La Imagen Del Mes Translate this page A manifestation of extrapontine myelinolysis confirmed by magnetic resonanceimaging. MR imaging of pontine and extrapontine myelinolysis. http://www.rnarg.com.ar/med/revista1/imagen.htm
Extractions: Article Table of Contents Full Text of this article Figures/Tables List Services Send comment/rapid response letter Notify a friend about this article Alert me when this article is cited Add to Personal Archive ... ACP Search PubMed Articles in PubMed by Author: Laureno, R. Karp, B. I. Related Articles in PubMed PubMed Citation ... PubMed Robert Laureno, MD and Barbara Illowsky Karp, MD Myelinolysis is a neurologic disorder that can occur after rapid correction of hyponatremia.Initially named "central pontine myelinolysis," this disease is now known to also affect extrapontine brain areas. Manifestations of myelinolysis usually evolve several days after correction of hyponatremia. Typical features are disorders of upper motor neurons, spastic quadriparesis and pseudobulbar palsy, and mental disorders ranging from mild confusion to coma. Death may occur. The motor and localizing signs of myelinolysis differ from the generalized encephalopathy that is caused by untreated hyponatremia.
Syndrome Of Inappropriate ADH Pontine and extrapontine myelinolysis a neurologic disorder following rapidcorrection of hyponatremia. Karp BI, Laureno R. http://www.thedoctorsdoctor.com/diseases/siadh.htm
Extractions: Background SIADH stands for syndrome of inappropriate anti-diuretic hormone. The abnormal production of this hormone ADH, leads to salt wasting, or hyponatremia. The result is a profound metabolic disturbance which may result in coma and death. The pathologist is often called upon to investigate a laboratory abnormality of serum hypo-osmolality, an unexpectedly high urinary specific gravity, an absence of edema or dehydration, hyponatremia, and an elevation of plasma vasopressin. Usually there is normal adrenal, thyroid, and renal function. Occasionally the syndrome is due to head trauma or a tumor. In these cases, the pathologist may be called upon to evaluate a tissue biopsy to confirm the diagnosis. OUTLINE Epidemiology Amiodarone Pneumonia Laboratory/Radiologic/Other Diagnostic Testing Gross Appearance and Clinical Variants Geriatric Differential Diagnosis Cerebral salt wasting syndrome Prognosis Central pontine myelinolysis Treatment Vasopressin Receptor Antagonist Commonly Used Terms Internet Links EPIDEMIOLOGY CHARACTERIZATION SYNONYMS Schwartz-Bartter syndrome INCIDENCE/PREVALENCE Probably more common than reported AGE
Journal Of Clinical Neurophysiology - UserLogin CENTRAL PONTINE AND extrapontine myelinolysis TOP. Central pontine myelinolysis (CPM)occurs at an increased rate in liver transplant recipients. http://www.clinicalneurophys.com/pt/re/jclnneurophys/fulltext.00004691-199601000
Royal Hospital For Neuro-disability A case of central pontine myelinolysis and extrapontine myelinolysis during rapidcorrection of hypernatremia. Japanese http://www.rhn.org.uk/doc.asp?docId=300&catId=257
IM Abstract 39-11 Case Reports 11 showed a signal increase in the central pons, thalamus and striatum on T2weighted images compatible with central pontine and extrapontine myelinolysis. http://www.naika.or.jp/im/im39/ab3911/c391111.html
Extractions: Home Table of Issues Vol.39 No.11 Slowly Progressive Dystonia Following Central Pontine and Extrapontine Myelinolysis A 28-year-old woman was hospitalized with dysarthria and oro-mandibular and upper limb dystonia. Approximately 8 years prior to the current admission, the woman became severely hyponatremic due to traumatic subarachnoid hemorrhage-related SIADH. Brain MRIs showed a signal increase in the central pons, thalamus and striatum on T2 weighted images compatible with central pontine and extrapontine myelinolysis. From a few months after that event, dystonia progressed slowly over the subsequent 8 years. We speculate that the particular damage chiefly to the myelin structures by myelinolytic process may have caused an extremely slow plastic reorganization of the neural structures, giving rise to progressive dystonia.
