During late adult life, the number of muscle fibers diminishes and variation in fiber size increases as mentioned in Chap. 28 on aging. The variations are of 2 types: group atrophy, in which clusters of 20 to 30 fibers are all reduced in diameter to about the same extent, and random single-fiber atrophy. Also, muscle cells, like other cells of postmitotic type, are subject to aging changes (lipofuscin accumulation, autophagic vacuolization, enzyme loss) and to death. Group atrophy, present to a slight degree in the gastrocnemii of almost all individuals older than 60 years, represents denervation effect from an aging-related loss of lumbar motor neurons and peripheral nerve fibers. Further comments regarding muscle and aging can be found in the work of Tomlinson and colleagues and in Chap. 28.
Denervation from spinal motor neuron or nerve disease at every age has roughly the same effect; namely, atrophy of muscle fibers (first in random distribution, then in groups) and later, degeneration. Muscle necrosis at all ages excites a regenerative response from sarcolemmal and satellite cells in any intact parts of the fibers. If this occurs repeatedly, the regenerative potential wanes, with ultimate death of the fiber leading to permanent depopulation of fibers with the expected muscle weakness.
The number and diversity of diseases of striated muscle greatly exceed the number of symptoms and signs by which they express themselves clinically; thus, different diseases share certain common symptoms and syndromes. To avoid excessive repetition in the description of individual diseases, we discuss here, in one place, the broad clinical manifestations of muscle disease.
The physician is initially put on the track of a myopathic disease by eliciting complaints of muscle weakness or fatigue, pain, limpness or stiffness, spasm, cramp, twitching, or a muscle mass or change in muscle volume. Of these, the symptom of weakness is by far the most frequent and at the same time the most elusive. As remarked in Chap. 23, when speaking of weakness, the patient often means excessive fatigability and poor endurance. Although fatigability in the strict sense of gradually reduced power with ongoing use of a muscle may be a feature of muscle diseases, particularly those affecting the neuromuscular junction such as myasthenia gravis, it is far more frequently a complaint of patients with chronic systemic disease or with anxiety or depression. As stated in Chap. 23, fatigue is an abstruse symptom, always requiring analysis and interpretation. When not attended by manifest reduction in muscle power, it is usually nonmuscular in origin. It may, on medical investigation, prove to be a systemic manifestation of infection, metabolic or endocrine disorder, severe anemia, reduced cardiopulmonary function, or neoplasia. More often, when expressed as a feeling of poor endurance, weariness, and disinclination to undertake or sustain mental and physical activity, it is indicative of neurasthenia, a psychiatric manifestation common to states of chronic anxiety and depression. On the other hand, a rare example of a physiologic muscle disorder that simulates lassitude is lifelong exercise intolerance, often accompanied by muscle cramps during exercise, which has been traced to mutations in the cytochrome b gene of the mitochondrial DNA (Andreu et al). The subject of fatigue as a physiologic phenomenon and as a clinical feature of many psychiatric and medical diseases, including those that are predominantly myopathic, is considered fully in Chap. 23.
Evaluation of Muscle Weakness and Paralysis