Sierra Acai Company was launched with the goal to revolutionize the sale of MonaVie. We have dedicated ourselves to changing your shopping experience by providing an easy to use website, a wealth of product information, outstanding customer service, incredible in stock selection, great prices, prompt service, and fast shipping online. We have become one of the largest most respected online retailers. Remember you are not buying from some disreputable retailer but from a professional mainstream company that you can trust.

News

News About Acute_disseminated_encephalomyelitis

20-September-2008 10:08:29 - Acute disseminated encephalomyelitis Acute disseminated encephalomyelitis Classification and external resources ICD-10 G04.0 ICD-9 323.61 DiseasesDB 158 eMedicine neuro/500 MeSH D004673 Acute disseminated encephalomyelitis ADEM is an immune mediated disease of the brain123. It usually occurs following a viral infection but may appear following vaccination, bacterial or parasitic infection, or even appear spontaneously. As it involves autoimmune demyelination, it is similar to multiple sclerosis, and is considered part of the Multiple sclerosis borderline45 The incidence rate is about 0.8 per 100,000 people per year6. Although it occurs in all ages, most reported cases are in children and adolescents, with the average age around 5 to 8 years old789. The mortality rate may be as high as 5%, full recovery is seen in 50 to 75% of cases, while up to 70 to 90% recover with some minor residual disability10. The average time to recover is one to six months. ADEM produces multiple inflammatory lesions in the brain and spinal cord, particularly in the white matter. Usually these are found in the subcortical and central white matter and cortical gray-white junction of both cerebral hemispheres, cerebellum, brainstem, and spinal cord11, but periventricular white matter and gray matter of the cortex, thalami and basal ganglia may also be involved. When the patient suffers more than one demyelinating episode, it is called Recurrent disseminated encephalomyelitis12 or Multiphasic disseminated encephalomyelitis13MDEM. Contents 1 Causes, Antecedent History 2 Presentation 3 Treatment 4 Prognosis 4.1 Motor deficits 4.2 Neurocognitive 5 ADEM MS 6 Acute Hemorrhagic Leukoencephalitis 7 Experimental Allergic Encephalomyelitis 8 See also 9 References 10 External links Causes, Antecedent History Viral infections thought to induce ADEM include influenza virus, enterovirus, measles, mumps, rubella, varicella zoster, Epstein Barr virus, cytomegalovirus, herpes simplex virus, hepatitis A, and coxsackievirus; while the bacterial infections include Mycoplasma pneumoniae, Borrelia burgdorferi, Leptospira, and beta-hemolytic Streptococci14. The only vaccine proven to induce ADEM in the Semple form of the rabies vaccine, but hepatitis B, pertussis, diphtheria, measles, mumps, rubella, pneumococcus, varicella, influenza, Japanese encephalitis, and polio vaccines have all been implicated1516176181920212223 24. In rare cases, ADEM seems to follow from organ transplantation18. The risk of ADEM from measles vaccination is about 1 to 2 per million17, which is far lower than the risk of developing ADEM from an actual measles infection, which is about 1 per 1000 for measles and 1 per 5000 for rubella2519. Measles infection also appears to lead to worse ADEM outcomes than cases associated with measles immunization. Some vacines, later shown to have been contaminated with host animal CNS tissue, have ADEM incident rates as high as 1 in 60026. Presentation ADEM has an abrupt onset and a monophasic course. Symptoms usually begin 1-3 weeks after infection or vaccination. Major symptoms include fever, headache, drowsiness, seizures and coma. Although initially the symptoms are usually mild, they worsen rapidly over the course of hours to days, with the average time to maximum severity being about four and a half days18. Treatment No controlled clinical trials have been conducted on ADEM treatment, but aggressive treatment aimed at rapidly reducing inflammation of the CNS is standard. The widely accepted first-line treatment is high doses of intravenous corticosteroids 27, such as methylprednisolone or dexamethasone, followed by 3-6 weeks of gradually lower oral doses of prednisolone. Patients treated with methylprednisolone have shown better outcomes than those treated with dexamethasone18. Oral tapers of less than three weeks duration show a higher chance of relapsing2829, and tend to show