No environmental, dietary, or activity-related changes are known to alter the course of the illness.
In the usual forms of MS—that is, in those with a relapsing and remitting course and evidence of disseminated lesions in the CNS—the diagnosis is rarely in doubt. Vascular malformations such as cavernous angiomas of the brainstem or spinal cord with multiple episodes of bleeding, brain lymphoma, lupus erythematosus, the antiphospholipid antibody syndrome, and Behçet disease all may simulate relapsing MS, and each has its own characteristic and diagnostic features. The list can be expanded by the inclusion of corticosteroid-responsive intravascular lymphoma and the other numerous causes of multiple, well-demarcated white matter abnormalities on MRI, such as embolic infarcts, PML, migraine-associated white matter lesions, Lyme disease, sarcoidosis, Susac syndrome, and tumors. Difficulties are most likely to arise when the standard clinical criteria for the diagnosis of MS are lacking, as occurs in the acute initial attack of the disease and in cases with an insidious onset and slow, steady progression. Other features that call for caution in diagnosis of MS are an absence of symptoms and signs of optic neuritis, the presence of widespread amyotrophy, entirely normal eye movements, a hemianopic field defect, pain as the predominant symptom, or a progressive nonremitting illness that begins in youth. Other points against MS are fever and nonneurologic features such as joint inflammation, skin rash, sicca syndrome, or evidence of peripheral neuropathy. The differentiation from Devic disease is discussed further on.
As has been stated, the initial attack of MS (clinically isolated syndrome) may mimic acute labyrinthine vertigo or tic douloureux (trigeminal neuralgia). Careful neurologic examination of such patients usually discloses other signs of a brainstem lesion; the CSF examination may be particularly helpful in these circumstances. Extensive brainstem demyelination of subacute evolution, involving tracts and cranial nerves sequentially, may be mistaken for a pontine glioma. With brainstem symptoms of acute onset, there may be difficulty in distinguishing an MS plaque from a small infarction because of a basilar branch occlusion. In several patients who we have observed, recurrent bleeding from cavernous vascular malformations and small brainstem arteriovenous malformations simulated MS clinically. Only with MRI, visualization of blood products surrounding the small vascular lesions may the diagnosis be clarified. Sequential MRIs and the course of the illness usually settle the matter.
Acute disseminated encephalomyelitis (ADEM; see further on) is an acute illness with widely scattered small demyelinating lesions but it is self-limited and monophasic. Furthermore, fever, stupor, and coma, which are characteristic of severe cases, rarely occur in MS. The encephalomyelitis may, however, progress for several weeks, making the distinction from MS difficult.
In systemic lupus erythematosus and less often in other autoimmune diseases (mixed connective tissue disease, Sjögren syndrome, scleroderma) there may be multiple lesions of the CNS white matter. These may parallel the activity of the underlying immune disease or the level of autoantibodies, particularly those against native DNA or phospholipids but myelitis or lesions in the cerebral hemispheres are known to occur before other organ systems are affected. Conversely, between 5 and 10 percent of MS patients have antinuclear or anti-double stranded DNA antibodies without signs of lupus, but the significance of this finding is not at all clear. In addition, as discussed in the introductory section, relatives of patients with MS in some series have a higher than expected incidence of autoantibodies of various types, suggesting an as yet unproved connection between systemic autoimmune disease and MS.