Intenal Medicine Contents Vol.39 No.11 Slowly Progressive Dystonia Following Central Pontine and extrapontine myelinolysisAbstract; Bilirubin Adsorption Therapy and Subsequent Liver http://www.naika.or.jp/im/im39/im3911.html
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Water Balance - Slide Notes 23. pontine and extrapontine myelinolysis clinical manifestations. 24.central pontine myelinolysis white areas in the middle of the pons indicate massive http://22.214.171.124/video/panteq/neworleans2004/verbalis/caption.htm
Extractions: Researchers at Cedars-Sinai Medical Center report that high amounts of Hepatitis C (HCV) in the blood and simultaneous co-infection with the human immunodeficiency virus (HIV) may be linked to a greater risk of developing AIDS and AIDS related death. affiliate alternative medicine antioxidants auction ... zoo Injection drug users constitute the largest group of persons infected with the hepatitis C virus (HCV) in the United States, and most new infections occur in drug users. Fortunately, a substantial body of research and clinical experience exists on the prevention and management of chronic viral infections among injection drug users, especially HIV infection, and effective principles have been developed for engaging drug users in health care relationships (Table 2). http://www.stressgen.com/news/pr-010417-hepb.PDF
BrainTF19 -Porphyria_Text MRI may show central pontine and extrapontine myelinolysis and/or cortical laminarnecrosis. These are not common in AIP, but may be due to rapid correction http://www.mribhatia.com/braintf19/braintf19text.html
Extractions: BrainTF19 -Porphyria Clinical Profile: Patient is a fourteen year old boy who is a known case of porphyria. He presented with weakness of the right upper extremity, seizures and abdominal cramps. Findings: There are hyperintense areas on the Proton, T2W and FLAIR images along the cortex and subcortical white matter in the left fronto-parieto-temporal lobes and in the right centrum semiovale. These are hypointense on the T1W images. Similar signal changes are seen in the lentiform and caudate nuclei, bilaterally, in a symmetric fashion. These changes would be most likely ischemic in etiology. Discussion: Porphyria is a group of at least eight disorders that differ considerably from each other. A common feature in all is the accumulation in the body of "porphyrins" or "porphyrin precursors". Though normal body chemicals, they normally do not accumulate. Which of these chemicals builds up depends upon the type of porphyria. The symptoms arise mostly from effects on the nervous system or the skin. Effects on the nervous system occur in the acute porphyrias. Skin manifestations can include burning, blistering and scarring of sun-exposed areas. The terms "porphyrin" and "porphyria" are derived from the Greek word "porphyrus" meaning purple. Urine from some porphyria patients may be reddish in color due to the presence of excess porphyrins and related substances, and the urine may darken after standing in light. In each type of porphyria there is a deficiency of a specific "enzyme". These enzymes are involved in the synthesis of heme (found in largest amounts in the bone marrow, red blood cells and the liver). Heme exists as hemoglobin in the bone marrow and red blood cells but has other functions in other tissues such as the liver. The type of porphyria present is determined by which enzyme is deficient. These enzyme deficiencies are usually inherited. The different type of porphyrias are as follows:
Untitled Document In severe cases, the lesion becomes necrotic and extends to the cerebralhemispheres (extrapontine myelinolysis). CPM is usually an incidental autopsy http://www.akronchildrens.org/neuropathology/Chapter6 files/chapter6.html
