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Central pontine myelinolysis secondary to rapid correction of hyponatremia historical perspective with Doctor Robert Laureno
- Source :
- Neurological Sciences. 42:3479-3483
- Publication Year :
- 2021
- Publisher :
- Springer Science and Business Media LLC, 2021.
-
Abstract
- Central pontine myelinolysis (CPM) is a neurological disorder characterized by damage to the myelin and oligodendrocytes in the pons. This review focuses on the history of CPM and the discovery of its association with the treatment of hyponatremia. The author reviewed original publications regarding CPM, hyponatremia, and the treatment of hyponatremia. The author interviewed Dr. Robert Laureno who was a pioneer in CPM research with his animal work in dogs. Animal models demonstrated the role of the rapid correction of hyponatremia as causative of pontine and extrapontine myelinolytic lesions. Nevertheless, the importance of the speed of correction was widely denied. There were years of debates and only slow changes in expert guidelines. CPM occurs as a consequence of a rapid rise in serum sodium in individuals with chronic hyponatremia. It is recommended to increase plasma sodium concentration by no more than 8 to 10 mmol/L per 24 h in chronic hyponatremia.
- Subjects :
- Pediatrics
medicine.medical_specialty
Neurology
Dermatology
Neurological disorder
Chronic hyponatremia
03 medical and health sciences
Dogs
0302 clinical medicine
Physicians
Pons
parasitic diseases
medicine
Animals
Humans
030212 general & internal medicine
Neuroradiology
business.industry
nutritional and metabolic diseases
General Medicine
medicine.disease
Magnetic Resonance Imaging
Psychiatry and Mental health
Rapid rise
Myelinolysis, Central Pontine
embryonic structures
Central pontine myelinolysis
Neurology (clinical)
Neurosurgery
Hyponatremia
business
human activities
030217 neurology & neurosurgery
Subjects
Details
- ISSN :
- 15903478 and 15901874
- Volume :
- 42
- Database :
- OpenAIRE
- Journal :
- Neurological Sciences
- Accession number :
- edsair.doi.dedup.....6978b426022cda418cf7a8655df260b1
- Full Text :
- https://doi.org/10.1007/s10072-021-05301-3