I think the Internet may have saved Dr. Zamboni’s career. It seems there is a trail of broken careers and missed opportunities in doctors who happened upon strikingly similar vascular theories in the years before the power of social media and the Internet. These doctors found no or few colleagues willing to listen to their ideas about widened veins, impaired blood flow, and irregularities of **(Juurlink). And, of course, researchers need interest and collaboration in order to attract research dollars. Without funding, most researchers cannot initiate a large enough program of research to get their work taken seriously, nevermind published. Finally, there’s something to be said for getting peer acceptance and respect regardless of whether funding follows.
The following doctors got little positive attention and significant negative attention when they launched their theories. And now, there’s a new name on this list, Dr. William Hammesfahr.
Dr. Roy Swank – Best known for his dietary approach to managing multiple sclerosis, Dr. Swank was given funding to study MS in 1948. His “…four months of intense study of MS led to three possible leads:
- Usually the onset of severe attacks developed rapidly.
- The onset of most individual attacks suggested vascular origins.
- The disease was found worldwide but particularly common in the industrial countries. “ (1)
Building on his observational skill that people with MS on fat-restricted diets through the Second World War did better than those who didn’t restrict fats, Dr. Swank developed his famous diet plan. His results on slowing disease progression, now with over 60 years of research, are impressive.
However, Dr. Swank didn’t find early acceptance of his ideas by doctors treating MS patients. He was marginalized and lumped into those “alternative therapy” groups that doctors love to discredit and raise an eyebrow over, even though Dr. Swank was simply talking about FOOD. His fatal flaw was his compassion – he didn’t do a double-blind trial. Dr. Swank’s study had all subjects go on his diet and didn’t deny anyone the opportunity to improve by following a control group (no diet change), as is required for experimental research. Thus, his results fell victim to ”placebo effect” accusations. When I was diagnosed in the early 1990s, I asked what more I could do after suffering a rapid series of exacerbations. I was told I could “give up red meat” (which I did), but that was the extent of dietary advice given at the time, despite the Swank diet’s lengthy track record of outperforming all DMDs on forestalling disease progression.
Next victim: Dr. F. A. Schelling. Over 30 years stomping the global pavement trying to get anyone to listen to his theory about a venous connection to MS yielded nothing. It wasn’t until Dr. Schelling heard about Dr. Zamboni’s work (through the Internet!) that the two scientists got together and collaborated results. They are both founding Board members of the new International Society of Neurovascular Disease. See CTV’s coverage of Dr. Schelling here when they did their original story about Dr. Zamboni: http://csvi-ms.net/en/content/ctv-news-ms-vein-theory-has-roots-rejected-research. Dr. Schelling has the misfortune to develop his theory on the etiology of MS at the same time as a new imaging technology was born, MRI. With this ability to see lesions on the brain and spinal cord, the immunodeficiency theory of MS became firmly entrenched.
Sadly, a Canadian connection, i.e., another researcher gets ignored: Dr. Bernardt Juurlink used to be the Head of the Department of Anatomy and Cell Biology at the University of Saskatchewan. That was before he tried convincing his colleagues to look at the veins in people with MS. WaYnE (2) put Dr. Juurlink’s words into a Quote of the Day (below) that sum up the state of affairs:
Dr. Juurlink’s research looked at the cells that form myelin in our brains and a potential connection to impaired blood flow through our veins. He has not sought out fame or attention with the current interest in CCSVI. He left the University of Saskatchewan in 2008 and took a faculty position in Saudi Arabia.
I found another unwilling member of this fraternity of shunned theories: Dr. William Hammesfahr. Dr. Hammesfahr has little online presence, but what is there shows a disturbing trend. Like Dr. Juurlink,, Dr. Hammesfahr switched from multiple sclerosis research to stroke research when he hit the brick wall of neurology.
The final attack on his credibility came with his involvement in a very high profile case, the legal battle to euthanize Terry Schiavo in 2002 by her ex-husband. Dr. Hammesfahr “examined Terri Schiavo, the woman at the center of a debate in the United States about euthanasia. Testifying on behalf of Schiavo's parents, Hammesfahr told a court that, contrary to majority medical opinion, which stated that Schiavo was in an irreversible persistent vegetative state, she was in a minimally conscious state and might recover. He testified that his treatment might improve her to the point of being able to communicate, a statement not regarded as credible by the other neurologists involved in the case” (3)(4).
Dr. Hammesfahr has been called a quack and snake oil salesman (my research found he was selling nothing other than an approach to stroke that uses a large number of available drugs to treat their underlying vascular issues).
