Recovery from symptoms during remissions is due mainly to the restoration of axonal function, either by remyelination, the resolution of inflammation, or the restoration of conduction to axons which persist in the demyelinated state. Conduction in the latter axons shows a number of deficits, particularly with regard to the conduction of trains of impulses and these contribute to weakness and sensory problems. The clinical course of the disease is discussed, together with its relationship to the evolution of lesions as revealed by magnetic resonance imaging and spectroscopy. The earliest detectable event in the development of most new lesions is a breakdown of the blood-brain barrier in association with inflammation. Inflammation resolves after approximately one month, at which time there is an improvement in the symptoms.
Demyelination occurs during the inflammatory phase of the lesion.
An important mechanism determining persistent neurological deficit is axonal degeneration, although persistent conduction block arising from the failure of repair mechanisms probably also contributes. J Neurol Sci. These are considered to be mediated by ectopic impulses generated at the site of demyelination, whereas negative symptoms are caused by conduction block. Conduction block at a demyelinated segment should reduce positive symptoms, but worsen negative ones. As reported previously, lidocaine, an Na channel blocker unmasks silent negative symptoms presumably by further reducing the action current in demyelinated portions and blocking conduction.