what is muscular dystrophy and what are the symthoms?
111473
The most common form is Duchenne muscular dystrophy. This form is caused by mutations of the gene for the dystrophin protein. The dystrophin is the second largest gene in mammals.\n\nThe dystrophin gene is located on the X chromosome, thus making it a 'sex-linked' disorder. Accordingly, muscular dystrophies are much more common in males, as females have two copies of the X chromosome while males have only one.\n\nDuchenne muscular dystrophy is caused by an X-linked gene. This means that only boys are affected but that their mothers may be carriers. In almost half of all affected boys, the faulty gene has arisen by mutation in the boy himself and no other family member carries it. However, this may be difficult to prove and can be decided only after careful and expert assessment of the family.\n\nIn the remaining cases (somewhat over half of all cases), the mother carries the gene but is usually not herself affected by it. Such women are known as ‘carriers’. Each subsequent son of a carrier has a 50:50 chance of being affected and each daughter has a 50:50 chance of being a carrier herself. A small number of female carriers of the gene have a mild degree of muscle weakness themselves and are then known as ‘manifesting carriers’.\n\nOne of the most important things that needs to be done soon after the diagnosis of a boy with Duchenne muscular dystrophy is to seek genetic advice and appropriate tests for those family members who are at risk of being carriers.\n\nFemale carriers of muscular dystrophy who are considering having children should be aware that prenatal diagnosis is available. Tests can be carried out during pregnancy, to try to find out if the fetus (unborn child) is affected.\n\nA couple may want to consider whether or not to continue the pregnancy if the fetus is affected. Alternatively, they may wish to know if the fetus is affected so that they can carry on with the pregnancy armed with knowledge that will help them to prepare and plan for the future.\n\nDifferent types of prenatal tests can be carried out after about 10 weeks of pregnancy. Chorionic villus sampling (CVS) can be done at 10-12 weeks, and amniocentesis at about 14-16 weeks, while placental biopsy and fetal blood sampling can be done at about 18 weeks. \n\nAbout 100 boys with Duchenne muscular dystrophy are born in the UK each year. There are about 1,500 known boys with the disorder living in the UK at any one time. For the general population the risk of having an affected child is about one in every 3,500 male births.\n\nThe most frequent symptoms are muscle weakness (frequent falls, walking problems, drooping eyelid) and skeletal and muscle deformities. Neurologic examination often reveals loss of muscle tissue (wasting), muscle contracture, pseudohypertrophy, and weakness. Diagnosis is usually established by muscle biopsy, elevated serum creatine kinase levels and electromyography, which is consistent with myogenic involvement. Some types of muscular dystrophies may result with additional cardiac diseases, intellectual deterioration and infertility.
810376
Cardiomyopathy, which literally means "heart muscle disease", is the deterioration of the function of the myocardium (i.e., the actual heart muscle) for any reason. People with cardiomyopathy are often at risk of arrhythmia and/or sudden cardiac death.[1]\n\nCardiomyopathies can generally be categorized into two groups, based on World Health Organization guidelines: extrinsic cardiomyopathies and intrinsic cardiomyopathies.\n\nsee link for more details\n\nhttp://en.wikipedia.org/wiki/Cardiomyopathy
41298
It's cool;\n\nDystrophic calcification is the mineralization of soft tissue without a systemic mineral imbalance. This occurs as a reaction to tissue damage, including as a consequence of medical device implantation.
838196
I believe you mean Rhabdomyolysis,which is a rare disease in which serious muscle damage results in the release of muscle cell contents into the blood stream. In rare cases, it may result in fatal damage to kidneys and other organs. Some drugs have been withdrawn from the "market" because the "risks" were high.\n\nMuscle problems can occur with statins and other lipid lowering drugs is an accepted problem. While some people seem unable to take statins because of muscle soreness or weakness, the vast majority are unaffected. There is something of a biological progression, from muscle soreness, through more severe muscle problems, to increased levels of creatinine kinase enzymes, to rhabdomyolysis, and even death from rhabdomyolysis (in about 1 in 15 cases). \nMost of the spontaneous reports of rhabdomyolysis to the FDA were associated with cerivastatin, now withdrawnThe problem with spontaneous reporting is that while it may identify cases, there is always uncertainty about denominators, so rates of adverse events are imprecise. Randomised trials are poor at finding rare but serious adverse events, because the events do not occur in sufficient numbers. Only 12 cases of rhabdomyolysis were reported in 30 RCTs reviewed .
