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STROKE

Acute Stroke and Heart Attack due to Cardiac Embolism - BR

Swallowing Disorder related to Embolic Brain Stem Stroke - ZD

MME 16 years out from Embolic Stroke - CJ

Acute Stroke and Heart Attack due to Cardiac Embolism - BR

We didn't set out with our MME program to treat acute stroke, but when a favorite patient presents with a stroke and a heart attack on the same day, we move into high gear, and high gear in our practice now includes MME. We treat all our patients as equals, but BR may be a little more equal than most. First, there is a family connection. Second, and most important, BR brings cookies to each office visit (This is a secret, passed down from generation to generation in medical families - if you want really good care, bring food. Even better, bring a large plate for the staff, and a second, smaller plate, labeled "for the doctor". Otherwise the staff will eat all the good stuff and the doctor will never know what a good cook you are).

BR awoke one morning with the vertigo complex, a sensation that the world was spinning wildly about her, along with intense nausea and a loss of balance. Benign vertigo is not an uncommon malady, and typically reflects a transient viral infection of the inner ear. I might see three patients in a month with vertigo, which resolves in 3-4 days, and then I won't see another for 6 months, until another wave of viral vertigo presents itself. But BR wasn't experiencing benign viral vertigo; her symptom complex was more consistent with stroke, and this was confirmed by MRI. BR wasn't troubled by chest pain, but she felt terrible overall, and her EKG was diagnostic of acute heart attack involving the front wall of her heart.

What was going on? How could an 84 year old non-hypertensive, non-diabetic women with an LDL of 100 and an HDL of 70, and no past history of coronary or cerebrovascular disease, experience a stroke and a heart attack on the same day? BR had been under my care for 15 years. A screening stress echo study in 1997 had returned normal, and I had never heard a bruit (shrill noise consistent with a blocked artery) over her carotid arteries on physical exam. She had been troubled by atrial fibrillation, where the pacemaker cells of the heart fail and the atria, the blood storage chambers that prime the pumping chambers, the ventricles, loose their intrinsic rhythm and begin to beat like a sack of worms. Overall cardiac function can fall off by 20% when atrial fibrillation develops, but BR's heart was otherwise normal, and even in atrial fib she could carry out all desired activities without difficulty. The real danger of atrial fibrillation in patients like BR is the danger of clot formation within the cardiac atria, where blood flow is stagnant. A clot in the atria causes little trouble, but if it breaks off and travels to the brain (causing what is termed an embolic stroke or stroke due to cardiac embolism), then it can ruin your life. The risk of embolism due to atrial fibrillation is low, maybe less than 2 % per year in young people, while in BR's age range, the risk is more like 6 % per year. Thus BR was put on coumadin anticoagulation a decade ago. We check her anticoagulation values every 2 to 3 months (all cookie opportunities), and she has done well.

BR was taken off Coumadin for five days in preparation for a minor surgical procedure. It is common practice to take patients with non-valvular atrial fibrillation off Coumadin for up to five days to allow normal clotting with a surgery, but for BR this proved to be a mistake. She had the surgery, Coumadin was resumed the next day, and the next morning, before the Coumadin anticoagulation effect had set back in, she experienced a stroke and a heart attack at the same time. A clot had formed in BR's atria, then had broken off in two or more pieces, one lodging in the Cerebellum, the area of the brain that controls coordination and balance, producing the vertigo, and the other(s) in the coronary arteries serving the heart. When the ER called me, I suspected cardiac embolism, but I couldn't know for sure that BR was not in the midst of a conventional, atherosclerotic or blocked vessel heart attack, one that might respond to stent placement. BR received a dose of heparin, a rapidly acting IV blood thinner, and urgent coronary angiography was carried out. BR felt awful, but looked good heart wise when I first saw her, and I was shocked to see that the muscle serving the front wall of her heart, essentially half of the heart muscle, wasn't working. A clot was seen, sub-totally occluding one the the arteries involved. The other artery serving this region was open, and I felt that it had also been affected but that it's clot had already dissolved. So what do you do in a situation like this?

We couldn't be totally sure, right at the time, that BR was not bleeding into her brain, and it appeared from her coronary study that the clots were dissolving on their own, so we did not give her a blood clot dissolving agent. We did treat BR with an infusion of Heparin, to prevent the formation of new clots, and a program of agents known to improve post-heart attack outcome, including Carnitine, Co-Enzyme Q, Antioxidants, and Coreg (a b-Blocker, anti-adrenaline pharmacologic agent). BR cruised through her heart attack as is nothing had happened (which can happen when you combine the best of pharmacologic and nutritional medicine). It was a different matter regarding the stroke. BR's vertigo didn't just persist, it worsened. She could barely keep food down. She couldn't walk across the room. She couldn't sit in a chair the dizziness was so bad. The neurologist who saw her advised only patience, rehab, and physical therapy, as no specific therapy existed to hasten recovery of the brain cells involved. Actually, no specific therapy existed to allow recovery of the brain cells at all. But he didn't know about MME - we did.

