عرض مصدر إدمان

{{عن|3=إدمان (توضيح)}}
{{معلومات مرض
| اسم أصلي= Addiction
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| مرادفات = ''Severe substance use disorder''<ref name="Surgeon General severe SUD">{{استشهاد ويب | عنوان=Facing Addiction in America: The Surgeon General's Report on Alcohol, Drugs, and Health | مسار= https://addiction.surgeongeneral.gov/sites/default/files/surgeon-generals-report.pdf | موقع = Office of the Surgeon General | ناشر=US Department of Health and Human Services | تاريخ=November 2016 | تاريخ الوصول=28 January 2017 | صفحات = 35–37, 45, 63, 155, 317, 338 | اقتباس = |مسار أرشيف= https://web.archive.org/web/20200209152236/https://addiction.surgeongeneral.gov/sites/default/files/surgeon-generals-report.pdf|تاريخ أرشيف=2020-02-09}}</ref>
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| اختصاص = [[طب نفسي]]
| بديل = PET images showing brain metabolism in drug addicts vs controls
| تعليق = [[التصوير المقطعي بالإصدار البوزيتروني للدماغ|تصوير مقطعي بالإصدار البوزيتروني للدماغ]] images that compare [[دماغ بشري]] in a healthy individual and an individual with a cocaine addiction
| صورة = Brain metabolism and drug addiction.jpg
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}}[[ملف:Bayer Heroin bottle.jpg|تصغير|يسار|200px|زجاجة تحتوى على [[مخدر]] [[هيروين|الهروين]].]]
'''الإدمان''' هو [[أمراض الجهاز العصبي المركزي|اضطراب في الدماغ]] يتسم بارتباط قهري بمحفزات [[نظام المكافأة في الدماغ]] بالرغم من النتائج الضارة.{{refn|<ref name="pmid18790142">{{استشهاد بدورية محكمة |عدة مؤلفين=Angres DH, Bettinardi-Angres K | عنوان = The disease of addiction: origins, treatment, and recovery | صحيفة = Disease-a-Month | المجلد = 54 | العدد = 10 | صفحات = 696–721 |تاريخ=October 2008| pmid = 18790142 | doi = 10.1016/j.disamonth.2008.07.002 | مسار = }}</ref>}}رغم تورط عدد من العوامل النفسية والاجتماعية في الإدمان، إلا أن العملية الحيوية (البيولوجية) - العملية التي يسببها التعرض المتكرر لمحفز للإدمان - هي العلة المرضية الأساسية التي تدفع تطور الإدمان واستمراره.<ref>{{استشهاد ويب
| مسار = https://www.asam.org/for-the-public/definition-of-addiction
| عنوان = Definition of Addiction
| سنة = 2012
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| مؤلف = American Society for Addiction Medicine
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| المجلد = 
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|مسار أرشيف= https://web.archive.org/web/20191213092924/https://www.asam.org/for-the-public/definition-of-addiction|تاريخ أرشيف=2019-12-13}}</ref> السمتان المميزتان لجميع محفزات الإدمان هما: [[تعزيز (علم النفس)|التعزيز]] (أي أن المحفز يزيد احتمال سعي الشخص إلى التعرض المتكرر له)، و[[نظام المكافأة في الدماغ|مكافئ]] في ذاته (أي يُنظر إلى المحفز على أنه بطبيعته إيجابي ومرغوب وممتع).

الإدمان هو اضطراب في [[نظام المكافأة في الدماغ|نظام المكافآت في الدماغ]] ينشأ من خلال آليات [[نسخ (وراثة)|النسخ]] و[[علم التخلق|علم التخلُق]]، ويتطور مع مرور الوقت نتيجة التعرض المزمن بمستويات عالية لمحفز للإدمان (مثل تناول الطعام، واستخدام [[كوكايين|الكوكايين]]، والانخراط في النشاط الجنسي، والمشاركة في الأنشطة الثقافية التشويقية مثل [[قمار|لعب القمار]]، وما إلى ذلك).<ref name="What the ΔFosB?">{{استشهاد بدورية محكمة|مؤلف=Ruffle JK|عنوان=Molecular neurobiology of addiction: what's all the (Δ)FosB about?|صحيفة=Am. J. Drug Alcohol Abuse|المجلد=40|العدد=6|صفحات=428–37|تاريخ=November 2014|pmid=25083822|doi=10.3109/00952990.2014.933840|اقتباس=<br />The strong correlation between chronic drug exposure and ΔFosB provides novel opportunities for targeted therapies in addiction (118), and suggests methods to analyze their efficacy (119). Over the past two decades, research has progressed from identifying ΔFosB induction to investigating its subsequent action (38). It is likely that ΔFosB research will now progress into a new era – the use of ΔFosB as a biomarker.&nbsp;...<br />Conclusions<br />ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a ''molecular switch'' (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction.}}</ref><ref name="Natural and drug addictions">{{استشهاد بدورية محكمة|مؤلف=Olsen CM|عنوان=Natural rewards, neuroplasticity, and non-drug addictions|صحيفة=Neuropharmacology|المجلد=61|العدد=7|صفحات=1109–22|تاريخ=December 2011|pmid=21459101|pmc=3139704|doi=10.1016/j.neuropharm.2011.03.010|اقتباس=Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm (Komisaruk et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004).&nbsp;... Cross-sensitization is also bidirectional, as a history of amphetamine administration facilitates sexual behavior and enhances the associated increase in NAc DA&nbsp;... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. The transcription factor delta FosB is increased in the NAc, PFC, dorsal striatum, and VTA following repeated sexual behavior (Wallace et al., 2008; Pitchers et al., 2010b). This natural increase in delta FosB or viral overexpression of delta FosB within the NAc modulates sexual performance, and NAc blockade of delta FosB attenuates this behavior (Hedges et al, 2009; Pitchers et al., 2010b). Further, viral overexpression of delta FosB enhances the conditioned place preference for an environment paired with sexual experience (Hedges et al., 2009).&nbsp;... In some people, there is a transition from "normal" to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a).&nbsp;... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al, 2006; Aiken, 2007; Lader, 2008)."}}<!--The following link is outside the template to make it hyperlinked while appearing to be part of the quote.-->[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139704/table/T1/ Table 1: Summary of plasticity observed following exposure to drug or natural reinforcers]"</ref>