Fibromyalgia and myofascial pain (MP) are among the most common musculoskeletal disorders from which older adults suffer. These disorders represent opposite ends of the pain spectrum with the discrete character of MP at one extreme and the widespread symptoms of fibromyalgia at the other. MP may be acute or chronic, and is associated with taut muscle bands and hypersensitive areas called trigger points. Fibromyalgia syndrome includes symptoms of sleep disruption, fatigue, and psychological distress in addition to widespread pain. Both fibromyalgia and MP syndromes may result in significant functional impairment and cause suffering and disability comparable to that of rheumatoid arthritis and osteoarthritis. Diagnosis of these disorders is grounded in appropriately targeted history and physical examination; these are the tools required to avoid unnecessary ordering of “diagnostic” tests and foster implementation of appropriate management strategies.

Definition and Epidemiology

While a number of fibromyalgia classification criteria have been proposed, the criteria developed by the American College of Rheumatology are used most commonly. These criteria, which are 81% sensitive and 88% specific, allow fibromyalgia patients to be distinguished from patients with widespread pain caused by other rheumatological disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis). They include a history of generalized body pain (i.e., pain in at least three of four body quadrants) for at least 3 months duration and at least 11 out of 18 specific tender points on physical examination. Although initially developed for classification of fibromyalgia, practitioners tend to regard them as required for diagnosis, although this is not accurate. Older adults who present with widespread pain and other supportive clinical features (see below) should be considered to have fibromyalgia even if they do not precisely fulfill the ACR criteria. These criteria are best used as a general guide and to allow for study enrollment, not for strict use in the office setting.

The incidence of fibromyalgia syndrome (the proportion of new cases or first ever episodes) is difficult to measure in part because symptoms seem to ebb and flow over time. According to five large population studies, approximately 10% of the population has widespread pain. Of those with widespread body pain, approximately 2% meet ACR diagnostic criteria for fibromyalgia. Women are four to seven times as likely to have fibromyalgia compared to men, with the greatest prevalence in those 60 to 79 years of age. Patients with fibromyalgia also have been estimated to have a two- to sevenfold greater risk of suffering from depression, anxiety, headache, irritable bowel syndrome, chronic fatigue syndrome, systemic lupus erythematosus, and rheumatoid arthritis compared to healthy individuals.

Pathogenesis

While recent studies have added to our understanding of the pathogenesis of fibromyalgia, the exact cause is still unknown. Most studies suggest that abnormal central nervous system pain processing, known as central sensitization, plays a key role in fibromyalgia pathogenesis. Abnormal peripheral pain processing, peripheral sensitization, also contributes to fibromyalgia pathogenesis. The cause of sensitization is not known, but a variety of neuroendocrine and biochemical abnormalities are believed to be involved.

Peripheral Tissue Abnormalities

Early studies of fibromyalgia patients failed to consistently show abnormalities in the peripheral tissues. However, reexamination of this issue has uncovered differences between muscle samples from fibromyalgia subjects and healthy controls. One difference is higher levels of nitric oxide in muscles of fibromyalgia patients that may result in increased cell death. Other abnormalities that have been identified in muscles of fibromyalgia patients as compared with healthy individuals include lower phosphorylation potential and oxidative capacity as evidenced by lower levels of muscle phosphocreatine and ATP, as well as increased substance P, DNA fragmentation, interleukin-1, and perfusion deficits (see Staud reference). While the exact meaning of these abnormalities is unclear, the findings suggest an underlying difference in muscle metabolism of fibromyalgia patients as compared to people without fibromyalgia. Further study is needed to establish a relationship between these findings and the pain and fatigue fibromyalgia patients report.

