Fibromyalgia - Wikipedia
The defining symptoms of fibromyalgia are chronic widespread pain, fatigue, sleep disturbance, and heightened pain in response to tactile pressure (allodynia).[21] Other symptoms may include tingling of the skin (paresthesias),[21] prolonged muscle spasms, weakness in the limbs, nerve pain, muscle twitching, palpitations,[23] and functional bowel disturbances.[3][24]
Many patients experience cognitive dysfunction[6][21] (known as "fibrofog"), which may be characterized by impaired concentration,[25] problems with short[7][25] and long-term memory, short-term memory consolidation,[7] impaired speed of performance,[7][25] inability to multi-task, cognitive overload,[7][25] and diminished attention span. Fibromyalgia is often associated with anxiety and depressive symptoms.[7]
Other symptoms often attributed to fibromyalgia that may possibly be due to a comorbid disorder include myofascial pain syndrome, also referred to as chronic myofascial pain, diffuse non-dermatomal paresthesias, functional bowel disturbances and irritable bowel syndrome, genitourinary symptoms and interstitial cystitis, dermatological disorders, headaches, myoclonic twitches, and symptomatic hypoglycemia.
Although fibromyalgia is classified based on the presence of chronic
widespread pain, pain may also be localized in areas such as the shoulders, neck, low back, hips, or other areas. Many sufferers also experience varying degrees of myofascial pain and have high rates of comorbid temporomandibular joint dysfunction. 20–30% of patients with rheumatoid arthritis and systemic lupus erythematosus may also have fibromyalgia.[26]
Patients with fibromyalgia may have alterations of normal neuroendocrine function, characterized by mild hypocortisolemia,[68] hyperreactivity of pituitary adrenocorticotropin hormone release in response to challenge, and glucocorticoid feedback resistance.[69]
Other abnormalities include reduced responsivity of thyrotropin and thyroid hormones to thyroid-releasing hormone,[70] a mild elevation of prolactin levels with disinhibition of prolactin release in response to challenge[71] and hyposecretion of adrenal androgens.[72]
These changes might result from chronic stress, which, after being perceived and processed by the central nervous system, activates hypothalamic corticotrophin-releasing hormone neurons. Chronic overactivity of these neurons could disrupt normal function of the pituitary-adrenal axis and cause an increased stimulation of hypothalamic somatostatin secretion, which, in turn, could inhibit the secretion of other hormones.[73]
The defining symptoms of fibromyalgia are chronic widespread pain, fatigue, sleep disturbance, and heightened pain in response to tactile pressure (allodynia).[21] Other symptoms may include tingling of the skin (paresthesias),[21] prolonged muscle spasms, weakness in the limbs, nerve pain, muscle twitching, palpitations,[23] and functional bowel disturbances.[3][24]
Many patients experience cognitive dysfunction[6][21] (known as "fibrofog"), which may be characterized by impaired concentration,[25] problems with short[7][25] and long-term memory, short-term memory consolidation,[7] impaired speed of performance,[7][25] inability to multi-task, cognitive overload,[7][25] and diminished attention span. Fibromyalgia is often associated with anxiety and depressive symptoms.[7]
Other symptoms often attributed to fibromyalgia that may possibly be due to a comorbid disorder include myofascial pain syndrome, also referred to as chronic myofascial pain, diffuse non-dermatomal paresthesias, functional bowel disturbances and irritable bowel syndrome, genitourinary symptoms and interstitial cystitis, dermatological disorders, headaches, myoclonic twitches, and symptomatic hypoglycemia.
Although fibromyalgia is classified based on the presence of chronic
widespread pain, pain may also be localized in areas such as the shoulders, neck, low back, hips, or other areas. Many sufferers also experience varying degrees of myofascial pain and have high rates of comorbid temporomandibular joint dysfunction. 20–30% of patients with rheumatoid arthritis and systemic lupus erythematosus may also have fibromyalgia.[26]
Cause
The cause of fibromyalgia is unknown. However, several hypotheses have been developed including "central sensitization".[21] This theory proposes that fibromyalgia patients have a lower threshold for pain because of increased reactivity of pain-sensitive nerve cells in the spinal cord or brain.[1] Neuropathic pain and major depressive disorder often co-occur with fibromyalgia – the reason for this comorbidity appears to be due to shared genetic abnormalities, which leads to impairments in monoaminergic, glutamatergic, neurotrophic, opioid and proinflammatory cytokine signaling. In these vulnerable individuals psychological stress or illness can cause abnormalities in inflammatory and stress pathways which regulate mood and pain. Eventually a sensitisation and kindling effect occurs in certain neurones leading to the establishment of fibromyalgia and sometimes a mood disorder.[10] The evidence suggests that the pain in fibromyalgia results primarily from pain processing pathways functioning abnormally. In simple terms it can be described as the volume of the neurones being set too high and this hyper-excitability of pain processing pathways and under-activity of inhibitory pain pathways in the brain results in the affected individual experiencing pain. Some of the neurochemical abnormalities that occur in fibromyalgia also regulate mood, sleep and energy, thus explaining why mood, sleep and fatigue problems are commonly co-morbid with fibromyalgia.[14]Neuroendocrine disruption
Levels of hormones under the direct or indirect control of growth hormone (GH), including insulin-like growth factor 1 (IGF-1), cortisol, leptin and neuropeptide Y may be abnormal in people with fibromyalgia.[63] Several authors have demonstrated low growth hormone levels or low IGF-I levels in patients with fibromyalgia compared with controls. Moreover, fibromyalgia patients have an abnormal sleep pattern involving stages 3 and 4 of non REM sleep during which growth hormone is predominantly secreted.[64] Further support for a causal role for growth hormone deficiency comes from observations that such deficiency in adults has been associated with many of the symptoms described by fibromyalgia patients. Growth hormone is important in maintaining muscle homeostasis, and it has been suggested that low levels may be responsible for delayed healing of muscle microtrauma in fibromyalgia.[65] Low (IGF-1) levels in some fibromyalgia patients have led to the theory that these patients may actually have a different, treatable syndrome, adult growth hormone deficiency.[66] However, there remains some disagreement about the role of HGH in fibromyalgia.[67]Patients with fibromyalgia may have alterations of normal neuroendocrine function, characterized by mild hypocortisolemia,[68] hyperreactivity of pituitary adrenocorticotropin hormone release in response to challenge, and glucocorticoid feedback resistance.[69]
Other abnormalities include reduced responsivity of thyrotropin and thyroid hormones to thyroid-releasing hormone,[70] a mild elevation of prolactin levels with disinhibition of prolactin release in response to challenge[71] and hyposecretion of adrenal androgens.[72]
These changes might result from chronic stress, which, after being perceived and processed by the central nervous system, activates hypothalamic corticotrophin-releasing hormone neurons. Chronic overactivity of these neurons could disrupt normal function of the pituitary-adrenal axis and cause an increased stimulation of hypothalamic somatostatin secretion, which, in turn, could inhibit the secretion of other hormones.[73]
