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07-SEPTEMBER-2008 03:17:44 - polio syndrome Post-polio syndrome Classification and external resources ICD-10 B91. ICD-9 138 eMedicine pmr/110 MeSH D016262 Post-polio syndrome PPS is a condition that affects survivors of poliomyelitis, a viral infection of the nervous system, after recovery from an initial paralytic attack of the virus. Typically the symptoms appear 20-40 years after the original infection, at an age of 35 to 60. Symptoms include new or increased muscular weakness, pain in the muscles, and fatigue.1 The precise mechanism that causes post-polio syndrome is unknown. It shares many features in common with myalgic encephalomyelitis, a form of chronic fatigue syndrome that is apparently caused by viral infections, but unlike those disorders it tends to be progressive, and can cause tangible loss of muscle strength. 2 Treatment is primarily limited to adequate rest, conservation of available energy, and to supportive measures, such as leg braces and energy-saving devices such as powered wheelchairs, plus pain relievers, sleep aids, etc. Contents 1 Diagnosis 1.1 Symptoms 1.2 Causes 1.2.1 Neural fatigue 1.2.2 Mitochondrial disruption 1.2.3 Reticular activating system damage 1.2.4 Mechanical overwork 1.2.5 Reactivated polio 1.2.6 Relationship with ME/CFS 1.3 Treatment 1.4 See also 1.5 References 1.5.1 Further reading 1.6 External links Diagnosis Diagnosis of post-polio syndrome can be difficult, since the symptoms are hard to separate from the original symptoms of polio and from the normal infirmities of aging. There is no laboratory test for post-polio syndrome, nor is there any other specific diagnostic, and diagnosis is usually a diagnosis of exclusion whereby other possible causes of the symptoms are eliminated.3 PPS may be difficult to diagnose in some because it is hard to determine what component of a neuromuscular deficit is old and what is new: neurological examination aided by other laboratory studies can help to exclude all other possible diagnoses. Objective assessment of muscle strength in PPS patients may not be easy. Changes in muscle strength are determined in specific muscle groups using various muscle scales which quantify strength, such as the Medical Research Council MRC scale. Magnetic resonance imaging MRI, neuroimaging, and electrophysiological studies, muscle biopsies, or spinal fluid analysis may also be used in establishing a PPS diagnosis.3 In general, PPS is not life-threatening. The only exception is in patients left with severe residual respiratory difficulties, who may experience new severe respiratory impairment. Studies have proven that, compared to control populations, PPS patients lack any elevation of antibodies against the poliovirus, and because no poliovirus is excreted in the feces, it is not considered a recurrence of the original polio. Further, there is no evidence that the poliovirus can cause a persistent infection in humans. PPS can be confused with Amyotrophic lateral sclerosis ALS, which progressively weakens muscles. PPS patients do not have an elevated risk of ALS. Symptoms Symptoms include new or increased muscular weakness, pain in the muscles, and fatigue.1 Fatigue is often the most disabling symptom, as often even slight exertion can produce disabling fatigue and also increase other symptoms.4 Some post-polio patients report having memory problems, or various other cognitive difficulties that are difficult to distinguish from normal aging. Some physicians have suspected that post-polio patients have an increased sensitivity to anesthetics, but rigorous work on the subject remains to be done. Weight gain is also a frequently noted symptom, though it is hard to tell if this is due to the disorder directly or due to the decreased level of physical activity that usually accompanies the disorder. Causes Several theories have been proposed to explain post-polio symptoms. One theory of the mechanism behind the disorder is that it is due to neural fatigue from overworked neurons. The original polio infection generally results in the death of a substantial fraction of the motor neurons controlling skeletal muscles, and the theory is that the remaining neurons are thus overworked and eventually wear out. Another theory holds that the original viral infection damages portions of the lower