You can hear a recent interview (May 24, 2011) with Dr. Hammesfahr discussing stroke and inflammatory disease by clicking below. Move the slider in the Flash player to underneath the “K” in “Talk O Zone.com” to find the lengthy interview.
http://www.talkzone.com/mp3FlashPlayer.php?channelid=199&showid=586&Eid=333&Sid=9698
Dr. Hammesfahr’s work is so important, so fundamental to our understanding of CCSVI, I am putting most of it here in its entirety. Please read it all! Although he focuses on arteries, not veins, his theory keeps bumping into what Dr. Zamboni and others hypothesize about CCSVI. Yes, he approached treatment by looking at drug therapies, but the principles are sooo similar…it’s uncanny. I bolded some of the many significant parts and bolded and italicized thoe most important bit at the end.
And let’s add Dr. Hammesfahr to our list of doctors who all came to the same conclusion. It was Dr. Zamboni who finally put a name to this – CCSVI – and, through the Internet, cannot be silenced.
To a new understanding of personality, behavior and neurological disease
W. Hammesfahr, M.D.
D. Adkins, REEG.T
Hammesfahr Neurological Institute
With a long history of medical investigation behind, diseases affecting the brain, nervous system, and psyche have been named, categorized, classified and recategorized again. The diseases bear names of those who first described them, a common pathological finding, or bear the name of their primary clinical symptom. Such naming protocols rarely name aetiology or cause, as the cause is rarely known.
Yet we have found that a large number of apparently diverse neurological, psychological, or psychiatric diseases share a common underlying disorder, that of chronic or intermittent ischemia1 of the brain. The disparate clinical manifestations of that disorder2, depends on the acute or chronic onset of the disorder, the rapidity of the evolution of an underlying vascular disorder, the age of the patient when the disorder develops, other medications that the patient may be on which helps to limit or aggravate the underlying vascular disorder, and the body's ability to compensate for this disorder.
We have further found that all of these disorders2 respond similarly to techniques that correct the underlying vascular/ischemic disorder.
In essence, most of the neurological diseases associated with chronic ischemia result in either cognitive disorders or chronic degenerative neurological states. Thus Autism, Attention Deficit Disorder and similar syndromes, including Tourette's, many cases of Depression, psychosis, and other neuropsychiatric disorders are frequently seen in a chronic ischemia. In some cases, the chronic ischemic state results in a degenerative neurological condition. Thus, ongoing ischemia may mimic what we more commonly diagnose patients with diagnosis of Alzheimer's, Multiple Sclerosis, and Parkinson's. In others with these diagnoses, there may be an underlying chronic vascular ischemia which also aggravates the original condition, and is clinically indistinguishable. That vascular portion of their disease may be entirely reversible. When the problem develops rapidly, physical symptoms predominate. Thus patients are diagnosed as Migraine Headache, Stroke, Closed Head Injury, Ataxia, Vertigo, Tinnitis, Fibromyalgia, etc.
As few will read beyond these opening remarks, the headache deserves special mention. In our experience, it is the equivalent of Angina. In Angina, blood vessels downstream from a partial blockage dilate as one of the body's most important mechanism to compensate for a decrease in blood flow. As such, this dilations helps to preserve blood flow to the tissue. This dilation stretches the nerve fibers in the walls of the arteries, which results in pain. Similarly, the headache in our patients represents one of the body's compensatory mechanisms used to increase blood flow in response to a blockage. As the patient's vascular disorder becomes chronic, the body develops other compensatory mechanisms. By developing these other mechanisms, the headache becomes a more infrequent and less noticed clinical problem. As the body develops the ability to compensate, the physical symptoms become less noticeable, and the cognitive/emotional/behavioral disturbances become the major problems3. Thus, as the patient recovers, it becomes vitally important to be aware that the patient's symptoms will vary and alter as the vascular disorder improves. Indeed, many of these symptoms become less of one specialty's province, and becomes that of another's. Thus, the managing physician and patient need to continue to consider the entire range of symptoms as "ischemia/vascular equivalents", and continue to treat all symptoms aggressively. The present or past history of headache or family history of migraine, becomes incredibly important in understanding that patient's disorder may have a vascular component. [Sandra’s comment: Does your family have a history of migraine?]
What follows is a discussion of the development of our experience.