339895
If you have Myopathy because of an HIV infection, there is a website called \nhttp://www.aidsmeds.com/Fusetalk/messageview.cfm?catid=6&threadid=25017\nThey have a community forum.\n\nGood luck. Stay well.
92570
Until the 1980s, little was known about the cause of any kind of muscular dystrophy. In 1986, MDA-supported researchers identified the gene that, when flawed - a problem known as a mutation - causes DMD. In 1987, the protein associated with this gene was identified and named dystrophin.\nGenes contain codes, or recipes, for proteins, which are very important biological components in all forms of life. DMD occurs when a particular gene on the X chromosome fails to make the protein dystrophin. BMD results from different mutations in the same gene. People with BMD have some dystrophin, but it's not enough or it's poor in quality. Having some dystrophin protects the muscles of those with Becker from degenerating as badly or as quickly as those of people with Duchenne.
372719
go to wikipedia and look up minimata disease
722254
www.mda.org\nwww.mdausa.org\nwww.ninds.nih.gov\nwww.muscular-dystrophy\n\nWikipedia info \nGenetics\n\n\n\nDuchenne dystrophy is a type of dystrophinopathy which includes a spectrum of muscle disease caused by mutations in the DMD gene, which encodes the protein dystrophin. Becker's muscular dystrophy is a milder type of dystrophinopathy. Although it is caused by a defective gene, it often occurs in people from families without a known family history of the condition.\n\nDuchenne muscular dystrophy is inherited in an X-linked recessive pattern. Because of random X inactivation, some women carriers can actually be partially affected by this disease, despite its recessive nature. X inactivation leads to women being in a state of X0, not XX as is usually thought (see below). Women who carry the defective gene can pass an abnormal X on to their sons. Since boys have an X from their mother and a Y from father, there is no second X to make up for the defective gene from the carrier mother. The sons of carrier females each have a 50% chance of having the disease, and the daughters each have a 50% chance of being carriers. Daughters of men with Duchenne will always be carriers, since they will inherit an affected X chromosome from their father (note that the diagram only shows the results from an unnaffected father). Some females will also have very mild degrees of muscular dystrophy, and this is known as being a manifesting carrier.\n\nPrenatal testing, such as amniocentesis, for pregnancies at risk is possible if the DMD disease-causing mutation has been identified in a family member or if informative linked markers have been identified.\n\nIn 30% of the cases, the disease is a result of a spontaneous mutation.\n\nIn some female cases, DMD is caused by skewed x inactivation. In these cases, two copies of the x chromosome exist, but for reasons currently unknown, the flawed x chromosome manifests instead of the unflawed copy. In these cases, a mosaic form of DMD is seen, in which some muscle cells are completely normal while others exhibit classic DMD findings. The effects of a mosaic form of DMD on long-term outlook is not known.\n\n[edit]\nPatho-mechanism\nDuchenne muscular dystrophy is caused by a mutation of the dystrophin gene whose protein product is responsible for linking the actin filaments of muscle fibres to the extracellular matrix through a protein complex containing many subunits. As a result, the sarcolemma is damaged through shearing forces and muscle fibres undergo necrosis and are ultimately replaced with adipose and connective tissue.\n\n\n\n\n[edit]\nSymptoms\nMuscle weakness \nRapidly progressive \nFrequent falls \nDifficulty with motor skills (running, hopping, jumping) \nProgressive difficulty walking \nAbility to walk can be lost by age 11 \nFatigue \nIntellectual impairment (in approx. 30% of Duchenne's patients) \nSkeletal deformities \nChest and back (scoliosis) \nMuscle deformities \nContractures of heels, legs \nPseudohypertrophy of tongue and calf muscles \nMild mental retardation in some cases \nScoliosis in some cases \n\nSymptoms usually appear before age 6 and may appear as early as infancy. There is progressive muscle weakness of the legs and pelvis, which is associated with a loss of muscle mass (wasting). Muscle weakness also occurs in the arms, neck, and other areas, but not as severely or as early as in the lower half of the body. Calf muscles initially enlarge -- the enlarged muscle tissue is eventually replaced by fat and connective tissue (pseudohypertrophy). Muscle contractures occur in the legs, rendering the muscles unusable because the muscle fibers shorten and fibrosis occurs in connective tissue.\n\n[edit]\nSigns and tests\nThe pattern of symptom development resembles that of Duchenne's muscular dystrophy, but with a much slower rate of progression. Muscle wasting begins in the legs and pelvis, then progresses to the muscles of the shoulders and neck, followed by loss of arm
682091
Atrophy is the partial or complete wasting away of a part of the body. Causes of atrophy include poor nourishment, poor circulation, loss of hormonal support, loss of nerve supply to the target organ, disuse or lack of exercise or disease intrinsic to the tissue itself.
