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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. CCNAPI Newsletter
at a rapid ( 0.5 mEq/L/hour) rate may be more dangerous than hyponatremia itself,resulting in central pontine and extrapontine myelinolysis manifested by
  • Cerebral edema of type I diabetic ketoacidosis
  • Often a potentially preventable complication of treatment of DKA. It is easier to prevent than to treat. Asymptomatic increase in brain size during treatment of DKA is rule rather then an exemption Worsening cerebral function (headache, lethargy, irritability, combativeness, responsiveness) with improving biochemical parameters is characteristic Early recognition and prompt management can successfully reverse encephalopathy. Conversely, if untreated, early manifestations may rapidly progress to seizures, respiratory arrest, brain herniation, and death. Associated with hypotonic fluid overload and rapid decrease in serum osmolality Therapeutic pitfalls in dehydration of patient with DKA:
  • Underestimation: hyperosmolality (traditional teaching) Overestimation: hyperventilation - dry lips and mouth
    Acidosis - myocardial performance and tissue perfusion
    Assessment - 5%, 10%, 15% (infants) vs. 3%, 6%, 9% (older children and adults)
  • 62. Conditions And Diseases: E | Treasure Coast Health
    Erythema Multiforme@ (3); Erythromelalgia@ (4); Esophageal Diseases@ (47); EssentialTremor@ (3); extrapontine myelinolysis@ (3); Eye Cancer@ (14). Our Sponsers.
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    63. f’fŒ‹‰Êƒgƒbƒv
    aberrant right subclavian artery. central pontine myelinolysis (CPM) +extrapontine myelinolysis (EPM). L4/5 . L5/S1 .
    aberrant right subclavian artery
    central pontine myelinolysis (CPM) + extrapontine myelinolysis (EPM)
    nutcracker phenomenon
    rounded atelectasis
    ˆÝ’×ᇂ̐úE‚É‘±”­‚µ‚½• –Œ‰Š
    ‰ºs‘å“®–¬‚Ì•Ç“àŒŒŽî(intramural thrombus of the descending aorta)
    ŠÌ×–EŠà”j—ô‚É‚æ‚é• o“àoŒŒ
    ‹CŠÇŽx“®–¬– óŒŒŠÇŽî(racemose hemangioma of the bronchial artery)
    ‚»‚Ì‚P ‚»‚Ì‚Q
    ŒŒ‹C‹¹A”牺‹CŽîAtraumatic pneumatocele
    Œ‹’°ŒeŽº‚̐úE‚É‚æ‚é‹C• ‚ÆŒÀ‹Ç«• –Œ‰Š
    ‚“x•nŒŒ‚É‚æ‚鍜‘‚Ì reconversion
    Œã• –ŒüˆÛÇ(retroperitoneal fibrosis)

    64. Chang Gung Memorial Hospital
    Central and extrapontine myelinolysis in a patient in spite of a careful correctionof hyponatremia. Clin Nephrol 2001;5524853. 15. Pirzada NA, Ali II.
    No.199, Tunghwa Rd.,
    Taipei, Taiwan, R.O.C
    Chang Gung Medical Journal Vol.25 No.12 Treating Hyponatremia in an Empty Sella Syndrome Patient Complicated with Possible Myelinolysis Wen-Chin Lee, MD
    Yuan-Fu Cheng, MD
    Jin-Bor Chen, MD
    (Chang Gung Med J 2002;25:838-43)
    glucocorticoid substitution, hyponatremia, empty sella, myelinolysis.
    CASE REPORT This 44-year-old woman, a housewife, was admitted because of hyponatremia and disturbed consciousness. She had no liver disease and never drank alcohol. She also denied any history of using diuretics. She had a history of postpartum hemorrhage which had occurred 13 years previous. Amenorrhea and failure to lactate developed thereafter. Fatigue and cold intolerance were also found. She neglected these problems and received no treatment. She lived an uneventful life until 1 day prior to this admission when she suffered from vomiting and diarrhea. Drowsiness developed the next day. She was then sent to our hospital for further management. After hormonal substitution of 50 mg cortisone acetate in 2 divided doses and 0.1 mg/day L-thyroxin, the hyponatremia no longer recurred.

