Corticospinal tract involvement occurs with the initial attack of MS in 32% to 41% of patients (36-39), but it is present to a significant degree in 62% (37,39) of patients with chronic disease. Symptoms may also include "heaviness," ''stiffness,'' or even, pain in an extremity. The legs are much more frequently involved than the arms; when both are involved, symptoms in the legs usually appear earlier. Involvement often begins with one leg, but in most patients, both are eventually affected, although the severity may be quite asymmetric. Signs of corticospinal tract pathology may be as minimal as abnormal reflex activity, but the disease frequently progresses to severe spastic paraparesis. Hyperactivity of the deep tendon reflexes, often including crossed tibioadductor and puboadductor reflexes, is seen in most patients. Clonus, which may be sustained and severe, is often present. This is most common at the ankle, but it may be found at other sites as well. The Babinski reflex is frequently present, at times as the only manifestation of corticospinal tract dysfunction.
Spasticity is very commonly seen in the legs, but may also occur in the arms. At times this abnormality actually helps a paretic patient walk (40,41), but in other patients it may produce discomfort or pain, cause flexor or extensor spasm (42,43), or interfere with personal hygiene (adductor spasticity). In addition, spasticity may result in disturbed sleep or interference with sitting. If inadequately addressed and treated, it may ultimately result in irreversible joint contractures. Patients themselves complain of stiffness, cramps, spasm, or pain. In the upper extremity, weakness often predominates in the distal musculature. At times, this is accompanied by extensive atrophy, presumably reflecting demyelination in the root entry zones of the spinal cord (36).
Corticospinal tract involvement most often results from demyelination within the spinal cord, although other sites, including the medullary pyramids, basis pontis, cerebral peduncles, and deep hemispheric white matter, may also be involved (44). A hemiparetic pattern of motor weakness may be seen, but is uncommon. Indeed, on occasion MS may present with the acute onset of hemiparesis including the face (45) and may clinically look like lacunar infarction. Despite an initial appearance suggesting a vascular etiology, MRI may lead to the diagnosis of MS, with lesions most often evident in the posterior limb of the internal capsule. Subtle abnormalities of bimanual coordination have recently been reported in MS, presumably from involvement of the corpus callosum (46).
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