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Ingenta: Table Of Contents -- Reactions, 2003, Volume 1, Issue 950 20. Cyclosporin Central and extrapontine myelinolysis case reportReactions, 2003, vol. 1, iss. 950, pp. 88(1) Adis International http://www.ingenta.com/isis/browsing/TOC/ingenta?issue=pubinfobike://adis/rea/20
Hyponatraemia: Common Causes Were Heart Failure And Iatrogenic. part due to overly rapid correction of patients with chronic hyponatremia which probablyresulted in central pontine and extrapontine myelinolysis causing coma http://www.eboncall.org/CATs/2109.htm
Extractions: Clinical bottom line (level 4) Mortality was higher in patients with acute onset hyponatraemia or symptomatic hyponatraemia. The commonest causes of hyponatraemia were congestive heart failure, iatrogenic causes (fluid overload or diuretics) and SIADH. Arieff et al: Medicine 1976; 55 (2): 121-129 Outcomes studied: mortality with chronic symptomatic hyponatraemia mortality with asymptomatic hyponatraemia cause: congestive heart failure cause: SIADH cause: post-surgical (overtransfusion with 5% dextrose) fluid overload cause: dieuretic use usually due to diuretic use cause: chronic renal failure cause: acute renal failure
AJNR -- Abstracts: Ho Et Al. 14 (1): 163 of Neuroradiology. ARTICLES. Resolving MR features in osmotic myelinolysis(central pontine and extrapontine myelinolysis). VB Ho, CR http://www.ajnr.org/cgi/content/abstract/14/1/163
Extractions: Department of Radiology, Walter Reed Army Medical Center, Washington, DC 20307-5001. Osmotic myelinolysis is a distinctive clinical syndrome with characteristic MR features in the central pons (central pontine myelinolysis) and in other locations (extrapontine myelinolysis). We describe the resolving MR features in an adolescent who has experienced complete neurologic recovery. Regions of involvement manifested increased T2 signal intensity. The extrapontine involvement was noted to resolve earlier with interim-increased T1-weighted signal. The mechanism for the variable
Questia Online Library - New Search NeuropsychiatryResearch. 2. Methylphenidate Treatment of NeuropsychiatricSymptoms of Central and extrapontine myelinolysis(*). Journal article http://www.questia.com/SM.qst?act=search&subjects=Neuropsychiatry&subjectsSearch
Murat Aydin Yayinlar. 1. Ozturk F, Gork S, Aydin M, Incesu L, Baysal K. extrapontine myelinolysisin a nineyear-old child. Turk J Pediatr. 1998 Oct-Dec;40(4)579-84. http://www.omucocuk.gen.tr/ogretim/aydin/aydin.htm
Extractions: Hazýrlayan: Dr. Aliþan YILDIRAN Prof. Dr. Murat AYDIN Doðum Yeri-Tarihi Sürmene, Trabzon 06.02.1959 Ýlkokul Ýskender Paþa Ýlkokulu, Trabzon, 1966-1970 Ortaokul Mimar Kemal Ortaokulu, Ankara, 1970-1973 Lise Mimar Kemal Lisesi, Ankara, 1973-1976 Üniversite Hacettepe Üniversitesi, Trabzon Týp Fakültesi, 1976-1982 Karadeniz Üniversitesi Týp Fakültesi 1982 - 1983 Uzmanlýk Hacettepe Üniversitesi Týp Fakültesi Çocuk Saðlýðý ve Hastalýklarý Anabilim Dalý, 1986-1990 Yan Dal Uzmanlýðý Hacettepe Üniversitesi Týp Fakültesi Çocuk Saðlýðý ve Hastalýklarý Anabilim Dalý, Endokrinoloji Ünitesi, 1994-1996 Yardýmcý Doçent Doçent Profesör Yabancý Dil Ýngilizce Çalýþtýðý kurumlar 1984-86 Ýskenderun Çimento Fabrikasý, Ýþ yeri hekimi Mecburi Hizmet) 1986 90 Hacettepe Üniversitesi Týp Fakültesi Çocuk Saðlýðý ve Hastalýklarý Anabilim Dalý, Araþtýrma Görevlisi (Asistanlýðýnýn son yýlýnda baþasistan olarak görev aldý) 2000 - Ondokuz Mayýs Üniversitesi Hastanesi Baþhekim Yardýmcýlýðý Medeni Hali Evli, iki çocuklu.
