Several exciting nerv therapies for erectile dysfunction (ED) have bee
n released or will shortly appear for the management of erectile failu
re in diabetes and other conditions, These are the result of significa
nt advances in knowledge about the pathophysiology of ED, which have a
llowed a targeted approach to each of the elements involved in produci
ng an erection, Diabetes results in ED in 50-75% of men, Ln men,vith d
iabetes, the incidence of ED is 9% from age 20 to 29 years and increas
es to 95% by ap 70, It mag be the presenting symptom of diabetes. More
than 50% of men develop ED within 10 years of the diagnosis, and it m
ay precede the other complications of diabetes. Neuropathy, vascular d
isease, glycation of cavernosal elastin, nutrition, endocrine disorder
s, and psychogenic factors, ns well as drugs used in the treatment of
diabetes and its complications, are among the multiple etiologies of E
D in diabetes. Gradual onset and progression are the hallmarks of orga
nic ED, Decreased rigidity and incomplete tumescence occur before toto
l failure; morning or dream-related erections are lost along with spon
taneous, tactile, visual, or fantasy-induced erections. Organic En is
present with all partners and with masturbation, and there is no loss
of libido, Sudden loss of erections with a particular partner while ma
intaining morning erections and nocturnal penile tumescence suggests a
psychogenic cause. The neurological manifestations are those of dysfu
nction of the autonomic nervous sq stem (ANS) or peripheral sensory ne
rves, both of the AF and C fiber types, Buttock claudication is the us
ual manifestation of vascular disease, but this make; be absent, when
the stenotic vessel is the internal pudendal artery. A genile/brachial
index of <0.7 indicates diminished blood supply Unresponsiveness to v
asodilators is the harbinger of a venous leak; this requires evaluatio
n by penile Doppler sonography A logical stepwise progression is used
for making a diagnosis of the cause of ED (see algorithm). In all inst
ances, a careful history; for the rapidity of onset of ED, presence of
absence of morning erections, uniformity of sexual dysfunction with a
ll partners and in all situations, evidence of autonomic or sensory; n
erve dysfunction, vascular insufficiency hormonal inadequacy and drugs
used in the treatment of satellite disorders must be appraised. Oral
therapies can be used in any form of ED; failure should lead to intrac
avernous injection of a vasodilator as part of thr: evaluation, both f
or diagnostic purposes and as an aid in choosing among the therapeutic
options. Only problematic cases need be tested for nocturnal penile t
umescence (NPT), Normal NPT defines psychogenic ED, and a negative res
ponse to vasodilators implies vascular insufficiency. Antihypertensive
and cardiovascular drugs should be changed to those with no or a lowe
r potential for ED, and glycemic control should be optimized. For psyc
hogenic dysfunction, the patient should be referred to a therapist wit
h expertise in treating sexual dysfunction. Oral regimens will be must
acceptable as initial therapy and can include the alpha 2 antagonist
yohimbine, trazadone, Or the apparently mort: frequently successful ty
pe V phosphodiesterase inhibitor seldinafil, Vacuum erection devices a
re satisfactory for many patients, Men responsive to intracavernous in
jections have this as a therapeutic option, but those who are unrespon
sive usually have vascular disease or venous leaks and require prosthe
ses or vascular surgery. No attempt should ever be made to treat IID w
ithout first consulting the significant other.