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Abstract Details

Osmotic Demyelination Syndrome: Not just a Sodium Problem
Neurohospitalist
P10 - Poster Session 10 (8:00 AM-9:00 AM)
2-005
To describe a case of Osmotic Demyelination Syndrome (ODS) in context of normonatremia with alternate osmolytes. Our case underscores the wide range o metabolic disturbances resulting in osmotic shifts leading to ODS.


ODS is a rare, debilitating, and frequently irreversible neurological disorder most commonly linked to rapid correction of severe chronic hyponatremia. The syndrome primarily affects the central pons, although extrapontine regions such as the thalami, hippocampi but also the basal ganglia may also be involved. Recent literature documents ODS occurring in the context of normonatremia and fluctuations in alternative osmolytes and may be underdiagnosed, particularly as initial MRI brain may be negative. We report a case of ODS associated with Glucose fluctuations and chronic alcohol dependence.


NA
A 52-year-old man with poorly controlled diabetes mellitus type 2 (A1c 11.7), chronic alcohol dependence recently discharged from rehab and reporting relapse, medication non-adherence, presented to the hospital with encephalopathy, gait instability, vision changes and memory loss. He was normonatremic however his glucose level fluctuated widely within 24 hours after presentation. MRI brain without contrast demonstrated central diffusion restriction in the pons suggesting of ODS.  Despite acute management including immediate treatment with high-dose IV thiamine and management of all comorbidities, the patient cognitive impairment and episodic memory deficits remained. 

This case highlights the need to maintain a high suspicion for ODS in context of any osmotic shifts. Fluctuating glucose and chronic alcohol use can cause demyelination through astrocyte and oligodendrocyte injury, excitotoxicity, and energy-dependent disruption of osmotic homeostasis.

ODS can result from shifts in osmolytes other than sodium and a high level of suspicion is required for timely recognition. Imaging changes may initially be subtle and repeat MRI should be considered to define the full extent of demyelination including in extrapontine regions like the hippocampi or thalami.
Authors/Disclosures
Alok Govind Ravishankar Komari, MBBS
PRESENTER
Dr. Ravishankar Komari has nothing to disclose.
Abdul Rehman R. Nasir, MBBS Mr. Nasir has nothing to disclose.
Claire E. Delpirou Nouh, MD (University of Oklahoma Health Science Center, Department of Neurology) The institution of Dr. Delpirou Nouh has received research support from Oklahomas Nathan Shock Center. Dr. Delpirou Nouh has a non-compensated relationship as a Volunteer/Board member with Oklahoma Alzheimer Association that is relevant to AAN interests or activities.