Kemal Baysal Ozturk F, Gork S, Aydin M, Incesu L, Baysal K. extrapontine myelinolysisin a nineyear-old child. Turk J Pediatr. 1998 Oct-Dec;40(4)579-84. http://www.omucocuk.gen.tr/ogretim/baysal/baysal.htm
Health/Conditions And Diseases/E Multiforme@ 3 Erythromelalgia@ 4 Esophageal Diseases@ 47 Essential Tremor@2 Excessive Crying in Infants@ 7 extrapontine myelinolysis@ 3 Eye Cancer http://www.ebroadcast-info.com/information/Health/Conditions_and_Diseases/E/reso
¥xÆW¯«¸g¾Ç¥»¤g¸ê®Æ 51. CJ Chen, ChinChang Huang, LS Lo. Evolution of pontine and extrapontine myelinolysisclinical correlation with serial CT and MRI studies. Eur Neurol. http://www.neuro.org.tw/study/mov06.htm
Extractions: ¹B°Ê»Ùª¾Ç²Õ ¶ÀÀA³¹ ¦^¤W¤@¶ ½s¸¹ Yung-Kuei Soong, Horng-Yuan Huang, Chin-Chang Huang , Nai-Shin Chu: Successful pregnancy after D-penicillame theraphy in a patient with Wilson's disease. J Formosan Med Assoc 1991;90:693-696. Nai-Shin Chu, Chen-Chung Chu, Shu-Chen Tu, Chin-Chang Huang EEG spectral analysis and tographic mapping in Wilson's disease. J Neurol Sci Chin-Chang Huang , Nai-Shin Chu: Wilson's disease: Resolution of cerebral white matter lesions following long-term penicillamine therapy. J Formosan Med Assoc 1992;91:627-629. Chin-Chang Huang, Nai-Shin Chu: Wilson's disease: Clinical analysis of 71 cases and comparison with previous Chinese series. J Formosan Med Assoc 1992;91:502-507. Chin-Chang Huang , Chin-Song Lu, Nai-Shin Chu, F.H.Hochberg, D. Lilienfeld, D.B. Calne: Pathogensis of idiopathic Parkinsonism. In: Controversies in the treatment of Parkinson's disease. U.K. Rinne, N Yanagisawa, eds. PMSI, Tokyo. pp.7-13,1992.
Ô˶¯ÕÏ°ÐÔ¼²²¡---www.sunbinmd.com of Neurology, 3ed , McGrawHill Kook Co, New York , 1985, 778-780 2 Menger H,Jorg J. Outcome of central pontine and extrapontine myelinolysis J Neurol. http://www.sunbinmd.com/newsinfo.asp?nid=108
Radiology Abstracts Miller Et Al. 168 (3) 795 One patient never had a demonstrable pontine lesion but did have symmetric basalganglia abnormalities, which were consistent with extrapontine myelinolysis. http://intl-radiology.rsnajnls.org/cgi/content/abstract/168/3/795
Health, Conditions And Diseases, E extrapontine myelinolysis@ (3); Eye Cancer@ (34). This category in other languagesDanish (0), Dutch (0), German (0). Spanish (0). SPONSORED LINKS. PARTNERS LINKS. http://www.klevze.si/browse/Health/Conditions_and_Diseases/E/
Extractions: Gyr/ Haefeli/ Schoenenberger: Internistische Notfälle , ISBN 3135106071 Adrogue HJ, Madias NE. Aiding fluid prescription for the dysnatremias. Intens Care Med 1997;23:309-16 Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med 2000;342:1581-9 Berl T. Treating hyponatremia: damned if we do and damned if we don't. Kidney Int 1990;37:1006-18 Gross P, Reimann D, Neidel J et al. The treatment of severe hyponatremia. Kidney Int Suppl 1998;64:S6-S11 Karp BI, Laureno R. Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia. Medicine (Baltimore) 1993;72:359-73 Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte disorders. 5th ed. New York: McGraw-Hill 2001; p. 716-20; 761-4 Sterns RH. Severe symptomatic hyponatremia: Treatment and outcome. A study of 64 cases. Ann Intern Med 1987;107:656-64 Sterns RH, Cappuccio JD, Silver SM, Cohen EP.
Extractions: (advertisement) Synonyms, Key Words, and Related Terms: osmotic myelinolysis Background: Adams et al described central pontine myelinolysis (CPM) as a unique clinical entity. They published their findings in 1958, observing that patients who suffered from alcoholism or malnutrition developed spastic quadriplegia, pseudobulbar palsy, and varying degrees of encephalopathy or coma from acute, noninflammatory demyelination that centered within the basis pontis. Contemporary physicians recognize that CPM occurs inconsistently as a complication of severe and prolonged hyponatremia, particularly when corrected too rapidly. Standard of care requires judicious treatment of electrolyte disturbances to reduce the incidence of osmotic myelinolysis. Pathophysiology: CPM is concentrated, frequently symmetric, noninflammatory demyelination within the central basis pontis. In at least 10% of patients with CPM, demyelination also occurs in extrapontine regions, including the mid brain, thalamus, basal nuclei, and cerebellum. The exact mechanism that strips the myelin sheath is unknown. One theory proposes that in regions of compact interdigitation of white and gray matter, cellular edema, which is caused by fluctuating osmotic forces, results in compression of fiber tracts and induces demyelination. Prolonged hyponatremia followed by rapid sodium correction results in edema. During the period of hyponatremia, the concentration of intracellular charged protein moieties is altered; reversal cannot parallel a rapid correction of electrolyte status. The term "osmotic myelinolysis" is more appropriate than "central pontine myelinolysis" for demyelination occurring in extrapontine regions after the correction of hyponatremia.
