 Today, one of every seven Americans will experience movement disorders. Movement disorders encompass a number of debilitating conditions including Parkinson’s Disease, dystonia, torticollis, hemifacial spasm, tremors, and many other involuntary movements or muscle spasm from conditions like MS, stroke and cerebral palsy. Often symptoms do not manifest until later in life, and are growing in occurrence. The most common treatments pursued by doctors typically depend on oral medications. While sometimes successful in reducing motor symptoms, the effects of medications vary from person to person. Some drugs may be ineffective on certain individuals, and many trigger serious or disabling side effects. Experimenting with medications and treating corollary ailments can result in medical bills that add up into the thousands each month. Furthermore, in advanced cases, and even some mild cases, side effects resulting from medications may be more severe than the symptoms being treated. NSC offers innovative medications, nerve blocks and effective surgical options for better muscular control and improved quality of life. These advanced interventions offer patients a significant reduction in oral medications, relief from behavioral and cognitive side effects, and more effective motion control, which is essential for the successful treatment of movement disorders. As the first sub-specialty movement disorder clinic of its kind in central Texas, NSC also provides general neurologists and primary care physicians access to the latest services and treatments available today.
Excerpt from NINDS (National Institute of Neurological Disorders and Stroke) NIH Deep brain stimulation (DBS) is a surgical procedure used to treat a variety of disabling neurological symptoms—most commonly the debilitating symptoms of Parkinson’s disease (PD), such as tremor, rigidity, stiffness, slowed movement, and walking problems. The procedure is also used to treat essential tremor, a common neurological movement disorder. At present, the procedure is used only for patients whose symptoms cannot be adequately controlled with medications. DBS uses a surgically implanted, battery-operated medical device called a neurostimulator—similar to a heart pacemaker and approximately the size of a stopwatch—to deliver electrical stimulation to targeted areas in the brain that control movement, blocking the abnormal nerve signals that cause tremor and PD symptoms. Before the procedure, a neurosurgeon uses magnetic resonance imaging (MRI) or computed tomography (CT) scanning to identify and locate the exact target within the brain where electrical nerve signals generate the PD symptoms. Some surgeons may use microelectrode recording—which involves a small wire that monitors the activity of nerve cells in the target area—to more specifically identify the precise brain target that will be stimulated. Generally, these targets are the thalamus, subthalamic nucleus, and globus pallidus. The DBS system consists of three components: the lead, the extension, and the neurostimulator. The lead (also called an electrode)—a thin, insulated wire—is inserted through a small opening in the skull and implanted in the brain. The tip of the electrode is positioned within the targeted brain area. The extension is an insulated wire that is passed under the skin of the head, neck, and shoulder, connectng the lead to the neurostimulator. The neurostimulator (the "battery pack") is the third component and is usually implanted under the skin near the collarbone. In some cases it may be implanted lower in the chest or under the skin over the abdomen. Once the system is in place, electrical impulses are sent from the neurostimulator up along the extension wire and the lead and into the brain. These impulses interfere with and block the electrical signals that cause PD symptoms. Select this link to view a list of studies currently seeking patients. Prepared by: Baclofen acts by stimulating GABA type B receptors in the spinal cord and oral baclofen is often helpful in the treatment of spasticity. In order to avoid the side effects of high oral doses of baclofen, the medicine may be continuously administered into the space surrounding the spinal cord via a pump. The pump is implanted in the abdomen and connected to a small tube. This tube is tunneled under the skin around the back and then inserted into the space around the spinal cord (the intrathecal space). Very small doses are given. The pump is refilled approximately every three months by injection directly through the skin into the pump's reservoir. This technique is extremely effective for some