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         Central Pontine Myelinolysis:     more detail
  1. Thiamine Deficiency and Associated Clinical Disorders (Contemporary Clinical Neuroscience) by David W. McCandless, 2009-09-15

61. Brainstem Strokes
MRI scan of person with central pontine myelinolysis, axial view. Note the I shaped area in the center of the pons.
http://www.dizziness-and-balance.com/disorders/central/brainstem strokes.htm
Brainstem strokes associated with vertigo or hearing symptoms
Timothy C. Hain, MD Please read our Return to Index Search this site Page last modified: July 16, 2005
The purpose of this page is to consider the findings in brainstem strokes in detail. More general aspects of brainstem strokes and TIA's related to vertigo are considered elsewhere Vertigo is a common early symptom of brainstem strokes. However, because strokes are much less common than other sources of vertigo such as ear disorders, vertigo is only caused by central nervous system problems (including stroke) about 5% of the time. Migraine is a common cause of vascular vertigo. Hearing disturbance is a much less common symptom of brainstem stroke than vertigo. This may reflect the resilience of the wiring pattern of hearing in the brainstem which includes of both crossed and uncrossed pathways, or factors related to details of the blood supply or resistance of the ear to disturbances in blood supply.
Small Vessel Disease
PICA (posterior cerebellar artery syndrome).

62. Blackwell Synergy - Cookie Absent
Hyponatraemia and central pontine myelinolysis after elective colonoscopy central pontine myelinolysis (CPM) is a rare neurological disease of unknown
http://www.blackwell-synergy.com/doi/abs/10.1111/j.1468-1331.2004.00991.x
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63. Baylor Neurology Case Of The Month
The most wellknown of these disorders, central pontine myelinolysis, While central pontine myelinolysis was initially linked with alcoholism,
http://www.bcm.edu/neurology/challeng/pat75/summary.html
Patient #75
Summary and Discussion
Katie Noe, M.D., Ph.D..

Diagnosis:
Extrapontine myelinolysis following rapid correction of iatrogenic hyponatremia.
CLINICAL COURSE: DISCUSSION: Osmotic Demyelination Disorders
For these reasons, patients at risk of developing significant hyponatremia should be closely monitored. Treatment of symptomatic acute hyponatremia must balance the risk of development of osmotic demyelination with the risk of complications from the hyponatremia itself. Recent recommendations suggest that hyponatremia be corrected at a rate of not more than 8 mmol/L/day, although initial rates of correction may be as much as 1-2 mmol/L/hour until life-threatening symptoms resolve (Adrogue and Madias, 2000). Monitoring of sodium levels every 2-3 hours may be necessary in order that adjustments in treatment can be made to avoid overly rapid changes or reduce the impact of overcorrection. Chronic hyponatremia without life-threatening symptoms should be corrected very slowly. It is difficult at times, however, to distinguish chronic from acute alterations in the emergency setting. Diagnosis: clinical signs and imaging findings Diagnosis of osmotic demyelination syndromes begins with recognition of predisposing risk factors for hyponatremia, and a clinical course suggesting development of symptoms after a documented or suspected osmotic stress. Other disorders that could produce cortical, basal ganglia, or white matter injury, such as status epilepticus, hypoxic-ischemic events, hypertensive emergencies, and Wernicke encephalopathy, should be considered in the differential diagnosis.

64. Central Pontine Myelinolysis A Complication Of Hyponatremia Or Of Therapeutic In
Title central pontine myelinolysis A Complication of Hyponatremia or of Keywords alcoholism, central pontine myelinolysis, forensic science,
http://journalsip.astm.org/jofs/PAGES/837.htm
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Haibach H, Ansbacher LE, Dix JD
Title: Central Pontine Myelinolysis A Complication of Hyponatremia or of Therapeutic Intervention?
Keywords: alcoholism, central pontine myelinolysis, forensic science, hypernatremia, hyponatremia, hypothermia, malnutrition, pathology and biology, saline infusion
Abstract: We report four cases of central pontine myelinolysis (CPM) that illustrate important features of the disorder. The condition is described mainly in the neurological literature and, to our knowledge, is not discussed in the forensic science journals. This disorder must be recognized and understood by the forensic science expert who addresses issues of liability. In cases of multiple motor deficits and death with a history of hyponatremia, CPM must be included in the differential diagnosis. Careful examination of the pons and adjoining structures must be performed. Myelin stains are advisable. The association of CPM with major illnesses, hyponatremia and the correction of hyponatremia by intravenous saline infusions is discussed. Return to Search Page

