Like the modes of onset cited above, other early manifestations of MS may be unsteadiness in walking, brainstem symptoms (diplopia, vertigo, vomiting), paresthesias or numbness of an entire arm or leg, facial pain often simulating tic douloureux, and disorders of micturition. Vertigo of central type is also a frequent initial sign of MS, but it more often appears in established cases. Discrete manifestations such as hemiplegia, pain syndromes, facial paralysis, deafness, or seizures occur in an only small number of cases and suggest an alternative disorder to MS. Most often the disease presents with more than one of the aforementioned symptoms almost simultaneously or in rapid succession.
Not infrequently, a prominent feature of the disease is nystagmus and ataxia, with or without weakness and spasticity of the limbs, a syndrome that reflects involvement of the cerebellar and corticospinal tracts. Ataxia of cerebellar type can be recognized by scanning speech, rhythmic instability of the head and trunk, intention tremor of the arms and legs, and incoordination of voluntary movements and gait, as described in Chap. 5. The combination of nystagmus, scanning speech, and intention tremor is known as the Charcot triad. While this group of symptoms is often seen in the advanced stages of the disease, most neurologists would agree that it is not a common mode of presentation. The most severe forms of cerebellar ataxia, in which the slightest attempt to move the trunk or limbs precipitate a violent and uncontrollable ataxic tremor, are observed among patients with long-standing MS. The responsible lesion probably lies in the tegmentum of the midbrain and involves the dentatorubrothalamic tracts and adjacent structures. Cerebellar ataxia may be combined with sensory ataxia, owing to involvement of the posterior columns of the spinal cord or medial lemnisci of the brainstem. In most cases of this type, the signs of spinal cord involvement ultimately predominate; in others, the cerebellar signs are more prominent.
Diplopia is another common presenting complaint (see Prasad and Galetta). It is most often a result of involvement of the medial longitudinal fasciculi, producing an internuclear ophthalmoplegia (see Chap. 13). The signs are characterized by paresis of the medial rectus on attempted lateral gaze, with a coarse nystagmus in the abducting eye; in MS, this abnormality is usually bilateral (unlike small pontine infarcts, which cause a unilateral internuclear ophthalmoplegia [INO]). As a corollary, the presence of bilateral internuclear ophthalmoplegia in a young adult is virtually diagnostic of MS. Occasionally, internuclear ophthalmoplegia in one direction of gaze is combined with a horizontal gaze paresis in the other, although this “one-and-a-half syndrome” is more typical of brainstem stroke (Frohman). Other palsies of gaze (a result of interruption of supranuclear connections) or palsies of individual ocular muscles (because of involvement of the ocular motor nerves in their intramedullary course) also occur, but less frequently. Additional manifestations of brainstem involvement include myokymia or paralysis of facial muscles, deafness, tinnitus, vertigo—as noted above, vomiting (vestibular connections), and, rarely, stupor and coma. The occurrence of transient facial hypesthesia or anesthesia or of trigeminal neuralgia in a young adult should always suggest the diagnosis of MS implicating the intramedullary fibers of the fifth cranial nerve.