Osmotic Demyelination Syndrome Without Dyselectrolytemia- An Awareness in Type 1 Diabetes Mellitus

Sir, Osmotic Demyelination Syndrome is a rare entity characterized by acquired non-inflammatory demyelination of pons, basal ganglia, thalamus, cerebral cortex, cerebellum, and hippocampus.[1] We wish to report a case of an 18-year-old male, type 1 diabetic who presented to the casualty with difficulty in swallowing and speaking for 2 months, followed by difficulty in walking and frequent falls for 1 month. He was previously admitted 1 year back with DKA. He was doing well until 2 months back then his parents noticed change in his voice which progressed to difficulty in swallowing, associated more with solid food but could drink properly. Over 1.5 months back he noticed slipping off of his chappals while walking. He started complaining of his limbs getting stiff and he was unable to carry out his daily activities like riding a bicycle, using handpumps, etc. Over the last 20 days, his gait became ataxic with frequent falls but he could walk without support. He did not seek any healthcare advice meanwhile. He did not complain of any bladder or bowel disturbance. On examination, he had mild pallor with stable vitals. Neurological examination revealed hypertonia, hyperreflexia in both upper and lower limbs with bilateral extensor plantar. Power was 4/5 in bilateral upper and lower limbs. Bilateral patellar clonus and ankle clonus were present. Sensory examination was normal. Cerebellar signs, autonomic dysfunction, proximal muscle weakness was absent and Romberg sign was negative. Gait was ataxic with frequent falls without support. Other systems were unremarkable. A provisional diagnosis of spastic quadriparesis with truncal ataxia was made. Relevant investigations including MRI Brain [Figures 1-3] was done as in Table 1.Figure 1: A well defined oval shaped midline Hypointense lesion of size 15mm * 12mm * 14mm in pons (arrow) on T1WI, Hyperintense on T2WI, not suprressed on FLAIR imageFigure 2: Hyperintensity in Pons ( arrow) in Transverse, Sagittal and Coronal sectionsFigure 3: Restriction on Diffusion weighted imageTable 1: Laboratory investigationsExcluding other causes and in view of the above clinical findings and investigations, a diagnosis of diabetes-induced ODS was made. A slow progression of symptoms over 2 months in this case was atypical. He was revised for his basal-bolus insulin regimen maintaining a gradual control of his blood sugar levels. With time, he started showing improvement in his general condition, gait, speech, and swallowing. Later he was discharged with basal-bolus insulin, proper counseling, and training for self-blood glucose monitoring. We wish to highlight diabetes as an important harbinger of ODS, other than rapid correction of chronic hyponatremia,[2] alcoholism, and malnutrition.[1] Casey et al.[3] reported two cases of CPM in patients with long-standing poorly controlled diabetes. Overcorrection of metabolic acidosis in DKA with sodium bicarbonate causing rapid changes in serum osmolality leading to demyelinating changes in the brain has also been reported.[4] Regular monitoring of blood sugar levels, compliance with insulin therapy and high suspicion of this rare complication is important for diagnosis and management. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.