children with spasticity or dystonia that affects the arms and legs. If it is not effective, the pump and tubing may be removed without significant permanent effects. This therapy is associated with complications including pump infections, catheter problems, and spinal fluid leakage around the catheter into the subcutaneous tissues. Baclofen withdrawal is another potential complication. In spite of the complications, the majority of patients and families who are treated with ITB feel that the benefits of treatment outweigh the risks. Recent reports suggest that the baclofen pump may also be helpful in generalized dystonia, although the mechanism of this effect is not known. Intrathecal Pump Story from University of Texas at Houston Medical School BOTOX® is indicated for the treatment of cervical dystonia in adults to decrease the severity of abnormal head position and neck pain associated with cervical dystonia. Cervical dystonia (CD), also known as spasmodic torticollis, belongs to a group of disorders known as focal dystonias. These disorders are characterized by involuntary tonic contractions or intermittent spasms of the neck muscles, causing rotational (torticollis), lateral (laterocollis), forward (anterocollis), or backward (retrocollis) tilting of the head.1 CD is often associated with a high incidence of pain. In fact, one study showed that more than 90% of patients with CD experience pain.2 CD occurs in 9 out of every 100,000 individuals.3 Approximately 5% to 16% of patients with CD have a history of head or neck trauma preceding the onset of dystonia.4 The true cause of CD, however, is unknown at this time. The defining feature in dystonias is sustained muscle contractions leading to repetitive twisting movements and abnormal postures. Although onset may occur at any age, it typically occurs in adults between the ages of 30 and 70. Women are nearly twice as likely to be affected with CD as men.2 Symptoms usually appear gradually though an acute onset is not uncommon. Patients usually present with painful, tonic contractions or intermittent spasms of the sternocleidomastoid, trapezius, or other neck muscles that are limited to one side of their body. These contractions force the head into abnormal positions. The pain associated with CD is usually rated as moderate to severe. In severe cases, the disorder may impair a patient's ability to move or may lead to postural deformity. Generalized and focal forms of dystonia usually stabilize within 5 years of onset; however, symptoms may fluctuate, particularly during times of stress. Generally, late-onset dystonia usually progresses to a certain point then plateaus.5 A small percentage of CD patients (approximately 10% to 20%) may experience remission within 5 years of onset. Approximately 33% of CD patients show evidence of dystonia elsewhere on the body, such as the eyelids, face, jaw, or hand. Active spasms (ie, involuntary movements) disappear during sleep.6 BOTOX® (Botulinum Toxin Type A) Purified Neurotoxin Complex blocks the nerve impulses that trigger muscle hyperactivity. Although the exact mechanism of action is not yet known, the neurotoxin is thought to bind to certain receptors on cholinergic terminals on nerve endings. The neurotoxin is then absorbed into the nerve ending, where it interferes with the cholinergic vesicles that release acetylcholine. This interference leads to chemodenervation and reduced muscular contractions.7 In 2000, the FDA approved BOTOX® for the treatment of CD in adults to decrease the severity of abnormal head position and neck pain associated with CD.7 Each BOTOX® treatment lasts up to three months. Patients eventually return to pretreatment status at which point they can be reinjected over time with the neurotoxin as long as they continue to respond and do not have a serious allergic reaction.7 Patients with neuromuscular disorders may be at increased risk of clinically significant systemic effects including severe dysphagia and respiratory compromise from typical doses of BOTOX®. The effects of therapy may be increased with the use of aminoglycoside antibiotics or with other drugs that interfere with neuromuscular transmission. There have been rare spontaneous reports of death, sometimes associated with dysphagia, pneumonia, and/or other significant debility or anaphylaxis, after treatment with botulinum toxin. Patients with smaller neck muscle mass and patients who require bilateral injections into the sternocleidomastoid muscle have been reported to be at greater risk for dysphagia. Limiting the dose injected into the sternocleidomastoid muscle may reduce the occurrence of dysphagia. Injections into the levator scapulae may be associated with an increased risk of upper respiratory infection and dysphagia.