poorer outcomescitation needed. Other antiinflamatory and immunosuppressive therapies have been reported to show beneficial effect, such as plasmapheresis, high doses of intravenous immunoglobulin IVIg3031, mitoxantrone and cyclophosphamide. These are considered alternative therapies, used when corticosteroids cannot be used, or fail to show an effect. There is some evidence to suggest that patients may respond to a combination of methylprednisolone and immunoglobulins if they fail to respond to either separately32 In a study of 16 children with ADEM, 10 recovered completely after high-dose methylprednisolone, one severe case that failed to respond to steroids recovered completely after IVIg; the five most severe cases -with ADAM and severe peripheral neuropathy- were treated with combined high-dose methylprednisolone and immunoglobulin, two remained paraplegic, one had motor and cognitive handicaps, and two recovered30. A recent review of IVIg treatment of ADEM of which the previous study formed the bulk of the cases found that 70% of children showed complete recovery after treatment with IVIg, or IVIg plus corticosteroids33. A study of IVIg treatment in adults with ADEM showed that IVIg seems more effective in treating sensory and motor disturbances, while steroids seem more effective in treating impairments of cognition, consciousness and rigor34. This same study found one subject, a 71 year old man who had not responded to steroids, that responded to a IVIg treatment 58 days after disease onset. Prognosis Full recovery is seen in 50 to 75% of cases, ranging to 70 to 90% recovery with some minor residual disability typically assessed using measures such as mRS or EDSS, average time to recover is one to six months10. The mortality rate may be as high as 5%.10. Poorer outcomes are associated with unresponsiveness to steroid therapy, unusually severe neurological symptoms, or sudden onset. Children tend to have more favorable outcomes than adults, and cases presenting without fevers tend to have poorer outcomes35. The latter effect may be due to either protective effects of fever, or that diagnosis and treatment is sought more rapidly when fever is present. Motor deficits Residual motor deficits are estimated to remain in about 8 to 30% of cases, the range in severity from mild clumsiness to ataxia and hemiparesis 14. Neurocognitive Patients with demylinating illnesses, such as MS, have shown cognitive deficits even when there is minimal physical disability36. Research suggests that similar effects are seen after ADEM, but that the deficits are less severe than those seen in MS. A study of six children with ADEM mean age at presentation 7.7 years were tested for a range of neurocognitive tests after an average of 3.5 years of recovery. 37. All six children performed in the normal range on most tests, including verbal IQ and performance IQ, but performed at least one standard deviation below age norms in at least one cognitive domain, such as complex attention one child, short-term memory one child and internalizing behaviour/affect two children. Group means for each cognitive domain were all within one standard deviation of age norms, demonstrating that, as a group, they were normal. These deficits were less severe than those seen in similar aged children with a diagnosis of MS38. Another study compared nineteen children with a history of ADEM, of which 10 were five years of age or younger at the time average age 3.8 years old, tested an average of 3.9 years later and nine were older mean age 7.7y at time of ADEM, tested an average of 2.2 years later to nineteen matched controls39. Scores on IQ tests and educational achievement were lower for the young onset ADEM group average IQ 90 compared to the late onset average IQ 100 and control groups average IQ 106, while the late onset ADEM children scored lower on verbal processing speed. Again, all groups means were within one standard deviation of the controls, meaning that while effects were statistically reliable, the children were as a whole, still within the normal range. There were also more behavioural problems in the early onset group, although there is some suggestion that this may be due, at least in part, to the stress of hospitalization at a young age4041 ADEM MS While ADEM and MS both involve autoimmune demylenation, they differ in many clinical, genetic, imaging, and histopathological differences42. Some authors consider MS and its borderline forms to constitute a spectrum, differing only