brain, possibly including the thalamus and hypothalamus. This somehow upsets the hormones that control muscle metabolism, and the result is a metabolic disorder similar to mitochondrial disorder that causes muscle pain and injury via rhabdomyolysis and also causes the fatigue. Some also believe that the original polio caused the atrophying of some muscles and as the person ages the weakness caused by loss of muscle mass due to aging is accelerated due to the person starting off with less muscle. Another possibility is that post-polio symptoms are due to some combination of mechanisms. Neural fatigue The most widely accepted theory is the neural fatigue one. Motor neuron fibers were originally damaged by the polio virus and were subsequently over-stressed because too few surviving neurons activated too many muscles. Eventually these neurons become fatigued and die, leading to the slowly advancing loss of muscle function that is typical of post-polio. This scenario may be accelerated by the fall-off in production of nerve growth factor NGF that occurs with menopause/andropause. Mitochondrial disruption This theory assumes that the major symptoms of PPS are a result of some interference with the action of mitochondria in the muscles and possibly the nerves. Failure of the mitochondria to produce sufficient energy would result in the muscle pain typical of PPS, and would, over time, cause muscle death rhabdomyolysis due to exerting the muscle beyond its ability to recover. The cause of this interference with mitochondrial action is presumably a change in the body's hormone balance, as mediated by the hypothalamus and other lower brain areas that control hormones and which were, presumably, damaged by the original polio virus infection. As with the neural fatigue theory, menopause/andropause accelerates the process, though this time by most likely disrupting the NOTCH pathway that controls cell differentiation and damage repair. One significant argument in favor of the mitochondrial disruption theory is that it explains the fatigue and cognitive difficulties brain fog symptoms that usually accompany post-polio better than the neural fatigue theory does. Reticular activating system damage Damage to the reticular activating system and related areas such as the thalamus can also produce most of the fatigue, brain fog, and dysautonomia symptoms of post-polio, and may be able to cause hormonal changes that result in progressive muscle weakness. Post-mortem examinations of polio patients have shown damage to these areas, and some PPS patients show lesions in these areas when examined by MRI. Many authorities believe that these areas are damaged by the initial polio infection, either as a direct result of the polio virus, or due to an autoimmune reaction following the polio infection. One problem with this theory, though, is that it doesn't easily explain the delayed onset of PPS. It may be that this theory needs to be combined with one of the others to explain delayed onset. Mechanical overwork The stresses placed on nerves, muscles, and joints in a polio survivor are in many cases several times those experienced by other people. Problems with gait, in particular, can greatly over-stress joints and the surviving muscles, and the polio survivor is also likely to compensate for weakened arms by jerking more when lifting/pulling something. Over time and again with menopause/andropause, this results in fatigue and damage. Reactivated polio An early theory stated that PPS is caused by reactivation of latent polio virus in the body, similar to the way that shingles is a reactivation of the chicken pox virus. This theory has been discred by laboratory studies that show no active polio virus in the body. Relationship with ME/CFS Partly due to association with past epidemics there has long been hypotheses linking ME/CFS with polio. From the very first well documented epidemic in 1934 labelled Atypical poliomyelitis the question has arisen concerning the relationship between an infection and immnunization. Many ME patients prior to 1956 suffered a paralytic association along with typical ME/CFS symptoms, however post 1956 ME/CFS patients have been spared paralysis, and it was hypothesised that polio immunization altered the symptoms common in earlier epidemics. Despite polio having been first described in 1881 there was no mention of PPS or even named until about 1979, the same time ME/CFS catapulted into public attention, and the rise in numbers of PPS closely parallels the rise in ME/CFS. It has also been noted that patients who had previously fallen ill with Akureyri disease a synonym for ME/CFS in 1948, and the general population of that particular area, of Iceland failed to succumb to the polio epidemic that swept that country at the time. Which raised the questions; are many ME/CFS patients simply PPS patients who had contracted a subclinical case of polio years earlier or is ME/CFS in subgroups, a poliomyelitis variant? 