Central and Extrapontine Myelinolysis: Then…and Now

Kleinschmidt-DeMasters, B. K.; Rojiani, Amyn M.; Filley, Christopher M.

doi:10.1097/01.jnen.0000196131.72302.68

Cited by 145 publications

(149 citation statements)

References 73 publications

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“…6 It is believed that osmotic change due to decreased intake of food or water during heavy drinking or alcohol withdrawal may put alcoholics at a greater risk of cell shrinkage and hence demyelination. 3,7 There are three possible types of myelinolysis: CPM alone, EPM alone, and CPM and EPM together.…”

Section: Discussionmentioning

confidence: 99%

Recovery from a Complicated Case of Central Pontine and Extrapontine Myelinolysis by Dopaminergic Treatment: One-Year Follow-up: A Case Report

Seo

et al. 2014

Brain Neurorehabil

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Central pontine and extrapontine myelinolysis are well-recognized osmotic demyelination syndromes related to the rapid correction of hyponatremia, chronic alcoholism, and malnutrition. They are reported to show brain stem signs and various movement disorders. A 58-year-old man with a history of chronic alcoholism was admitted for dysarthria, dysphagia, and gait disturbance that had developed five days after a right forearm cellulitis. Magnetic resonance imaging revealed demyelinating patterns in the central portion of the pons and both thalami. He showed severe extrapyramidal symptoms with truncal swaying and postural instability that resulted in severe gait disturbance. Postural instability showed little improvement after conventional physical therapy, but his symptoms markedly improved after five days of dopamine administration. Cessation of dopamine agents was attempted two times, but postural instability and gait disturbance recurred. Therefore, medication was continued for one year. The patient showed stable gait and no further deterioration

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Section: Discussionmentioning

confidence: 99%

Recovery from a Complicated Case of Central Pontine and Extrapontine Myelinolysis by Dopaminergic Treatment: One-Year Follow-up: A Case Report

Seo

et al. 2014

Brain Neurorehabil

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“…This serves as a protective mechanism from swelling during chronic conditions of hypoosmolality that usually takes two days to be completed. In the absence of hyponatremia ODS is proposed to occur as a result of a relatively hypertonic insult in which ODS can result if the serum or the extracellular space becomes hypertonic faster than the rate at which the brain cells can compensate [3][4][5]23,24 .This consequently leads to disruption of the blood-brain barrier allowing inflammatory mediators to enter the central nervous system and damage oligodendrocytes, which may further release myelin toxin and produce vasogenic edema in the central pons 25 . Nevertheless, the breakdown concept of the blood-brain barrier as a result of osmotic stress has also been subject to debate.…”

Section: Discussionmentioning

confidence: 99%

Osmotic Demyelination Syndrome Occurs Early in The Course of Hyperosmolar Hyperglycemic State.

Das¹,

A.S²,

Mossang³

et al. 2017

IOSR JDMS

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Osmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome. The association of ODS with hyperosmolar hyperglycaemic state (HHS) has been seldom reported. The aim of this study was to show that Osmotic Demyelination Syndrome occurs early in the course of Hyperosmolar I. BackgroundOsmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome, which usually occurs in the setting of a rapid correction of severe chronic hyponatremia 1,2 .ODS is a clinical syndrome characterized by altered mental status, quadriparesis, dyspnoea, dysarthria, and dysphagia which all occur characteristically five to seven days after the correction of serum sodium 3 . The pathogenesis is still to be clearly understood, it is known that rapidly increasing serum osmolality shifts water out of the cells as a response to correct solute imbalance resulting in shrinkage of glial cells that can consequently lead to disruption of the blood-brain barrier allowing inflammatory mediators to enter the central nervous system damaging oligodendrocytes and myelin 4-7 . Even though ODS has been classically thought to be exclusively secondary to a rapid correction of hyponatremia, it has also been described, even though rarely, in various other situations such as malnutrition, liver transplantation, alcoholism, hypokalemia, hypophosphatemia, AIDS, lithium toxicity, hypoglycemia, and folate deficiency, among others [8][9][10][11][12][13][14][15] . In all cases a growing body of evidence demonstrates that more than sodium per se, the key factor, in ODS pathogenesis, is a rapid change in serum osmoles. The association of ODS with hyperosmolar hyperglycemic state (HHS) has been seldom reported with less than five cases in the literature [16][17][18][19][20] . Previous cases have been in the clinical scenario of concomitant hypernatremia, chronic hyperglycemia/epilepsy, and after HHS treatment.Herein we present the case of a patient with HHS who presented with ODS early in the course of her illness. A review of previous cases and pathophysiological mechanisms involved in ODS secondary to HHS will be presented and discussed. Case PresentationA 45 year old female with poorly controlled Type2 Diabetes Mellitus came to the emergency room due to loss of consciousness. She was a known case of Type2 Diabetes Mellitus on Tab.Glipizide 5mg and Metformin 500mg for 10years and long acting Isophane Insulin(30:70) for 5years and she was a known Hypertensive on Tab Amlodipine 5mg for 5 years. She had irregular Medication.On Physical examination, her BP was 100/60 mmHg. Heart rate was 140/min and SpO 2 was 90% in Room air. Her BMI was 27.2. Mucus membranes were dry. ECG showed Right Axis Deviation. She had a Glasgow Coma Scale of 3/15 and muscle power was 0/5 in all the limbs and plantars were flexor B/L.There was no neck rigidity. Blood Glucose levels were 600mg%. Plasma and urinary ketones were negetive. ABG analysis showed pH 7.31. HbA1C was 14.1%, Serum Calcium 7.9mg/dL. Serum creatinine was 4.5mg/dL. Her eGFR

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“…This syndrome has extremely diverse clinical manifestations ranging from a mild tremor or dysarthria to locked-in syndrome and the prognosis can be highly heterogeneous from complete recovery to progression and death (2,3). The cause and pathogenesis of ODS remain unclear.…”

Section: Central Pontine Myelinolysis (Cpm) and Extrapontine Myelinolmentioning

confidence: 99%

Central Pontine and Extrapontine Myelinolysis that Developed during Alcohol Withdrawal, without Hyponatremia, in a Chronic Alcoholic

Park

Han

et al. 2010

Intern. Med.

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Central and Extrapontine Myelinolysis: Then…and Now

Cited by 145 publications

References 73 publications

Recovery from a Complicated Case of Central Pontine and Extrapontine Myelinolysis by Dopaminergic Treatment: One-Year Follow-up: A Case Report

Recovery from a Complicated Case of Central Pontine and Extrapontine Myelinolysis by Dopaminergic Treatment: One-Year Follow-up: A Case Report

Osmotic Demyelination Syndrome Occurs Early in The Course of Hyperosmolar Hyperglycemic State.

Central Pontine and Extrapontine Myelinolysis that Developed during Alcohol Withdrawal, without Hyponatremia, in a Chronic Alcoholic

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