65. Effect Of Hypothermia On Breath-Alcohol Analysis
We report four cases of central pontine myelinolysis (CPM) that illustrate alcoholism, central pontine myelinolysis, forensic science, hypernatremia,
http://journalsip.astm.org/JOURNALS/FORENSIC/PAGES/926.htm
Volume 32, Issue 2 (March 1987)
ISSN:
Published Online:
Page Count:

PDF not available for download View License Agreement Effect of Hypothermia on Breath-Alcohol Analysis
Fox GR, Hayward JS
Abstract
, and support previous recommendations that temperature monitoring be included in procedures for breath-ethanol testing. We recommend that mouth temperature be obtained before breath sampling to screen for abnormal body temperature and to allow for potential use of a temperature correction factor. This modification to existing analytical procedures would help to optimize the reliability of breath-ethanol analysis in predicting blood-ethanol concentration.
Keywords:
alcohol, BAC, breath analysis, breath-alcohol testing devices, cold, criminalistics, ethanol, exposure, forensic science, hypothermia, temperature
ASTM International is a member of CrossRef. Author Fox GR, Hayward JS Title Effect of Hypothermia on Breath-Alcohol Analysis Symposium , Committee on Site Map Online Support Contact IP Policy ASTM International, 100 Barr Harbor Drive, PO Box C700, West Conshohocken, PA, 19428-2959 USA

66. Clinical Neuropharmacology - UserLogin
Although the exact pathogenesis of central pontine myelinolysis (CPM) is unknown, central pontine myelinolysis, a rare condition with generally poor
http://www.clinicalneuropharm.com/pt/re/clnneupharm/fulltext.00002826-200003000-
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67. Radiology, University Of Rochester Medical Center
central pontine myelinolysis (CPM), first described in 1959 by Adams et al. central pontine myelinolysis. Arch Neurol Psychiatry 1959;81154–72.
http://www.urmc.rochester.edu/smd/Rad/neurocases/Neurocase100.htm

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68. Disease - Central Pontine Myelinolysis - Detroit, Michigan
Disease central pontine myelinolysis - courtesy of Henry Ford Health System ofDetroit, Michigan.
http://www.henryfordhealth.org/15368.cfm
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Disease - Central pontine myelinolysis
Central nervous system Definition: Central pontine myelinolysis is a condition characterized by nerve damage caused by the destruction of the covering layer ( myelin sheath) of nerve cells in the brainstem (pons). Alternative Names: CPM Causes And Risk: The destruction of the myelin sheath that coats nerves inhibits impulse conduction within the cell and thus decreases its ability to communicate with other cells. The most common cause of central pontine myelinolysis is a rapid, drastic change in sodium levels in the body. Most commonly, this occurs when someone is being treated for low levels of sodium ( hyponatremia ) and the levels rise too fast, but it can occasionally occur when high levels of sodium in the body (hypernatremia) are corrected too quickly. This condition does not occur spontaneously; it is a complication of either treatment for other conditions or the other conditions themselves.

69. Health/Conditions And Diseases/Neurological Disorders/Brain Diseases/Metabolic/C
Drkoop Medical Encyclopedia central pontine myelinolysis A definition of centralpontine myelinolysis, including the causes, risks, prevention, symptoms,
http://www.thedoctorslounge.net/dir/Health/Conditions_and_Diseases/Neurological_
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  • Drkoop: Medical Encyclopedia: Central Pontine Myelinolysis A definition of central pontine myelinolysis, including the causes, risks, prevention, symptoms, diagnosis, treatment, prognosis and complications. url: www.drkoop.com/ency/article/000775.htm E-Medicine Central Pontine Myelinolysis: An introduction, clinical features, differencials, work up, treatment and follow up. url: www.emedicine.com/neuro/topic50.htm Pediatric Database A definition of central pontine myelinolysis, the epidemiology, pathogenesis, clinical features, investigations and management. url: www.icondata.com/health/pedbase/files/CENTRALP.HTM mozilla.org url: mozilla.org/
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    70. Central Pontine Myelinolysis
    central pontine myelinolysis is nerve damage caused by the destruction of thelayer (myelin sheath) covering nerve cells in the brainstem (pons).
    http://www.pennhealth.com/ency/article/000775.htm
    Appointments Medical Services Health Information Find a Doctor Search: Search Encyclopedia: List of Topics Print This Page  Cognitive Neurology
    Central pontine myelinolysis
    Central nervous system Definition: Central pontine myelinolysis is nerve damage caused by the destruction of the layer ( myelin sheath ) covering nerve cells in the brainstem (pons). Alternative Names: CPM Causes, incidence, and risk factors: The destruction of the myelin sheath that coats nerve cells prevents signals from being properly conducted within the nerve. This decreases its ability to communicate with other cells. The most common cause of central pontine myelinolysis is a rapid, drastic change in sodium levels in the body. Most commonly, this occurs when someone is being treated for low levels of sodium ( hyponatremia ) and the levels rise too fast. It also can occasionally occur when high levels of sodium in the body (hypernatremia) are corrected too quickly. This condition does not occur on its own. It is a complication of treatment for other conditions or the other conditions themselves. People at risk include those with low sodium levels from any cause

