i'm only on page 4 right now, SIAP. but here is some data:
Fibromyalgia (FM) is a chronic musculoskeletal pain syndrome which is characterised by clinical pain as well as widespread hyperalgesia/allodynia to mechanical, thermal, electrical, and chemical stimuli. Lack of consistent tissue abnormalities in FM patients has more and more shifted the focus...
pubmed.ncbi.nlm.nih.gov
Our study demonstrates that both somatic and nonsomatic dysfunction in FM, including clinical pain, pain catastrophizing, autonomic dysfunction, and amplified temporal summation, are closely linked with the degree to which evoked deep tissue pain alters S1 connectivity to salience/affective...
pubmed.ncbi.nlm.nih.gov
Brain imaging in fibromyalgia syndrome
R Staud 1
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Abstract
Fibromyalgia (FM) is a chronic musculoskeletal pain syndrome which is characterised by clinical pain as well as widespread hyperalgesia/allodynia to mechanical, thermal, electrical, and chemical stimuli. Lack of consistent tissue abnormalities in FM patients has more and more shifted the focus away from peripheral factors and towards central nervous system abnormalities including central sensitisation as well as aberrant pain facilitation and inhibition. Besides quantitative sensory testing, functional brain imaging has been increasingly utilised to characterise the abnormal pain processing of FM patients. Whereas initial work in FM patients identified abnormally increased pain-related brain activity within the thalamus, insula, anterior cingulate, S1, and prefrontal cortex (so-called 'pain matrix'), more recent research focused on altered 'connectivity' between multiple interconnected brain networks in these patients. Additionally, magnetic resonance spectroscopy studies demonstrated high concentration of the excitatory neurotransmitter glutamate in FM patients in pain-related brain areas which correlated not only with experimental but also with clinical pain ratings. Overall, functional brain imaging studies have provided compelling evidence for abnormal pain processing in FM, including brain activity that correlated with patients' augmented pain sensitivity (hyperalgesia/allodynia), temporal summation of pain, and prolonged pain aftersensations. Future imaging work needs to focus on identifying the neural correlates of FM patients' abnormal endogenous pain modulation which will likely not only shed more light on this important pain regulatory mechanism but may also provide useful information for future treatments of FM symptoms.
The somatosensory link in fibromyalgia: functional connectivity of the primary somatosensory cortex is altered by sustained pain and is associated with clinical/autonomic dysfunction
Jieun Kim 1 2,
Marco L Loggia 1 3,
Christine M Cahalan 3,
Richard E Harris 4,
Florian Beissner Dr Phil Nat 1 5,
Ronald G Garcia 1 6,
Hyungjun Kim 1 2,
Ajay D Wasan 7,
Robert R Edwards # 3 8,
Vitaly Napadow # 1 3 9
Affiliations expand
Free PMC article
Abstract
Objective: Fibromyalgia (FM) is a chronic functional pain syndrome characterized by widespread pain, significant pain catastrophizing, sympathovagal dysfunction, and amplified temporal summation for evoked pain. While several studies have demonstrated altered resting brain connectivity in FM, studies have not specifically probed the somatosensory system and its role in both somatic and nonsomatic FM symptoms. Our objective was to evaluate resting primary somatosensory cortex (S1) connectivity and to explore how sustained, evoked deep tissue pain modulates this connectivity.
Methods: We acquired functional magnetic resonance imaging and electrocardiography data on FM patients and healthy controls during rest (the rest phase) and during sustained mechanical pressure-induced pain over the lower leg (the pain phase). Functional connectivity associated with different S1 subregions was calculated, while S1(leg) connectivity (representation of the leg in the primary somatosensory cortex) was contrasted between the rest phase and the pain phase and was correlated with clinically relevant measures in FM.
Results: During the rest phase, FM patients showed decreased connectivity between multiple ipsilateral and cross-hemispheric S1 subregions, which was correlated with clinical pain severity. Compared to the rest phase, the pain phase produced increased S1(leg) connectivity to the bilateral anterior insula in FM patients, but not in healthy controls. Moreover, in FM patients, sustained pain-altered S1(leg) connectivity to the anterior insula was correlated with clinical/behavioral pain measures and autonomic responses.
Conclusion: Our study demonstrates that both somatic and nonsomatic dysfunction in FM, including clinical pain, pain catastrophizing, autonomic dysfunction, and amplified temporal summation, are closely linked with the degree to which evoked deep tissue pain alters S1 connectivity to salience/affective pain-processing regions. Additionally, diminished connectivity between S1 subregions during the rest phase in FM may result from ongoing widespread clinical pain.
© 2015 American College of Rheumatology.