One week after an upper respiratory tract viral infection, a 36-year-old woman began to have progressive paresthesias of the lower extremities and right thorax. She sought medical evaluation 2 weeks later.
The patient was afebrile; vital signs were normal. Her history included irritable bowel syndrome; a single episode of postviral arthralgia accompanied by a nonspecific rash had occurred 3 years earlier.
No motor deficits were noted; deep tendon reflexes were brisk. Lower extremity sensory deficits to vibration, pinprick, and light touch at L3 through S5 and sensory deficits to temperature and pinprick at T5 through T9 dermatomes on the right anterior thorax were demonstrated. Abdominal reflexes and anal sphincter tone were decreased; anal sensory deficit to light touch was noted.
The patient's gait, coordination, and cranial nerves were intact; the Babinski sign was absent. Lower extremity nerve conduction studies, complete blood cell count, and serum chemistries were normal. An MRI of the head confirmed the diagnosis of multiple sclerosis (MS).
Dr John Godino of Fort Sam Houston, Tex, writes that MS is the most common of the CNS immune demyelinating disorders. It occurs most often in women; typical age at onset of symptoms is between 20 and 40 years. Initially, an otherwise healthy person suffers an acute or subacute attack of unilateral vision loss, vertigo, ataxia, paresthesias, incontinence, diplopia, dysarthria, or paralysis. The symptoms are caused by a focus of inflammatory demyelination that later scars to form a plaque (Figure, arrow) in the white matter of the brain (most frequently periventricular), brain stem, or spinal cord. The demyelination slows or blocks conduction of nerve impulses and causes neurologic dysfunction.
Classically, MS is characterized by exacerbations and remissions of neurologic dysfunction over many years. The symptoms usually are painless; they may persist for days or weeks and partially or completely resolve between exacerbations.
Some patients exhibit slowly progressive myelopathy with spasticity and ataxia; others may have only 1 or 2 attacks during their lifetime. On average, about 60% of patients with MS remain fully functional for a decade after the initial episode; 25% to 30% remain functional for 30 years or more.
The cause of MS is unknown, but immunologic or genetic factors are suspected. An infective agent acquired early in life may be the trigger. Inflammatory infiltrates that are sometimes seen in the perivascular areas of the demyelinated plaques and the decrease in the serum suppressor lymphocytes that precedes acute attacks suggest an immune disorder.
In persons of appropriate age, diagnosis rests on clinical evidence of lesions that have affected different areas of CNS white matter at intervals of at least 2 months. Certain symptoms strongly suggest the diagnosis; these include bilateral internuclear ophthalmoplegia, Lhermitte sign (electric shock-like sensation radiating to the extremities and initiated by neck flexion), and exacerbation of neurologic symptoms associated with acute febrile illness.
Laboratory examination is helpful but not definitive. Most patients have elevated cerebrospinal fluid g-globulin levels and discrete (oligoclonal) bands. CT scans are less elucidating than MRI, which usually reveals characteristic white-matter lesions scattered throughout the brain and/or spinal cord.
Acute bouts of neurologic dysfunction may resolve more quickly with short-term corticosteroid therapy. There is no evidence that this treatment brings long-term benefit.
This patient was treated with IV methylprednisolone (1 g, slow push, qd) for 3 days; then she was given PO prednisone 1 mg/kg/d on days 4 to 17, 20 mg on day 18, and 10 mg on days 19 to 21. After 2 months, her symptoms resolved except for mild lower extremity paresthesias.