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
Extractions: 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. PICA (posterior cerebellar artery syndrome).
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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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
Extractions: 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.
Extractions: 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
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
Extractions: , 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.
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-
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;8115472. http://www.urmc.rochester.edu/smd/Rad/neurocases/Neurocase100.htm
Extractions: Previous Case View Other Brain Degenerative/Demyelination Cases Next Case Xiang Liu, MD, PhD and PL Westesson, MD, PhD, DDS Clinical Presentation: A 54-year-old man, status-post liver transplant one month ago (end stage liver disease secondary to hepatitis C), presented with left facial droop, slurred speech, and had several falls. He was on Tacrolimus for immunosuppression. Radiological Findings: Axial CT images showed swelling in the central pons with low density, which caused the fourth ventricle compression ( Fig. 1 ). There were also several patchy lesions with low density in the periventricular and frontal subcortical areas ( Fig. 2
Extractions: 3D Tour of the Vattikuti Institute About the Institute The Vattikuti Institute Prostatectomy Prostate Cancer ... Health Encyclopedia Back to main Health Information page 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.
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
Extractions: Appointments Medical Services Health Information Find a Doctor Search: Search Encyclopedia: List of Topics Print This Page  Cognitive Neurology 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
Cerebral Demyelination Syndrome central pontine myelinolysis. Book. Home Page, Cardiovascular Medicine, Dentistry,Dermatology, Emergency Medicine, Endocrinology, Gastroenterology http://www.fpnotebook.com/REN91.htm
Extractions: 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 Search other websites for this topic Advertisement Please see the privacy statement regarding advertising on this page.
Extractions: Vol Page [Advanced] This Article Full Text Full Text (PDF) Submit a response ... Alert me if a correction is posted Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Download to citation manager PubMed PubMed Citation Articles by Martin, R J Related Collections Neurology in Practice 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.
Extractions: Vol Page [Advanced] This Article Extract Full Text (PDF) Submit a response ... Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Download to citation manager PubMed PubMed Citation Articles by Keswani, S C Articles by Wada, Y Related Collections Other Neurology
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
Extractions: Overview Symptoms Treatment ... Prevention CPM 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). 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.
Extractions: Abstract References (17) View full size inline images Transplantation Volume 61(4) 27 February 1996 pp 658-661 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 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.
Extractions: 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.
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
Extractions: 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.
Extractions: This Article Abstract Figures Only Full Text (PDF) ... Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager ... Cited by other online articles PubMed PubMed Citation Articles by Cramer, S. C. Articles by Maravilla, K. R. American Journal of Neuroradiology American Society of Neuroradiology 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.
Extractions: This Article Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager PubMed PubMed Citation Articles by Sztencel, J. Articles by Zegers de Beyl, D. 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.
