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This chapter provides information on the epidemiology of headache, with major sections devoted to migraine and tension-type headache. The clinical features of each headache type are discussed, and details of International Headache Society (IHS) criteria are described. This is followed by a summary of studies related to the incidence and prevalence, and a description of how headache frequency varies by age, sex, race, and geographic region. The chapter provides a summary of risk factors for headache, in addition to describing triggering factors among headache sufferers. The final section is devoted to a discussion of the impact of headaches, including frequency, severity, and health-related quality of life.

There can be no doubt that migraine is associated with changes in the cephalic (cerebral and non-cerebral) circulation; the doubts, however, concern the cause and nature of such changes. In a majority of migraine patients with ‘aura’, the cerebral blood flow decreases, but in ‘classical’ migraine patients both decreases and increases have been reported. In the non-cerebral cephalic circulation, vasodilatation and increased pulsations are observed principally on the side of the migraine headache, but the idea of simple vasodilatation is paradoxical to the facial pallor and laxity of tissues usually noticed during the headache. To resolve this paradox, Heyck suggested that vasodilatation involves cephalic arteriovenous anastomoses.

When the Arthritis Foundation tried to categorize the 150 different forms of musculoskeletal conditions in 1963, it created a classification known as soft tissue rheumatism. Included in this listing are conditions in which joints are not involved. Soft tissue rheumatism encompasses the supporting structures of joints (e.g., ligaments, bursae, and tendons), muscles, and other soft tissues. Fibromyalgia is a form of soft tissue rheumatism. A combination of three terms—fibro (from the Latin fibra, or fibrous tissue), myo- (the Greek prefix myos, for muscles), and algia (from the Greek algos, which denotes pain)—fibromyalgia replaces earlier names for the syndrome that are still used by doctors and other health professionals such as myofibrositis, myofascitis, muscular rheumatism, fibrositis, and gener­alized musculoligamentous strain. Fibromyalgia is not a form of arthritis, since it is not associated with joint inflammation. In the late 1980s, a Multicenter Criteria Committee under the direction of Dr. Frederick Wolfe at the University of Kansas was formed to define fibromyalgia. In their study, 293 patients with presumed fibromyalgia were compared with 265 patients who had other rheumatic diseases in 16 centers throughout North America. The groups were evaluated for a variety of symptoms, signs, and laboratory abnormalities in an effort to ascertain which factors were the most sensitive and specific for defining the disorder. In other words, the investigators wanted to identify the most frequently found features of fibromyalgia (sensitivity) that could help doctors differentiate it from other disorders (specificity). The list in Table 1 was 88.4 percent sensitive and 81.1 percent specific in identifying fibromyalgia patients. As a result, these criteria were endorsed in 1990 by the American College of Rheumatology (ACR), the association to which nearly all 5,000 rheumatologists in the United States and Canada belong. Focusing on Table 1 and Figure 3, fibromyalgia essentially is: 1. Widespread pain of at least 3 months’ duration (this rules out viruses or traumatic insults which resolve on their own). 2. Pain in all four quadrants of the body (picture cutting the body into quarters, as in a pie): right side, left side, above the waist, below the waist.

The autonomic nervous system (ANS) has already been introduced; let’s summarize what we know about it so far. Part of the peripheral nervous system, the ANS consists of the sympathetic nervous system (SNS), which consists of outflow from the thoracic and upper lumbar spine, and the parasympathetic nervous system (PNS), including outflow from the cranial nerves emanating from the upper spine and also from the mid-lumbar to the sacral areas at the buttock region. Several neurochemicals help transmit autonomic instructions. These include epinephrine (adrenaline), norepinephrine (noradrenalin), dopamine, and acetylcholine. This chapter will focus on how abnormalities in the regulation of the ANS cause many of the symptoms and signs observed in fibromyalgia. Our body has numerous receptors or surveillance sensors that detect heat, cold, and inflammation. These ANS sensors perform a function known as autoregulation. As an example of how the ANS normally works, why don’t we pass out when we suddenly jump out of bed? Because the ANS instantly constricts our blood vessels peripherally and dilates them centrally. In other words, as blood is pooled to the heart and the brain, the ANS adjusts our blood pressure and regulates our pulse, or heart rate, so that we don’t collapse. On the local level, these sensors dilate or constrict flow from blood vessels. They can secondarily contract and relax muscles, open and close lung airways, or cause us to sweat. For instance, ANS sensors can tone muscles, regulate urine, and regulate bowel movements, as well as dilate or constrict our pupils. The SNS arm of the ANS is our “fight or flight” system, releasing epinephrine and norepinephrine as well as a neurochemical called dopamine. Whereas the SNS often acts as an acute stress response, the PNS arm tends to protect and conserve body processes and resources. The SNS and PNS sometimes work at cross purposes, but frequently they work together to permit actions such as normal sexual functioning and urination. How do the workings of the ANS relate to fibromyalgia? The SNS is underactive in fibromyalgia in the sense that an increased ratio of excitatory to inhibitory responses from central sensitization results in lower blood flow rates, leaky capillaries, at relatively low baseline blood pressure.