Disturbances of sensation, motor disorders, gait difficulties and monocular loss of vision are the most common symptoms in multiple sclerosis at the time of initial examination, to the point that in their absence, and in the absence of a clear course of remissions and exacerbation, and in the presence of an entirely normal cerebrospinal fluid examination, the diagnosis of MS should be considered at least doubtful. The combination of symptoms and sign in established case can be quite varied and can mimic any syndrome attributable to central nervous system white matter disease. Symptoms and signs attributable to gray matter disease, such as seizures, aphasia, apraxia etc. are quite unusual, at least initially.

Although the diagnosis of MS is ultimately a clinical one, advances in laboratory, neurophysiologic and neuroimaging techniques have aided in the diagnosis of this disorder. At the current stage of our knowledge, however, no diagnostic test can be considered 100% specific.

Approximately 75% of all patient manifest a course of the disease characterized by remissions and exacerbations and approximately 25% have a chronically progressive course from the very onset of the disease. A very small percentage of patients have a rapidly fulminating course leading to death in only a few months. The emergence of new diagnostic techniques and our increasing diagnostic acumen may reveal in the future that what we now call MS may represent only the tip of an iceberg and that there may be a huge number of benign monosymptomatic or asymptomatic cases in the population at large which are as yet undiagnosed or not diagnosable.

It should again be emphasized that results of cerebrospinal fluid (CSF) studies and other test may be abnormal for various reasons; hence, these are not specific for MS.

• An abnormal evoked potential is not specific for MS; therefore, it must be interpreted in the contest of the clinical picture. Electromyographic and nerve conduction tests pointing to peripheral nerve or muscle diseases should steer away from the diagnosis of a primary CNS demyetinating process.

• IMAGING STUDIES

  • MAGNETIC RESONANCE IMAGING - Magnetic resonance imaging (MRI) currently is the preferred imaging technique for obtaining evidence in support of a diagnosis of MS. The typical abnormalities on NM most commonly are located in the supratentorial white matter, especially in the periventricular region. They may appear as multiple descrete lesions, or they may coalesce to form more homogeneous borders surrounding the ventricles. These abnormalities have a location similar to that of the demyelinating lesions observed at autopsy. Less commonly, lesions can be detected in the cerebellum and in the brainstem.
  • COMPUTED TOMOGRAPY (CT) - While CT is not as sensitive as NM in the detection of abnormalities in MS, it nevertheless may demonstrate a wide variety of findings. Cerebral atrophy is the most common and least specific abnormality. Hypodense lesions before administration of contrast agent may be present in periventriucular and deep white matter and, uncommonly, in the posterior fossa. Enhancement seems to correlate with acute disruption of the blood-brain barrier, and the areas of abnormal enhancement can be abolished by treatment with corticosteroids.
• DIFFERENTIAL DIAGNOSIS - Numerous disorders can potentially mimic MS. Conditions to be ruled out include coflagenvascular disorders, sarcoidosis, acute disseminated encephalomyelitis, Behcet's disease, cerebrovascular occlusive disease, meningovascular syphilis, paraneoplastic disorders. Other conditions to be considered are hereditary spinocerebellar ataxias, subacute combined degeneration of the spinal cord (Vitamin B12 deficiency), progressive spastic paraparesis secondary to retrovirus infection (HTLV I), primary CNS lymphomas, arterio-venous malformations of the brainstem and spinal cord, Amold-Chiari malformation. Psychiatric disorders almost always enter in the differential diagnosis early in the course of the disease.
• MANAGEMENT - The clinical therapeutic trials are all aimed at altering the patients' immune system, inasmuch as the demyelination in MS is thought to be immune mediated. Some author recommend the intravenous use of ACTH, or methylprednisolone for moderate to severe exacerbations, and oral administration of prednisone for mile exacerbation of MS. Low dose maintenance treatment with steroids should have no place in the therapeutic armamentarium of MS. The results of treatment of chronic progressive MS, whether slow or rapid in its course, is dismal. We consider azathioprine, cyclophosphamide, cyclosporine, lymphatic irradiation and plasmapheresis as experimental treatment modalities without important therapeutic effect.

Case studies