediating sexual experience and experience-induced facilitation of sexual performance. Animals with DeltaFosB overexpression displayed enhanced facilitation of sexual performance with sexual experience relative to controls. In contrast, the expression of DeltaJunD, a dominant-negative binding partner of DeltaFosB, attenuated sexual experience-induced facilitation of sexual performance, and stunted long-term maintenance of facilitation compared to DeltaFosB overexpressing group. Together, these findings support a critical role for DeltaFosB expression in the NAc in the reinforcing effects of sexual behavior and sexual experience-induced facilitation of sexual performance. ... both drug addiction and sexual addiction represent pathological forms of neuroplasticity along with the emergence of aberrant behaviors involving a cascade of neurochemical changes mainly in the brain's rewarding circuitry. 
  5. ^ Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. 61 (7): 1109–22. PMID 21459101. doi:10.1016/j.neuropharm.2011.03.010. 
  6. ^ "Diagnostic criteria for Substance Dependence: DSM IV–TR". BehaveNet. تمت أرشفته من الأصل في 12 June 2015. اطلع عليه بتاريخ 12 يونيو 2015. 
  7. ^ "Substance Dependence". BehaveNet. تمت أرشفته من الأصل في 13 June 2015. اطلع عليه بتاريخ 12 يونيو 2015. 
  8. ^ Malenka RC، Nestler EJ، Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A، Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (الطبعة 2nd). New York: McGraw-Hill Medical. صفحات 364–375. ISBN 9780071481274. 
  9. ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681Freely accessible. PMID 24459410. Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict. 
  10. ^ "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. اطلع عليه بتاريخ 09 فبراير 2015. 
  11. ^ Volkow ND، Koob GF، McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. 374 (4): 363–371. PMID 26816013. doi:10.1056/NEJMra1511480. Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
    Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
     

وصلات خارجية[عدل]