in chronocity, severity, and clinical course4344, while others consider them discretely different diseases5. Acute Hemorrhagic Leukoencephalitis Acute hemorrhagic leukoencephalitis AHL, or AHLE or Acute necrotizing encephalopathy ANE, Acute hemorrhagic encephalomyelitis AHEM, Acute necrotizing hemorrhagic leukoencephalitis ANHLE, or Weston-Hurst syndrome, or Hurst's disease, is a hyperacute and frequently fatal form of ADEM. AHL is relatively rare less than 100 cases have been reported in the medical literature as of 200645, it is seen in about 2% of ADEM cases18, and is characterized by necrotizing vasculitis of venules and hemorrhage, and edema46, death is common in the first week47 with mortality rate of about 70%45, but increasing evidence points to favorable outcomes after aggressive treatment with corticosteroids, immunoglobulins, cyclophosphamide, and plasma exchange14. About 70% of survivors show residual neurological deficits46, but some survivors have shown surprisingly little deficit considering the magnitude of the white matter affected47. Experimental Allergic Encephalomyelitis Main article: Experimental autoimmune encephalomyelitis Experimental Allergic Encephalomyelitis EAE is an animal model of CNS inflammation and demyelination frequently used to investigate potential MS treatments48. An acute monophasic illness, EAE is far more similar to ADEM than MS49. See also Optic neuritis Transverse myelitis References ^ Dale RC. 2003. Acute disseminated encephalomyelitis. Seminars in pediatric infectious diseases 14:90--95. ^ Garg RK. 2003 Acute disseminated encephalomyelitis. Postgraduate medical journal 79:11--17. ^ Jones CT. 2003. Childhood autoimmune neurologic diseases of the central nervous system. Neurologic Clinics 21:745--764. ^ Rust RS 2000. Multiple sclerosis, acute disseminated encephalomyelitis, and related conditions. Seminars in Pediatric Neurology 7:66--90. ^ a b Poser CM Brinar VV 2007. Disseminated encephalomyelitis and multiple sclerosis: two different diseases - a critical review. Acta Neurologica Scandinavica 116:201--206. ^ a b Leake JAD, Albani S, Kao AS, et al. Acute disseminated encephalomyelitis in childhood: epidemiologic, clinical and laboratory features. Pediatr Infect Dis J 2004;23:756-764. ^ Hynson JL, Kornberg AJ, Coleman LT, Shield L, Harvey AS Kean MJ. 2001. Clinical and neuroradiologic features of acute disseminated encephalomyelitis in children. Neurology 56:1308--1312. ^ Anlar B, Basaran C, Kose G, et al. 2003. Acute disseminated encephalomyelitis in children: outcome and prognosis. Neuropediatrics 34:194--199. ^ Schwarz S, Mohr A, Knauth M, Wildemann B Storch-Agenlocher B. 2001. Acute disseminated encephalomyelitis: a follow-up study of 40 adult patients. Neurology 56:1313--1318. ^ a b c Menge T, Kieseier BC, Nessler S, Hemmer B, Hartung HP, Stuve O 2007. Acute disseminated encephalomyelitis: an acute hit against the brain. Current Opinion in Neurology 20:247--254 ^ Wingerchuk DM. 2003. Postinfectious encephalomyelitis. Current Neurology and Neuroscience Reports 3:256-264. ^ Poser CM May 2008. Multiple sclerosis and recurrent disseminated encephalomyelitis are different diseases. Arch. Neurol. 65 5: 674; author reply 674-5. doi:10.1001/archneur.65.5.674-a. PMID 18474749. ^ Citation is missing a title. Either specify one, or click here and a bot will try to complete the citation details for you. 1 . PMID 11099444. ^ a b c Tenembaum S, Chitnis T, Ness J, Hahn JS 2007. Acute disseminated encephalomyelitis. Neurology 68 Suppl 2:S23--S36. ^ Hemachudha T, Griffin DE, Giffels JJ, Johnson RT, Moser AB, Phanuphak P. 1987. Myelin basic protein as an encephalitogen in encephalomy elitis and polyneuritis following rabies vaccination. New England Journal of Medicine 316:369-374. ^ Hemachudha T, Griffin DE, Johnson RT, Giffels JJ. 1988. Immunologic studies of patients with chronic encephalitis induced by post-exposure Semple rabies vaccine. Neurology 38:42-44. ^ a b Murthy JM. 2002, Acute disseminated encephalomyelitis. Neurol India 50:238-243. ^ a b c d e Tenembaum S, Chamoles N, Fejerman N. 2002. Acute disseminated encephalomyelitis: a long-term follow-up study of 84 pediatric patients. Neurology 59:1224--1231. ^ a b Fenichel GM. 1982. Neurological complications of immunization. Annals of Neurology 12:119-128. ^ Takahashi H, Pool V, Tsai TF, Chen RT. Adverse events after Japanese encephalitis vaccination: review of post-marketing surveillance data from Japan and the United States. The VAERS Working Group. Vaccine 