    65. MDS International Congress Of Parkinson's Disease And Movement Disorders
    cause of tardive dyskinesia a report of five cases P. Hogarth P1090 Reversibleextrapontine myelinolysis with Parkinsonism in a 25year-old female V. Ries, K
    The Movement Disorder Society's
    International Congress of Parkinson's Disease and Movement Disorders
    Abstract Poster Sessions Poster Session Schedule Poster Instructions Presenting Authors ... 2002 Abstract/Poster Session Information
    Poster Session
    Thursday, November 14, 2002
    7:00 am – 8:30 am
    Ataxia, Chorea, Drug-Induced Movement Disorders, Myoclonus, Spasticity, Stereotypies, Tics, Tremor
    Poster Numbers 1021-1182
    Abnormal striatal dopaminergic function in SCA2 revealed by beta-CIT and IBZM SPECT
    S.M. Boesch, M. Schocke, K. Seppi, P. Hollosi, W. Poewe, G.K. Wenning
    Antioxidant treatment of patients with Friedreich's Ataxia: 3 year follow up P.E. Hart, R. Lodi, B. Rajagopalan, J.L. Bradley, D.J. Taylor, J.M. Cooper Ataxia: a common movement disorder in central nervous system Whipple's Disease L.K. Jones, K. Josephs, D.A. Saad, A. Aksamit, J.E. Ahlskog Cerebellar degenerative ataxias - terminology, classification and diagnostic criteria

    66. Les Troubles Métaboliques
    Translate this page 7. Karp BI, Laureno R. Pontine and extrapontine myelinolysis a neurologicdisorder following rapid correction of hyponatremia.
    Les complications métaboliques Les troubles métaboliques associés aux affections néoplasiques sont nombreux et variés et certains peuvent conduire le patient à l’USI dans un contexte de grande urgence (1).
  • L’hypercalcémie
  • Très fréquente, l’hypercalcémie est causée soit par des métastases osseuses, soit par un syndrome paranéoplasique (2). Le tableau clinique débutera par une polyurie et de la soif et évoluera vers la déshydratation, les nausées et vomissements, les troubles du comportement, la confusion et les troubles de la conscience. Il faudra envisager le transfert du patient en réanimation si la calcémie est supérieure à 14 mg/dl ou si le malade présente des arythmies cardiaques, de l’insuffisance cardiaque ou des troubles de la conscience. Le traitement (3) consiste d’une part à réhydrater le patient en 24 à 48 heures avec du sérum physiologique et en suivant la diurèse et l’ionogramme et d’autre part à administrer après réhydratation un biphosphonate (acide zolédronique 4 mg) pour bloquer la lyse osseuse. En cas d’extrême urgence, de la calcitonine sera injectée pour avoir un contrôle très rapide de la calcémie.
  • L’hyponatrémie L’acidose lactique
  • Si elle s’observe le plus souvent dans le contexte d’hypoxie tissulaire (choc de toute cause, sepsis) ou d’une insuffisance hépatique fulminante, l’acidose lactique peut être due à l’affection néoplasique, qu’il s’agisse d’une hémopathie maligne

    67. Center For Children With White Matter Disorders
    Central pontine and extrapontine myelinolysis Vitamin B12 deficiency Folate deficiencyMarchiafavaBignami disease Malnutrition Toxic encephalopathies
    Classification of white matter disorders I n the classification of white matter disorders, the first big divider is whether the disease is inherited or not. This difference has major implications for the tests to be performed, for risk of recurrence in the family, and for potential therapeutic strategies. The causes of the acquired forms can be subdivided according to type of cause into infectious-inflammatory, noninfectious-inflammatory, toxic-metabolic, traumatic and hypoxic-ischemic Hereditary disorders Lysosomal disorders Metachromatic leukodystrophy
    Krabbe’s disease (globoid cell leukodystrophy)
    GM1 gangliosidosis (infantile variant)
    GM2 gangliosidosis (infantile variant)
    Infantile neuronal ceroid lipufuscinosis
    Fabry’s disease
    Sialic acid storage disorder, Salla disease
    Mucoploysaccharidoses Peroxisomal disorders Zellweger syndrome
    Neonatal adrenoleukodystrophy
    Infantile Refsum disease Zellweger-like syndrome Pseudo-Zellweger syndrome Pseudo-neonatal adrenoleukodystrophy Bifunctional protein deficiency X-linked adrenoleukodystrophy and adrenomyeloneuropathy Refsum disease Mitochondrial disorders Respiratory chain defects Cerebrotendinous xanthomatosis DNA repair disorders Cockayne’s disease PIBD or Tay syndrome Defects in myelin proteins Pelizaeus-Merzbacher disease syndrome Amino acidopathies and organic acidopathies