Blepharospasm is a localized movement disorder (focal dystonia) that affects the muscles that control eyelid movement. The disorder is characterized by increased blinking caused by involuntary spasms of the muscles controlling the eyelid. Blepharospasm usually affects both eyelids and can progress to functional blindness (ie, an inability to open the eyelids for any significant period of time). Approximately 75% of patients with blepharospasm are female and the average age at onset is 56 years.1 Although the exact cause of this disorder is unknown, experts believe that it may be caused by a defect in the basal ganglia–a group of nerve cells in the central nervous system.2 BOTOX® injected directly in the affected eye muscles relieves the muscle spasm within 48 hours. The duration of effect lasts up to three months at which time the neurotoxin can be reinjected as long as the patient continues to respond and does not have a serious allergic reaction.3
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| ANTIINFLAMMATORY AND ANTIOXIDANT STRATAGIES Brain Defense Supplements by Rob Izor, MD, MS April 12, 2008 Supplements or “nutraceuticals” and other “alternative medicine” approaches have potential to significantly influence our health, sometimes for the better. However, some approaches may cause unintended side effects and even irreversible damage. The goal of this brief summary is to explain the basis for certain antioxidant and anti-inflammatory strategies for neurodegenerative disease, particularly Parkinson's Disease.Because “food supplements” do not undergo FDA testing for safety and efficacy, the benefits and risks of any given supplement or brand of supplement are much less certain than with regulated prescription medications. On the other hand, prescription medications may also have unintended dangers that do not surface until many have been injured, sometimes irreversibly. A good example is the prescription pain medication Vioxx, which increased risk for strokes and heart attacks. Prescription drug makers have legal requirements which motivate them to report severe side effects or complications to the FDA. This sometimes helps identify problems early so recalls can be implemented before more people are injured. Supplements do not have these reporting requirements, and therefore serious complications are not necessarily identified or reported. As with prescription medications, patients and doctors must weigh risks and benefits before proceeding with any treatment plan. Weighing risks can be more difficult with nutritional supplements and non-FDA approved uses of prescription medications. Research over the last several years indicates neuroinflammation and free radical oxidative stress play major roles in the propagation, if not underlying cause, of neurodegenerative diseases. There are multifactorial genetic, environmental, and age related processes which may promote loss of brain function. However, the presence of inflammation adds fuel to the fire. A genetic study implicates two inflammatory local hormones (cytokines); TNFa and IL-1b increase the risk for Parkinson's Disease1. Recent experiments in patients using a drug that blocks TNFa (etanercept) has shown remarkable improvement in cognitive function in advanced Alzheimer's disease (AD). AD is another neurodegenerative disease in which neuroinflammation plays a major role.2 Oxidizing free radical byproducts of metabolism have also been implicated, triggering production of potentially damaging inflammatory cytokines.3 Antioxidant and anti-inflammatory nutritional supplements may have a preventive role by modifying cytokines and associated signals which lead to programmed cell death (apoptosis). A few supplements in particular have been found to mitigate damage caused by oxidative stress and/or reduce the activity of TNFa and other inflammatory cytokine pathways. These supplements include B12, Folate, N-acetyl-L-cysteine, alpha lipoic acid, and DHA (omega-3) fatty acids. Dextromethorphan and the prescription drug naltrexone (non-FDA approved use) also have important anti-inflammatory and potentially neuroprotective properties which should be considered. B12/Folate/B6/Homocysteine Vitamins B12, B6 and folate are metabolic cofactors important for cellular metabolism and maintenance of all tissue cell types, but particularly important to nerve cells. B12 is found in animal products, meats, and fish. Folate is found in green vegetables. B6 is present in whole grain foods and animal