Central Pontine Myelinolysis sometimes be present. extrapontine sites of myelinolysis in the basalganglia and midbrain, and subcortical white matter may also occur. http://www.amershamhealth.com/medcyclopaedia/medical/Volume VI 1/CENTRAL PONTINE
Extractions: Amershamhealth.com Search for: Type a word or a phrase. All forms of the word are searchable. Browse entry words starting with: A B C D ... Other characters Central pontine myelinolysis, (also called osmotic demyelination), demyelinating disorder found in alcoholics or in association with many systemic disorders with electrolyte abnormalities. Because of the common association with rapidly corrected hyponatraemia, the term "osmotic demyelination syndrome" has been proposed. The symptoms of central pontine myelinolysis are quadriparesis, pseudobulbar palsy and changing levels of consciousness, including coma and death. Histologically, the area of myelin breakdown is sharply demarcated and displays extensive loss of oligodendrocytes, infiltration with foamy macrophages and reactive astrocytosis. At MR the lesion is characterized by T2 hyperintensity in a central pontine location ( Fig.1 ); gadolinium enhancement may sometimes be present. Extrapontine sites of myelinolysis in the basal ganglia and midbrain, and subcortical white matter may also occur. Many entities can be considered in the differential diagnosis, including ischaemia, multiple sclerosis, encephalitis, toxic exposures, radiation therapy effects and brain stem gliomas. When present, the key to the MRI diagnosis is the bilateral involvement of the deep and capsular white matter, often accompanied by abnormalities in the thalami and basal ganglia.
Central Pontine Myelinolysis Was First Described By Adams Et Al... myelinolysis in the pons is frequently associated with demyelination in other areasof These extrapontine lesions are thought to coexist with CPM in 10% of the http://www.indegene.com/Neu/ClinRound/indNeuCase10.html
Extractions: Hospital: Depatment of Medicine, Maulana Azad Medical College, New Delhi Introduction Central pontine myelinolysis was first described by Adams et al in 1959 during the course of studying the neuropathology of alcoholism. The lesion was localized to the central rostral part of the pons and consisted of a sharply outlined focus of myelin destruction. Quadriplegia and pseudobulbar palsy were the main clinical findings. CPM was usually a postmortem diagnosis till the advent of the CT and the MRI. We report this interesting case of a young lady who developed CPM following hemodialysis. Case Report A young 26-year-old lady, a diagnosed case of Hypertension with MPGN with Chronic Renal Failure, was admitted with complaints of sudden onset loss of consciousness. The patient had developed altered sensorium 4 days before presentation, for which she was taken to a private nursing home and was hemodialysed twice. Following dialysis she developed drooping of the right eyelid and progressive paraparesis. Following this the patient developed loss of consciousness, when she was brought to our hospital. There was no other significant history. On examination the patient was unconscious, not responding to painful stimulus and a blood pressure of 180/130. The general physical examination showed pallor and facial puffiness but no icterus, clubbing or lymphadenopathy. Chest, CVS and per abdomen examination was normal. CNS examination revealed deep comatose state, a right third nerve palsy, paraparesis, which later progressed to quadriparesis, with bilateral up-going plantars.
Extractions: Cases in the BRAIN: Non-neoplastic II section: 100 MR2001 Amyotrophic lateral sclerosis MR2002 Gray matter heterotopia MR2003 Cryptococcal meningitis, hydrocephalus and shunting with resulting subdural hematomas; subependymal cryptococcal cerebritis MR2004 Cysticercosis MR2005 Herpes encephalitis MR2006 Viral cerebellaritis MR2007 Nocardiosis MR2008 Toxoplasmosis MR2009 Cysticercosis MR2010 Brain abscess MR2011 Brain abscess MR2012 Cryptococcosis MR2013 Intracranial sarcoidosis MR2014 Tuberculous meningitis MR2015 Deep white matter and PICA infarct MR2016 Left middle cerebral artery infarction with Wallerian degeneration of the left corticospinal tract MR2017 Acute left hemispheric infarct and incidental corpus callosum lipoma MR2018 Occlusion of the left internal carotid artery with chronic infarction involving the left middle cerebral artery territory and Wallerian degeneration of the left corticospinal tract MR2019 Putaminal hypertensive hemorrhage and small left subdural hygroma MR2020 Watershed infarcts between the distributions of the middle and posterior cerebral arteries MR2021 Bilateral watershed infarcts between the distributions of the anterior and middle cerebral arteries MR2022 Subacute hemorrhagic cortical infarcts MR2023 Chronic right temporal lobe infarct with macrocystic encephalomalacia MR2024 Infarction due to right middle cerebral artery occlusion MR2025 Acute infarction in the distribution of the right middle cerebral artery MR2026 Pontine infarct MR2027 PICA infarction MR2028 Extensive cerebral vasculitis secondary to systemic lupus erythematosus
