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Review
. 2011 Apr;25(2):141-54.
doi: 10.1016/j.berh.2011.02.005.

Central pain mechanisms in chronic pain states--maybe it is all in their head

Kristine Phillips  1 , Daniel J Clauw
Affiliations
Review

Central pain mechanisms in chronic pain states--maybe it is all in their head

Kristine Phillips et al. Best Pract Res Clin Rheumatol. 2011 Apr.

Abstract

Mechanisms underlying chronic pain differ from those underlying acute pain. In chronic pain states, central nervous system (CNS) factors appear to play particularly prominent roles. In the absence of anatomical causes of persistent pain, medical sub-specialities have historically applied wide-ranging labels (e.g., fibromyalgia (FM), irritable bowel syndrome, interstitial cystitis and somatisation) for what now is emerging as a single common set of CNS processes. The hallmark of these 'centrally driven' pain conditions is a diffuse hyperalgesic state identifiable using experimental sensory testing, and corroborated by functional neuroimaging. The characteristic symptoms of these central pain conditions include multifocal pain, fatigue, insomnia, memory difficulties and a higher rate of co-morbid mood disorders. In contrast to acute and peripheral pain states that are responsive to non-steroidal anti-inflammatory drugs (NSAIDs) and opioids, central pain conditions respond best to CNS neuromodulating agents, such as serotonin-norepinephrine reuptake inhibitors (SNRIs) and anticonvulsants.

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References

    1. Woolf CJ. Dissecting out mechanisms responsible for peripheral neuropathic pain: implications for diagnosis and therapy. Life Sci. 2004;74:2605–2610. - PubMed
    1. Kroenke K, Krebs EE, Bair MJ. Pharmacotherapy of chronic pain: a synthesis of recommendations from systematic reviews. Gen Hosp Psychiatry. 2009;31:206–219. - PubMed
    1. Bennett RM. Fibrositis: misnomer for a common rheumatic disorder. West J Med. 1981;134:405–413. - PMC - PubMed
    1. Simms RW. Fibromyalgia is not a muscle disorder. Am J Med Sci. 1998 Jun;315(6):346–50. - PubMed
    1. Moldofsky H, Lue FA. The relationship of alpha and delta EEG frequencies to pain and mood in ‘fibrositis’ patients treated with chlorpromazine and L-tryptophan. Electroencephalogr Clin Neurophysiol. 1980;50:71–80. - PubMed

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