Central and Peripheral Sensitization and Pain Amplification

Abnormalities of peripheral and central pain processing are well established in fibromyalgia. In the periphery, tissue sensitization results from changes in primary nociceptive afferents, increased neuronal excitability, and enlarged neuronal receptive fields. Central sensitization involves neuroplasticity in the brain and spinal cord. “Windup,” a normal finding of increased pain sensations after repeated exposures to a painful stimulus, is an example of central sensitization. In studies of fibromyalgia patients, the “windup” response is exaggerated compared to controls. Staud and colleagues studied fibromyalgia patients and healthy controls after repeated exposure to heat stimuli. While both groups had higher pain ratings after repeated exposures to heat, the degree of windup and temporal summation was significantly greater in fibromyalgia subjects. In addition, the fibromyalgia subjects had more prolonged after sensations compared with control subjects. Peripheral and central sensitizations contribute to the exaggerated pain response of fibromyalgia patients.

Neuroendocrine Abnormalities

Altered activity of the hypothalamic–pituitary–adrenal axis (HPA), and abnormal levels of adrenocortical trophic hormone (ACTH) and urinary cortisol have been demonstrated in patients with fibromyalgia. Evidence suggests that the HPA axis may be less resilient than normal in fibromyalgia patients and that this and other HPA axis abnormalities may underlie the impaired response to stress that many of these patients exhibit. The review by Crofford provides an expanded discussion of the neuroendocrine abnormalities in fibromyalgia syndrome.

Biochemical Abnormalities

While there are no serologic tests to assist practitioners with making a diagnosis of fibromyalgia, a number of biochemical abnormalities have been identified in the context of research studies. Russell and colleagues have identified lower levels of serum serotonin and norepinephrine in patients with fibromyalgia compared to controls. Low platelet serotonin levels have also been identified. While cerebrospinal fluid (CSF) serotonin has not been measured in patients with fibromyalgia, its precursor and metabolic products have been demonstrated to exist at significantly lower levels in the CSF of fibromyalgia patients compared to controls. Norepinephrine’s metabolite, methoxyhydroxyphenyglycol, and dopamine’s metabolite, homovanillic acid, are also reduced in fibromyalgia patients. Further discussion of the biochemical abnormalities found in fibromyalgia patients is found in the review by Mease.

Abnormal levels of nociceptive neurochemicals have also been found in patients with fibromyalgia. Several studies have shown that substance P, a neuropeptide involved in pain transmission, exists in significantly higher levels in the CSF of fibromyalgia patients compared to those without fibromyalgia (see the Russell reference). Nerve growth factor (NGF), which promotes production of substance P, also is elevated in the CSF of fibromyalgia patients.

Functional Imaging of Pain

Researchers have used functional magnetic resonance imaging (fMRI) to help understand fibromyalgia pathogenesis. Functional MRI measures regional blood flow in the central nervous system in response to various environmental stimuli and fMRI studies have demonstrated increased central nervous system activity that corresponds to fibromyalgia patients’ subjective pain reports. In response to stimuli, which do not cause pain in controls, fibromyalgia patients report high pain scores and have augmented regional cerebral blood flow on fMRI.

Genetics

Mounting evidence points to fibromyalgia as a heritable disorder. This evidence includes familial aggregation of fibromyalgia as well as a reduced pain threshold in the first-degree female relatives of fibromyalgia patients, even in those without overt clinical symptoms. Gene polymorphisms in the serotonergic and dopaminergic systems and a higher prevalence of polymorphisms in the promoter region of the serotonin transporter gene (5HTT) in fibromyalgia patients as compared to healthy controls also have been identified.

Clinical Presentation

Patient History

Fibromyalgia patients often report that they feel pain “all over.” Pain diagrams, on which patients are asked to shade painful areas of a human figure, are helpful in making a diagnosis. For fibromyalgia patients, these diagrams show diffuse shading on the right and left sides of the body as well as above and below the waist. We observe that some fibromyalgia patients shade, circle, or put an X through the entire figure. Patients generally rate their pain as moderate to severe in intensity. Over time, pain will fluctuate in severity but typically does not resolve completely. The quality of the pain may be variably described as deep aching, mild tenderness, or sharp sensations. Symptoms are generally constant throughout the day but often are worse in the morning and the evening. Triggers, including stress, cold weather, illness, and unaccustomed exertion, will likely increase pain. In addition to pain, 75% of patients report stiffness and over 50% report a sensation of swelling. Low back pain and chronic whiplash are relatively common, affecting 20% to 30% of the patients with fibromyalgia.