I have a baseline practice consisting of mainly post-traumatic, closed-head injuries and post-traumatic migraine disorders of which many have attention deficit disorders, (ADD). However, several years ago I had a large number of patients who presented with ADD of which the origin of their problems was associated with silicon breast implants (silicon toxicity). What became evident in evaluating of these patients was that the neuropsychological tests, computerized EEG and Transcranial Artery Doppler results were essentially identical. Another common characteristic in these patients was the waxing and waning nature of at least some of their complaints. Those patients with Attention Deficit Disorder both post-traumatic and in particularly those patients with silicon breast implant disease with MS-like syndrome would have normal neurological examination one day and on another day the exam would be abnormal. This finding substantiated the patients' complaints of waxing and waning of symptoms and seemed to be related to the degree of physiological or psychological stress the patient experienced when being interviewed or tested.
The degree of abnormality of neurological exams would extend to the point of normal or abnormal Romberg and Tandem Gaits, reflex examinations and Babinski examinations in the same patient. Evoked potential test results varied from normal to abnormal on different days and the testing was performed by the same examiners.
In this same time frame, a series of new medications were developed to treat migraine headaches. As headache was a major complaint of many of my patients, we tried these medications out including Imitrex (Sumatriptan), IM Toradol (Ketoralac) and other medications under direct monitoring. As my patients tend to be intractable, it was not expected that any of these medications would have dramatic results. Rather, it was expected that one or another set of medications might help point the way into using specific classes of medications or approaches. Accordingly, each of these patients, equivalent of a large number of patients, were monitored continuously across the day. The patients would come in and be hooked up with EEG's or Brain Stem Auditory Evoked Responses, or VEP's, or Transcranial Dopplers, and across the day would have many of the different short-acting medications tried on them to see which would work and which monitoring tool would be most effective in identifying the improvement.
With respect to the different monitoring tools, some were more helpful than others. It was found that the EEG was not very sensitive. The Brain Stem Auditory Evoked Response and other evoked potential tests were very insensitive tools for monitoring, because of the length of time required to perform the test after short-acting medications were given in IM or sublingual or nasal spray administration route. The Transcranial Doppler consistently appeared to give the best indication as to which medications would work. If an ultrasound showed improvement, the patient invariably also reported improvement in their clinical symptoms. These symptoms included not only headache, but also sensations of confusion, balance disorder, abnormal Romberg or Tandem Gait or other neurological abnormalities. If the medications showed evidence of increasing vasoconstriction on the doppler, the patients who had a headache, frequently reported improvement in the headache, but a worsening of their confusional state or a worsening of other neurological symptoms. Those patients were identified as having improvement on ultrasound with doppler also showed resolution of their headache, but did not show the deterioration in other neurological effects.
This was completely unexpected. The general approach towards migraine and headache has always been that the headache represents a vasodilation and frequently a hyperperfusion state. The aura, of course, represents a vasoconstrictive phase. What our results seemed to suggest was that the doppler, which looks at essentially the area of blood vessels around the base of the brain, was showing vasoconstriction. Vasoconstrictive medicines would relieve the headache presumably through a similar mechanism, as a vasoconstrictive medication probably relieved coronary artery disease. It would relieve it by decreasing the vasodilation that occurs downstream from the area we are able to directly insonate. Unfortunately, if cerebral artery disease is anything like coronary artery disease, that downstream dilation represents an attempt by the body to compensate and maintain perfusion to thus becoming ischemic.
In my patient population all medications which resulted in vasoconstriction, relieved the headache, but caused neurological deterioration. As the medication wore off, as documented by the patient's clinical symptoms, sonography data, the patient's neurological abnormalities improved. Similarly, those medicines which resulted in direct vasodilation such as Hydralazine (Apresoline), Nitroglycerin and other medications all resulted in improvement in the patient's headache, but also resulted in improvement of any other neurological abnormalities including balance disorders, gait disorders, hemiparesis, abnormal Babinski's and abnormal reflexes.
It was found that with aggressive treatment to result in radiological and clinical vasodilation of the vasculature, patients frequently became neurocognitively, psychologically, and symptomatically cured. However, if the medications, and monitoring was then stopped, whatever underlying disorder that caused the vasospasm in the first place, caused it to re-occur. When the patient's clinical ischemia first re-occurred, it generally was not with the same symptoms as they first presented. Rather, the symptoms were generally more mild and in the neurocognitive arena or mild physical disability. Thus, the first symptoms to re-occur tended to be mild confusional/distraction states, or disorders of mood. These disorders of mood, attention, and concentration could vary across the day as well as across longer periods of time. Thus patients frequently showed emotional lability or other disorders of attention, memory, and mood that were intermittent or chronic depending on the degree of the chronicity of the vasospasm and its severity or periodicity. Occasionally, mild ataxias, apraxias, or visual blurring would predominate in these early phases. If left untreated, the patient's symptoms usually slowly deteriorated over months into similar symptoms as they first presented.
