Brain, a gluco-dependent organ: toxic effects of hypoglycaemia and hyperglycaemia
Radermecker, R.R.; Philips, J.C.; Jandrain, B.J.; Paquot, N.; Lefèbvre, P.J.; Scheen, A.J.
Revue Medicale de Liege 63(5-6): 280-286
2008
ISSN/ISBN: 0370-629X PMID: 18669193 Document Number: 620911
Glucose is almost the only energy substrate for the brain. Such glucose dependence explains why any large variation of plasma glucose levels could lead to cerebral dysfunction, which may be severe and progress to a coma. Hypoglycaemic coma, the most common one, has a pure metabolic origin (neuroglucopenia) whereas hyperglycaemic coma is more complex and mainly due to osmotic disturbances. Besides acute changes of plasma glucose concentrations, it is generally recognized that more subtle chronic or recurrent glucose abnormalities could also result in brain dysfunction. However, such clinical consequences are more difficult to assess in clinical practice. Nevertheless, learning perturbations in young patients with type 1 diabetes and memory losses, sometimes severe and subject to progress to dementia ("diabetic encephalopathy") in older type 1 or type 2 diabetic patients, have been reported, although with some controversy. The present paper summarizes the current knowledge of both acute and chronic cerebral dysfunctions following perturbations of blood glucose levels in diabetic patients.