Hyperglycemia Identified as Rare Cause of Quadriplegia in Osmotic Demyelination Syndrome: Case Study
India: A recent case report published in the Journal of the Association of Physicians of India has highlighted hyperglycemia as a rare and unusual cause of quadriplegia, shedding light on the potential neurological complications of uncontrolled blood sugar levels.
Osmotic demyelination syndrome (ODS), particularly central pontine myelinosis (CPM), is typically associated with the rapid correction of hyponatremia, a condition in which sodium levels in the blood are dangerously low. However, according to the authors, the case marks the first known instance of ODS triggered by hyperglycemia, where both the pontine and extrapontine regions of the brain were affected.
Mahesh Shinde, Consultant Physician, Department of Medicine, Carewell Superspeciality Hospital, Aurangabad, Maharashtra, India, and colleagues describe the case of a young male who presented with acute-onset altered mentation, quadriplegia, and urinary retention. On examination, he was stuporous with a Glasgow Coma Scale (GCS) of 6/15 and signs of dehydration, including tachycardia. Neurologically, he exhibited hypotonic quadriplegia, absent reflexes, and normal-sized pupils that reacted to light. Investigations revealed significantly high blood sugar (550 mg/dL), cerebrospinal fluid (CSF) sugar (149 mg/dL), and urine sugar (3+), with normal cell count in CSF but elevated protein levels. The serum osmolality was 330 mOsm/kg H2O, and Electroencephalogram (EEG) showed mild to moderate dysfunction. Further tests indicated severe hyperglycemia with a hemoglobin A1c of 11%. Despite normal findings in initial imaging, including an MRI of the brain and spine, the patient’s condition worsened, requiring mechanical ventilation.
After one week, the patient’s clinical condition raised suspicion of pontine involvement, leading to a repeat MRI, which confirmed hyperintensity lesions in both pontine and extrapontine areas, indicating osmotic demyelination syndrome, including central pontine myelinosis and extrapontine myelinosis (EPM). Over the next three weeks, his mental state and limb power improved, and he was eventually weaned off the ventilator. After 35 days, he was discharged with antidiabetic treatment. On follow-up, he had fully recovered, except for reduced lower limb power and the presence of a urinary catheter.
In conclusion, the authors have presented a rare case of osmotic demyelination syndrome where both central pontine myelinosis and extrapontine myelinosis were identified as initial manifestations of hyperglycemia. This rare etiology and presentation, with its characteristic clinical and radiological findings, is seldom reported in the literature.
The authors emphasize that acute changes in osmolality and subsequent subacute changes can contribute to the development of ODS. Given this, hyperglycemia should be considered a potential cause of quadriplegia due to ODS, even in the absence of hyponatremia, diabetic ketoacidosis, or hyperosmolar hyperglycemic state. While there is no definitive treatment for ODS at present, the authors highlight that symptomatic management and comfort care have improved patient outcomes.
Reference:
Shinde M, Rathod V, Wahatule R, et al. Hyperglycemia as a Rare Cause of Quadriplegia: A Case Report. J Assoc Physicians India 2025;73(1):66-69.
