what is guilambres (gee-ohm-brays) disease? where do i find info on it?
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Guillain-Barre Syndrome     proper name and spelling\nWhat is Guillain-Barre Syndrome?\n\nGuillain-Barre Syndrome is a disease of the nervous system due to damage to the myelin sheath around nerves. The myelin sheath acts as an insulator the same as rubber or plastic around electrical wires.\n\nGuillain-Barre Syndrome is the most frequent acquired (as opposed to inherited) nerve disease (neuropathy). In many cases it follows shortly after a virus infection. It is also rarely associated with immunizations, surgery, and childbirth.\n\nWhat causes Guillain-Barre Syndrome?\n\nThe cause of Guillain-Barre Syndrome is unknown, but it appears that there is an autoimmune (one's own immune system attacks the body) reaction.\n\nWhat are symptoms of Guillain-Barre Syndrome?\n\nSymptoms of Guillain-Barre Syndrome include weakness, typically beginning in the legs and progressing upward. The weakness is accompanied by decreased feeling (paresthesia). Reflexes are lost, for example, the hammer to the front of the knee will not induce a kick. In severe cases breathing can be affected enough to require a ventilator and rarely the heart can be affected. The maximal degree of weakness usually occurs within the first 2-3 weeks.\n\nHow is Guillain-Barre Syndrome treated?\n\nThe majority of patients can expect a slow but progressive recovery over several months. In severe cases the primary concern is maintaining vital functions and passively exercising the muscles. This sometimes requires temporary artificial breathing machines for severely affected patients.\n\nPlasmapheresis is a method to remove toxic substances from the blood and has been shown to improve outcome and shorten the disease. Intravenous immunoglobulin is also beneficial
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try these:\n\nhttp://www.mda.org.au/\n\nhttp://www.myotonicdystrophy.org/\n\nhttp://ghr.nlm.nih.gov/condition=myotonicdystrophy
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Guillian Barre syndrom.. is a inflammatory dises of unknow origin that involves degeneration of the stuff that helps you nerve impulses move faster. You get weak generally starting in your lower extremeties and then it moves up.. fourtunatly its recoverable and most people recover in 6 months but it can take up to 2 years ..
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Menetrier Disease \nMeniere's Disease\nMeniere's Syndrome \nMeningeal Plague\nMeningioma\nMeningiomas, Multiple\nMeningiomatosis\nMeningitis, Bacterial\nMeningitis, Viral\nMenkes Kinky Hair Syndrome\nMenkes Syndrome\nMenopause\nMenstruation Disorders \nMenstruation Disturbances\nMenstruation, Retrograde\nMental Disorders\nMental Retardation
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Introduction \nGuillain-Barre syndrome (GBS) is also called as acute idiopathic polyradiculoneuritis. This is the most common aquired demyelinating disease. This disease is characterized by the inflammatory disorder of the peripheral nerves. The incidence of Guillain-Barre syndrome is one in 100,000. The life time risk for any one individual getting Guillain-Barre syndrome (GBS) is 1/1000. All age group may affected by GBS. Both sexes are equally affected. The disease is characterized by weakness of limbs and numbness and tingling sensation over the limbs, body and the face. Mild cases of Guillain-Barre syndrome may present only with ataxia (difficulty in walking and balancing), whereas severe cases may present with difficulty in respiration due to paralysis the respiratory muscles and cranial nerves. \n\nWhat causes Guillain-Barre Syndrome? \nThe actual cause for Guillain-Barre syndrome is still not known. It may be an autoimmune disease; in which antibodies are directed against the peripheral myelin (myelin is the sheath covering of the peripheral nerves and is responsible for faster conduction of nerve signals). \nA mild respiratory or gastrointestinal infection may be present 1-3 weeks before the onset of neurological symptoms in 60% of the patients.   Infection with Campylobacter jejuni is the most often found association with Guillain-Barre syndrome. \nViral infection, minor surgery, immunization, mycoplasma infection may also be a preceding event in Guillain-Barre syndrome.  High frequency of occurrence of this Guillaine-Barre syndrome is found in the following conditions than in the normal population: Hodgkin's disease, lymphoma, systemic lupus erythematosis. \n\nWhat are the symptoms of Guillaine-Barre syndrome? \nMost of the patients present with numbness and tingling of the limbs in the initial phase of the disease.   The major complaint is the weakness of limbs which will be mostly symmetrical. Both proximal and distal parts of the limbs are affected. The lower limbs are affected first. Then the weakness spreads to trunk, respiratory muscles, upper limbs, neck muscles and cranial muscles.  Sometimes the weakness may progress to complete paralysis of the body leading to respiratory difficulty and death in a few days. About 50% of the patients, complaint of pain and aching discomfort of the hip, thigh and back muscles. \nFacial muscle weakness may be present in 50% of the cases. Facial muscle weakness usually comes after the upper arm weakness.  Difficulty in passing urine (urinary retention) occurs in 15% of the patients. \n\nHow do you diagnose Guillaine-Barre syndrome? \nMost of the time, a thorough neurological examination with laboratory investigation will clinch the diagnosis of Guillaine-Barre syndrome. \n\nFeatures required for diagnosis of Guillain-Barre syndrome (GBS) : \nProgressive motor weakness of more than one limb: \nFrom minimal weakness with or without ataxia (difficulty if balancing) to complete paralysis, which may include cranial nerves. Proximal muscles are more affected than distal ones. \nAreflexia(loss of muscle stretch reflexes)-usually universal \n\nFeatures strongly supportive of diagnosis of Guillain-Barre syndrome (GBS) : \nProgression of the motor weakness in the patient peaks at 2 weeks in 50%, by 3 weeks in 80% and by 4 weeks in 90%. \n\nThere is relative symmetry of weakness in the body. That is, both half of the body are equally affected. \n\nMild sensory symptoms-mild tingling and numbness in hand and feet. \n\nCranial nerve involvement: Facial weakness in 50%, usually bilateral. \n\nOropharyngeal muscles (muscles of the oral cavity and throat) may be affected. \n\nRecovery of the patient starts usually by 2-4 weeks after the progression stops, but may be delayed by months \n\nTachycardia (increase in heart rate), postural hypotension \nFever, sensory loss with pain, bladder paralysis (urinary retention) \n\nLumbar puncture is done and the Cerebrospinal fluid (brain fluid) is e
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This is the official Mad Cow Disease home-page...\nhttp://www.mad-cow.org/\nWith over 7,650 articles on mad cow and new variantCreutzfeldt-Jakob disease, prions, bovine spongiform encephalopathy, scrapie, BSE, CJD, CWD, TME, and TSE.