    71. Cerebral Demyelination Syndrome
    central pontine myelinolysis. Book. Home Page, Cardiovascular Medicine, Dentistry,Dermatology, Emergency Medicine, Endocrinology, Gastroenterology
    http://www.fpnotebook.com/REN91.htm
    Home About Links Index ... Editor's Choice document.write(code); Advertisement Nephrology Neurology Sodium Cerebral Demyelination Syndrome Cerebral Demyelination Syndrome Central Pontine Myelinolysis Book Home Page Cardiovascular Medicine Dentistry Dermatology Emergency Medicine Endocrinology Gastroenterology Geriatric Medicine Gynecology Hematology and Oncology HIV Infectious Disease Jokes Laboratory Neonatology Nephrology Neurology Obstetrics Ophthalmology Orthopedics Otolaryngology Pediatrics Pharmacology Practice Management Prevention Psychiatry Pulmonology Radiology Rheumatology Sports Medicine Surgery Urology Chapter Nephrology Index Acid and Base Disorders Calcium Chloride Cardiovascular Medicine Dermatology Edema Endocrinology Examination Failure Glomerulus Laboratory General Pulmonology Magnesium Neurology Pharmacology Phosphorus Potassium Prevention Radiology Sodium Surgery Tubule Page Neurology Index Sodium CPM
  • See Also Hyponatremia Pathophysiology Lethal Cerebral edema from rapid electrolyte correction Over-correction of Serum Sodium Too rapid correction of Serum Sodium Related to chronicity of electrolyte disturbance Associated with rapid correction chronic Hyponatremia Not associated with correction of acute Hyponatremia
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    72. Central Pontine And Extrapontine Myelinolysis: The Osmotic Demyelination Syndrom
    Keywords central pontine myelinolysis; extrapontine myelinolysis; central pontine myelinolysis (CPM) was described by Adams and colleagues in 1959 as
    http://jnnp.bmjjournals.com/cgi/content/extract/75/suppl_3/iii22

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    Journal of Neurology Neurosurgery and Psychiatry
    CENTRAL PONTINE AND EXTRAPONTINE MYELINOLYSIS: THE OSMOTIC DEMYELINATION SYNDROMES
    R J Martin Correspondence to:
    Dr R J Martin
    Department of Neurology, Gloucestershire Royal Hospital, Great Western Road, Gloucester GL1 3NN, UK; roswell.martin@gloucr-tr.swest.nhs.uk Keywords: central pontine myelinolysis; extra-pontine myelinolysis; osmotic demyelination syndromes The first 150 words of the full text of this article appear below.

    73. Central Pontine Myelinolysis Associated With Hypokalaemia In Anorexia Nervosa *
    Keywords central pontine myelinolysis; posterior reversible encephalopathy He was thought to have asymptomatic central pontine myelinolysis (CPM).
    http://jnnp.bmjjournals.com/cgi/content/full/75/4/663

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    CORRESPONDENCE
    Central pontine myelinolysis associated with hypokalaemia in anorexia nervosa
    S C Keswani Department of Neurology, Johns Hopkins Hospital, Baltimore, MD, USA Correspondence to:
    Dr S C Keswani
    Pathology 509, The Johns Hopkins Hospital, 600 North Wolfe St, Baltimore, MD 21287, USA; Keywords: central pontine myelinolysis; posterior reversible encephalopathy syndrome; diffusion weighted imaging

    74. Health Encyclopedia
    central pontine myelinolysis is a condition characterized by nerve damage causedby the destruction of the covering layer ( myelin sheath) of nerve cells in
    http://healthcontent.baptisteast.com/adamcontent/ency/article/000775.asp
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    Disease
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    Central pontine myelinolysis
    Central nervous system

