OBJECTIVES: Diabetic impotence is generally due to peripheral neuropathy, but a central pathway impairment has also been suggested. We evaluated somatosensory transmission in a group of impotent diabetic men to assess the role of central nervous system (CNS) involvement. MATERIALS AND METHODS: Somatosensory evoked potentials (SEPs) of pudendal (pdn) and posterior tibial (ptn) nerves were recorded in 74 patients. Type and duration of diabetes, severity of sexual dysfunction, medium term metabolic control, occurrence of microangiopathic chronic complications and autonomic neuropathy were evaluated. RESULTS: Our data show an impairment of central conduction times in pdn (25.7%) and ptn (39.2%) greater than peripheral nervous impairment (pdn 12.2%, ptn 8.1%), in impotent diabetic patients without any further major complication. Central nervous conduction delay resulted to be correlated with poor glycemic control. Significant evident autonomic dysfunction was found only in a minority of cases. CONCLUSION: Our data might suggest that altered conduction along CNS and somatic peripheral neuropathy might develop independently. We confirm the hypothesis of a "central diabetic neuropathy" and suggest that central sensory pathways involvement, not related to peripheral impairment, could play a role in the pathogenesis of erectile dysfunction in diabetic patients.
OBJECTIVES:Diabetic impotence is generally due to peripheral neuropathy, but a central pathway impairment has also been suggested. We evaluated somatosensory transmission in a group of impotent diabeticmen to assess the role of central nervous system (CNS) involvement. MATERIALS AND METHODS: Somatosensory evoked potentials (SEPs) of pudendal (pdn) and posterior tibial (ptn) nerves were recorded in 74 patients. Type and duration of diabetes, severity of sexual dysfunction, medium term metabolic control, occurrence of microangiopathic chronic complications and autonomic neuropathy were evaluated. RESULTS: Our data show an impairment of central conduction times in pdn (25.7%) and ptn (39.2%) greater than peripheral nervous impairment (pdn 12.2%, ptn 8.1%), in impotent diabeticpatients without any further major complication. Central nervous conduction delay resulted to be correlated with poor glycemic control. Significant evident autonomic dysfunction was found only in a minority of cases. CONCLUSION: Our data might suggest that altered conduction along CNS and somatic peripheral neuropathy might develop independently. We confirm the hypothesis of a "central diabetic neuropathy" and suggest that central sensory pathways involvement, not related to peripheral impairment, could play a role in the pathogenesis of erectile dysfunction in diabeticpatients.