Change search
ReferencesLink to record
Permanent link

Direct link
Reward deficiency and anti-reward in pain chronification
Boston Childrens Hosp, Ctr Pain & Brain, Boston, MA 02115 USA.;Massachusetts Gen Hosp, Boston, MA 02114 USA.;Boston Childrens Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA USA.;Mclean & Massachusetts Gen Hosp, Dept Psychiat, Boston, MA USA.;Harvard Med Sch, Boston, MA USA..
Boston Childrens Hosp, Ctr Pain & Brain, Boston, MA 02115 USA.;Massachusetts Gen Hosp, Boston, MA 02114 USA.;Boston Childrens Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA USA.;Harvard Med Sch, Boston, MA USA..
Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Psychology. Boston Childrens Hosp, Ctr Pain & Brain, Boston, MA 02115 USA.;Massachusetts Gen Hosp, Boston, MA 02114 USA.;Boston Childrens Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA USA.;Harvard Med Sch, Boston, MA USA..
Beth Israel Deaconess Med Ctr, Dept Anesthesia Crit Care & Pain Med, Boston, MA USA.;Harvard Med Sch, Boston, MA USA..
Show others and affiliations
2016 (English)In: Neuroscience and Biobehavioral Reviews, ISSN 0149-7634, E-ISSN 1873-7528, Vol. 68, 282-297 p.Article, review/survey (Refereed) Published
Abstract [en]

Converging lines of evidence suggest that the pathophysiology of pain is mediated to a substantial degree via allostatic neuroadaptations in reward- and stress-related brain circuits. Thus, reward deficiency (RD) represents a within-system neuroadaptation to pain-induced protracted activation of the reward circuits that leads to depletion-like hypodopaminergia, clinically manifested anhedonia, and diminished motivation for natural reinforcers. Anti-reward (AR) conversely pertains to a between-systems neuroadaptation involving over-recruitment of key limbic structures (e.g., the central and basolateral amygdala nuclei, the bed nucleus of the stria terminalis, the lateral tegmental noradrenergic nuclei of the brain stem, the hippocampus and the habenula) responsible for massive outpouring of stressogenic neurochemicals (e.g., norepinephrine, corticotropin releasing factor, vasopressin, hypocretin, and substance P) giving rise to such negative affective states as anxiety, fear and depression. We propose here the Combined Reward deficiency and Anti-reward Model (CReAM), in which biopsychosocial variables modulating brain reward, motivation and stress functions can interact in a 'downward spiral' fashion to exacerbate the intensity, chronicity and comorbidities of chronic pain syndromes (i.e., pain chronification).

Place, publisher, year, edition, pages
2016. Vol. 68, 282-297 p.
Keyword [en]
Reward, Motivation, Aversion, Analgesia, Amygdala, Habenula, Nucleus accumbens, Dopamine, Addiction, Stress, Pain
National Category
Psychiatry Neurology
Identifiers
URN: urn:nbn:se:uu:diva-306057DOI: 10.1016/j.neubiorev.2016.05.033ISI: 000383293500020PubMedID: 27246519OAI: oai:DiVA.org:uu-306057DiVA: diva2:1039702
Available from: 2016-10-25 Created: 2016-10-24 Last updated: 2016-10-25Bibliographically approved

Open Access in DiVA

fulltext(2507 kB)13 downloads
File information
File name FULLTEXT01.pdfFile size 2507 kBChecksum SHA-512
b84a2ee127d1f184706dbb690c37c5dc5ec416b6eb96d6cae84171e2cc436ad544df730b23e7eb31a90b4b1eefa1d5c102457850c4c50d12190c29f0cc438bde
Type fulltextMimetype application/pdf

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Faria, Vanda
By organisation
Department of Psychology
In the same journal
Neuroscience and Biobehavioral Reviews
PsychiatryNeurology

Search outside of DiVA

GoogleGoogle Scholar
Total: 13 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 49 hits
ReferencesLink to record
Permanent link

Direct link