    Overview
    Symptoms Treatment ... Prevention
    Alternate Names
    CPM
    Definition
    Central pontine myelinolysis is a condition characterized by nerve damage caused by the destruction of the covering layer ( myelin sheath) of nerve cells in the brainstem (pons).
    Causes and Risk
    The destruction of the myelin sheath that coats nerves inhibits impulse conduction within the cell and thus decreases its ability to communicate with other cells. The most common cause of central pontine myelinolysis is a rapid, drastic change in sodium levels in the body. Most commonly, this occurs when someone is being treated for low levels of sodium ( hyponatremia ) and the levels rise too fast, but it can occasionally occur when high levels of sodium in the body (hypernatremia) are corrected too quickly. This condition does not occur spontaneously; it is a complication of either treatment for other conditions or the other conditions themselves.

    75. Transplantation - Fulltext: Volume 61(4) February 27, 1996 P 658-661 CENTRAL PON
    central pontine myelinolysis AND CYCLOSPORINE NEUROTOXICITY FOLLOWING LIVERTRANSPLANTATION. Fryer, Jonathan P. 1,2; Fortier, Marielle V. 3; Metrakos,
    http://www.transplantjournal.com/pt/re/transplantation/fulltext.00007890-1996022
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    Abstract
    References (17) View full size inline images Transplantation Volume 61(4) 27 February 1996 pp 658-661
    CENTRAL PONTINE MYELINOLYSIS AND CYCLOSPORINE NEUROTOXICITY FOLLOWING LIVER TRANSPLANTATION
    Fryer, Jonathan P. ; Fortier, Marielle V. ; Metrakos, Peter ; Verran, Deborah J. ; Asfar, Sami K. ; Pelz, David M. ; Wall, William J. ; Grant, David R. ; Ghent, Cameron N. Multiorgan Transplant Service and Department of Radiology, University Hospital, University of Western Ontario, London, Ontario, Canada Multiorgan Transplant Service. Department of Radiology. Address correspondence to Dr. Jonathan P. Fryer, Department of Surgery, Northwestern University, 303 East Superior, Suite 532, Chicago, IL 60611. Received 7 June 1995. Accepted 5 September 1995. Article Outline Figures/Tables
    Abstract TOP
    In a recent series of 44 liver transplants we identified both extrapontine myelinolysis (EPM)-characteristic of cyclocosporine neurotoxicity-and central pontine myelinolysis (CPM) in 5 recipients posttransplant. An additional 2 recipients had EPM only posttransplant. MRIs performed in 4 asymptomatic recipients were normal. Large perioperative shifts in serum sodium, hypomagnesemia, and high cyclosporine levels may play a role in the development of these lesions, although the evidence from this study is inconclusive. In addition to supportive care, dilantin was started in patients who had seizures; aggressive magnesium replacement was initiated for hypomagnesemia, and cyclosporine levels were reduced in all patients. All patients demonstrated a slow steady recovery and all but 2 are home at the time of writing. CPM may be more prevalent than previously appreciated following liver transplantation, although its prognosis may not be as dismal.

