Pathophysiological aspects of the formation of neurological deficit in multiple sclerosis.

The results of complex studies were used to formulate a concept of the development of neurological impairments in multiple sclerosis (MS). Acutely developing impairments to spike propagation, reaching the level of conduction blockade, due to the active pathological process with demyelinating and axonal damage to the CNS lead to the formation of neurological impairments in exacerbations of MS, while complete or partial reversion (regression) of these symptoms in the stage of remission results from compensatory changes in the nature of conduction, which were not, however, accompanied by recovery of electrophysiological measures. The development of stable neurological deficit in secondary-progressive MS is determined by impairments to spike conduction processes associated with significant levels of demyelination and atrophic changes in the CNS, with myelin loss and axon death.

[A comparative analysis of rebif 22-mcg and copaxone efficacy in multiple sclerosis].

A comparative analysis of efficacy and tolerability of such immunomodulating compounds as rebif 22-mcg and copaxone used in the treatment of multiple sclerosis is presented. The analysis was based on the data obtained in the 2-year study of copaxone (145 patients) and rebif 22-mcg (74 patients) therapy carried out in the Neurology Institute, Russian Academy of Medical Sciences.

[Mechanisms of lability of neurological symptoms in multiple sclerosis].

Pathophysiological peculiarities of demyelinated axons determine their high sensitivity to different exogenous factors and are the reason of instability of neurological signs in MS. One of the typical MS sing is high sensitivity to elevated temperature of the body. Even temporary elevation in body temperature may cause changes in impulse conduction in demyelinated fibres, which was proved by studies of evoked potentials and stabilometric studies.