Diabetic Autonomic Neuropathy

Aaron I. Vinik, MD, PhD.; Roy Freeman, MB, ChB.; Tomris Erbas, MD


Semin Neurol. 2003;23(4) 

In This Article

Genitourinary Autonomic Neuropathy

Erectile Dysfunction

Erectile dysfunction (ED) is the most common form of organic sexual dysfunction in males with diabetes, with an incidence estimated to be between 35 and 75%.[39,40,41] ED is defined as the consistent inability to attain and maintain an erection adequate for sexual intercourse, usually qualified by being present for several months and occurring at least half the time. ED in diabetes is multifactorial, including neuropathy, vascular disease, metabolic control, nutrition, endocrine disorders, psychogenic factors, and drugs. In diabetes, the development of autonomic neuropathy is partly responsible for the loss of cholinergic activation of the erectile process. In the penis, acetylcholine acts upon the vascular endothelium to release nitric oxide and prostacyclin, both of which participate in relaxation of the corpora cavernosa necessary for the increase in blood flow that causes an erection and both of which are impaired in ED. There is also evidence that nonadrenergic/noncholinergic nerve function is hampered with decreased content of vasoactive intestinal polypeptide, substance P, and other vasodilatating neurotransmitters.[42] ED is a marker for the development of generalized vascular disease and for premature demise from a myocardial infarct, and penile failure may be a portent of upcoming and possible preventable cardiovascular events.[39] ED should alert physicians to perform cardiovascular evaluations for these patients. Retrograde ejaculation is caused by damage to efferent sympathetic nerves that coordinate the simultaneous closure of the internal vesicle sphincter and relaxation of the external vesicle sphincter during ejaculation. Absence of spermatozoa in the semen and presence of motile sperm in a postcoital specimen of urine confirm the diagnosis.

Neurogenic Bladder

Symptoms of bladder dysfunction have been observed in 37 to 50% of diabetic patients. Afferent nerve impulses of bladder sensation and reflex bladder contraction are carried by sympathetic, parasympathetic, and somatic nerves to the spinal cord. The earliest bladder autonomic dysfunctions are sensory abnormalities that result in impaired bladder sensation, an elevated threshold for initiating the micturition reflex, and an asymptomatic increase in bladder capacity and retention. When there is damage to the efferent parasympathetic fibers to the urinary bladder, symptoms such as hesitancy in micturition, weak stream, and dribbling ensue with a reduction in detrusor activity. This leads to incomplete bladder emptying, an increased postvoid residual, decreased peak urinary flow rate, bladder overdistension, and urine retention. Finally, overflow incontinence occurs because of denervation of the external and internal sphincter.[43] A postvoiding residual volume of more than 150 mL is diagnostic of neurogenic bladder. Neurogenic bladder may put patients at risk for urinary infections. More than two urinary tract infections per year should alert the physician to possible neurogenic bladder and elicit appropriate diagnostic procedure.


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