Central Pontine Myelinolysis Secondary to Hyperglycemia in a Young Patient.

Wasey Ali Yadullahi Mir,Dhan B Shrestha,Vijay K Reddy,Mir Arshad Ali Yadullahi,Barun B Aryal

doi:10.7759/cureus.18495

Abstract

Central pontine myelinolysis (CPM) is a neurological disorder typically caused by rapid correction of severe chronic hyponatremia. Conditions causing a hyperosmolar state can also cause CPM, but it is rarely seen in diabetes.Here we describe a case of a 34-year-old female with longstanding uncontrolled diabetes mellitus who presented with bilateral upper and lower limb weakness and dysphagia. Examination showed decreased muscle strength, and laboratory investigations showed high HbA1c, high blood glucose, increased serum osmolality, and normal sodium. A diagnosis of CPM was made after MRI showed restricted diffusion in the bilateral pons and CT showed pontine hypodensities. The patient was started on insulin therapy, and she showed clinical improvement with improving blood glucose levels. After five days of hospital stay, she was discharged home with appointments to neurology and endocrinology clinics.This case shows that CPM is a potential complication of uncontrolled diabetes mellitus in the presence of normal serum sodium. Timely treatment of hyperglycemia can lead to improvement of symptoms, but it is a potentially fatal condition. Thus, a diagnosis of CPM should be considered in diabetic patients who present with neurological symptoms and hyperglycemia.

Highlights

Osmotic demyelination syndrome (ODS) is a rare neurological disorder classically described in the rapid correction of severe hyponatremia [1]
ODS typically involves the destruction of myelin sheath in the pons, termed central pontine myelinolysis (CPM), but extrapontine neurons can be affected, leading to various neurological symptoms
We have described a case of central pontine myelinolysis in a young female with type 2 diabetes mellitus for 13 years

Summary

Introduction

Osmotic demyelination syndrome (ODS) is a rare neurological disorder classically described in the rapid correction of severe hyponatremia [1]. Laboratory investigations revealed an HbA1c of 12.3%, random blood glucose of 278 mg/dL, and erythrocyte sedimentation rate of 33 mm/h Her corrected sodium level was 138, and thyroid-stimulating hormone, liver function parameters, lipid profile, complete blood counts, vitamin B12, folate, and creatine phosphokinase were within normal limits. The day, despite a further increase in insulin dosage to 26 units of glargine and 11 units of lispro thrice daily, her blood sugar levels remained above 200 mg/dL. She could get up from bed and walk on her own but needed to rest after a short period of activity. The patient was discharged home with instructions to follow up with a neurologist on an outpatient basis

Discussion

Conclusions

Disclosures

Martin RJ