An impressive polymyalgia follows excessive exercise. Often, the patient observes that aching pain occurs not at the time of activity but some hours or even a day or two later, resembling the discomfort following the excessive use of unconditioned muscles. The muscles are sore and there is an intolerance of exercise and physical exertion. The serum CK concentration is mildly to moderately elevated. This is a natural phenomenon and is self-limiting. When such a state persists indefinitely and a program of conditioning exercises does not alleviate the pain, it represents a special category of disease. In a few instances an increased sedimentation rate or other laboratory aids may clarify the diagnosis, and muscle biopsy may reveal a nonspecific interstitial nodular myositis or the giant cell arteritis associated with polymyalgia rheumatica. Whether or not patients on lipid-lowering statin medications are particularly susceptible to this problem is not clear. A few individuals go on to have the features of the previously described fibromyalgic syndrome. However, this cluster of symptoms most often occurs without explanation, and one can only suspect an obscure infection or a subtle aberration of muscle metabolism, presently impossible to demonstrate. Reference has been made in the literature to the controversial finding of a myoadenylate deaminase deficiency in some of these cases. There is also a group of patients who have idiopathic leg pain during rest after activity. Some families afflicted in this way are forced to live a sedentary existence. The condition does not respond to analgesics. In 2 cases, a deficiency of calcium ATPase was found and reportedly alleviated by a calcium channel blocker such as verapamil, 120 mg (Walton). It must be distinguished from the syndromes of painful legs and moving toes, and from the restless leg syndrome discussed in Chap. 18.
Before dismissing vague muscle aches as an excessive somatic concern, hypothyroidism, hyperparathyroidism, and renal tubular acidosis, hypophosphatemia, hypoglycemia, and the intrinsic phosphorylase or phosphofructokinase defects should be considered. Patients with these latter diseases often complain of soreness, stiffness, and lameness after strenuous muscular effort. The most valuable screening tests are the sedimentation rate and serum CK concentration. Some patients probably have an obscure metabolic myopathy, presently undiagnosable. In every reported series, such as that of Serratrice and coworkers, half of the cases with diffuse myalgia are of this uncertain type. This coincides with, or is more optimistic than, our own experience.
Masses may be found in one or many muscles in a variety of clinical settings, and the clinical findings in each one have a different significance.
Muscle or tendinous rupture is usually caused by a violent strain attended by an audible snap and then a bulge, which appears when the muscle contracts. A very focal weakening in contractile power and mild discomfort are usually noted by the patient. The biceps brachii and soleus muscles are most often affected. Treatment is by surgical repair; if that is delayed, little can be done for the condition.
Hemorrhage into muscle may occur as a consequence of trauma, as a complication of the use of anticoagulants, in hematologic diseases, in severe myotonia, or after a minor trauma to a patient with Zenker degeneration of muscle who is convalescing from typhoid fever or some other infection. Runners may acquire painful localized hematomas in leg muscles.