Some of you might have missed Dr. William Hammesfahr`s 1997 theory about MS and how he feels one third is of vascular origin, one third both vascular and neurological, and one third strictly neurological. Here`s the excerpt from his writing (link to my p...revious Note on this follows): The case of Multiple Sclerosis is especially instructive for understanding the role of Vasospasm in multiple neurological disorders, as our experience with Multiple Sclerosis highlights that these neurological syndromes are frequently multifactorial.
The vascular component can exist in isolation as the cause of the entire disorder in some patients, and in other patients, it may be a concommitant disorder.
These cases will be discussed further in future articles, however, an overview of our clinical experience is relevant now. Virtually all patients with the diagnosis of Multiple Sclerosis referred to me have had Vasospasm on Transcranial Doppler. The diagnosis of Multiple Sclerosis in all cases were confirmed by outside neurologists before referral to me.
Approximately one third of these patients had dramatic improvement, including MRI improvement of plaques, with medication to control the vasospasm. None of these patients had relapses as long as they stayed on their vasodilating medications and all abnormalities on TCD were successfully treated and prevented from returning by the use of ongoing monitoring during clinically asymptomatic periods.
A second third suggests that the neurological deficit is a combination of vascular injury and direct attack on the nervous system. These patients, during acute attacks, had significant improvement in neurological functioning with reduction of the vasospasm identified on ultrasound. However, they continued to have new neurological deficits from the new attack on the nervous system. Those deficits required alternative therapies such as steroids to treat ( with respect to steroids, monitoring with TCD is vital, as in some patients, the steroid itself could cause vasospasm. Steroids, of course, have complex and myriad effects on the nervous system, some of their effects may increase neurological functioning and efficiency of activity, thus improving a patient clinically, even as the concommitant vasospasm is aggravating the underlying neurological injury). These patients probably had a degree of autoimmune attack on both the vasculature and the nervous system. The degree of residual dysfunction, which sometimes continued to progress in spite of successful control of the vasospasm in the clinical outbreak, suggests that the autoimmune attack continued on the nervous system. Their clinical course, however, also suggests that the underlying autoimmune attack on the nervous system was aggravated by an ongoing ischemia brought on by a concommitant attack on the blood vessels. It was this vascular aspect of the disease that was altered.
The third group had successful control of the vasospasm, but without significant clinical improvement. The time course and progress of the acute attack continued without any significant clinical change. This suggests that there was a concommitant antibody attack to the blood vessels, as vasospasm was identified on the ultrasounds, but that this vasospasm was not clinically significant.
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