What is thereby consistently left out of consideration is the question as to the forces which would be required for any blood- and otherwise fluid-borne corpuscles to (be) spread according to the patterns in which the multiple sclerosis-specific lesions evolve. Instead, researchers have directly proceeded to promulgate ideas on the activities by which the one or other (ultra-) microscopic agent might be imagined to bring about the condition's demyelinations. As regards the principles governing the particular incriminated agents' spread, no more than a random involvement of the brain's and spinal cord's blood vessels and surfaces to the cerebrospinal fluid in terms of a certain "inflammatory process" is customarily spoken of.

If multiple sclerosis-specific lesion spread is thus directly ascribed to a scattering of corpuscular elements evolving in connection with certain injurious "inflammatory events", it must be asked: Can -- and if so, how can -- a dissemination of corpuscles according to the dynamics of the body's fluid circulations create such lesion patterns as those which Carswell's and Charcot's first illustrations of spinal respectively cerebral multiple sclerosis so unmistakably testified to? Without answering these questions, we can never be sure whether the currently prevailing views on the causation of multiple sclerosis really explain the specific lesion developments in the proper ways.