18:2963-2969. ^ Tourbah A, Gout O, Liblau R, et al. 1999. Encephalitis after hepatitis B vaccination: recurrent disseminated encephalitis or MS? Neurology 53:396-401. ^ Karaali-Savrun F, Altintas A, Saip S, Siva A. 2001 Hepatitis B vaccine related-myelitis? European Journal of Neurology 8:711-715. ^ Sejvar JJ, Labutta RJ, Chapman LE, Grabenstein JD, Iskander J, Lane JM. 2005. Neurologic adverse events associated with smallpox vaccination in the United States, 2002-2004. Journal of the American Medical Association 294:2744-2750. ^ Ozawa H, Noma S, Yoshida Y, Sekine H, Hashimoto T. 2000. Acute disseminated encephalomyelitis associated with poliomyelitis vaccine. Pediatric Neurology 23:177-179. ^ Miller HG, Stanton JB, Gibbons JL 1956. Parainfectious encephalomyelitis and related syndromes. Quarterly Journal of Medicine 25:427-505. ^ Hemachudha T, Griffin DE, Giffels JJ, et al. 1987. Myelin basic protein as an encephalitogen in encephalomyelitis and polyneuritis following rabies vaccination. New England Journal of Medicine 316:369--374. ^ Shahar E, Andraus J, Savitzki D, et al. 2002. Outcome of severe encephalomyelitis in children: effect of high-dose methylprednisolone and immunoglobulins. Journal of Child Neurology 17:810--814. ^ Dale RC, de Sousa C, Chong WK, Cox TC, Harding B, Neville BG. 2000. Acute disseminated encephalomyelitis, multiphasic disseminated encephalomyelitis and multiple sclerosis in children. Brain 123:2407-2422. ^ Anlar B, Basaran C, Kose G, et al. 2003. Acute disseminated encephalomyelitis in children: outcome and prognosis. Neuropediatrics 34:194-199. ^ a b Shahar E, Andraus J, Savitzki D, et al. 2002. Outcome of severe encephalomyelitis in children: Effect of high-dose methylprednisolone and immunoglobulins. Journal of Child Neurology 17:810-814 ^ Ravaglia S, Piccolo G, Ceroni M, Franciotta D, ichiecchio A, Bastianello S, Tavazzi E, Minoli L, Marchioni E 2007. Severe steroid-resistant post-infectious encephalomyelitis: General features and effects of IVIg. Journal of Neurology 254:1518-1523. ^ Straussberg R, Schonfeld T, Weitz R, Karmazyn B, Harel L. 2001. Improvement of atypical acute disseminated encephalomyelitis with steroids and intravenous immuneglobulins. Pediatric Neurology 24:139-143. ^ Feasby T, et al. 2007. Guidelines on the Use of Intravenous Immune Globulin for Neurologic Conditions. Transfusion Medicine Reviews 21:S57-S107. ^ Ravaglia, S. et al. 2007 Severe steroid-resistant post-infectious encephalomyelitis: General features and effects of IVIg. Journal of Neurology 254:1518-1523 ^ Lin C-H, Jeng J-S, Hsieh S-T, Yip P-K, Wu R-M 2007 Acute disseminated encephalomyelitis: a follow-up study in Taiwan. Journal of Neurology Neurosurgery and Psychiatry 78:162--167. ^ Foong J, Rozewicz L, Quaghebeur G, et al. 1997. Executive function in multiple sclerosis. The role of frontal lobe pathology. Brain 120:15-26. ^ Hahn CD, Miles BS, MacGregor DL, Blaser SI, Banwell BL Hetherington CR. 2003. Neurocognitive outcome after acute disseminated encephalomyelitis. Pediatric Neurology 29:117-123. ^ Banwell BL Anderson PE. 2005. The cognitive burden of multiple sclerosis in children. Neurology 64:891--894. ^ Jacobs RK, Anderson VA, Neale JL, Shield LK, Kornberg AJ. Neuropsychological outcome after acute disseminated encephalomyelitis: impact of age at illness onset. Pediatr Neurol 2004;31:191--197. ^ Douglas JWB. 1975. Early hospital admissions and later disturbances of behavior and learning. Devel Med Child Neurol 17:456-80. ^ Daviss WB, Racusin R, Fleischer A, Mooney D, Ford JD McHugo GJ. 2000. Acute stress disorder symptomatology during hospitalization for pediatric injury. J Am Acad Child Adol Psychiatry 2000;39:569-75. ^ Wingerchuk DM Lucchinetti CF. 2007. Comparative immunopathogenesis of acute disseminated encephalomyelitis, neuromyelitis optica, and multiple sclerosis. Current Opinion in Neurology 20:343--350. ^ Weinshenker B, Miller D. 1999. Multiple sclerosis: one disease or many? In: Siva A, Kesselring J, Thompson A, eds. Frontiers in multiple sclerosis. London: Dunitz, p37--46. ^ Hartung H-P, Grossman R. 2001. ADEM: distinct disease or part of the MS spectrum? Neurology 56:1257-12-60. ^ a b Davies NWS, Sharief MK Howard RS 2006. Infection-associated encephalopathies: their investigation, diagnosis, and treatment. Journal of Neurology 253:833--845. ^ a b Stone MJ Hawkins CP 2007 A medical overview of encephalitis. Neuropsychological Rehabilitation 17:429-449. ^ a b Archer H all R 2003. Acute Haemorrhagic Leukoencephalopathy: Two case reports and review of the literature. Journal of Infection 46:133-137. ^ Rivers TM Schwentker FF. 1935. Encephalomyelitis accompanied by myelin destruction experimentally produced in monkeys. Journal of Experimental Medicine 61:689 -701. ^ Sriram S Steiner I 2005 Experimental Allergic Encephalomyelitis: A misleading model of Multiple Sclerosis. Annals of Neurology 58:939 -945. External links Acute Disseminated Encephalomyelitis ADEM at myelitis.org v d e Multiple sclerosis Signs and symptoms Ataxia · Depression · Diplopia · Dysarthria · Dysphagia · Fatigue · Incontinence · Neurological fatigue · Nystagmus · Optic neuritis · Pain · Uhthoff's phenomenon Diagnosis and evolution following McDonald criteria · EDSS Investigation Pathophysiology · Experimental autoimmune encephalomyelitis Treatment Interferon · Glatiramer acetate · Mitoxantrone · Natalizumab · Therapies under investigation Borderline forms Acute disseminated encephalomyelitis · Balo concentric sclerosis · Devic's disease · Guillain-Barré syndrome · Marburg multiple sclerosis · Schilder's disease Other List of people with multiple sclerosis · List of multiple sclerosis organizations v d e Pathology of the nervous system, primarily CNS G00-G47, 320-349 Inflammatory Meningitis Arachnoiditis - Encephalitis - Myelitis - Encephalomyelitis Acute disseminated - Tropical spastic paraparesis - Cavernous sinus thrombosis Systemic atrophies Huntington's disease - Spinocerebellar ataxia Friedreich's ataxia, Ataxia telangiectasia, Herary spastic paraplegia - Spinal muscular atrophy: Werdnig-Hoffman - Kugelberg-Welander - Fazio-Londe - MND ALS, PMA, PBP, PP, PLS Extrapyramidal and movement disorders Parkinson's disease - Neuroleptic malignant syndrome - Postencephalitic parkinsonism - Pantothenate kinase-associated neurodegeneration - Progressive supranuclear palsy - Striatonigral degeneration - Dystonia/Dyskinesia Spasmodic torticollis, Meige's, Blepharospasm - Essential tremor - Myoclonus - Lafora - Chorea Choreoathetosis - Restless legs - Stiff person Other degenerative/ demyelinating diseases dementia: Alzheimer's - Pick's - Dementia with Lewy bodies - Frontotemporal lobar degeneration mitochondrial disease: Leigh's demyelinating: Multiple sclerosis - Devic's - Central pontine myelinolysis - Transverse myelitis - Marchiafava-Bignami disease - CAMFAK syndrome - Alpers' Seizure/epilepsy Focal - Generalised - Status epilepticus - Myoclonic epilepsy Headache Migraine Familial hemiplegic - Cluster - Vascular - Tension Vascular Transient ischemic attack Amaurosis fugax, Transient global amnesia Cerebrovascular disease MCA, ACA, PCA, Foville's, Millard-Gubler, Lateral medullary, Weber's, Lacunar stroke Sleep disorders Insomnia - Hypersomnia - Sleep apnea Obstructive, Ondine's curse - Narcolepsy - Cataplexy - Kleine-Levin - Circadian rhythm sleep - Delayed sleep phase - Advanced sleep phase Intracranial hypertension Hydrocephalus Normal pressure - Idiopathic intracranial hypertension Other encephalopathy Brain herniation - Cerebral edema - Reye's Other spinal cord disease Syringomyelia - Syringobulbia - Morvan's syndrome - Spinal cord compression Retrieved from http://en..org/wiki/Acute_disseminated_encephalomyelitis Categories: Multiple sclerosis | Autoimmune diseases | Neurological disorders | NeurologyHidden categories: All articles with statements | Articles with statements since March 2008 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 Suomi This page was last modified on 7 August 2008, at 15:49

Videos and Links

39 Reasons to Drink Acai Juice Every Day
What is MonaVie - Watch the 8-minute video
Discovering MonaVie Video
The Power of You Video
Effects of MonaVie Active on Antioxidant Capacity in Humans
Log into your Wholesale MonaVie Account

Why Drink MonaVie?

So many of us do not eat a balanced diet, get enough sleep, have too much stress, or are impacted with toxins and pollutants. Drinking 2 ounces of MonaVie twice a day will help your body detoxify as well as build your immune system. Its the smartest thing you can do for yourself, so start today. Buying MonaVie through our company guarantees you support 7 days a week and, if you would like to share MonaVie with your family and friends we will guide you from start to finish.

The Best Way to Buy MonaVie is Wholesale

1. Click on Enroll Now (30 - 55% off retail price)
2. Pay $39 for your Wholesale ID number.
3. NO minimum order required.
4. MonaVie is delivered to your door in 3 to 5 days.


Sierra Acai Company | Site Map |