Abstract

Objetives:
Cerebellar ataxia is a rarely reported complication of severe hypoglycemia, usually related with CPM, a central pons osmotic demyelinating lesion. The CPM etiology is diverse, more frequently related to
rapid corrections of severe hyponatremia. However, it is also described in diseases resulting in rapid and significant shifts in plasma osmolality in absence of abnormalities of sodium homeostasis.
Maerials and Methods:
A 45­years­old woman, with diabetes type 1 and Graves­Basedow disease presented with abrupt speech disturbance, ataxia and impairment to swallow after a severe hypoglycemic episode (30mg/dl). She
referred recurrent severe hypoglycemic episodes. Examination revealed slurred speech, upper and lower limbs dysmetria, weak left limbs reflexes, and a wide based unsteady gait ataxia with no Romberg’s sign. 
Results:
Cerebral CT and extensive blood test were normal. Brain MRI showed a non contrast- enhancing central pontine lesion, hyper- intense on T2 and FLAIR, and isointense on T1 sequences. A MRI after two months showed significant decrease in the lesion size. Few months later, only minimal residual neurological deficit with light unsteadiness on walking and slurred speech persisted.
Conclusion: 
Neurological manifestations of hypoglycemia include behavioural change, confusion, loss of consciousness and seizures, but ataxia is unusual because cerebellum is protected by the glucose uptake.
CPM secondary to hypoglycemia is a rare entity, associated with continue neurologic dysfunction, however, our case showed improvement despite the lesion. 
Proposed pathophysiology is a cytotoxic edema secondary to impairment of the cellular ion pumps. Changes of blood glucose concentrations can be as brisk and profound as to cause significant serum tonicity changes leading to CPM.