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14-September-2008 12:50:27 - Chronic inflammatory demyelinating polyneuropathy Chronic inflammatory demyelinating polyneuropathy Classification and external resources ICD-9 357.81 OMIM 139393 DiseasesDB 30084 eMedicine neuro/467 MeSH D020277 Chronic Inflammatory Demyelinating Polyneuropathy CIDP is an acquired immune-mediated inflammatory disorder of the peripheral nervous system but often can have central nervous system involvement. The disorder is sometimes called chronic relapsing polyneuropathy. CIDP is closely related to Guillain-Barre syndrome and it is considered the chronic counterpart of that acute disease. Its symptoms are also similar to progressive inflammatory neuropathy. Contents 1 Overview 2 Diagnosis 3 Treatment 4 Prognosis 5 See also 6 References 7 External links Overview The pathologic hallmark of the disease is loss of the myelin sheath the fatty covering that protects nerve fibers of the peripheral nerves. Chronic inflammatory demyelinating polyneuropathy is disease believed to be due to immune cells, cells which normally protect the body from foreign infection, but here begin incorrectly attacking the nerves in the body instead. As a result, the affected nerves fail to respond, or respond only weakly, to stimuli causing numbing, tingling, pain, progressive muscle weakness, loss of deep tendon reflexes areflexia, fatigue, and abnormal sensations. The likelihood of progression of the disease is high. CIDP is under-recognized and under-treated due to its heterogeneous presentation both clinical and electrophysiological and the limitations of clinical, serologic, and electrophysiologic diagnostic criteria. Despite these limitations, early diagnosis and treatment is important in preventing irreversible axonal loss and improving functional recovery.1 Lack of awareness and treatment of CIDP is also due to limitations of clinical trials. Although there are stringent research criteria for selecting patients to clinical trials, there are no generally agreed-on clinical diagnostic criteria for CIDP due to its different presentations in symptoms and objective data. Application of the present research criteria to routine clinical practice often miss the diagnosis in a majority of patients, and patients are often left untreated despite progression of their disease.2 In some cases electrophysiological studies fail to show any evidence of demyelination. Though conventional electrophysiological diagnostic criteria are not met, the patient may still respond to immunomodulatory treatments. In such cases, presence of clinical characteristics suggestive of CIDP are critical, justifying full investigations, including sural nerve biopsy.3 Diagnosis Clinical neurological examination Patients usually present with a history of weakness, numbness, tingling, pain and difficulty in walking. They may additionally present with fainting spells while standing up or burning pain in extremities. Some patients may have sudden onset of back pain or neck pain radiating down the extremities, usually diagnosed as radicular pain. These symptoms are usually progressive and may be intermittent. On examination the patients may have weakness, and loss of deep tendon reflexes rarely increased or normal. There may be atrophy shrinkage of muscles, fasciculations twitching and loss of sensation. Patients may have Multi-Focal Motor neuropathy, as they have no sensory loss. The patient may present with a single cranial nerve or peripheral nerve dysfunction. Autonomic system dysfunction can occur; in such a case, the patient would complain of orthostatic dizziness, problems with bowel and bladder functions, and cardiac problems. Most experts consider the necessary duration of symptoms to be greater than 8 weeks for the diagnosis of CIDP to be made. Electrodiagnostics - electromyography EMG and nerve conduction study NCS. In usual CIDP, the nerve conduction studies show demyelination. These findings include: a reduction in nerve conduction velocities b; the presence of conduction block or abnormal temporal dispersion in at least one motor nerve; prolonged distal latencies in at least two nerves; absent F waves or prolonged minimum F wave latencies in at least two motor nerves. In some case EMG/NCV can be normal. Serum test to discard other autoimmune deseases. Spinal tap and serum test for Anti-ganglioside antibodies, wich are one branch of the CIDP diseases, as anti-GM1 anti-GD1a anti-GQ1b. Sural nerve biopsy Biopsy is considered for those patients in whom the diagnosis is not completely clear, when other causes of neuropathy eg, herary, vasculitic cannot be excluded, or when profound axonal involvement is observed on EMG. Treatment First line treatment for CIDP includes corticosteroids such as prednisone, plasmapheresis plasma exchange and intravenous immunoglobulin IVIg which may be prescribed alone or in combination with an immunosuppressant drug. IVIG and plasmapheresis have proven benefit in randomized, double-blind, placebo-controlled trials. Despite less definitive published evidence of efficacy, corticosteroids are considered standard therapies because of their long history of use and cost effectiveness. Immunosuppressive drugs are often of the cytotoxic