products. B12 absorption from the intestine is a complicated process and tends to diminish with age. Several metabolic disturbances are known to deplete B12. B12 deficiency can damage the nervous system leading to neuropathy, myelopathy, and dementia. Furthermore, B12, B6, and folate work together to regulate homocysteine levels. Deficiencies in B12 or folate can raise homocysteine levels. Elevated homocysteine levels have been associated with a higher risk for vascular disease, dementia, and directly or indirectly increases in oxidative stress. The role in neurodegenerative disease is unclear, but elevated homocysteine has been associated with PD and may aggravate the neurodegenerative process.4 B12 deficiency is typically diagnosed by blood tests. However, one study in Alzheimer's patients demonstrated normal blood levels, when in fact cerebrospinal fluid levels were low compared to control subjects.5 Testing blood B12 levels is probably not a good indicator of the true B12 status in the central nervous system. B12 and folate supplementation has not been adequately studied in Parkinson's Disease; however, due to potentially shared mechanisms in neurodegeneration, active supplementation of B12, folate, and other antioxidants may be beneficial in promoting better neurological health. N-acetyl-L-cysteine (NAC) NAC is a precursor to glutathione, the body’s most important cellular antioxidant. NAC supplementation has been shown to increase cellular glutathione levels. NAC relieves oxidative stress, reduces the apoptotic effects of TNFa, and has many other documented benefits. Glutathione function diminishes with aging and is particularly reduced in neurodegenerative states. In Parkinson's research, NAC has been shown to reduce MPTP toxin induced TNFa and associated apoptosis in mice.6 Early studies in Alzheimer's disease indicate improvement in cognitive scores after 6 months treatment.7 Human studies in Parkinson's Disease are lacking at this time. Alpha Lipoic Acid (ALA) ALA is an essential cofactor in normal cellular metabolism and cellular energy production. ALA is also an antioxidant free radical scavenger and heavy metal chelator. ALA has the capability of regenerating the antioxidant function of glutathione, vitamin C, and vitamin E and can reverse symptoms caused by vitamin C and E deficiencies. The use of ALA as a supplement is under investigation, and has demonstrated improvements in peripheral neuropathy8, Alzheimer's disease9, and insulin resistant type II diabetes10. Several studies indicate ALA inhibits TNFa induced apoptosis which may support a neuroprotective effect11. ALA has not yet been studied in Parkinson's disease in humans; however, MPTP toxic animal models of PD have shown evidence of neuroprotection from MPTP12. There are two forms of ALA, called R and S enantiomers. The R version is considered the more active form. Most supplements are a 50/50 mixture of R/S. Opioid Antagonists (Dextromethorphan and low dose naltrexone (LDN)) Naltrexone is actually a prescription drug, but can be compounded into a lower dose form, LDN, which imparts significant indirect anti-inflammatory properties. Dextromethorphan may also have similar properties and is available over-the-counter as a cough suppressant. LDN shows promising results in early studies of MS and Crohn’s Disease, both characterized by abnormal inflammation. Effects on the endogenous opioid system (endorphins, enkephalins) inhibit many inflammatory mediators, including TNFa and IL-6. A few studies support a potential neuroprotective effect of LDN and dextromethorphan.13, 14, 15 The mechanism whereby LDN or dextromethorphan reduces inflammation is thought related to modulation of endorphin receptors and related immunomodulatory effects.16 Opiod receptors have also been implicated as important modulators of neurotrophic growth factors, GDNF and BDNF.17 Use of antioxidant supplements and/or low dose opioid antagonists may have important neuroprotective and anti-inflammatory effects which might benefit PD and other neurodegenerative and inflammatory conditions. All these supplements should be considered drugs and only used only under the supervision of a physician. More research is needed before any can be safely recommended as an effective treatment for any neurodegenerative disease. Until such research becomes available, I believe patients should be made aware of these potential benefits and proceed cautiously in choosing to take these drugs as an adjunct to standard medical treatments. So far, data does not support significant short term risks at dosing ranges used in human studies. However, long term daily usage may surprise us with unknown and unpredictable complications. Therefore risks, both known and unknown, must be weighed carefully with the potential benefits. Unfortunately, standard treatments for most neurodegenerative diseases like PD confer little if any neuroprotective benefit, which makes alternative strategies very attractive in spite of limited data supporting efficacy. .
