Author response: The changing face of osmotic demyelination syndrome: A retrospective, observational cohort study
WhitneyFitts, Resident Physician in Child Neurology, Children's Hospital of Philadelphia
Andre CVogel, Clinical Research Coordinator, Massachusetts General Hospital
Farrah JMateen, Associate Professor of Neurology, Harvard Medical School and Massachusetts General Hospital
Submitted November 30, 2020
We thank Dr. Sterns for his thoughtful response to our publication.1 In his letter, he stated that osmotic demyelination syndrome (ODS) is defined by being caused by over-correction of serum sodium, and therefore the term should not be used in the absence of an over-correction of serum sodium.
When the term ODS was initially used in 1986,2 the understanding of myelinolysis of the observed pontine and extrapontine lesions was limited. The studies, showing an association with a rapid correction of sodium, demonstrated one of the first potential explanations of the underlying etiology. As time has passed, we have come to learn that other factors influence this disorder. Rather than creating new terminology, the literature, including several large studies,3,4,5 have used the term ODS as an umbrella term to describe both central pontine myelinolysis and extrapontine myelinolysis, even in the absence of a rapid change in serum sodium. We used the term ODS in the same way that these recent articles have done. While this may not have been how the term was originally intended to be used, it has come to be commonly used this way and is thus appropriate based upon the current literature.
Notwithstanding the lexicon, our manuscript1 contributes additional information about the current clinical characteristics of ODS, which have changed since it was originally described in 1959,6 and since the Stern et al. paper in 1986. Guidelines and awareness surrounding sodium correction have likely led to fewer cases of rapid electrolyte correction. Increased use of MRI may also allow us to identify cases earlier and with less severe pathology. In Dr. Stern’s article in 1986, the patients were predominantly diagnosed based on having profound neurologic dysfunction after rapid sodium correction. His initial sample included only patients who were hyponatremic on admission. Of these 8 patients, 7 had normal head CT scans and MRI was not part of routine clinical care. In our study, >90% of patients had brain MRI. It is likely that our sample included individuals with more subtle neurologic findings who would not have been diagnosed in the pre-MRI era. As brain MRI is now commonly used in inpatient clinical practice, our cohort demonstrates the clinical characteristics that physicians will likely encounter today. Accordingly, our study provides value to clinicians that prior studies, which were predominantly pathology and CT-based, could not.
Disclosure
The author reports no relevant disclosures. Contact [email protected] for full disclosures.
References
Fitts W, Vogel AC, Mateen FJ. The changing face of osmotic demyelination syndrome: A retrospective, observational cohort study. Neurol Clin Pract Epub 2020 Aug 26.
Sterns RH, Riggs JE, Schochet Jr SS. Osmotic demyelination syndrome following correction of hyponatremia. N Engl J Med 1986 Jun 12;314:1535–1542.
Aegisdottir H, Cooray C, Wirdefeldt K, Piehl F, Sveinsson O. Incidence of osmotic demyelination syndrome in Sweden: A nationwide study. Acta Neurol Scand 2019 Epub 2019 Aug 19.
Kallakatta RN, Radhakrishnan A, Fayaz RK, et al. Clinical and functional outcome and factors predicting prognosis in osmotic demyelination syndrome (central pontine and/or extrapontine myelinolysis) in 25 patients. J Neurol Neurosurg Psychiatry 2011;82:326-331.
Siegler JE, Wang AR, Vanderwerf JD. Normonatremic osmotic demyelination in the setting of acquired immune deficiency syndrome and malnutrition: case report and literature review. J Neurovirol 2016;22:876-879.
Adams RD, Victor M, Mancall EL. Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patients. AMA Arch Neurol Psychiatry. 1959;81:154-72.
We thank Dr. Sterns for his thoughtful response to our publication.1 In his letter, he stated that osmotic demyelination syndrome (ODS) is defined by being caused by over-correction of serum sodium, and therefore the term should not be used in the absence of an over-correction of serum sodium.
When the term ODS was initially used in 1986,2 the understanding of myelinolysis of the observed pontine and extrapontine lesions was limited. The studies, showing an association with a rapid correction of sodium, demonstrated one of the first potential explanations of the underlying etiology. As time has passed, we have come to learn that other factors influence this disorder. Rather than creating new terminology, the literature, including several large studies,3,4,5 have used the term ODS as an umbrella term to describe both central pontine myelinolysis and extrapontine myelinolysis, even in the absence of a rapid change in serum sodium. We used the term ODS in the same way that these recent articles have done. While this may not have been how the term was originally intended to be used, it has come to be commonly used this way and is thus appropriate based upon the current literature.
Notwithstanding the lexicon, our manuscript1 contributes additional information about the current clinical characteristics of ODS, which have changed since it was originally described in 1959,6 and since the Stern et al. paper in 1986. Guidelines and awareness surrounding sodium correction have likely led to fewer cases of rapid electrolyte correction. Increased use of MRI may also allow us to identify cases earlier and with less severe pathology. In Dr. Stern’s article in 1986, the patients were predominantly diagnosed based on having profound neurologic dysfunction after rapid sodium correction. His initial sample included only patients who were hyponatremic on admission. Of these 8 patients, 7 had normal head CT scans and MRI was not part of routine clinical care. In our study, >90% of patients had brain MRI. It is likely that our sample included individuals with more subtle neurologic findings who would not have been diagnosed in the pre-MRI era. As brain MRI is now commonly used in inpatient clinical practice, our cohort demonstrates the clinical characteristics that physicians will likely encounter today. Accordingly, our study provides value to clinicians that prior studies, which were predominantly pathology and CT-based, could not.
Disclosure
The author reports no relevant disclosures. Contact [email protected] for full disclosures.
References