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Diabetes Mellitus, prolonged hyperglycemia, causes peripheral and central nervous system dysfunction.  Chronic hyperglycemia causes changes in the sorbitol, inositol and taurine content of peripheral and central nervous system tissue.  The proteins in these tissues are also altered by glycosylation end products. The changes in metabolites impair growth and development of nerves and the increased glycosylation end products make the proteins stiff, sticky and prone to physical injury.  This activity stimulated by hyperglycemia impairs the normal function of the peripheral and central nervous system.  Manifestations of this tissue injury have been loss of sensation and increased pain in the extremities, loss of proprioception when standing, dysregulation of gastrointestinal motility, and heart rate.  Also noted in children are delayed maturation of cognitive function during childhood and more rapid decline of cognitive function with increasing age and increasing HbA1c. 

Sleep apnea has become an important cause of heart failure and death commonly linked to type 2 diabetes and obesity.  Continuous pressure airway pressure (CPAP) does overcome the periods of obstruction and prevents the morbidity associated with obstructive sleep apnea (OSA).  Forty-Six percent of type 1 diabetic patients have absence of effort sleep apnea which means it is a central lack of drive to breath.  There is evidence of change of structure in the medulla of subjects with type 1 diabetes as well as evidence of injuries in the medulla that cause cessation of breathing.  These observations indicate that central neuropathy caused by hyperglycemia does cause central sleep apnea and possibly death.