5 6 7 Treatment Treatment for post-polio is primarily palliative, as very few reliable therapies to reverse symptoms are known. Very often fatigue is the most disabling symptom of PPS, and many of those with the disease have discovered that by carefully managing energy expenditure they can prevent or reduce the worst fatigue episodes. Further, for many this energy management approach appears to reduce pain. Though most authorities agree that rest is an important component of post-polio treatment, there is significant disagreement as to how much rest is necessary. Some hold that the best approach is to expend the absolute minimum amount of energy necessary to enjoy a reasonable lifestyle, while others feel that there is some threshold below which energy conservation is not helpful and may in fact be harmful due to the general effects caused by lack of exercise. Leg braces and other orthotics can reduce the stress on joints and, in some cases, muscles, and so may slow the progression of joint and muscle damage related to PPS. However, some authorities feel that many PPS patients rely on such items too much and for too long when they should be graduating to a wheelchair. Wheelchairs particularly powered wheelchairs and scooters small battery-powered vehicles are useful both to conserve energy and to reduce the stress on weakened joints and muscles. Non-powered wheelchairs, however, are not generally recommended since they place too much stress on arm muscles and joints and may take too much energy to operate. In some cases even the scooters are not recommended since operating the tiller of the typical scooter can be tiring to arm muscles. A standing frame can be used in conjunction with the wheelchair to provide alternative positioning and prevent secondary complications. Post-polio syndrome often causes significant levels of pain, sometimes in specific muscles or joints, and sometimes body-wide. Various forms of narcotic and non-narcotic pain-relievers, muscle relaxants, tranquilizers, and sleep medications may help to deal with the pain and related sleep problems. In some cases surgery can be used to repair joint deformities, or to fuse joints as in the back or ankle that have become too weak. Very few non-palliative treatments for post-polio syndrome have shown any promise, and none have been subjected to any sort of rigorous clinical testing. There are, however, a few treatments that have developed some following in the PPS community: Bio-Electric Stimulation Therapy BEST, also known as micro current electro therapy MET, has been proven to relieve pain and fatigue symptoms in early clinical trials. BEST is a very specific form of electro therapy that delivers extremely small amounts of current to the body less than one milliAmpere, 100 times less than a typical TENS machine. BEST mimics what happens within human cells by working to enhance the physiological processes. The amino acid, L-carnitine has several functions in the body, one of the most important being the transport of fatty acids into the mitochondria. Researchers in Australia have had some success using doses of several grams per day. Coenzyme Q10is a general antioxidant, but it also plays a critical role in the function of the mitochondria, transporting electrons between the complexes that participate in the energy conversion cycle. A shortage of CoQ10 can cause the fatigue and muscle pain much like that experienced with PPS. Some PPS patients have reported significant improvements in their symptoms when taking several hundred milligrams of CoQ10 per day. The pentose sugar D-ribose is the R in RNA and a critical component of DNA, RNA, and enzymes. It is also a component of ATP, the energy-transporting molecule