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Kartageners syndrome\n\nciliary dyskinesia
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i think you mean Guillain-Barre Syndrome....
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Do a Yahoo search on Lou Gherig disease.
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Background: Orf is a viral disease that is widespread in sheep and goats. It can be transmitted to humans by contact with an infected animal or contaminated fomites. Reindeer have also caused similar lesions in humans. It is frequently seen in farming communities and meat handlers. Clinically, reddish weeping nodules are seen on the dorsa of the hands and the fingers that heal spontaneously in about 35 days.\n\n\nPathophysiology: Orf is primarily a disease involving the skin, though the lymph nodes are occasionally involved.\n\n\nFrequency: \n\n\nInternationally: A higher frequency of reports has occurred from Europe and New Zealand compared with North America, but this is of unknown significance. \nMortality/Morbidity: The natural course of the disease is spontaneous recovery in 3-6 weeks. \n\nImmunocompromised patients can have progressive, destructive lesions requiring medical interventions such as antiviral therapy and surgical debridement. However, reports exist of immunosuppressed individuals with large, fungating lesions that have been refractory to treatment. \nMortality has not been reported.\nRace: Orf has been reported exclusively in whites. \n\nSex: No sexual predilection is reported. \n\nAge: No age predilection is described. \n\n\n \n\n  CLINICAL  Section 3 of 10      \nAuthor Information Introduction Clinical Differentials Workup Treatment Follow-up Miscellaneous Pictures Bibliography\n \n \n\nHistory: \n\nOrf usually appears as a small papule on the dorsum of the index finger 1 week following contact with an infected animal or contaminated fomite.\nLow-grade fever may occur and usually subsides within 3-4 days.\nPhysical: Orf appears as a solitary lesion or as a few lesions on the fingers, the hands, or the forearms, and it has even been reported on the face. The lesion starts as a small, firm, red-to-blue papule that grows to form a hemorrhagic, flat-topped pustule or bulla. The bulla may have a crust in its umbilicated center. The fully developed lesion is typically 2-3 cm in diameter, but it may reach 5 cm. It is often tender and may bleed easily.\n\nRegional adenitis and/or mild lymphangitis may be found.\nMild fever and malaise may be associated.\nLarge, fungating lesions have been reported in patients who are immunosuppressed and in patients with atopic dermatitis.\nThe infection goes through 6 clinical stages, each lasting about 1 week.\nStage 1 (maculopapular) - A red elevated lesion\nStage 2 (targetoid) - A bulla with an irislike configuration (nodule with a red center, a white middle ring, and a red periphery)\nStage 3 (acute) - A weeping nodule\nStage 4 (regenerative) - A firm nodule covered by a thin crust through which black dots are seen\nStage 5 (papillomatous) - Small papillomas appearing over the surface\nStage 6 (regressive) - A thick crust covering the resolving elevation\nCauses: The disease is caused by infection with the orf virus that belongs to the Parapoxvirus genus, which also includes the milker's nodule virus. Parapoxvirus is a member of the family Poxviridae, which contains double-stranded DNA viruses known to be the largest viruses.\n\nThe orf virus is a cylindrical virus measuring 260 X160 nm. Its surface tubules form a long crisscross design that is seen on negatively stained preparations by electron microscopy. This virus resists physical damage and persists through the winter months on hedges, feeding troughs, and barns.\nOrf is transmitted by direct contact inoculation. Humans acquire the infection from contact with infected animals, carcasses, or contaminated, nonliving material. It is very common among shepherds, veterinary surgeons, and farmers' wives who bottle-feed young lambs, as well as in butchers and meat porters from handling infected carcasses.\nNo transmission occurs to cattle, and no human-to-human transmission occurs.
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http://www.jhu.edu/\n\nmedical references\nhttp://webapps.jhu.edu/jhuniverse/medicine/diseases/
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There appears to be more than one type of amyotrophy. See the links.
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here's a site that might help you http://www.diseasesdatabase.com/ddb31745.htm
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Tibial hemimelia-split hand/foot syndrome (TH-SHFM) is a rare constellation of multiple congenital malformations which includes Ectrodactyly (Lobster claw deformity or Cleft hand/foot) with a wide range of phenotypes of absent tibia/tibial hemimelia or long bone deficiency\n\ncc
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TRY\n\nwww.wrongdiagnosis.com\n\nor \n\nwww.merck.com
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Go to OMIM at the NCBI http://www.ncbi.nlm.nih.gov/, it is a database of inherited diseases, ie diseases that are affected by genetics (just about everything).  It's an excellent reference.  You can pick pretty much any disease, the topic doesn't matter.  What matters is how well you known the subject and how deep you explore it.  Ie genetics, hx, treatement, dx, etc.
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You can find all the answrs to your questions on the web site:Webmd.com\nJust enter"mumps" in the Search bar.  There are several good  articles.  Thefirst one explains the incubation period and duration of the illness.