(do not take any supplements without reviewing with your physician, and obtaining written instructions on dosages and side effects) THE BRAIN DEFENSE DIET by Rob Izor MD, MS January 1, 2007 Scientific literature outlines serious health risks caused by diets containing processed “trans” unsaturated fat, high saturated fat and high omega 6 fat. Replacing these bad fats with foods containing a better ratio of monounsaturated and natural “cis” unsaturated fats will significantly reduce risk for heart disease, stroke and many chronic diseases like Parkinson's and dementia. Until the general population demands healthy fast foods and restaurant ingredients, we will need to take individual responsibility for our health, and spend the time and resources necessary to insure a healthy diet. My goal with this brief summary is to give you my best current opinion regarding dietary recommendations after reviewing and compiling readily available literature on this subject. There are still controversies about best recommendations, complicated by many myths. But choosing an active, vital role in your dietary health is in your best interest. Eating processed food blindly is dangerous to your long term health and will likely accelerate disability from chronic disease. Food suppliers have been forced by the FDA to expand labeling of fat content, and to at least partly recognize the dangers of certain fats. “Trans” unsaturated fat, also called partially hydrogenated fat, intentionally created during commercial food processing for fat stabilization, has now been linked to heart disease, stroke and contributes to many other health risks. Some food companies are reducing or eliminating “trans” fats. However, labeling flexibility from the FDA allows many foods to be labeled as 0 grams “trans” fats per serving, but actually contain up to 0.5 grams per serving. This could still add up to significant exposure with multiple servings per day. There are other dangerous ingredients present in commercially processed and refined foods which should be avoided for the most part. Healthier, unrefined foods with good fats tend to cost more for ingredients and preparation, and are therefore less available in restaurants, if at all. Our fast food western diet is typically high in saturated fats and simple carbohydrates like starch and enriched wheat. Polyunsaturated omega 6 to omega 3 fat ratios are as high as 40:1 (heavily lopsided toward omega 6 with very little or no omega 3 fat.) Large amounts of saturated fats are physiologically destructive, and should be minimized. Replacing saturated fats with monounsaturated and polyunsaturated fats lowers LDL cholesterol, raises healthy HDL cholesterol, and is protective for your health. Higher omega 3 fat intake is protective, and too much omega 6 increases health risks. Ratios of these fat subtypes vary widely in different foods which makes choosing the right combination of food ingredients even more complex. A simplistic answer to avoid the dangers of certain fats might be to seek a “low fat” diet, even substituting natural foods with processed, low fat food substitutes and/or health shakes or bars. However, avoiding good fat (favorable omega 3:6 ratios, and monounsaturated omega 9 fats) is also unhealthy, and most food substitutes are too low in the good fats. In retrospect, low fat diets generally favor consumption of higher calorie, less filling, refined carbohydrates which also increase bad “LDL” cholesterol and triglycerides. Eventually, high LDL cholesterol, high triglycerides and high simple carbohydrates are associated with obesity, diabetes, hypertension and reduced circulation. These risk factors lead to vascular disease, heart attacks, strokes and dementia. Stroke and heart disease are the leading causes of death, and stroke is the leading cause of disability in the United States. These same dietary risks increase risk for vascular and Alzheimer's dementia, Parkinson's disease, and perhaps other neurodegenerative diseases which are also important causes of disability. EATING a balance of GOOD FATS, protein and complex carbohydrates (whole grain, unrefined foods,) while AVOIDING BAD FATS (saturated and high ratio omega 6 fats) and limiting REFINED CARBOHYDRATES, STARCHES AND