Rapid Development of Central Pontine Myelinolysis after Recovery from Wernicke Encephalopathy: A Non-alcoholic Case without Hyponatremia

Kishimoto, Yuui; Ikeda, Ken; Murata, Kiyoko; Kawabe, Kiyokazu; Hirayama, Takehisa; Iwasaki, Yasuo

doi:10.2169/internalmedicine.51.7498

Cited by 15 publications

(14 citation statements)

References 18 publications

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“…CPM is associated with cytotoxic edema, whereas in extra-pontine myelinolysis, the edema seems to be mainly vasogenic in origin [7]. Although osmotic demyelination is typically precipitated by rapid shifts in blood osmolality [111], CPM has been reported to occur in states of thiamine deficiency [75, 171]. In alcoholics, CPM and extrapontine myelinolysis occur with alcohol withdrawal, even in the absence of rapid correction of hyponatremia.…”

Section: White Matter Toxic Metabolic and Degenerative Brain Pathologymentioning

confidence: 99%

Human alcohol-related neuropathology

2013

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Alcohol-related diseases of the nervous system are caused by excessive exposures to alcohol, with or without co-existing nutritional or vitamin deficiencies. Toxic and metabolic effects of alcohol (ethanol) vary with brain region, age/developmental stage, dose, and duration of exposures. In the mature brain, heavy chronic or binge alcohol exposures can cause severe debilitating diseases of the central and peripheral nervous systems, and skeletal muscle. Most commonly, long-standing heavy alcohol abuse leads to disproportionate loss of cerebral white matter and impairments in executive function. The cerebellum (especially the vermis), cortical-limbic circuits, skeletal muscle, and peripheral nerves are also important targets of chronic alcohol-related metabolic injury and degeneration. Although all cell types within the nervous system are vulnerable to the toxic, metabolic, and degenerative effects of alcohol, astrocytes, oligodendrocytes, and synaptic terminals are major targets, accounting for the white matter atrophy, neural inflammation and toxicity, and impairments in synaptogenesis. Besides chronic degenerative neuropathology, alcoholics are predisposed to develop severe potentially life-threatening acute or subacute symmetrical hemorrhagic injury in the diencephalon and brainstem due to thiamine deficiency, which exerts toxic/metabolic effects on glia, myelin, and the microvasculature. Alcohol also has devastating neurotoxic and teratogenic effects on the developing brain in association with fetal alcohol spectrum disorder/fetal alcohol syndrome. Alcohol impairs function of neurons and glia, disrupting a broad array of functions including neuronal survival, cell migration, and glial cell (astrocytes and oligodendrocytes) differentiation. Further progress is needed to better understand the pathophysiology of this exposure-related constellation of nervous system diseases and better correlate the underlying pathology with in vivo imaging and biochemical lesions.

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Section: White Matter Toxic Metabolic and Degenerative Brain Pathologymentioning

confidence: 99%

Human alcohol-related neuropathology

2013

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“…[11] , hyponatremia due to Peritoneal Dialysis, Wernicke encephalopathy. [12] Only one of our case had history of hyponatremia. Other two cases were treated with IV fluids for hyperemesis gravidarum and generalised weakness respectively.…”

Section: Discussionmentioning

confidence: 73%

Central Pontine Myelinolysis in Patients With Inadvertent Intravenous Fluid Therapy: A Case Report Series

Gimhavanekar¹,

Dahiphale²,

Kaginalkar³

et al. 2016

jemds

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Central pontine myelinolysis is an acquired demyelinating disease. It is commonly associated with chronic alcoholics, electrolyte imbalance and chronically debilitated patients. It has predilection for involvement of central portion of basis pontis; however, it may involve axons in the putamina, caudate nuclei, thalami, cerebellum, splenium of the corpus callosum and subcortical white matter. [1] The term "osmotic demyelination syndrome" is similar to "central pontine myelinolysis," but also includes areas outside the pons. [2] It is characterised by loss of myelin and oligodendroglia with relative neuron sparing.

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“…Although CPM may not be associated with an acute correction of hyponatremia, in chronic alcoholics, CPM is often associated with severe liver disease and Wernicke encephalopathy [8]. However, these were ruled out in this case.…”

Section: Discussionmentioning

confidence: 95%

Central Pontine Myelinolysis Induced by Alcohol Withdrawal: A Case Report

Kim

Jeong

et al. 2017

Ann Rehabil Med

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Central pontine myelinolysis (CPM) is a demyelinating disorder characterized by the loss of myelin in the center of the basis pons, and is mainly caused by the rapid correction of hyponatremia. We report the case of a young woman who presented with gait disturbance and alcohol withdrawal, and who was eventually diagnosed with CPM. Generally, the cause and pathogenesis of CPM in chronic alcoholics remain unclear. In this cases, the CPM may be unrelated to hyponatremia or its correction. However, it is possible that the osmotic pressure changes due to refeeding syndrome after alcohol withdrawal was the likely cause in this case. This case illustrates the need for avoiding hasty, and possibly incomplete diagnoses, and performing more intensive test procedures to ensure a correct diagnosis.

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Rapid Development of Central Pontine Myelinolysis after Recovery from Wernicke Encephalopathy: A Non-alcoholic Case without Hyponatremia

Cited by 15 publications

References 18 publications

Human alcohol-related neuropathology

Human alcohol-related neuropathology

Central Pontine Myelinolysis in Patients With Inadvertent Intravenous Fluid Therapy: A Case Report Series

Central Pontine Myelinolysis Induced by Alcohol Withdrawal: A Case Report

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