TY - CHAP M1 - Book, Section TI - The Motor Examination: There Is Always More Than Weakness A1 - Brust, John C. M. PY - 1 T2 - Practice of Neural Science: A Case-Based Approach AB - 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.) SN - PB - CY - New York, NY Y2 - 2024/03/29 UR - neurology.mhmedical.com/content.aspx?aid=1180669232 ER -