Fibromyalgia patients are likely to report a wide variety of nonmusculoskeletal symptoms, most commonly fatigue and difficulty sleeping. Sixty percent of patients report psychological and neuropsychological symptoms including anxiety, mental distress, and cognitive dysfunction. Thirty percent of patients report current depression with over 50% of patients reporting a history of depression. Headaches are also common. Uncommon symptoms (<20% prevalence) include tinnitus, dizziness, vertigo, and Raynaud’s phenomenon. Fibromyalgia may also coexist in 20% of rheumatoid arthritis patients, 30% of patients with systemic lupus erythematosus, and 50% of those with Sjögren’s syndrome. Table 123-1 lists the symptoms and syndromes commonly associated with fibromyalgia.

Up to 80% of fibromyalgia patients report debilitating fatigue. This complaint encompasses mental fatigue and impaired concentration commonly referred to as “fibro fog,” physical fatigue after exertion, and general sleepiness. In fibromyalgia patients, these symptoms most often occur in the absence of other medical illnesses. Poor sleep quality seen in fibromyalgia patients is known as nonrestorative sleep. Patients awaken feeling unrefreshed even after a full night’s sleep. Other complaints include light sleep, frequent awakenings, and insomnia. As with other aspects of fibromyalgia, the cause of poor sleep and chronic fatigue is not fully known. Studies of sleep architecture in fibromyalgia patients have revealed abnormalities, which may account for daytime fatigue. One such finding is alpha wave intrusion into stage four sleep. In fibromyalgia patients, alpha waves, typically seen in stage one light sleep, are found in stage four slow wave deep sleep. In addition, fibromyalgia patients have a relative rapid eye movement (REM) sleep deficiency compared to healthy controls. These abnormalities, while not specific to fibromyalgia, may cause significant fatigue.

Physical Examination

When evaluating the older adult with widespread chronic pain, the practitioner should be cognizant of multiple rheumatological disorders in addition to fibromyalgia syndrome such as generalized osteoarthritis, pseudogout, gout, rheumatoid arthritis, systemic lupus erythematosus, and polymyalgia rheumatica, as summarized in Table 123-2. A careful history and thorough physical examination for synovial and extrasynovial findings can help differentiate these conditions from fibromyalgia. Table 123-2 lists a number of key features on history and physical examination that may aid in the diagnosis. Other diagnostic considerations include hypothyroidism, vitamin D deficiency, demyelinating polyneuropathies, and paraneoplastic syndromes. A targeted laboratory panel may be helpful in teasing out these differential diagnostic considerations.

The characteristic physical examination finding in patients with fibromyalgia is the presence of tender points at the specific locations outlined in Table 123-3. A tender point is defined as a spot on the body that is painful with 4 kg of pressure (the amount of pressure required to blanch the examiner’s thumbnail when palpating the palm of her own hand). Palpation of the tender points with 4 kg of pressure is needed, as below this level, most subjects will not report pain. Those who report pain when tested with 4 kg of pressure demonstrate a lower than normal pain threshold. Patients reporting pain in fewer than the 11 of 18 tender points included in the American College of Rheumatology classification criteria may still be diagnosed with fibromyalgia if they have otherwise supportive clinical features (e.g., sleep disturbance, fatigue, morning stiffness). Tender points exist in a number of conditions other than fibromyalgia, including cervical and lumbosacral facet arthrosis syndrome, sacroiliac joint syndrome, and chronic whiplash and therefore a careful history and examination are key diagnostic elements.