Diabetic community is vast enough, giving researchers a very good reason to explore more in their world. One of their rarely probed complications is brainstem dysfunction. In this study, we investigated brainstem auditory evoked potential studies (BAEPs) in diabetic patients, as well as its associations with diabetic complications, especially diabetic microangiopathy. Our study was conducted on 40 diabetic patients having type I or type II. They were classified into two groups; group I (< 5 years duration of illness) and group II (> 5 years duration of illness). Their ages ranged from 20 to 59 years. The patients were examined clinically, neurologically and electrophysiologically. Brainstem auditory evoked potential studies, nerve conduction studies and flash electroretinography were performed to all patients. Urine analysis, instantaneous random blood sugar and funduscopy were also performed for patients. The brainstem auditory evoked potential studies of patients were compared to values of 30 normal subjects and their ages ranged, also, from 20 to 59 years. The diabetic patients experience brainstem dysfunction early in their disease course (before 5 years duration of the illness) that is increased as the disease duration increases. This dysfunction is evident by significant delay of wave V in diabetic patients as compared to normal individuals. Later, after 5 years duration of the illness, delay of wave III, further delay of wave V, prolongation of I-V IPL and decrease in amplitude of wave V occur. Diabetes type, I or II, has no different effect on BAEPs results.Microangiopathic complications (retinopathy and nephropathy) are associated with increasing hearing threshold in diabetic patients, mainly after 5 years duration of the illness. Wave III is significantly delayed in presence of diabetic retinal affection; functionally and by funduscopy. Also, wave V is significantly delayed, in patients with abnormal skin and peripheral nervous system manifestations. In addition, wave V latency and III-V IPL are prolonged in patients having cardiovascular affection symptoms and postural hypotension. Finally, in patients with sweating abnormalities, wave I amplitude is significantly increased.So brainstem dysfunction occurs early in the course of diabetes (type I and II similarly) and it is further affected by its duration. It starts by affection at the midbrain level (inferior colliculus) then proceeds by time to lower levels; caudal pons (cochlear nucleus). Also, as diabetic microangiopathic complications occur, hearing threshold increases. Retinopathy is accompanied with brainstem disintegration, at the caudal pons level. In three situations, we questioned the occurrence of similar pathogenesis theories, intracranially and extracranially. First, diabetic patients, with abnormal skin or peripheral nervous system manifestations, experience midbrain dysfunction (in the vicinity of the inferior colliculus) as well. The presumed theory if microvascular or, less likely, autoimmune affection. Second, diabetic patients with cardiovascular affection symptoms and postural hypotension show retrocochlear dysfunction. The doubted theory is macrovascular affection. Finally, diabetic patients with sweating abnormalities show evidence of affection of olivocochlear bundle. The probable theory is small fiber neuropathy.