SUGARS may be the best way to maintain better health. Reducing saturated fats and simple carbohydrates, starches and refined sugars may also be important in reducing overall inflammation and supporting better immune function. Eating or supplementing more omega 3 may help offset health risks caused by too much omega 6. Therefore whenever possible, try to avoid, reduce and/or replace foods rich in saturated fat and omega 6 fat, with foods richer in omega 3 and monounsaturated fats (omega 9.) Aim to achieve a ratio of 1:1 omega 6 to omega 3 over the day. A 4:1 ratio has been suggested as adequate for good health, but foods with more omega 3 and less omega 6 fats are probably even better. So on average, for every one (to four) gram(s) of omega 6 in your diet, you should strive to eat foods which include at least one gram of omega 3. Supplementing your diet with omega 3 rich flaxseed oil and/or EPA/DHA fish oil supplements may also be a helpful strategy. The following AHA guidelines are reasonable targets for total fat intake and cholesterol. As previously outlined, eating foods with up to 0.5 grams of trans fat (which are labeled 0 grams) could easily overwhelm these recommendations if several servings add up over the day. Therefore, carefully look at the ingredients and avoid foods with any partially hydrogenated fats. “The American Heart Association's Nutrition Committee strongly advises these fat guidelines for healthy Americans over age 2: Limit total fat intake to less than 25–35 percent of your total calories each day; Limit saturated fat intake to less than 7 percent of total daily calories; Limit trans fat intake to less than 1 percent of total daily calories; The remaining fat should come from sources of monounsaturated and polyunsaturated fats such as nuts, seeds, fish and vegetable oils; and Limit cholesterol intake to less than 300 mg per day, for most people. If you have coronary heart disease or your LDL cholesterol level is 100 mg/dL or greater, limit your cholesterol intake to less than 200 milligrams a day. For example, a sedentary female who is 31–50 years old needs about 2,000 calories each day. Therefore, she should consume less than 16 g saturated fat, less than 2 g trans fat, and between 50 and 70 grams of total fat each day (with most fats coming from sources of polyunsaturated and monounsaturated fats, such as fish, nuts, seeds and vegetable oils).” 9 Steps for a Brain Defense Diet: 1.Eat more fish, beans, vegetables, nuts, fruits, and juices. Avoid farmed fish. Avoid foods or juices with added refined sugar or corn syrup. Consider diluting fruit juices and vegetable juices with 50% purified water to reduce total calories. 2.Avoid red meats from sedentary farm animals (high saturated fats, high omega 6.) Choose organic, free range, grass or flaxseed fed meats which have better omega 3 ratios and less saturated fat. Low fat cuts of game meats like venison are good too. Trim all excess fat before cooking. 3.Eat whole grain breads, brown rice and whole grain pastas while avoiding simple carbohydrates, starches and refined sugars. Limit white potatoes, french fries, white breads, white tortillas, white rolls, enriched pastas, white rice, refined corn products, and anything that has enriched wheat, starch or dextrose as a main ingredient. 4.Avoid foods and oils high in saturated fat (more than 10% of total fat.) Avoid foods with hydrogenated or partially hydrogenated oil listed in the ingredients, even if label states 0 grams “trans” fat. Use organic macadamia nut oil or canola oil for cooking or frying. Canola is low in saturated and omega 6 fats, and high in omega 3. Olive oil is higher in omega 6 and low in omega 3. Do not overheat oils, especially olive oil. If you see smoke, its too late. Buy cold pressed oils in small quantities (extra virgin olive oil) and replace every few months. Flaxseed oil cannot be heated and must be refrigerated. These types of oils are more expensive to produce. Better oil is expensive, so consider using smaller amounts when cooking or frying to help offset the cost. 5.Add ground flaxseeds, 1-2 tbs to whole grain cereal or oatmeal for breakfast using fat free skim milk. If too bitter, use a ½ tbs of cold pressed flaxseed oil instead. 6.Avoid regular egg yolks. Instead choose free range, flaxseed fed chicken eggs. 7.Limit foods or spreads with large amounts of saturated and omega 6 fats; (corn, safflower, soybean or other vegetable oils.) 8.Avoid foods with MSG (monosodium glutamate) and other preservatives “taste enhancers” (glutamic acid, amino acid derivatives.) 9.Use EPA/DHA omega 3 nutritional supplements low in omega 6. |