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    69. Artículo 7: Descripción Del Síndrome Pseudobulbar Por El Poeta Juan Ramón Ji
    Translate this page Striatal syndrome following hyponatremia and its rapid correction a manifestationof extrapontine myelinolysis confirmed by magnetic resonance imaging.
    Principal Mapa Presentación Artículos ... Novedades Descripción del síndrome pseudobulbar
    por el poeta Juan Ramón Jiménez Este artículo se publicó en papel en Revista de Neurología ; La referencia es la siguiente: D. Ezpeleta. Descripción del síndrome pseudobulbar por el poeta Juan Ramón Jiménez. Rev Neurol 1998; 27: 122-124 [ MEDLINE Léalo, es un artículo muy especial... Resumen Se presenta un caso de síndrome pseudobulbar que se ha identificado en uno de los personajes de una obra clásica de la literatura española, Platero y yo , de Juan Ramón Jiménez. En este poema en prosa, se puede apreciar que Darbón, el "médico" de Platero, padece los síntomas de un síndrome pseudobulbar típico; disartria, disfagia e incontinencia emocional. Se revisa escuetamente el síndrome pseudobulbar, así como otros antecedentes de descripciones de enfermedades neurológicas en la literatura clásica española no médica. Abstract We present a case of pseudo-bulbar syndrome, identified in one of the characters of a classic of Spanish literature, Platero y yo by Juan Ramon Jimenez. In this prose poem, it can be seen that Darbon, Platero's 'doctor' has the symptoms of a typical pseudo-bulbar syndrome: dysarthria, dysphagia and emotional incontinence. The pseudo-bulbar syndrome is briefly reviewed, as are other descriptions of neurological syndromes in the non-medical classical Spanish literature.

    70. Paper 19 - Postoperative Hyponatraemia
    pontine myelinolysis (CPM) or to a related and more diffuse condition known asosmotic demyelination syndrome, 9 or pontine and extrapontine myelinolysis.
    Paper 19 Postoperative Hyponatraemia Vida Viliunas FANZCA.
    Department of Anaesthesia and Pain Management,
    The Canberra Hospital,

    From AUSTRALASIAN ANAESTHESIA 1998 Summary Approach To Hyponatraemia Introduction Postoperative Hyponatraemia ... Sodium And Water Physiology
    Summary Hyponatraemia is a common and potentially dangerous metabolic perturbation in hospitalised patients. This essay reviews the aetiology, pathology and treatment of acute, severe postoperative hyponatraemia. It is not a comprehensive review article, but is a review of the literature based on a Medline search using the Medline database in English for the last 20 years. Major mesh headings of hyponatraemia, aetiology, pathophysiology and therapy were used, and human and animal studies were included. No meta-analysis of treatment options and outcomes was found in the literature that was surveyed. Although some studies were prospective, there were no controlled nor randomised studies found on this subject. Introduction Hyponatraemia is the most common electrolyte abnormality in hospitalised patients Its prevalence depends on which source one reads, but for hospitalised patients range estimates are that:

    71. EMedicine - Central Pontine Myelinolysis : Article Excerpt By: Christopher C Luz
    The term osmotic myelinolysis is more appropriate than central pontine myelinolysis for demyelination occurring in extrapontine regions after the
    Excerpt from Central Pontine Myelinolysis
    Synonyms, Key Words, and Related Terms: osmotic myelinolysis
    Please click here to view the full topic text: Central Pontine 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.

