A review of the causes of central pontine myelinosis: yet another apoptotic illness?

@article{Ashrafian2001ARO,
  title={A review of the causes of central pontine myelinosis: yet another apoptotic illness?},
  author={Hutan Ashrafian and Patrick Davey},
  journal={European Journal of Neurology},
  year={2001},
  volume={8}
}
One of the well recognized stimuli for central pontine myelinosis (CPM) is the rapid correction of chronic hyponatraemia. Conventionally this has been perceived to lead to pontine glial cell swelling through osmosis and eventually to cell death. However, although a purely osmotic argument has been central to any patho‐physiological understanding of CPM, there are deficiencies in this approach that do not account for why certain individuals develop CPM with relatively mild osmotic insults. Here… 
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TLDR
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  • Medicine, Biology
    The American journal of the medical sciences
  • 2010
TLDR
This finding suggests that the pathogenesis of ODS may be more complex and involve the inability of brain cells to respond to rapid changes in osmolality of the interstitial (extracellular) compartment of the brain, leading to dehydration of energy-depleted cells with subsequent axonal damage that occurs in characteristic areas.
Osmotic demyelination syndromes: Central and extrapontine myelinolysis
[A case of central pontine and extrapontine myelinolysis, without hyponatremia, during alcohol withdrawal with favorable outcome].
TLDR
Central pontine and extra-pontine myelinolysis is a rare neurological disorder that should be considered in the setting of any unexplained neurological symptoms during the course of alcohol withdrawal or for any patient with chronic alcohol abuse, as promptly as possible, given the potentially fatal outcome.
A case of asymptomatic pontine myelinolysis
TLDR
A 69-year-old Caucasian male presented intensive headache and underwent cranial MRI that showed the typical feature of central pontine myelinolysis, and the possible role in the etiopathogenesis of his chronic use of anti-depressive drugs and exposure to glue and chemical agents is discussed.
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TLDR
The view that a rapid rise in serum sodium may be responsible for the development of central pontine myelinolysis in man is supported.
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TLDR
A case of CPM where no hyponatremia was found is presented and it is hypothesize that iatrogenic sodium restoration may not in all cases be the putative mechanism, and normal admission sodium levels do not exclude the diagnosis of C PM.
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TLDR
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TLDR
Three, perhaps four, cases were observed in which the myelin sheaths of all the nerve fibers in the central part of the basis pontis had been destroyed in a single, large, symmetric focus, leading to death in about 13 and 26 days.
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TLDR
Observations in the case of a 36-year-old man who died with acute hemorrhagic pancreatitis with the autopsy findings of central pontine and extrapontine myelinolysis suggest that osmotic stress and oligodendrocyte topography rather than rapid correction of hyponatremia may be the key to the development of central Pope's disease (osmotic myelinelysis).
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TLDR
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TLDR
It is suggested that the osmotic demyelination syndrome is a preventable complication of overly rapid correction of chronic hyponatremia, which developed after the patients presented with severe hypon atremia.
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TLDR
An 18-year-old woman in her first pregnancy with hyperemesis gravidarum, presented dehydration, without hyponatremia, and a T2 weighted sagittal cranial-magnetic resonance imaging revealed a high signal within mid-pons suggesting central pontine myelinolysis.
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