P Schweinhardt, KM. Sauro, MC Bushnell
This article presents evidence that fibromyalgia patients have alterations in CNS anatomy, physiology, and chemistry that potentially contribute to the symptoms experienced by these patients. There is substantial psychophysical evidence that fibromyalgia patients perceive pain and other noxious stimuli differently than healthy individuals and that normal pain modulatory systems, such as diffuse noxious inhibitory control mechanisms, are compromised in fibromyalgia. Furthermore, functional brain imaging studies revealing enhanced pain-related activations corroborate the patients’ reports of increased pain. Neurotransmitter studies show that fibromyalgia patients have abnormalities in dopaminergic, opioidergic, and serotoninergic systems. Finally, studies of brain anatomy show structural differences between the brains of fibromyalgia patients and healthy individuals. The cerebral alterations offer a compelling explanation for the multiple symptoms of fibromyalgia, including widespread pain and affective disturbances. The frequent comorbidity of fibromyalgia with stress-related disorders, such as chronic fatigue, posttraumatic stress disorder, irritable bowel syndrome, and depression, as well as the similarity of many CNS abnormalities, suggests at least a partial common substrate for these disorders. Despite the numerous cerebral alterations, fibromyalgia might not be a primary disorder of the brain but may be a consequence of early life stress or prolonged or severe stress, affecting brain modulatory circuitry of pain and emotions in genetically susceptible individuals
NEUROSCIENTIST 14(5):415—421, 2008 (abstract only)
DOI: 10.1177/1073858407312521
Filed under: Fibromyalgia, Neuroscience | Leave a Comment »
The role of the brain in chronic pain conditions remains speculative. We compared brain morphology of 26 chronic back pain (CBP) patients to matched control subjects, using magnetic resonance imaging brain scan data and automated analysis techniques. CBP patients were divided into neuropathic, exhibiting pain because of sciatic nerve damage, and non-neuropathic groups. Pain-related characteristics were correlated to morphometric measures. Neocortical gray matter volume was compared after skull normalization. Patients with CBP showed 5-11% less neocortical gray matter volume than control subjects. The magnitude of this decrease is equivalent to the gray matter volume lost in 10-20 years of normal aging. The decreased volume was related to pain duration, indicating a 1.3 cm3 loss of gray matter for every year of chronic pain. Regional gray matter density in 17 CBP patients was compared with matched controls using voxel-based morphometry and nonparametric statistics. Gray matter density was reduced in bilateral dorsolateral prefrontal cortex and right thalamus and was strongly related to pain characteristics in a pattern distinct for neuropathic and non-neuropathic CBP. Our results imply that CBP is accompanied by brain atrophy and suggest that the pathophysiology of chronic pain includes thalamocortical processes.