Neurological fallout of hyperglycemia: A case report of a rare presentation of osmotic demyelination syndrome

Background: Osmotic demyelination syndrome (ODS) is a rare but potentially life-threatening neurological disorder. It is characterized by non-inflammatory demyelination, usually triggered by sudden shifts in serum osmolality. However, emerging evidence suggests that abrupt osmotic shifts caused by severe hyperglycemia, even in the absence of sodium imbalance, can also precipitate ODS.

Case presentation: A 57-year-old male with poorly controlled type 2 diabetes mellitus and chronic alcohol use presented with recurrent seizures and altered sensorium. Initial blood work revealed severe hyperglycemia (390 mg/dL), an elevated HbA1c level (15.2%), and a normal corrected serum sodium level (135 mEq/L). During hospitalization, the patient developed progressive neurological deterioration, culminating in quadriplegia.

Imaging findings: Initial non-contrast computed tomography (NCCT) of the brain was unremarkable. Magnetic resonance imaging (MRI) on day 11 showed symmetric T2/FLAIR (Fluid-Attenuated Inversion Recovery) hyperintensities in the central pons extending into the middle cerebellar peduncles. These findings, in the absence of diffusion restriction or enhancement, were characteristic of central pontine myelinolysis (CPM). No extrapontine involvement was observed.

Differential diagnosis: Radiological differentials considered included acute disseminated encephalomyelitis (ADEM), multiple sclerosis (MS), ischemic infarction, vasculitis, and brainstem glioma. However, the symmetric pontine involvement without enhancement or mass effect, along with the clinical context of hyperosmolar hyperglycemia, favored a diagnosis of ODS.

Management and outcome: Supportive therapy involving careful glucose correction, intravenous hydration, and close monitoring of metabolic parameters was initiated. The patient showed gradual neurological recovery during the hospital course.

Conclusion: This case highlights a rare presentation of CPM secondary to hyperosmolar hyperglycemia in the absence of hyponatremia. It underscores the importance of early recognition, neuroimaging, and cautious metabolic correction in diabetic patients presenting with new-onset neurological deficits.