produced by the mitochondria. A shortage of D-ribose can produce fatigue and muscle pain. Some PPS patients have reported significant improvement in pain and fatigue symptoms when taking on the order of 20 grams/day of D-ribose. See also Post-Polio Health International List of polio survivors References ^ a b Trojan D, Cashman N 2005. Post-poliomyelitis syndrome. Muscle Nerve 31 1: 6-19. doi:10.1002/mus.20259. PMID 15599928. ^ Bruno RL, Creange SJ, Frick NM September 1998. Parallels between post-polio fatigue and chronic fatigue syndrome: a common pathophysiology?. Am. J. Med. 105 3A: 66S-73S. doi:10.1016/S0002-93439800161-2. PMID 9790485. ^ a b Silver JK, Gawne AC 2003. Postpolio Syndrome. Philadelphia: Hanley Belfus. ISBN 1560536063. ^ Jubelt B, Agre JC 2000. Characteristics and management of postpolio syndrome. JAMA 284 4: 412-4. doi:10.1001/jama.284.4.412. PMID 10904484. ^ Nightingale Research Foundation; Goldstein, Jay E.; Byron M. Hyde 1992. The Clinical and scientific basis of myalgic encephalomyelitis/chronic fatigue syndrome. Ogdensburg, N.Y: Nightingale Research Foundation, xi-xii,3. ISBN 0-9695662-0-4. ^ Roberto Patarca-Montero 2004. Medical Etiology, Assessment, and Treatment of Chronic Fatigue and Malaise. Haworth Press, 6-7. ISBN 078902196X. ^ 1 AN OUTBREAK of encephalomyelitis in the Royal Free Hospital Group, London, in 1955 1957. Br Med J 2 5050: 895-904. PMID 13472002. Further reading Bruno, Richard L. 2002. The Polio Paradox. New York: Warner Books. ISBN 0446529079. Maynard, F.M., Headley, J.H. Eds. 1999. Handbook on the Late Effects of Poliomyelitis for Physicians and Survivors. Saint Louis, MO: GINI now Post-Polio Health International. Information on 90 post-polio topics; a compilation of the research and experience of over 40 experts. March of Dimes Birth Defects Foundation. 1999. Identifying Best Practices in Diagnosis Care. Warm Springs, GA: March of Dimes International Conference on Post-Polio Syndrome Nollet F. Perceived health and physical functioning in postpoliomyelitis syndrome. Vrije Universiteit Amsterdam, 2002. Nollet, F. Post-polio syndrome. Orphanet Ecyclopaedia, 2003 Silver, Julie K. 2001. Post-Polio Syndrome: A Guide for Polio Survivors and Their Families. New Haven: Yale University Press. Dr. Silver is Medical Director, Spaulding-Framingham Outpatient Center; Assistant Professor, Department of Physical Medicine and Rehabilitation, Harvard Medical School. External links National Institute of Neurological Disorders and Stroke Post-Polio Health International Polio Canada v d e Infectious diseases - Virus diseases A80-B34, 042-079 CNS Encephalitis/ meningitis DNA virus: Progressive multifocal leukoencephalopathy RNA virus: Subacute sclerosing panencephalitis - Lymphocytic choriomeningitis - Tick-borne meningoencephalitis unknown: Encephalitis lethargica Eye DNA virus: Cytomegalovirus retinitis Other RNA virus: Rabies - Myelitis: Poliomyelitis Post-polio syndrome - Tropical spastic paraparesis Skin and mucous membrane lesions DNA virus, Herpesviridae: Herpes simplex - Chickenpox - Herpes zoster - KSHV DNA virus, other: Poxviridae Smallpox, Monkeypox, Cowpox, Vaccinia, Molluscum contagiosum - exanthem Roseola, Fifth disease - HPV Wart RNA virus: exanthem Measles, Rubella - picornavirus Hand, foot and mouth disease, Foot-and-mouth disease Digestive system Hepatitis DNA virus: B RNA virus: A - D - C - E - G Gastroenteritis DNA virus: Adenovirus RNA virus: Rotavirus - Norovirus - Astrovirus - Coronavirus Respiratory system RNA virus, IV: Acute viral nasopharyngitis - Severe acute respiratory syndrome RNA virus, V: Influenza/Avian influenza - Human parainfluenza viruses - RSV - hMPV Other/varied: Infectious mononucleosis - Viral pneumonia Sexually transmitted DNA virus: HPV Genital warts, Cervical cancer RNA virus, retrovirus: HIV AIDS, AIDS dementia complex - Adult T-cell leukemia Oncovirus DNA virus: Hepatitis B - HPV - Kaposi's sarcoma-associated herpesvirus RNA virus: Hepatitis C - HTLV Systemic DNA virus: Cytomegalovirus RNA virus: Mumps - Bornholm disease - Coxsackie B Retrieved from http://en..org/wiki/Post-polio_syndrome Categories: Poliomyelitis | Motor neuron disease Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Deutsch Nederlands 日本語 Suomi This page was last modified on 20 June 2008, at 18:25
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