Motor symptoms often occur early in the disease. Patients may complain of weakness or heaviness of the involved limb. They may initially complain of weakness on exertion, gradually increasing until it is constantly present. They may describe a tendency to trip or fall or may drag the affected limb (Hickey, 1992). The symptoms may last for minutes to hours and therefore cannot always be observed during an ordinary clinical exam (Matthews, 1991). There may be no abnormal signs on the clinical exam at rest except for the absence of abdominal reflexes, an indication of cortical tract dysfunction. On exercise, weakness, spasticity, and extensor plantar reflexes rapidly appear, only to become reversible at rest (Matthews, 1991). Uhthoff’s phenomenon is a worsening of motor function after a hot shower or a hot bath. This can be of diagnostic significance.

Pyramidal tract involvement produces characteristics of upper neuron disease: spasticity, hyperreflexia, clonus, and extensor plantar responses. Deep tendon reflexes are exaggerated, sustained clonus may be elicited (usually at the ankles), and extensor plantar responses may be observed. Commonly, these signs are asymmetric. Deep tendon reflexes can be decreased if the reflex arc has been interrupted by a lesion at a certain segmental level of the spinal cord. The Achilles reflex may be absent, and sphincter and sexual dysfunction may be present if lesions are found in sacral segments (Gordon et al, 1991).

Triceps jerks are lost more frequently in the upper extremities; ankle jerks are lost more frequently than knee jerks. In established disease in the upper limbs, biceps and supinator jerks may be associated with finger flexion and Hoffman’s sign. Flicking or nipping the nail of the second, third, or fourth finger, if the reflex is present, causes flexion of these fingers and possibly the thumb. Its presence indicates that the tendon reflexes are hyperactive. An increased jaw jerk suggests involvement above the level of the foramen magnum (Matthews, 1991).

Increased muscle tone is an important factor in this disease. In less severe cases, there is spasticity of the extensor muscles of the legs. This occurs in bed at night or when trying to rise in the morning. The legs are held rigidly extended, usually for several minutes. These spasms are seldom painful but are inconvenient. As the disease progresses, the flexor muscles become spastic. The patient may fall without warning while walking. Flexor spasms are frequently painful (Matthews, 1991).

Bilateral involvement of the corticobulbar tracts occurs in some patients; this leads to dysarthria, dysphagia, hyperactive jaw jerks, bifacial paralysis, and apparent emotional lability. Spastic weakness of the muscles of speech is common. In the early stages, speech is often slurred. As the disease progresses, speech becomes explosive or staccato and unintelligible. Scanning speech—slow and measured speech with pauses between syllables—is seen in later stages of the disease (Hickey, 1992).

Sensory symptoms are the most common initial features of MS and occur throughout the course of the disease. These symptoms are varied and the onset may be symmetrical. The sensations are described as tingling, numbness, a pins-and-needles sensation, tightness, coldness, or swelling of the limbs or trunk. Complaints of tight bands or straps around the trunk or limbs are characteristic symptoms (Gordon et al, 1991). A common pattern is for unusual sensations to begin in one foot and spread to both lower limbs, the buttock, the perineum, and the trunk within a few days.

The normal sensation of micturition and defecation may be affected, but control remains normal. Vaginal sensation is also diminished. The exam may reveal no loss of light touch or pinprick, but the pinprick may feel distant, as if something is between the pin and the skin. An intensely itching pain, especially in the cervical dermatomes, usually unilateral and occurring in young women, is suggestive of MS (Gordon et al, 1991).

The most frequent sensory signs are varying degrees of impairment of vibration and joint position sense, decrease of pain and light touch in a stocking-and-glove distribution in the four extremities, and patchy areas of reduced pain and light touch perception in the limbs and trunk (Gordon et al, 1991).

Lhermitte’s sign consists of an electric feeling passing down the back to the legs on flexing the neck. This is common in MS but can occur in other conditions (compressive myopathies). The usual course of a sensory episode is toward complete remission within 6 to 8 weeks; for patients who have frequent attacks, these episodes may clear in 10 days. Observant patients may recognize sensory symptoms of a more localized nature that last for only 1 to 2 days, unrelated to exercise, infection, or environmental temperatures (Matthews, 1991). Sensory symptoms tend to remit more frequently than do symptoms involving other systems.

Cerebellar dysfunction is characterized by gait imbalances, difficulty in performing coordinated actions with the arms, and slurred speech. Cerebellar signs are usually uncommon at the
onset of the disease (Matthews, 1991). The early appearance of cerebellar ataxia is an indication of a poor prognosis, and cerebellar signs often persist. There may be difficulty in distinguishing cerebellar signs from those of weakness, spasticity, sensory loss, and vertigo. Cerebellar ataxia naturally affects the gait, but spasticity and weakness are more important causes of disability.

Conventional heel–knee shin tests are poorly performed by weak and spastic legs. Truncal ataxia and gait are not obvious when sitting but contribute to poor balance. These abnormalities may be observed by having the patient stand or walk normally. Cerebellar incoordination in the upper limbs may be terribly disabling, especially when combined with any significant degree of intentional tremor. Severe degrees of intentional tremor may render the hands useless; voluntary movement can be disturbed by violent deviations of the arms that may render the patient unapproachable (Matthews, 1991).

Many patients with MS display abnormalities of vision. These defects are the result of lesions of the optic nerve or chiasm. Even patients who do not demonstrate a clinically detectable visual defect often do so electrophysiologically through the measurement of visual evoked potentials. Evoked potentials are considered extensions of the clinical exam and allow objective measurement of lesions in specific pathways (Rudnick, 1996).