    72. Central Pontine Myelinolysis
    sometimes be present. extrapontine sites of myelinolysis in the basalganglia and midbrain, and subcortical white matter may also occur. VI 1/CENTRAL PONTINE MYELINO
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    *For Medical Professionals only, registration required 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

    73. 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
    Central Pontine Myelinolysis Following Hemodialysis Author: Dr R Dewan, Dr Rahul Rai, Dr Praveen Gupta, Dr Rahul Anand, Dr Pankaj Mehta,
    Dr Sameer Gulati
    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.

    74. Issues: Volume 102: January - December 1979: Issue 2: June 1979
    ED . Bird , ES . Spokes and LL . Iversen Pages 347 360. Pontine and extrapontinemyelinolysis. DG . Wright , R . Laureno and M . Victor Pages 361 - 386.
    Volume 102: January - December 1979
    Issue 2: June 1979
    Table of Contents
  • Loss and recovery of reactivity to noxious stimuli in monkeys with primary spinothalamic cordotomies, followed by secondary and tertiary lesions of other cord sectors
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  • Pinealoblastoma with retinoblastomatous differentiation
  • SZ Stefanko and WA Manschot Pages:
  • An analysis of factors influencing measurements of dopamine, noradrenaline, glutamate decarboxylase and choline acetylase in human post-mortem brain tissue
  • EGS Spokes Pages:
  • Increased dopamine concentration in limbic areas of brain from patients dying with schizophrenia
  • ED Bird ES Spokes and LL Iversen Pages:
  • Pontine and extrapontine myelinolysis
  • DG Wright R Laureno and M Victor Pages:
  • Control of the saccadic and smooth pursuit systems after cerebral hemidecortication
  • JA Sharpe AW Lo and HE Rabinovitch Pages:
  • Different types of disturbed motor control in gait of hemiparetic patients
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    75. Thammasat Medical Journal
    ? 3 ? Central Pontine and ExtrapontineMyelinolysis A study of 3 cases in Ramathibodi hospital.
    Central Pontine and Extrapontine Myelinolysis : A study of 3 cases in Ramathibodi hospital
    Study on health behaviors concerning Helminthiasis in different age groups
    Factors affected acceptance of screening for thalassemia in pregnant women
    at Thammsat Hospital
    Knowledge attitude and experience of thai traditional medicine of Thammasat University
    (Student - centred learning)
    Communication skill in critical situation

