Bull Mem Acad R Med Belg 2002;157(7-9):391-8; discussion 398-400
Service de Neurologie, Cliniques universitaires Saint-Luc, U.C.L.
The complex pathogenesis of multiple sclerosis includes inflammation and potentially disabling focal lesions that are associated with heterogeneous, often destructive pathologic changes disseminated throughout the white matter of the central nervous system.
Genetic and environmental factors may trigger the movement of autoreactive T cells, from the systemic circulation into the central nervous system through disruption of the blood-brain barrier.
In the brain, local factors may enhance the immune reaction, resulting in the proliferation of pro-inflammatory CD4+ type 1 T cells, and ultimately in immune-mediated injury of oligodendrocytes and myelin.
The exposed axon segments may be susceptible to further injury from soluble mediators such as cytokines, chemokines, complement and proteases, resulting in irreversible axonal lesions.
Partial remyclination may occur by differentiation of resident oligodendrocyte precursor cells.
Decreases in the volume of the brain and spinal cord, indicating atrophy, correlate with both the loss of axons and the occurrence of extensive demyelination, and are markers of the degenerative phase of the disease.
Besides classical motor and sensory signs and symptoms, cognitive impairment is frequently observed and increases the burden of the disease.