All patients in this series presented within 3 months from the date of their acute cervical cord injury (hyperextension-hyperflexion injury in automobile accidents and hyperextension-rotational injury in industrial or environmental accidents). The diagnosis of definite MS in all the cases was confirmed by the neurologists prior to their referral to one of us (POB). There were a total of 39 cases, 24 of which were of new onset. These latter cases had new disease, without any history of neurological symptoms and were previously in excellent health. There were 12 males and 12 females, whose ages ranged from 19 to 55 years with a mean age of 32 years. They were all in excellent physical health previously. The onset of the symptoms occurred within a range of 12 h-12 weeks post-trauma with the maximum number of new cases reaching their peak between 2 and 3 weeks. Their expanded disability status scale (EDSS) scores ranged from 1.5 to 8.5 with a median score of 5.0. A further 15 cases, three male and 12 female, were of mild MS which rapidly accelerated to a progressive form following their injury. Their ages ranged from 21 to 51 years with a mean of 38.6 years. Their pre-trauma EDSS score had a range of 1-3 with a mode of 1, whilst their post-trauma EDSS at the time of examination were between 3 and 8.5 with a median score of 5.5. The worsening of their MS, i.e. the onset of new symptoms occurred between 1 and 12 weeks post-trauma with a mean maximum incidence of 1-2 weeks.
The severity of soft tissue injury was assessed retrospectively on an arbitrary scale of 1-15 (Table 3). There was no apparent correlation between the individual severity of injury as measured in this arbitrary scale and the subsequent deterioration of MS symptoms. In this series, none of the cases had any cervical vertebral fracture, dislocation or spinal cord compression."
In our paper, we have sought to draw the attention of the readers to the role of certain CNS-specific focal trauma (cervical cord injury, stereotactic brain surgery like thalamotomy and electrical injury) in precipitating the symptoms of undeclared MS and adversely affecting the course of benign MS. Like infection, which will trigger MS symptoms only in a proportion of patients [10% (McAlpine et al., 1965)-48% (Sibley and Foley, 1965)], cervical cord hyperextension-hyperflexion injury is likely to unmask or worsen the natural course of MS in a subgroup of affected patients with an underlying diathesis. This may be important because the prevalence of asymptomatic (silent) MS has been estimated to be about 25% of that diagnosed in vivo (Engell, 1989).
We must make it clear that we do not propose physical trauma in any form causes MS per se. Physiologically, CNS-specific trauma produces focal breaches in the BBB and induces metabolic changes by activating the stress response. In addition, focal trauma also enhances the expression of nitric oxide synthase in the CNS microvasculature (Cobbs et al., 1997). In susceptible individuals, these effects might unleash critical changes in the levels of pro-inflammatory cytokines and nitric oxide, thus triggering MS symptoms ab initio or aggravating symptoms of pre-existing latent disease. The mechanism of MS is still unknown and research must focus on the role of traumatic breakdown of BBB, stress and nitric oxide pathways in the MS symptom exacerbation for a better understanding of this common, disabling neurological disorder."http://www.mult-sclerosis.org/news/Jan2 ... AndMS.html