The role of trauma in the pathogenesis of multiple sclerosis: a review

The suggestion that an alteration of the blood-brain barrier (BBB) is an obligatory step in the pathogenesis of the multiple sclerosis (MS) lesion has been amply confirmed by innumerable magnetic resonance scans. There also exists a large body of clinical, neuropathologic, neuropsychologic, radiologic and experimental evidence that shows that trauma, in particular mild concussive injury to the head, neck or upper back, thus impinging on the brain and spinal cord, may result in an increase in BBB permeability. It is only logical therefore to infer that when such mild trauma to those parts of the body affects MS patients, the resulting alteration of the BBB leads to the formation of new lesions or the enlargement and activation of old ones. In such situations trauma acts as a facilitator of the postulated but still not fully understood pathogenetic mechanism of lesion formation. Because of the extremely poor correlation between site and size of the lesions and clinical manifestations of MS, one cannot expect that every episode of trauma will result in the appearance of new symptoms in an hitherto asymptomatic individual, or the recurrence of old symptoms in an MS patient. It is inappropriate to attempt to prove or disprove a causal relationship between physical trauma and MS exacerbations or clinical onset by means of epidemiologic studies. The unpredictability and variability of the clinical manifestations of the disease, the differences in the genetic and immunologic backgrounds of individuals, as well as in their degree of clinical and pathologic involvement and level of activity, render such investigations pointless.