Extractions: CHAPTER SIX DEMYELINATIVE DISEASES Demyelinative diseases of the central nervous system are characterized by loss of myelin with variable loss of axons. In contrast, infarcts, contusions, encephalitis, and other conditions destroy myelin and axons equally. The main demyelinative disease of the CNS is multiple sclerosis (MS) and its variants. Its counterpart in the peripheral nervous system is inflammatory demyelinative polyradiculoneuropathy ( Guillain-Barré syndrome-GBS ) and its chronic variants. MS and GBS are autoimmune inflammatory diseases. There are also virus-induced demyelinative diseases, such as progressive multifocal leukoencephalopathy. Demyelinative diseases should be distinguished from leukodystrophies, which are inherited metabolic disorders of myelin lipids and proteins. MULTIPLE SCLEROSIS AND VARIANTS MS affects one in every 500 persons, women twice as frequently as men. It is more common in young adults and causes a variety of neurological deficits (visual loss, paralysis, sensory loss, ataxia, nystagmus, psychiatric disorders, dementia). The clinical course of MS is unpredictable. Many cases have a long course (20-30 years) with remissions and exacerbations. Some cases have an acute, fulminant, even fatal course and others go into a relentlessly progressive phase after a period of remissions and exacerbations. The pathology of MS is characterized by multifocal lesions, the
HONG KONG COLLEGE OF RADIOLOGISTS Osmotic Myelinolysis (central pontine myelinolysis extrapontine myelinolysis).HISTORY PREVIOUS MTHS HOME CURRENT MTH http://www.hkcr.org/CaseOfMonth/2001/feb01/feb01a.html
JKMS Vol 13, No. 1 A case of central pontine and extrapontine myelinolysis with early hypermetabolismon 18FDGPET scan. Roh JK, Nam H, Lee MC http://jkms.kams.or.kr/1998/abstract/99a.html
Extractions: We report a 63 year-old woman who developed central pontine and extrapontine myelinolysis after rapid correction of hyponatremia. Lesions on brain MRI showed hypermetabolism on 18FDG-PET scan in the early stage of the disease and became hypometabolic on the follow-up scan. We suggest that active microglia and astrocytes are the main cause of the increased glucose metabolism.
Directory Of Open Access Journals Title, Pontine and extrapontine myelinolysis following rapid correction ofhyponatremia. Author, Srivastava T ; Singh P ; Sharma B http://www.doaj.org/abstract?id=86102&toc=y
Directory Of Open Access Journals Pontine and extrapontine myelinolysis following rapid correction of hyponatremia.Author Srivastava T ; Singh P ; Sharma B Journal Neurology India Year http://www.doaj.org/openurl?genre=journal&issn=00283886&volume=48&issue=1&date=2
Hyponatremia : Epilepsy.com/Professionals and extrapontine myelinolysis, characterized by spastic quadriparesis,pseudobulbar palsy, and an encephalopathy ranging from confusion to coma.1517,19 http://professionals.epilepsy.com/page/electroab_hyponatremia.html
Extractions: Search epilepsy.com/professionals: WHO IS EPILEPSY.COM DONATE PROFESSIONAL FORUM CO-EXISTING DISORDERS ... RESOURCE LIBRARY Hyponatremia Co-Existing Disorders Metabolic Disorders Electrolyte abnormalities Hyponatremia Author: SC Schachter and MR Lopez Hyponatremia is relatively common in hospitalized patients. It occurs when an imbalance between the intake and excretion of water results in excess water relative to sodium. This imbalance may be the consequence of impaired water excretion or fluid intake that exceeds the excretory capacity of the kidneys (as in primary polydipsia or iatrogenic administration Water excretion may be deficient because of renal dysfunction, or it may be inhibited by the persistent release of ADH induced by volume depletion or the secretion of inappropriate ADH. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) has many possible causes: Central nervous system disorders Pulmonary disorders Drugs Hyponatremia may also be seen in cerebral or renal salt-wasting conditions. Sodium depletion from the kidneys is associated with adrenal insufficiency (Addisons disease) and the use of thiazide diuretics. Extrarenal sodium loss occurs with vomiting, diarrhea, or third-spacing. Other causes of hyponatremia are hypothyroidism, hyperlipidemia and hyperproteinemia (in which serum osmolality is normal), and hyperglycemia (in which the serum is hyperosmolar).