Glucose is the preferred metabolite of the brain with 25% of circulating blood glucose in adults destined for cerebral metabolism. It is intuitive then that type 1 diabetes mellitus (T1DM), a disorder characterised by perturbations in blood glucose, should cause acute and chronic brain dysfunction. These cognitive and affective impacts appear to be greatest in the developing brain of children and adolescents with T1DM. Whilst both hyperglycaemia and ketoacidosis also have impact upon brain function, this presentation will focus upon the acute and chronic consequences of hypoglycaemia on the developing brain. In humans mild hypoglycaemia results in cognitive dysfunction. Preliminary MR data from a study of subjects experiencing controlled hypoglycaemia undertaking cognitive tasks indicates that even mild hypoglycaemia results in disrupted cortical function that is slow to recover. Recurrent or chronic episodes of mild hypoglycaemia are mostly unrecognised and occur within a broader neurotoxic milieu of hyperglycaemia and glycaemic variation. Thus in the context of T1DM it impossible to quantitate the impacts of recurrent chronic mild hypoglycaemia per se. Severe hypoglycaemia can cause loss of consciousness and significant alterations in brain biochemistry. In animal models a single episode of significant hypoglycaemia results in neuronal apoptosis. The one study that has captured episodes of severe hypoglycaemia in humans undergoing continuous glucose monitoring indicates that many hours of hypoglycaemia must occur before a seizure event follows. Such events are readily identifiable and statistically associated with disturbed brain function and morphology in an age dependent manner after controlling for other diabetes variables. In summary, the full spectrum of mild to severe hypoglycaemia has an associated spectrum of acute and chronic impacts upon function and development of the paediatric brain.