chemotherapy class, including Rituximab Rixutan which targets B Cells, and cyclophosphamide, a drug which reduces the function of the immune system. Ciclosporin has also been used in CIDP but with less frequency as it is a newer approach.4 Ciclosporin is thought to bind to immunocompetent lymphocytes, especially T-lymphocytes. Non-cytotoxic immunosuppressive treatments usually include Imuran and Cellcept. Anti-thymocyte globulin ATG, an immunosuppressive agent that selectively destroys T lymphocytes is being studied for use in CIDP. Anti-thymocyte globulin is the gamma globulin fraction of antiserum from animals that have been immunized against human thymocytes. It is a polyclonal antibody. Although chemotherapeutic and immunosuppressive agents have shown to be effective in treating CIDP significant evidence is lacking, mostly due to the heterogeneous nature of the disease in the patient population in addition to the lack of controlled trials. Physiotherapy may improve muscle strength, function and mobility, and minimize the shrinkage of muscles and tendons and distortions of the joints. Prognosis As in Multiple Sclerosis, a similar demyelinating condition, it is not possible to predict with certainty how CIDP is going to affect an individual in the future. The pattern of relapses and remissions varies greatly with each patient. A period of relapse can be very disturbing, but many patients make significant recoveries. If diagnosed early, initiation of early treatment to prevent loss of nerve axons is recommended. However, many individuals are left with residual numbness, weakness, fatigue and other symptoms which can lead to long-term morbidity and diminished quality of life. 5 It is important to build a good relationship with doctors, both primary care and specialist. Because of the rarity of the illness, many doctors will not have encountered it before. Each case of CIDP is different, and relapses, if they occur, may bring new symptoms and problems. Because of the variability in severity and progression of the disease, doctors will not be able to give a definite prognosis. A period of experimentation with different treatment regimes is likely to be necessary in order to discover the most appropriate treatment regimen for a given patient. See also Autoimmune diseases Neurology References ^ Toothaker TB, Brannagan TH 2007. Chronic inflammatory demyelinating polyneuropathies: current treatment strategies. Curr Neurol Neurosci Rep 7 1: 63-70. PMID 17217856. ^ Latov N 2002. Diagnosis of CIDP. Neurology 59 12 Suppl 6: S2-6. PMID 12499464. ^ Azulay JP 2006. The diagnosis of chronic axonal polyneuropathy: the poorly understood chronic polyradiculoneuritides in French. Rev. Neurol. Paris 162 12: 1292-5. PMID 17151528. ^ Odaka M, Tatsumoto M, Susuki K, Hirata K, Yuki N 2005. Intractable chronic inflammatory demyelinating polyneuropathy treated successfully with ciclosporin. J. Neurol. Neurosurg. Psychiatr. 76 8: 1115-20. doi:10.1136/jnnp.2003.035428. PMID 16024890. ^ Kissel JT 2003. The treatment of chronic inflammatory demyelinating polyradiculoneuropathy. Semin Neurol 23 2: 169-80. doi:10.1055/s-2003-41130. PMID 12894382. External links cidp at NINDS Online CIDP booklets and information from the GBS Organisation of the UK The Neuropathy Association CIDP information from the GBS/CIDP Foundation Update 16 April 2008 among pork workers v d e Nervous system pathology, primarily PNS G50-G99, 350-359 Nerve, nerve root and plexus disorders Cranial nerve disease V Trigeminal neuralgia - VII Facial nerve paralysis, Bell's palsy, Melkersson-Rosenthal syndrome, Central seven - XI Accessory nerve disorder Radiculopathy, plexopathy Brachial plexus lesion - Thoracic outlet syndrome - Phantom limb Mono- neuropathy upper limb Carpal tunnel syndrome, Ulnar nerve entrapment, Radial neuropathy lower limb Meralgia paraesthetica, Tarsal tunnel syndrome, Morton's neuroma Causalgia - Mononeuritis multiplex Polyneuropathies HMSN Charcot-Marie-Tooth disease - Dejerine Sottas syndrome - Refsum's disease Polyradiculoneuropathy autoimmune Guillain-Barré syndrome, Chronic inflammatory demyelinating polyneuropathy - Alcoholic polyneuropathy Diseases of muscle myopathy/ neuromuscular disease Neuromuscular junction disease autoimmune Myasthenia gravis, Lambert-Eaton myasthenic syndrome Muscular dystrophy Congenital - dystrophin Becker's, Duchenne - Distal - Emery-Dreifuss - Facioscapulohumeral - Limb-girdle muscular dystrophy - Myotonic - Oculopharyngeal Myotonia Myotonic dystrophy - Myotonia congenita - Thomsen disease - Neuromyotonia - Paramyotonia congenita Congenital myopathy Bethlem myopathy - Central core disease - Centronuclear myopathy - Nemaline myopathy - Zaspopathy Mitochondrial myopathy MELAS - MERRF - KSS - PEO Periodic paralysis Hypokalemic - Hyperkalemic Dysautonomia/ Autonomic neuropathy HSAN Familial dysautonomia - Horner's syndrome - Multiple system atrophy Shy-Drager syndrome, Olivopontocerebellar atrophy Retrieved from http://en..org/wiki/Chronic_inflammatory_demyelinating_polyneuropathy Categories: Autoimmune diseases | Neurological disorders 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 日本語 Polski This page was last modified on 2 September 2008, at 15
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