The aetiology proposed for the development of chronic cerebrospinal venous insufficiency (CCSVI) associated with multiple sclerosis (MS) has been the presence of congenital truncular venous malformations. However, this hypothesis is not consistent with the epidemiology or geographical incidence of MS and is not consistent with many of the ultrasonographic or radiographical findings of the venous disturbances found in MS patients. However, the probability of a venous aetiology of MS remains strong based on evidence accumulated from the time the disorder was first described.
The method used in this review was to search PubMed (Database of scientific publications) for all past medical publications related to vascular, venous, haematological, epidemiological, biochemical, and genetic investigations and treatments of MS. Epidemiological and geographical findings of prevalence of MS indicate the involvement of an infective agent. This review of the venous pathology associated with MS describes a hypothesis that the pathogenesis of the venous disease could be initiated by a respiratory infective agent such as Chlamydophila pneumonia, (Chlamydia) which causes a specific chronic persistent venulitis affecting the cerebrospinal venous system. Secondary spread of the agent would initially be via the lymphatic system to specifically involve the azygos, internal jugular and vertebral veins.
The hypothesis proposes mechanisms by which an infective venous vasculitis could result in the specific neural damage, metabolic, immunological and vascular effects observed in MS. The hypothesis described is consistent with many of the known facts of MS pathogenesis and therefore provides a framework for further research into a venous aetiology for the disease. If MS does result from a chronic infective venulitis rather than a syndrome involving congenital truncular venous malformations, then additional therapies to the currently used angioplasties will be required to optimize results.
Mad as a Hatter or a Genius in the Making?
Everyweek/month or so, someone comes up with a new idea about "this or that" concerning MS. You read and buy into them or not. This person has read and not bought into the CCSVI concept, will people buy into this idea. Some will, some will not and for many it will not be that important.
We can all be armchair pundits, but the way to see if your novel idea has any legs is to get up and do something to disprove your hypothesis. It is usually possible to find studies to support your idea, where you often forget those that do not support it.
This idea suggests that an infective agent alters the blood vessel architecture. However, some would argue that demonstrating that the blood vessel architecture is actually altered is the first element to demonstrate. Others may question whether cross reactivity between human and bacterial Heat shock protein 60 (Hsp60) is important when MSers react predominantly against a Hsp27. Others will question if there is any evidence that Chlamydia actually causes any blood vessel damage in the way that pathology in MS occurs. Furthermore whether Chlamydia is the infective agent associated with MS is debatable and after initial studies claiming it to be the infective agent in MS, many have put it to the test and found this idea wanting. Even though the presence of Chlamydia may be more likely in MS patients, these findings are insufficient to establish a causative relationship. Progressive disease is linked to ongoing infection. One would think that immunosuppression would accelerate this, but I do not think that this holds either.
The answer is for the author to do something (some hands-on work rather than just cerebral work) about it, as there may be holes in the story. This would maybe a new venture as the author has no track record concerning multiple sclerosis research so I will "watch this space" before binning my teaching notes. No doubt this will stimulate some people to investigate this further.