    76. “ú‘åˆãŠwŽGŽ@2000”N5ŒŽE59Šª5†
    The summary for this Japanese page contains characters that cannot be correctly displayed in this language/character set.
    “쐳”V@Žu•û‚¦‚肳@…’J’q•F 54ÎA—« Žå‘i: ˆÓŽ¯áŠQ “Á‹L‚·‚ׂ«‚±‚Æ‚È‚µB 1992”N‚æ‚萸_•ª—ô•aB Œ»•a—ð: ‚ª•`o‚³‚êACPM‚¨‚æ‚Ñ extrapontine myelinolysis(EPM)‚ÆŠmf‚µ‚½B¸¸‰Á—–Ú “I‚É‚Ä7ŒŽ21“úA“–_Œo“à‰È‚É“]‰@‚µ‚½B Œo‰ß:
    ‹´’†S‘â•ö‰óÇ(central pontine myelinolysis:CPM) ‚́A1959”NAAdams‚炪‹´’ê•”‚É”ñ‰ŠÇ«’E‘‚ð”F‚ß‚½ 4—á‚Ì–«ƒAƒ‹ƒR[ƒ‹’†“ÅŠ³ŽÒ‚ð‰‚ß‚Ä•ñ‚µAŽ¾Š³ŠT ”O‚ªŠm—§‚³‚ꂽB—Տ°“I‚ɂ́AŽlŽˆ‚Ìáz«–ƒáƒE‹…–ƒáƒ EˆÓŽ¯áŠQ‚È‚Ç‚ð’悵A_Œo•a—Šw“I‚ɂ́AŽå•a•Ï‚Æ ‚µ‚Ä‹´’ê•”‚Ì’†S•”‚ɑΏ̐«‚Ì”ñ‰ŠÇ«’E‘‚ªŒ©‚ç‚êA ’E‘•”•ª‚Ìoligodendrocyte‚ÍŒ¸­‚·‚邪A_Œo×–EEŽ² õEŒŒŠÇ‚Í”äŠr“I—Ç‚­•Û‚½‚êA‹´‚ÌŽü•Ó•”‚à•Û‚½‚ê‚鎖 ‚ð“Á’¥‚Æ‚·‚éA‚Ü‚½AdÇ—á‚ł́A‹´”íŠW•”‚â’†”]E¬ ”]‹r‚É‚Ü‚Å•a•Ï‚ª‹y‚Ô‚±‚Æ‚ª‚ ‚éB‚È‚¨A‹´ˆÈŠO‚É‘å”] Šî’êŠjEŽ‹°E‘å”]‚⏬”]‚̔玿‚¨‚æ‚є玿‘Ž¿‹«ŠE •”EÒ‘‚È‚Ç‚É’E‘•a•Ï‚ªŒ©‚ç‚ê‚邱‚Æ‚ª‚ ‚èA‹´ŠOŒ^ ‘â•ö‰óÇ(extrapontine myelinolysis:EPM)‚ƌĂ΂ê‚Ä‚¢ ‚éB ‚Å‚à“¯—l‚̏ŠŒ©‚ª ŠÏŽ@‚³‚ꂽBCPMEEPM‚Ì•a•Ï‚Í‘Šú‚©‚çMRI‚Å”F‚ß ‚ç‚êAf’f‚É”ñí‚É—L—p‚Å‚ ‚邪A‰æ‘œŠŒ©‚̉ü‘P‚́A —Տ°Çó‚̉ü‘P‚æ‚è’x‚ê‚ÄŒ©‚ç‚ê‚邽‚߁i•¶Œ£17jAŒo‰ß‚ðŒ©‚é ‚É‚Í_ŒoŠw“IfŽ@ŠŒ©‚ªd—v‚Å‚ ‚éB
    1)Adams RD, Victor M, Mancall EL:Central pontine myelinolysis. A hitherto undescribed disease occurring in alcoholic and malnourished patients. Arch Neurol Psychiatry, 81:154-172 (1959)

    77. Privattandvård I Örebro, Tandläkaren Michel Deaibes, Sjukdomslista På Engels
    Erythema Infectiosum. Erythema Multiforme. Esophageal Diseases. ExtrapontineMyelinolysis. F. Fabry's Disease. Facial Differences. Facial Paralysis.
    A Aarskog Syndrome Aase Syndrome Abetalipoproteinemia Ablepharon-Macrostomia Syndrome Achilles Tendonitis Achondroplasia Acoustic Neuroma Acromegaly Activated Protein C Resistance Acute Idiopathic Polyneuritis ADD and ADHD Addiction and Recovery Addison's Disease Adiposis Dolorosa Adjustment Disorders Adrenoleukodystrophy Agnosia Agoraphobia Aicardi Syndrome AIDS Alagille Syndrome Albinism Alcoholism Alexander Disease Alkaptonuria Allergies Alopecia Alpers' Disease Alpha1 Antitrypsin Deficiency Alport Syndrome Alstrom Syndrome Alternating Hemiplegia Altophobia Alzheimer's Amblyopia Amputee Amyloidosis Amyoplasia Congenita Amyotrophic Lateral Sclerosis Anal Fissures Anemia Anencephaly Aneurysm Angina Pectoris Anophthalmos Anorexia Anosmia Anterior Knee Pain Syndrome Antiphospholipid Syndrome Anxiety Aortic Valve Disease Apert Syndrome Aphasia Aplastic Anemia Apnea, Sleep Appendicitis Arrhythmia Arteriohepatic Dysplasia Arthritis Arthrogryposis Asbestosis Asperger's Syndrome Aspergillosis Asthma Atherosclerosis Athlete's Foot Atrial Fibrillation Attachment Disorder Attention Deficit Disorder Autism Auto Immune Disorders Aviophobia Aviatophobia B Bacillary Angiomatosis Back Disorders Bad Breath Balanitis Baldness Barth Syndrome Bassen Kornzweig Syndrome Batten Disease Beckwith-Wiedemann Syndrome Behcet's Syndrome Bell's Palsy Benign Breast Lumps Benign Prostatic Hyperplasia Berger's Disease Beriberi Beryllium Disease Besnier Boeck Disease Betalipoprotein Deficiency Disease

