Article: Multiple Sclerosis - Medical Litigation News

MULTIPLE SCLEROSIS

Poser of the Department of Neurology, Harvard Medical School continues to argue[1] that an alteration in the permeability of the blood-brain barrier is both proven in the pathogenesis of Multiple Sclerosis and a demonstrable result of mild concussive injury to the head, neck or upper back. Ergo, such trauma causes onset or relapses of the disease. Chaudhuri and Behan[1a] in Glasgow, Scotland will be publishing a supportive case-study.

A case-study In the 1950s[1b] and a later pathological study [1c] had suggested a causal connection with spinal cord injury.

Empirical studies persistently and consistently refute a causal connection. A longitudinal, prospective study of a cohort of patients at the Mayo Clinic[2] found no cases occurring after head trauma or back surgery. The authors pointed out that a third of all people experience a memorable injury and that these will sometimes occur before onset and relapses of the disease. Further, disabilities arising from Multiple Sclerosis increase liability to injury.

Similarly designed research[3] at the University of Arizona could detect no overall causal effect of trauma on relapses. Using a three-month at-risk period for electrical injury, there was a significant association, but minor head injury caused no exacerbations. They found a significant decrease in activity of Multiple Sclerosis during the three months following surgical procedures and fractures.

Most recently, a much smaller study at the University of British Columbia[4] looked at infection, emotional stress and physical trauma. The authors were unable to demonstrate a statistical correlation with fluctuations in disease activity.

PRACTICE POINT
There is theoretical basis for traumatic provocation of relapse of Multiple Sclerosis but no empirical evidence.

Poser's explanation of the lack of empirical evidence is that trauma is only one facilitating factor in the ill-understood pathogenesis of Multiple Sclerosis, and that there is a poor correlation between the presence and size of lesions and the occurrence of symptoms.

However, absence of proof is not proof of absence, and prospective epidemiological studies of whiplash have yet to be undertaken or reported.