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The motor examination has many components, which should be performed systematically. A lesion causing weakness can affect any level of the corticospinal (pyramidal) system from the frontal lobe to the spinal cord (Figure 4–1). It can also affect anterior horn cells, motor nerve roots, peripheral nerves, the neuromuscular junction, or muscles themselves. By looking for abnormalities other than weakness, the examiner often identifies the level of the neuraxis that is involved. Weakness secondary to frontal lobe or corticospinal tract lesions (upper-motor-neuron-type weakness) may be accompanied acutely by reduced muscle tone (flaccidity), but over days or weeks, muscle tone increases (spasticity) with hyperactive tendon reflexes. As a result of disuse, loss of muscle bulk (atrophy) can evolve over time, but marked atrophy would be unusual with upper-motor-neuron-type weakness, and chronic muscle fasciculations are not a feature. Weakness secondary to anterior horn cell, nerve root, nerve plexus, or peripheral nerve lesions (lower-motor-neuron-type weakness) is accompanied by reduced muscle tone and hypoactive tendon reflexes. After 2 or 3 weeks, atrophy develops, and if a muscle is completely denervated, atrophy rapidly becomes marked. Particularly with lesions directly involving anterior horn cells such as amyotrophic lateral sclerosis (ALS), muscle fasciculations may be prominent. (The fact that ALS involves both upper and lower motor neurons means that hyperreflexia, atrophy, and fasciculations can affect the same limb or even the same muscle, a nearly pathognomonic combination.)

Figure 4–1.

A significant number of fibers in the corticospinal tract originate in the primary motor cortex and terminate in the ventral horn of the spinal cord. The same axons are at various points in their projection part of the internal capsule, the cerebral peduncle, the medullary pyramid, and the lateral corticospinal tract. (Reproduced with permission from Kandel ER, Koester JD, Mack SH, Siegelbaum SA. 2021. Principles of Neural Science, 6th ed. New York: McGraw Hill.)


A 55-year-old man notices difficulty buttoning and turning keys.”

In myopathic disorders such as polymyositis or muscular dystrophy, atrophy can eventually develop, but usually over years, not weeks. In fact, in Duchenne muscular dystrophy (a hereditary sex-linked recessive disorder affecting boys), the muscles may appear larger than normal despite severe weakness.


A 15-year-old boy, weak since early childhood, has been wheelchair-bound for 3 years.”


Cerebral injury during infancy can result in deficient growth of contralateral limbs, which may be weak and hypertonic but usually maintain normal muscle contours. Diffuse muscle atrophy can be a consequence of malnutrition or malignancy, and reduced muscle bulk follows prolonged disuse of a limb from any cause.

Muscle atrophy in association with neurological disease suggests denervation or ...

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