OBSERVATIONS NOTED CONCERNING TRANSCRANIAL DOPPLERS
As alluded to earlier, we have found that Transcranial Dopplers are the most cost effective means of monitoring the vasospasm and guiding medical therapy. Due to their importance, a special word about Transcranial Doppler needs to be made.
We found that morphology of a Transcranial Doppler Artery Ultrasound is as important as mean flow velocities. In our patients, as they became more normal, and as their fixed deficits and neuropsycho-logical abnormalities resolved etc., the morphology of the wave form would be similar to that of an internal carotid artery tracing. We did not find that there would be elevation of flow readings throughout diastole, as is more commonly published. It is important to identify that the original normative data obtained in 1979, used for "Normals" patients with post-traumatic migraine disorders, "psychogenic seizures", and the interictal migraine phase may not be appropriate. It is important to note that other labs which have done less extensive studies of normal versus non-normal, may have unknowingly used many patients with a history of migraines or whiplash headaches. [Sandra: Dr. Hammesfahr has issues with the “normal” subjects recruited for studies.]
Some have not identified the close relationship between degree of vasospasm and clinical abnormalities. This may be due to less lengthy monitoring or evaluations being carried out by those labs in comparison to our own. Equally, the trend clinical correlation is a general one. Remembering hemodynamics, it is important to note that if the blood vessel is constricted, patients do have a limited ability to compensate for the effects of that vasoconstriction by dilating distally to the constricted area. Patients will not be abnormal clinically during the early stages of constriction of an artery. It is only once the downstream area is no longer able to dilate to a degree enough to maintain a significant pressure gradient across the vasoconstricted area that the patient will develop symptoms. It is important to continue to monitor and treat these patients until the sonographic studies return to normal and beyond. Realizing that blood vessels constrict across the day in response to sympathetic nervous system variability, internal steroid release, physiological and psychological stress, including the physiological stress of photic stimulation, driving etc., and thus to obtain an ultrasound at one moment, must be correlated with the patient's clinical symptoms and any complaints of variability across the day.
We also found that over time, chronic, untreated patient studies frequently falsely appear to normalize with a dropping of mean flow velocities. This occurs as the body develops compensating mechanisms to relieve the ischemia. Thus morphology becomes extremely important in identifying those who have ongoing vasoconstrictive disorder intracranially. The development of a pattern as time goes on is to have a blunted upstroke in the systolic portion of the ultrasound, but with an overall mean flow velocity of less than .6 meters per second. That blunting, which is also seen in disseminated vascular disease from any cause, is highly suspicious for severe vasospastic disorder. A computerized EEG or standard EEG consistent with brain dysfunction or ischemia, and/or neuropsych testing consistent with variability of cognitive injury (especially with fluctuating cognitive deficits across several hours or days of testing) with ischemia is often helpful as a corraborating study. These are patients who should not be treated initially with Nitroglycerin or other potent medications, but should first have other medications which are direct vasodilators instituted at low doses and slowly advanced as the patient is able to tolerate it. This institution with alternative vasodilators, tends to decrease the incidence of a potentially dangerous nitric oxide sensitivity reaction.
Specifics of Experience with Medications: [I deleted Dr. Hammesfahr’s extensive list of vasodilators he used to attempt to control what he thought were spasms in arteries causing hypertension and decreased blood flow to the brain. You can find the full list in the article here: http://www.autismtoday.com/articles/To-a%20new-understanding.asp. Most interestingly, his drug of choice is Nitroglycerin, which has the same action as Viagra to relax local blood vessels by producing nitric oxide. Sound familiar? See Joan's discussion of Viagra here: http://www.facebook.com/note.php?saved&¬e_id=10150191153207734&id=182832983940#!/notes/ccsvi-in-multiple-sclerosis/viagra-in-the-ms-news-again/10150191290612211]
CONCLUSION:
It is important to realize that for centuries we have been treating neurological diseases as though each symptom or symptom complex represented a different disease. Our office has found that many of these diseases represent the same disorder with different manifestations. The cause of the disorder and the treatment of that cause may vary widely. However, the treatment of the patient is the same.
We strongly advocate searching for any vascular component of any patient’s neurological disorder, and aggressive treatment of that vascular component. It has been our experience that until the vascular disorder is reversed, it is impossible to identify the portion of the patient's neurological problems that are left behind.
1. Ischemia: Loss of sufficient oxygenation to an organ, as may be seen with a loss of blood flow from that required for the health of an organ.