I consulted with Dr. Bonlie, and began BR on MME on her 6th post-stroke day. At this early point, she hadn't had a chance to heal on her own to a new steady state, but at that point we couldn't be sure that she would heal at all, and her symptoms were debilitating. Rather than discharging BR from the hospital to a rehab facility for physical therapy, we discharged BR home, and began her on 12 hours-per-session night-time MME. Two of BR's daughters and her grand-daughter are nurses; they helped BR at home and this arrangement worked well. BR received 200 hours of MME, and during this time she improved, but not fully; the vertigo did not fully resolve and she still required assistance with walking. After 200 hours of MME, BR entered a rehab facility, and received 10 days of intensive physical therapy. Coumadin anticoagulation was continued, and BR's medical and nutritional regimen was adjusted as required. BR's cardiac echo was repeated, and looked a lot better (While we treated BR's brain with MME, there is some scatter of the magnetic field to the region of the heart, and I think that the clots had dissolved rapidly and spared some of the muscle at risk. The nutritional therapies had helped as well - in any event, BR was left with a nearly normal heart). Now three months out from a combined heart attack and stroke, BR is back at home, living independently. Her balance is still not normal and vertigo has not fully resolved, but both conditions have improved. She had the family in for Christmas, and BR helped with the cooking (there was no way she was going to let her kids do all the cooking). At her last Coumadin blood check BR brought in a plate of cookies, a sure sign that things are going well.

BR got better. As we treated her with MME well before a new neurological steady state could be achieved, we can't say that it was the MME that helped, or whether it was the physical therapy, or weather BR just needed more time. Probably it was the combination of the above. On day six post-stroke/heart attack, when she was still experiencing symptoms, we didn't know, and really couldn't know, just what BR's eventual outcome would be, whether she would get better on her own or not. We had MME, essentially a no-risk therapy that has helped patients late post-stroke regain function. It made sense to treat BR with MME so we did. I think we did help BR, and that it wasn't obvious early on as it takes the brain time to recover, and that MME added to BR's eventual positive outcome. I don't know for sure but BR is doing much better, and I'm now back in cookies - chocolate chip, oatmeal, and sometimes peanut butter.

Swallowing Disorder related to Embolic Brain Stem Stroke - ZD

ZD couldn't swallow properly. Food would "go down the wrong pipe", leading to repetitive aspiration pneumonia. A percutaneous gastric feeding tube was placed, resolving the problem of recurrent pneumonia, but depriving ZD the enjoyment of normal eating. This now 88 year-old man had undergone mitral valve replacement 6 years earlier; a metallic valve was utilized, mandating life-long Coumadin anticoagulation. When out of town (and presumably on a different diet), ZD's level of blood thinning fell. A clot formed on his prosthetic valve, broke off, and lodged in the blood vessel serving the swallowing centers in ZD's midbrain. ZD's thinking and speech were intact, but coordinated swallowing was lost.

ZD had learned of MME in a health newsletter, and was already sleeping on a magnetic sleep pad. Previously he had received 25 IV EDTA (binds Lead and Cadmium) treatments, and his amalgam fillings had been removed. ZD had undergone three hyperbaric oxygen treatments, but none of this had solved his problem. We treated ZD with 250 hours of MME over a 6 week period; he received 500 mg of oral DMSA with each session. We also did not solve his problem. Vision in his right eye (related to a local vascular problem) improved a little, but swallowing function, ZD's primary problem, did not. This was a total treatment failure.

We feel good about our victories, but we learn from our failures. So what factors prevented us from helping ZD with 250 hours of MME? What can we learn from our experience with ZD?

1. Treatment duration - The brain stem is fairly distant from the Hippocampus, and perhaps 250 hours of MME is not enough to stimulate the Hippocampal stem cells to proliferate and then migrate all the way to the brain stem. Dr. Bonlie treats stroke patients for 12 hours a day. We treated ZD in 8 hour blocks, but towards the end of his MME regimen, ZD was receiving only 4-6 hours per session. Our problem was keeping ZD under the magnet long enough, while at the same time ensuring adequate nutrition. ZD typically took his tube feedings every four hours; then he would need to remain upright for several hours to prevent regurgitation of his liquid meal back through his esophagus and into his airway. This was a logistical problem as we needed ZD flat on his back during MME. We did our best here, but in retrospect, I don't feel that ZD got enough MME, and not enough MME per session. From now on we will push our stroke patients to receive MME on a 12 hour per day schedule.

2. Aging stem cells - The kids with cerebral palsy (CP) respond better to MME than do adults with prior stroke. The stem cells, and the residual brain cells in general, are otherwise pristine in the child with CP are otherwise pristine. Old stem cells don't proliferate as readily as do infant stem cells, and the cells of an 88 year old have soaked up a lifetime of toxins and wear-and-tear free radical stress. It thus makes sense that treating stroke in adults is going to be more challenging than treating CP in kids.