    76. Transplantation - Abstract: Volume 61(4) February 27, 1996 P 658-661 CENTRAL PON
    central pontine myelinolysis AND CYCLOSPORINE NEUROTOXICITY FOLLOWING LIVERTRANSPLANTATION. Transplantation. 61(4)658661, February 27, 1996.
    http://www.transplantjournal.com/pt/re/transplantation/abstract.00007890-1996022
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    Fulltext
    CENTRAL PONTINE MYELINOLYSIS AND CYCLOSPORINE NEUROTOXICITY FOLLOWING LIVER TRANSPLANTATION.
    Transplantation. 61(4):658-661, February 27, 1996.
    Fryer, Jonathan P. 1,2; Fortier, Marielle V. 3; Metrakos, Peter 1; Verran, Deborah J. 1; Asfar, Sami K. 1; Pelz, David M. 2; Wall, William J. 1; Grant, David R. 1; Ghent, Cameron N. 1 Abstract:
    In a recent series of 44 liver transplants we identified both extrapontine myelinolysis (EPM)-characteristic of cyclocosporine neurotoxicity-and central pontine myelinolysis (CPM) in 5 recipients posttransplant. An additional 2 recipients had EPM only posttransplant. MRIs performed in 4 asymptomatic recipients were normal. Large perioperative shifts in serum sodium, hypomagnesemia, and high cyclosporine levels may play a role in the development of these lesions, although the evidence from this study is inconclusive. In addition to supportive care, dilantin was started in patients who had seizures; aggressive magnesium replacement was initiated for hypomagnesemia, and cyclosporine levels were reduced in all patients. All patients demonstrated a slow steady recovery and all but 2 are home at the time of writing. CPM may be more prevalent than previously appreciated following liver transplantation, although its prognosis may not be as dismal.
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    77. Untitled Document
    central pontine myelinolysis is a disorder characterized pathologically bydissolution of the myelin sheaths of fibers within the central aspect of the
    http://spinwarp.ucsd.edu/NeuroWeb/Text/br-840cpm.htm
    Central Pontine Myelinolysis Central pontine myelinolysis is a disorder characterized pathologically by dissolution of the myelin sheaths of fibers within the central aspect of the basis pontis. In extreme cases there may be extension to the pontine tegmentum, midbrain, thalamus, internal capsule and cerebral cortex. The myelinolysis occurs with relative sparing of the nerve cells and axon cylinders. Many patients are asymptomatic, and at the other extreme are patients whose symptoms are masked by coma. Most clinically diagnosed cases present with spastic quadriparesis, pseudobulbar palsy, and acute changes in mental status with progression possible to altered levels of consciousness and death. Survival is possible with varying residual neurologic deficits. Although initial reports were largely confined to chronic alcoholics, central pontine myelinolysis has also been seen in patients with electrolyte disturbances, particularly hyponatremia which has been rapidly corrected. The lesions on MR are seen best as areas of hypointensity on IR images and hyperintensity on T2-weighted images in the central pons with sparing of the pontine tegmentum and ventrolateral pons. Lesions have an oval shape on sagittal images, a bat-wing configuration on coronal images and various shapes on the axial images. The extrapontine lesions often resolve completely, leaving some residual pontine abnormality. Enhancement is not a feature of this disease, but severe cases may show peripheral enhancement of the pontine lesions.

    78. Decreased Diffusion In Central Pontine Myelinolysis -- Cramer Et Al. 22 (8): 147
    central pontine myelinolysis (CPM) is an uncommon consequence of certain Early Diagnosis of central pontine myelinolysis with DiffusionWeighted Imaging
    http://www.ajnr.org/cgi/content/full/22/8/1476
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    American Society of Neuroradiology
    ARTICLE
    Decreased Diffusion in Central Pontine Myelinolysis
    Steven C. Cramer a Keith C. Stegbauer a Alex Schneider a John Mukai a and Kenneth R. Maravilla a a From the Departments of Neurology (S.C.C., A.S.), Bioengineering (K.C.S.), and Radiology (K.R.M.), University of Washington, Seattle, WA, and Kennewick General Hospital (J.M.), Kennewick, WA.
    Abstract TOP
    Abstract
    Introduction
    Case Reports
    Discussion
    References Summary: Two patients with central pontine myelinolysis (CPM) were studied with diffusion-weighted MR imaging 1 week after onset of tetraplegia. In both patients, affected white matter

    79. Central Pontine Myelinolysis: Correlation Between CT And Electrophysiologic Data
    central pontine myelinolysis correlation between CT and electrophysiologic data.J Sztencel, D Baleriaux, S Borenstein, E Brunko and D Zegers de Beyl
    http://www.ajnr.org/cgi/content/abstract/4/3/529
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    ARTICLES
    Central pontine myelinolysis: correlation between CT and electrophysiologic data
    J Sztencel, D Baleriaux, S Borenstein, E Brunko and D Zegers de Beyl
    Because of the nature and location of the lesion in central pontine myelinolysis, considerable difficulties in diagnosis may arise. Computed tomography (CT) and brainstem auditory-evoked potentials are useful in following the spread and regression of the pontine lesion. The correlation between clinical evolution, serial CT scans, and brainstem auditory-evoked potentials is considered in a patient with central pontine myelinolysis and subsequent complete recovery with special emphasis on the evolution of the CT scan after recovery.

    80. Alcohol Research Center - Marchiafava-Bignami Sydrome - Louisiana
    Korsakoff s psychosis Alcoholic dementia central pontine myelinolysis What about central pontine myelinolysis and MarchiafavaBignami s disease?
    http://alcoholresearch.lsuhsc.edu/effects/bignami.asp

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