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         Extrapontine Myelinolysis:     more detail
  1. Methylphenidate Treatment of Neuropsychiatric Symptoms of Central and Extrapontine Myelinolysis(*).: An article from: Journal of Studies on Alcohol by Denise Bridgeford, David B. Arciniegas, et all 2000-09-01

61. 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

62. Myelinolysis After Correction Of Hyponatremia -- Laureno And Karp 126 (1): 57 --
These lesions have been called extrapontine myelinolysis 2. Laureno R.Experimental pontine and extrapontine myelinolysis. Trans Am Neurol Assoc.
http://www.annals.org/cgi/pmidlookup?view=long&pmid=8992924

63. Myelinolysis After Correction Of Hyponatremia -- Laureno And Karp 126 (1): 57 --
Catatonia due to central pontine and extrapontine myelinolysis case report J.Neurol. Neurosurg. Psychiatry, November 1, 1999; 67(5) 692 693.
http://www.annals.org/cgi/content/abstract/126/1/57
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Myelinolysis after Correction of Hyponatremia
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.

64. Alcoholism: Clinical And Experimental Research - UserLogin
such as extrapontine myelinolysis or pontine ischemic rarefaction recovery after extensive pontine and extrapontine myelinolysis (abstract).
http://www.alcoholism-cer.com/pt/re/alcoholism/fulltext.00000374-200108000-00017
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65. 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
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
Psychotropic drugs
Vincristine Disease Associations Head and neck cancer
Lung cancer
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
Chronic idiopathic hyponatremia in older people due to syndrome of inappropriate antidiuretic hormone secretion (SIADH) possibly related to aging.

66. 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
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67. The American Journal Of The Medical Sciences - UserLogin
Lateral pontine and extrapontine myelinolysis associated with hypernatremia andhyperglycemia. Clin Neuropathol 1989; 8 2848.
http://www.amjmedsci.com/pt/re/ajms/fulltext.00000441-200212000-00006.htm
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68. The American Journal Of The Medical Sciences - Abstract: Volume 323(5) May 2002
Magnetic resonance imaging of the brain clearly showed typical features of pontineand extrapontine myelinolysis. We suggest that the aggressive KCl
http://www.amjmedsci.com/pt/re/ajms/abstract.00000441-200205000-00005.htm
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PDF (474 K) Osmotic Demyelination Syndrome after Correction of Chronic Hyponatremia with Normal Saline.
American Journal of the Medical Sciences. 323(5):259-262, May 2002.
Lin, Shih-Hua MD; Chau, Tom MD; Wu, Chia-Chao MD; Yang, Sung-Sen MD Abstract:
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69. 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

70. 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
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.
(Internal Medicine 39: 956-960, 2000) Yukie Yoshida, Jun Akanuma, Sanae Tochikubo, Akihiko Hoshi, Yutaka Matsuura, Mari Homma and Teiji Yamamoto
From the Department of Neurology, Fukushima Medical University, Fukushima
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71. 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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72. 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://65.56.1.66/video/panteq/neworleans2004/verbalis/caption.htm
Disorders of Water Balance Endocrine Fellows Foundation June 15, 2004
body fluid compartments
neurohypophysis
two major nuerohypophyseal peptides
increased osmolality...
higher AVP levels are necessary.....
AVP receptor subtypes
AVP receptor diagram 1
antidiuresis is accomplished by shuttling of vesicular aquaporin-2 water channels into the apical membrane of collecting duct cells in response to AVP-mediated increases in intracellular cAMP levels
three relationships determine urine volume....
disorders of inappropriately increased AVP or AVP effect Hyponatremia - Incidence Hyponatremia can be caused by dilution.... ECF Volume Status.... a spot urine [Na+] <30 mEq/L generally identifies patients who respond to isotonic saline, and therefore are volume depleted, from those who do not, and therefore are more likely to have SIADH SIADH: essential criteria plasma AVP levels in patients with SIADH: 10-15% are below typical detection limits tumors pulmonary mediastinal extrathoracic requirements for producing hyponatremia neurological symptoms are roughly correlated with the level of hyponatremia, but with considerable individual variability across patients

73. Food: Contaminated Bivalve Shellfish, Salads, Fresh Fruits And Vegetables, Water
and the literature contains only two reports of infants under 2 years of agewho have been diagnosed with pontine and/or extrapontine myelinolysis 3.
http://www.clickerado.com/h/hepatitis/water.htm
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74. 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
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:

75. 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
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

76. 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
CASE OF THE MONTH
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Figure 1 Figure 3 Figure 2
Figure 3 There are also T2 hyperintense lesions in the bilateral basal ganglia and thalami.
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77. 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
Abstract Full-text 1998 Feb;13(1):99-102
A case of central pontine and extrapontine myelinolysis with early hypermetabolism on 18FDG-PET scan.
Roh JK, Nam H, Lee MC
Department of Neurology, Seoul National University Hospital, Korea.
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.

78. 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

79. 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

80. Hyponatremia : Epilepsy.com/Professionals
and extrapontine myelinolysis, characterized by spastic quadriparesis,pseudobulbar palsy, and an encephalopathy ranging from confusion to coma.15–17,19
http://professionals.epilepsy.com/page/electroab_hyponatremia.html
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
Causes
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:
  • Malignant neoplasia
      Carcinoma: bronchogenic, pancreatic, duodenal, ureteral, prostatic, bladder Lymphoma and leukemia Thymoma and mesothelioma
    Central nervous system disorders
      Trauma Infection Tumors Porphyria
    Pulmonary disorders
      Tuberculosis Pneumonia Fungal infections Lung abscesses Ventilators with positive pressure
    Drugs
      Desmopressin Oxytocin Vincristine Chlorpropamide Nicotine Cyclophosphamide Morphine Amitriptyline Selective serotonin reuptake inhibitors (SSRIs)
    Hyponatremia may also be seen in cerebral or renal salt-wasting conditions. Sodium depletion from the kidneys is associated with adrenal insufficiency (Addison’s 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).

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