In addition to strictly sensory-discriminative elements of nociception and afferent input from somatic reflexes, major contributions from pathways and regions of the brain that are associated with emotional, motivational, and cognitive aspects of pain are evident and help determine the subjective intensity of pain. The 2 principal effectors of the stress response, the hypothalamic-pituitary-adrenocortical (HPA) axis and the sympathetic nervous system (SNS), are also activated. Although normally adaptive, the stress response may become maladaptive in patients with chronic pain and fatigue syndromes such as fibromyalgia.[18, 19, 20, 21] Negative emotions (eg, depression and anxiety) and other negative psychological factors (eg, loss of control, unpredictability in ones environment) and certain cognitive aspects (eg, negative beliefs and attributions, catastrophizing) can all function as stressors with actions in these systems. Furthermore, negative emotions, such as anger and sadness, have been shown to be direct amplifiers of pain in women with and without fibromyalgia.[22] Thus, therapeutic approaches to regulate emotion may attenuate pain sensitization in patients with fibromyalgia. In some patients with fibromyalgia, such negative emotional, motivational, and cognitive stressors may dominate the clinical picture, potentially leading to a self-sustaining neuroendocrine cascade that contributes to flulike symptoms, depressed mood, fatigue, myalgias, cognitive difficulties, and poor sleep. The important biologic elements here include proinflammatory cytokines, the HPA axis, other neuroendocrine axes, and the autonomic nervous system. Growth hormone abnormalities are also thought to contribute to symptoms in fibromyalgia.[23] Pain in patients with fibromyalgia derives partly from a generalized decrease in the pain perception threshold, with reduced discrimination of nociceptive sensations from nonnociceptive sensations (eg, touch, warmth, cold), and in the threshold for pain tolerance, resulting in an unwillingness to receive more-intense stimulation.[24] These phenomena can be demonstrated clinically by pressure algometry (dolorimetry) or in research settings with quantitative sensory testing (QST) using pressure, heat, cold, or electricity as stimuli or functional magnetic resonance imaging (fMRI) using pain stimuli.[4] Underlying these changes in thresholds is altered processing of nociceptive stimuli in the CNS (central sensitization). A number of abnormalities in pain processing have been demonstrated in fibromyalgia.[25, 26, 27, 28, 29] Among them are the following: Excess excitatory (pronociceptive) neurotransmitters (eg, substance P, glutamate levels in the insula) Low levels of inhibitory neurotransmitters (eg, serotonin and norepinephrine) in descending antinociceptive pathways in the spinal cord Maintained enhancement of temporal summation of second pain Altered endogenous opioid analgesic activity in several brain regions known to play a role in pain modulation Dopamine dysregulation
Posted on: Fri, 12 Dec 2014 07:03:14 +0000
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