    78. David B
    Methylphenidate Treatment of Neuropsychiatric. Symptoms of Central and ExtrapontineMyelinolysis. Journal of Studies on Alcohol, 61657660, 2000. 12.
    David B. Arciniegas, M.D.
    Assistant Professor of Psychiatry and Neurology
    University of Colorado Health Sciences Center, Denver, Colorado
    To conact, e-mail: RESEARCH AND PROFESSIONAL EXPERIENCE: Experience: 1992 – 1993 Internship in Community Medicine, University of Colorado Health Sciences Center (UCHSC) 1993 – 1996 Residency in Adult Psychiatry, UCHSC 1995 – 1996 Chief Resident in Consultation-Liaison Psychiatry, UCHSC 1996 – 1998 Instructor/Fellow in Psychiatry, UCHSC 1996 – 1999 Fellowship in Neuropsychiatry and Clinical Neuroscience Research, UCHSC 1996 – 1999 Fellowship in Neuroscience Research and Traumatic Brain Injury, Denver VAMC 1996 – 1998 Associate Director of Medical Student Education, Department of Psychiatry, UCHSC 1997 – Director, Neuroscience Course, Adult Psychiatry Residency Training Program, UCHSC 1998 – 1999 Instructor/Fellow in Psychiatry and Neurology, UCHSC 1998 – Member, Behavioral Neurology Section, Department of Neurology, UCHSC 1998 – Director of Medical Education, Colorado Mental Health Institute at Pueblo, Pueblo, CO

    79. Clinical Nephrology, Vol. 55, 3/01
    Contents. Clinical Nephrology, Vol. 55, No. 3/2001 (248253). Central and extrapontinemyelinolysis in a patient in spite of a careful correction of hyponatremia.
    Volume 55, No. 3/2001 (March) Contents Originals Regulation of in situ complement activation via the lectin pathway in patients with IgA nephropathy
    M. Endo, H. Ohi, A. Satomura, M. Hidaka, I. Ohsawa, T. Fujita, K. Kanmatsuse, M. Matsushita and T. Fujita Corticosteroid therapy in patients with IgA nephropathy and impaired renal function
    S. Tamura, K. Ueki, H. Ideura, Y. Tsukada, A. Maezawa, H. Kawai, R. Wakamatsu, S. Yano, Y. Nojima and T. Naruse Do patients with obstructive sleep apnea have clinically significant proteinuria?
    E.A. Iliescu, M. Lam, J. Pater and P.W. Munt An evaluation of the physicochemical risk for renal stone disease during pregnancy
    C.L. Smith, C. Kristensen, M. Davis and P.A. Abraham The effect of i.v. iron alone or in combination with low-dose erythropoietin in the rapid correction of anemia of chronic renal failure in the predialysis period
    D.S. Silverberg, M. Blum, Z. Agbaria, V. Deutsch, M. Irony, D. Schwartz, R. Baruch, T. Yachnin, S. Steinbruch and A. Iaina Interferon therapy in hemodialysis patients with chronichepatitis C virus infection induces a high rate of long-term sustained virological and biochemical response
    M. Espinosa, M. Rodriguez, A. Martin-Malo, M.A. Alvarez de Lara, R. Gonzalez, F. Lopez-Rubio, M. de la Mata and P. Aljama

    80. [Dysphagia] CPM
    Here are a couple of abtracts that may be useful Central Pontine and ExtrapontineMyelinolysis After Correction of Hyponatremia Neurologist 2000 ;6255266

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