Neurologic consequences of hypoglycemia and pathogenic mechanisms involved in diabetic neuropathy.
Although the limitations of human experimental models of hypoglycemia have hampered investigation, it is generally accepted that a reversible deterioration in cognitive function occurs at a plasma glucose concentration of around 3.5 mmol/L, above the glycemic threshold for symptoms. It is unclear whether this threshold varies in those with hypoglycemia unawareness. Repeated severe hypoglycemia may cause chronic impairment although the clinical significance and the contribution of other factors remains unclear. There is increasing evidence that microvascular abnormalities are the major factor in the pathogenesis of peripheral neuropathy. This may be why there is still little experimental support from human clinical studies for the use of aldose reductase inhibitors in its treatment.
Heller
S
S
Northern General Hospital, Sheffield, UK.
Ward
J D
JD
D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000503:physiopathology; D001925:Brain Damage, Chronic / Q000503:physiopathology*; D001928:Brain Diseases, Metabolic / Q000503:physiopathology*; D003929:Diabetic Neuropathies / Q000503:physiopathology*; D006801:Humans; D007003:Hypoglycemia / Q000503:physiopathology*; D009460:Neurologic Examination
D001786:Blood Glucose