3. Cellular toxicity - ZD was not pre-treated with a metal chelator. Given his prior IV chelation therapy (and aiming to minimize costs) I had assumed that heavy metals had been cleared from his system. This was an error on my part. Given ZD's poor response to MME, a DMPS/DMSA challenge study was carried out, and returned with a spill of several metals, most noticeably Tungsten. I had never seen a Tungsten spill of this quantity. ZD had worked machining metal, and this is likely the cause of his exposure. Our plan will be for ZD to take oral DMSA in cyclic fashion, while sleeping on a negative field only sleep pad, and in the future we may repeat his challenge study, and after the metals have cleared, try again with MME.

MME 16 years out from Embolic Stroke

At age 26, CJ presented to the hospital with incomplete visual loss in both eyes. CT scan revealed a stroke in the occipital lobe, the region in the back of the brain that mediates vision. The vertebral arteries serving the back of CJ's brain were intact, as were the carotid arteries serving the front. CJ's echo demonstrated Mitral Valve Prolapse, a common condition, one only rarely associated with stroke. A blood workup for abnormal clotting factors returned negative. It was our impression that CJ had sustained an embolic stroke; that is that a blood clot had formed on CJ's mitral valve, from there breaking off and lodging in his brain. The neurologist involved in CJ's care recommended aspirin therapy to prevent the formation of further clots. CJ was sent home on aspirin, and returned several weeks later with a 2nd stroke. Further damage had occurred in the occipital lobe, and CJ's vision was further impaired. Aspirin clearly wasn't getting the job done; we switched from aspirin to coumadin anticoagulation, and on coumadin no further strokes have occurred. CJ's vision improved to the point that he could return to work, but its anything but normal. Over the years we detected elevations in CJ's homocysteine and cholesterol levels; both responded well to treatment. CJ's BP has never been elevated, nor has there been any change in the appearance of his mitral valve. CJ had a mouthful of Mercury amalgam fillings, but back then I had no idea that this might pose a problem to him.

CJ received 211 hours of MME over 18 evenings. DMSA (metal binder) was initiated several weeks prior to CJ's start date, but several days later CJ broke our with a generalized rash. The DMSA was stopped, and the rash slowly faded. We couldn't tell whether this was an allergic reaction to the DMSA, or instead related to Mercury detoxification through the skin. CJ had scheduled two weeks off from work to allow him to undergo MME; this could not be rescheduled so we treated him without concomitant metal binding therapy.

CJ didn't get any better. A formal visual fields analysis suggested a slight improvement, but this was within the range of measurement error for the technique. Functionally CJ couldn't see any better. As with ZD, abstracted above, we need to ask ourselves - What went wrong? What didn't we do right?

1. Treatment duration - In contrast to ZD, CK received 12 hours of MME per session, so insufficient treatment duration was not the problem. The distance from the Hippocampus to the occipital lobe is considerable, so perhaps 211 hours was not enough time, but still we would expect some return of vision by 211 hours. Treatment time likely wasn't the culprit.

2. Brain prioritization - This is a hypothesis, an idea that we can't back up with science, but perhaps CJ's brain directed the stem cells to repair a region that it felt to be more vital than CJ's vision. Mother Nature is far smarter than we are, and often does bright things that we don't understand. Maybe we helped CJ in ways that we cannot measure, or maybe not.

3. Cellular toxicity - This is more likely the problem. As I gain experience with MME, I am gaining the impression that one's response to MME is likely conditioned by the physiologic health of the still viable cells, and the stem cells, in the region under treatment. We are fairly certain that alcohol intake during MME compromises one's response, so it makes sense that other toxins, such as certain prescription drugs and heavy metals, may do the same. CJ doesn't consume alcohol, but he has a mouthful of amalgam fillings, and this means that his brain cells contain Mercury (well documented in the scientific literature). One of the benefits of MME, we feel, is clearance of heavy metals from the organ or body region under treatment, but without concomitant medical metal binding therapy, we probably didn't get the job done for CJ. Maybe the stem cells can't proliferate and migrate until the metals are cleared. Maybe a metal overloaded environment is toxic to the new cells. We don't know the answers to all of these questions, but we do know that we didn't solve CJ's problem.

We are not interested in not solving problems. We are in the process of slowly dealing with the Mercury issue in CJ, and later on he will undergo a 2nd round of MME. Recall that CJ broke out with a rash while on DMSA. DMPS, a Mercury binding agent previously available only in IV form, is now available as a topical preparation, complexed with Glutathione. CJ recently began a program of DMPS based Mercury detoxification. While the standard dose of topical DMPS is 50 drops every other day, we began CJ on one drop every other day. The dose will be slowly advanced, drop by drop. When a certain phenomena, the rash in CJ's case, is due to a detoxification reaction in a markedly metal overloaded individual, "plan B" involves the use of a chemically dissimilar agent, beginning with a low dose, then increasing the dose slowly as tolerated. After we "sneak out" a little of the metal, the detoxification process seems to proceed along a smoother course. This is our tentative plan with CJ. His DMPS dose will be advanced, his amalgams will be removed, and later we will try again with MME.

AMRI of NW Ohio provides MME treatment under the guidelines of an Investigational Review Board, consistent with FDA regulations.

Please note that MME treatment is considered to be experimental by the FDA. Although many patients have improved, no guarantee of success is implied.