Neurobiology Underlying Fibromyalgia Symptoms

Alan Edwards Centre for Research on Pain, McGill University, 3640 University Street, Room M19, Montreal, QC, H2A 1C1, Canada.
Pain Research and Treatment 01/2012; 2012(2):585419. DOI: 10.1155/2012/585419
Source: PubMed


Fibromyalgia is characterized by chronic widespread pain, clinical symptoms that include cognitive and sleep disturbances, and other abnormalities such as increased sensitivity to painful stimuli, increased sensitivity to multiple sensory modalities, and altered pain modulatory mechanisms. Here we relate experimental findings of fibromyalgia symptoms to anatomical and functional brain changes. Neuroimaging studies show augmented sensory processing in pain-related areas, which, together with gray matter decreases and neurochemical abnormalities in areas related to pain modulation, supports the psychophysical evidence of altered pain perception and inhibition. Gray matter decreases in areas related to emotional decision making and working memory suggest that cognitive disturbances could be related to brain alterations. Altered levels of neurotransmitters involved in sleep regulation link disordered sleep to neurochemical abnormalities. Thus, current evidence supports the view that at least some fibromyalgia symptoms are associated with brain dysfunctions or alterations, giving the long-held "it is all in your head" view of the disorder a new meaning.

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    • "Some experimental studies have identified a number of other abnormalities in FM patients, including increased sensitivity to multiple types of painful stimuli, increased sensitivity to other sensory modalities, and alterations in pain modulator mechanisms. [17] The quality of life in FM patients can be significantly compromised, as it can interfere with a patient's ability to work and perform regular daily activities. "
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    ABSTRACT: Fibromyalgia (FM) is a prevalent, chronic and disabling disorder, which etiology is unknown. It is characterized by widespread pain, diffuse tenderness, and a plethora of other symptoms. It is also considered the coexistence of tender points – painful points when a digital palpation of 4 kg/A of force is exercised - through the body. Technically, it can be defined as a history of widespread pain for at least 3 months and the existence of pain at least in 11 of 18 tender points. Its manifestations are not homogenous, making the diagnosis difficult. It shows varying proportions of anxiety and depression as comorbidities, which depend on the psychological features of each patient. Therefore, the medical evaluation must not include only the presence/absence of widespread pain or painful tender points, but also the existence of mood changes. Some studies show that the patients with FM have high rates of alexithymia and rage, and link depression, work stress and childhood traumatic events as contributors to its etiology, therefore, antidepressants could be an effective therapeutic handling. On the other hand, researchers have identified the influence of social effort and emotional context under the pain threshold in FM. These and other results led to conclude that there is an intrinsic bind between depressive disorders and FM. Other studiers classified them in a same wide category of stress disturbances. Finally, depression is a frequent (present in 28,6 to 70% of the patients) comorbidity associated with fibromyalgia, and brings worsening to its natural history of disease.
    Fibromyalgia: Risk Factors, Symptoms and Treatment, 01/2013: chapter Fibromyalgia: The Role of Antidepressant Agents: pages 63-86; Nova Publishers., ISBN: 978-1-62257-678-4
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    ABSTRACT: Fibromyalgia is a primary brain disorder or a result of peripheral dysfunctions inducing brain alterations, with underlying mechanisms that partially overlap with other painful conditions. Although there are methodologic variations, neuroimaging studies propose neural correlations to clinical findings of abnormal pain modulation in fibromyalgia. Growing evidences of specific differences of brain activations in resting states and pain-evoked conditions confirm clinical hyperalgesia and impaired inhibitory descending systems, and also demonstrate cognitive-affective influences on painful experiences, leading to augmented pain-processing. Functional data of neural activation abnormalities parallel structural findings of gray matter atrophy, alterations of intrinsic connectivity networks, and variations in metabolites levels along multiple pathways. Data from positron-emission tomography, single-photon-emission-computed tomography, blood-oxygen-level-dependent, voxel-based morphometry, diffusion tensor imaging, default mode network analysis, and spectroscopy enable the understanding of fibromyalgia pathophysiology, and favor the future establishment of more tailored treatments.
    Current Pain and Headache Reports 06/2012; 16(5):388-98. DOI:10.1007/s11916-012-0284-9 · 2.26 Impact Factor
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    ABSTRACT: Background: Irritable bowel syndrome and other gastrointestinal (GI) and non-GI disorders such as functional dyspepsia, fibromyalgia, temporomandibular joint disorder, interstitial cystitis/painful bladder syndrome, and chronic fatigue syndrome are known as functional pain syndromes. They commonly coexist within the same individual. The pathophysiologic mechanisms of these disorders are not well understood, but it has been hypothesized that they share a common pathogenesis. Purpose: The objective of this review is to discuss the proposed pathophysiologic mechanisms, which have been similarly studied in these conditions. These mechanisms include enhanced pain perception, altered regional brain activation, infectious etiologies, dysregulations in immune and neuroendocrine function, and genetic susceptibility. Studies suggest that these functional disorders are multifactorial, but factors which increase the vulnerability of developing these conditions are shared.
    Neurogastroenterology and Motility 08/2012; 24(10):895-913. DOI:10.1111/j.1365-2982.2012.01993.x · 3.59 Impact Factor
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