964460
I did not find it as a medicine. I found reference to it as a muscle disorder protei.
1068312
Parkinson's disease (also known as PD or Parkinson Disease) is a degenerative disorder of the central nervous system, that affects the control of muscles, and so may affect movement, speech and posture. Parkinson's disease belongs to a group of conditions called movement disorders. It is often characterized by muscle rigidity, tremor, a slowing of physical movement (bradykinesia), and in extreme cases, a loss of physical movement (akinesia). The primary symptoms are due to excessive muscle contraction, normally caused by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain.\n\nPD is both chronic, meaning it persists over a long period of time, and progressive, meaning its symptoms grow worse over time. It is not contagious. Although some PD cases appear to be hereditary, and a few can be traced to specific genetic mutations, most cases are sporadic — that is, the disease does not seem to run in families. Many researchers now believe that PD results from a combination of genetic susceptibility and exposure to one or more environmental factors that trigger the disease.\n\nPD is the most common form of parkinsonism, the name for a group of disorders with similar features and symptoms. PD is also called primary parkinsonism or idiopathic PD. The term idiopathic means a disorder for which no cause has yet been found. While most forms of parkinsonism are idiopathic, there are some cases where the cause is known or suspected or where the symptoms result from another disorder. For example, parkinsonism may result from changes in the brain's blood vessels.
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OMG!!!  Reasons for having one of the 40+ forms of MD has nothing to do with diet.  \n\nMuscular Dystrophies are caused from many different reasons as well as genetic problems but has nothing to do with what one eats.\n\nLearn the facts at MDA's website!
464570
down's syndrome is a disease that results from gaining an extra autosome through nondisjunction.  It effects autosome 21.
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myotonin protein kinase: gene product of myotonic dystrophy is localized in the sarcoplasmic reticulum of skeletal muscle. Also, may be located at the intercalated discs and have a different isoform in cardiac tissue.\n\nIt is quite important to know the exact localization and function of myotonin protein kinase (MtPK), identified as the gene product of myotonic dystrophy, the most prevalent disease with multisystem disorders among muscular dystrophies. To investigate the localization of MtPK, we raised a polyclonal antibody against a synthetic peptide chosen within the deduced sequence of MtPK. This antibody detected both a membrane-bound 70-kd protein and a soluble 55-kd protein on Western blots of human muscles. By using this antibody for immunohistochemical studies of both biopsied human skeletal muscle fibers and mature innervated cultured muscle fibers, we can now demonstrate by confocal laser scanning microscopy that MtPK is localized mainly in the I-band. By immunoelectron microscopy, it was determined that MtPK is a membrane-bound protein localized mainly in the terminal cisternae of the sarcoplasmic reticulum. To our knowledge, this is the first documentation of the ultrastructural localization of MtPK. This finding is quite important for clarifying the pathophysiological basis of myotonic dystrophy, which might be due to a dysregulation of calcium metabolism.
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Well the reason you didn't find anything is because the word is rhabdomyolsis. Not labdo. It's an expedited degeneration of the muscle tissue. Statin drugs like Lipitor in a small population are known to have this side effect although I've yet to witness it for myself.
678937
There appears to be more than one type of amyotrophy. See the links.
866726
It depends on the kind of muscular dystrophy your family has whether it will be passed on to what gender children you have, first of all. I'm guessing that they aren't all boys. If that is the case then there could be a chance that one of your X chromosomes (if you are a female) is carrying the latent form of the disease. \n\nMales are born with XY chromosomes and females with XX (if you did't already know this). That being the case, males tend to get diseases that are X-linked---that are 'carried' on the X chromosome because they don't have another X chromosome to block out the effects of the one bad X. \n\nAnother factor is whether you are a man or woman (I couldn't tell from your question). If you are female, your X chromosome COULD have a latent form of the disease on it. I dbout you do have a 'bad' X if you are female, however. If your father tested negative for muscular dystrophy, and he passed his X chromosome to you (which he did if you are female remember) you would have no underlying problems in your genes to pass on to your offspring. \nIf you are male, you recieved your X chromosome from your mother by default, so unless MD runs in that side of the famiy too, I think you don't have to worry about passing it to your children. \n\nIn conclusion, I think you are safe. But because I am NOT a doctor or geneticist and I rather not be blamed if your child does end up with muscular dystrophy one day, I suggest you see a doctor for more solid answers. \nI hope this helps you otherwise, and I included a link if you are interested.