Multiple sclerosis and interferon beta-1a

The commonly accepted treatment of relapsing multiple sclerosis consists of therapies for the symptoms of the disease, including treatment of acute exacerbations. However currently (1997) there is no therapy that modifies the progression of the physical disability associated with the disease.

The symptoms of multiple sclerosis are extremely changeable, the plaques have various topography, they appear at different times.

  1. The onset is varied, you can have a polysymptomatic start (55%), monosymptomatic (45%), it can occur in the order of motor fault frequency (s. pyramidal), paresthesie (spinobulbotalamic beam), optic neuritis (unilateral), ataxia (s. cerebellare), vertigo (nc. Vestibolari), marcia cerebellare.
  2. In the state period you have pyramidal signs (cortico-spinal bundle) characterized by early and acute voluntary motility disorder with greater fatigue, subjective motor hindrance, paresis, paralysis that with the progression of the disease tend to become evident, symmetric. Cerebellar signs with atax-shift and dysarthria. Visual disturbances with total and partial recovery. Retrobulbar optic neuritis with decreased visual acuity, central scotaoma, often residual, orbital pain. Cranial nerve disorders you can have diplopia, peripheral facial paralysis, vertigo. Sensitivity disorders in the form of paresthesias, changes in pallesthesia and sense of position, for lesions of the spinobulbotalamic bundles with dysesthesia in the form of heartburn, itch, cold, to be referred to the interest of the spinothalamic bundles.

A multicenter study was conducted in America to determine whether interferon beta-1a could slow the progressive and irreversible neurological disability of relapsing multiple sclerosis. Interferon beta-1a, at the dose of 6 million units, it was administered once a week by intramuscular injection, to patients with double-blind relapsing multiple sclerosis, placebo controlled. The primary evaluation variable of the study was the disability progression time maintained over time by at least one point on the expanded scale of Kurtzke's disability status. Interferon beta-1a treatment resulted in a statistically significant delay in disease progression time ( Lawrence D. Jacobs and others). The estimate according to the Kaplan-Meier method on the percentage of patients progressing at the end of the 104 weeks has been since 34,9% in the placebo group and the 21,9% in the group treated with interferon beta-1a. Patients treated with interferon beta-1a also experienced fewer exacerbations, significantly fewer brain lesions and volumes, highlighted by nuclear magnetic resonance with gadget. After two years, the rate of exacerbations per year was 0,9 in patients treated with placebo against 0,61 in patients treated with interferon beta-1a. No serious treatment-related side effects occurred. Interferon beta-1a had a significantly favorable impact on patients with relapsing multiple sclerosis by reducing the progression of permanent physical disability, the rate of exacerbations and disease activity assessed on the basis of the size of the brain lesions highlighted by MRI with a gadget. This treatment can modify the natural course of relapsing multiple sclerosis.

Reserved literary property, publication prohibited without written permission from the publisher.