2. We have successfully treated a large number of different diseases with the use of medication that dilates blood vessels leading to the brain.
The results are dramatic and reproducible. Indeed, when these techniques are applied across the country, the practitioners will feel that they have defeated many of these disorders. As I have experience in over 2000 cases of reversing these vascular disorders, I have learned that vasospasm/vascular ischemia is probably not the cause of any of these diseases. Rather, it is the cause of the diseases' symptoms. In treating these patients, we frequently get dramatic improvements from using the vasodilators or other agents that increase blood flow to the tissue. However, if the medication is stopped, decreased inappropriately, or the underlying disorder goes through an exacerbation, symptoms of vascular ischemia will return. These symptoms are only rarely the same symptoms with which the patient presented. Generally, they are other symptoms somewhere on the continuum of neurological and psychological changes that accompany ischemia. Thus, those symptoms may range from increased distractability, to behavioral/mood/memory/language/spatial disturbances, to sensorimotor disturbances such as visual/balance/motor problems, on to headache, or, in the most severe cases, stroke, seizure, syncope.
What follows is a partial listing of diseases that have been successfully treated:
In the Psychiatric/Psychological arena:
Depression, Impulsive Rage Disturbances, Irritability, Emotional Lability, Psychosis, Autism, Attention Deficit Disorder and its variants, Memory Loss, Tourette's Syndrome, Transient Global Amnesia
In the Neurological/Physical arena:
Stroke, Grand Mal Epilepsy, Absence or Petit Mal Epilepsy, Psychomotor Epilepsy, Headache, Closed Head Injury, Post Concussion Syndrome, Vertigo, Ataxia, Tinnitis, Aphasia, Apraxias, Visual Loss, Visual Blurring, Blindness, Stuttering, Vasospasm after Sub-Arachnoid Hemmorhage, Vasospasm after Intracranial surgery not associated with trauma or Sub-Arachnoid Hemmorhage, disturbances of Word substitution and Word Finding, Dyslexia, Photophobia, Hyperaccusis, Tremor, Multiple Sclerosis, Multiple Sclerosis-Like Syndrome, Post Traumatic Stress Syndrome, Vertebrobasilar Insufficiency, Vertigo, Cerebral Palsey, Vertebrogenic Syndrome, Syncope, Multi-Infarct Dementia, "Alzheimer's" Syndrome, Whiplash Induced Headaches, Headaches in general, TMJ Headaches6 Steroid Induced Migraines, Steroid Induced Psychosis, Fibromyalgia, Prinz-Metal Angina, Neuro-cognitive changes associated with electrical and lightning injuries.
3. The neurocognitive and behavioral disorders run the gamut from severe to mild, Autism, to depression, to mild disturbances of communication, interpretation of others' communication, and distractability. Although the more severe disorders in this range are easy to identify and recognize, the less severe disturbances result in difficulty with interpersonal relationships, work productivity and output. A common link in the histories is that most patients will describe variability in their cognitive and emotional abilities. Further, that these changes are frequently associated with stress or pain. This is due to the stress causing increasing vascular constriction, ischemia, and altered mood, personality change, and memory. As the stress or pain response or any other irritant of the sympathetic nervous system decreases, the personality and mood disorders will lessen. As patients are not always the best historians at identifying these links, the physician needs to be aware and obtain histories from those about the patient. A classic finding in these patients is increased rates of divorce or job changes. In the follow-up of these patients, attention must be spent looking at these issues of interpersonal and business activity.
Disorders in these areas are frequently related to early ischemia, in my practice from incompletely treated Vasospasm or narrowing of the arteries of the brain. This can be easily confirmed from a repeat ultrasound, computerized EEG, or neuropsychological tests. A classic finding on neuropsychological testing is the cognitive variability identified on testing. Treatment for any remaining vasospasm rapidly improves these disorders.
Patients who are successful in completing treatment in my practice generally show great job and social stability.
[Sandra’s note Dr. Hammesfahr’s 1/3, 1/3, 1/3 categorization of multiple sclerosis and patient responses to therapies. Sound familiar? You betcha!]
4. 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.
My experience with these results and clinical cases will be further discussed in future publications. [Sandra: I cannot find any future publications? Can you?]
Copyright Medforum 1997 [From Sandra: the medforum.com website is now registered by a reporter and appears to be inactive.]
- http://www.swankmsdiet.org/About%20Dr%20Swank
- http://www.flickr.com/photos/ccsvitoronto/5026928830/
- http://en.wikipedia.org/wiki/William_Hammesfahr
- http://www.lifenews.com/2005/06/20/bio-1041/
