Muscle Volume and Contour

Asearch for evidence of muscle atrophy or hypertrophy is an important part of the motor examination. There is normally an appreciable individual variation in muscular development, but noteworthy changes in the size or shape of individual muscles or muscle groups, especially when focal or asymmetric, may be significant.

Muscle atrophy (amyotrophy) causes a decrease in muscle volume or bulk, and is usually accompanied by changes in shape or contour. Neurologic conditions likely to cause muscle atrophy are primarily those that affect the anterior horn cell, the nerve root(s), the peripheral nerve, or the muscle. Neuromuscular junction disorders do not cause muscle atrophy. Atrophy may also result from such things as disuse or inactivity, immobilization, tendonotomy, muscle ischemia, malnutrition, endocrine disorders, and normal aging.

Muscle hypertrophy is an increase in the bulk, or volume, of muscle tissues. It may result from excessive use of the muscles (physiologic hypertrophy) or occur on a pathologic basis. Hypertrophied muscle is not necessarily stronger than normal. Persistent abnormal muscle contraction may cause hypertrophy. Patients with myotonia congenita have a diffuse muscularity without significant increase in strength. Patients with dystonia may develop hypertrophy of the abnormally active muscle. In cervical dystonia (spasmodic torticollis), it is common to see hypertrophy of one sternomastoid muscle. Muscular dystrophies, especially Duchenne dystrophy, often cause pseudohypertrophy of muscle, with enlargement due to infiltration of the muscle with fat and connective tissue without an actual increase in muscle fiber size or number.

EXAMINATION OF MUSCLE VOLUME AND CONTOUR

There is a great deal of individual variation in muscular development, in part constitutional and in part due to training, activity, and occupation. Certain individuals have small or poorly developed muscles, while others show outstanding muscular development. The sedentary, the elderly, and those with chronic disease may have small muscles without evidence of wasting or atrophy. Athletes may develop physiologically hypertrophic muscles. In normal individuals, the dominant side may exhibit an increase in the size of the muscles, even of the hand and foot. The appraisal of bulk and contour should be correlated with the other parts of the motor examination, especially with the evaluation of strength and tone.

Muscle volume and contour may be appraised by inspection, palpation, and measurement. Inspection generally compares symmetric parts on the two sides of the body, noting any flattening,
hollowing, or bulging of the muscle masses. A useful technique for comparing extremities is to look down the long axis. Hold the patient’s arms outstretched and close together, comparing “down the barrel” from fingertips to shoulders for any asymmetry.

Palpation assesses muscle bulk, contour, and consistency. Normal muscles are semi-elastic and regain their shape at once when compressed. When hypertrophy is present, the muscles are firm and hard; in pseudohypertrophy they appear enlarged but may feel doughy or rubbery on palpation. Atrophic muscles are often soft and pulpy in consistency. When degenerated muscles have undergone fibrotic changes, they may be hard and firm. Those infiltrated or replaced by fat may feel pliant and flabby.

Measurements may be very useful in assessing atrophy or hypertrophy. A pronounced difference in muscle size may be recognized at a glance, especially when confined to one side of the body, one extremity, or one segment of a limb. Slight differences are more difficult to detect, and measurements with a tape measure or calipers may be necessary. Measurements should be made from fixed points or landmarks, and the sites—such as the distance above or below the olecranon, anterior superior iliac spine, or patella—recorded. The extremities should be in the same position and in comparable states of relaxation. It may also be valuable to measure the length of the limbs.

Atrophy or hypertrophy may be limited to an individual muscle, to muscles supplied by a specific structure (e.g., a nerve or root), to those muscles supplied by certain spinal cord segments, or to one half of the body; or it may be multifocal or generalized. In atrophy related to arthritis and disuse there may be a pronounced decrease in volume with little change in strength. In myopathies, on the other hand, there is often little atrophy in spite of a striking loss of power.

ABNORMALITIES OF VOLUME AND CONTOUR

Muscular Atrophy

Muscular atrophy may be caused by many processes. Neurogenic atrophy follows disease of the anterior horn cell, root, or peripheral nerve. Atrophy due to other neurologic processes, such as the hemiatrophy associated with congenital hemiplegia, is not typically considered neurogenic atrophy even though it is related to nervous system disease. The term neurogenic atrophy as commonly used implies disease affecting some part of the lower motor neuron. Myogenic atrophy is that due to muscle disease, such as muscular dystrophy. As a generalization, when weakness and wasting are comparable the process is more likely to be neurogenic; when the weakness is disproportionately greater than the wasting the process is more likely to be myopathic. When a muscle appears wasted but is not weak the cause is likely to be non-neurologic, such as disuse.

Neurogenic Atrophy

When a lesion completely disrupts the lower motor neuron or its peripheral processes, the affected muscle lies inert and flaccid, and no longer contracts voluntarily or reflexively. Muscle fibers decrease in size, causing wasting or atrophy of the entire muscle mass. Without timely reinnervation the muscle may become fibrotic, with an increase in connective tissue and fatty infiltration. The more abrupt or extreme the interruption of nerve supply, the more rapid is the wasting. The atrophy may either precede or follow other signs, such as weakness. In rapidly progressing diseases weakness precedes atrophy, but in slowly progressive diseases the atrophy may precede appreciation of weakness. If the pathologic process is confined to the anterior horn cells or the spinal cord, the neurogenic atrophy is segmental in distribution. Some conditions cause rapid destruction of the anterior horn cells and atrophy in the distribution of the affected spinal cord segments that develops within a short period of time (e.g., poliomyelitis).

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