Erectile
dysfunction is classified as psychogenic, organic (neurogenic, hormonal,
arterial, cavernosal and drug induced) and mixed. Mixed erectile dysfunction is
the most common encountered having both a psychogenic and organic component (Cellek
et al., 2002).
a)
Psychogenic:
Psychogenic
impotence is the most common type, with about 90% of impotent men suffering
from this condition arising
from are depression, psychological stress, performance anxiety and relationship
problems (Steers, 1990). Sexual behavior and penile
erection are controlled by the hypothalamus, the limbic system, and the
cerebral cortex. Therefore, stimulatory or inhibitory messages can be relayed
to
the spinal erection centers to facilitate or inhibit erection. Two possible
mechanisms have been proposed to explain the inhibition of erection in
psychogenic dysfunction, these are; direct inhibition of the spinal erection
center by the brain as an exaggeration of the normal suprasacral inhibition and
excessive sympathetic outflow or elevated peripheral catecholamine levels,
which may increase penile smooth muscle tone to prevent the relaxation
necessary for erection (Steers,1990).
b)
Organic
i. Neurogenic
It has
been estimated that 10 to 19% of ED is of neurogenic origin (Abicht, 1999). Because erection is a
neurovascular event, any disease or dysfunction affecting the brain, spinal
cord, cavernous and pudendal nerves can induce dysfunction. Example are stroke,
Alzheimer’s disease, Parkinson’s disease (Sachs and Meisel, 1988),
encephalitis, dementia, spinal cord injury, diabetes, pelvic injury (Saenz
de-Tejade et al., 1989). These disorders interrupt neurotransmission causing failure to initiate
nerve impulse (Eardley and Kirby, 1991).
ii.
Hormonal
Hormonal abnormalities, such as hyperprolactinemia (whether from a pituitary
adenoma or drugs), results in both reproductive and sexual dysfunction.
Symptoms may include loss of libido, ED, galactorrhea, gynecomastia, and infertility.
Hyperprolactinemia is associated with low circulating levels of testosterone,
which appear to be secondary to inhibition of gonadotropin-releasing hormone
secretion by the elevated prolactin levels.(Leonard et al.,1989). ED may also be associated with
both the hyperthyroid and the hypothyroid state. Hyperthyroidism is commonly
associated with diminished libido, which may be caused by the increased
circulating estrogen levels, and less often with ED. In hypothyroidism, low
testosterone secretion and elevated prolactin levels contribute to ED. This leads to loss of libido due to inadequate NO (Nitric
Oxide) release from paraventricular nucleus
(PVN)
(Leonard et al., 1989).
iii.
Vasculogenic ( arterial and cavernosal)
Arteriogenic
cause decrease the perfusion pressure and arterial flow to the sinusoidal
spaces, thus increasing the time to maximal erection and decreasing the
rigidity of the erect penis (Michal, 1980). Common risk factors associated with
arterial insufficiency include hypertension, hyperlipidemia, cigarette smoking,
diabetes mellitus, blunt perineal or pelvic trauma, and pelvic irradiation (Goldstein
et al., 1984), (Rosen et al., 1990).
Cavernosal
(Venogenic) Failure of adequate venous occlusion has been proposed as one of
the most common causes of vasculogenic impotence. Veno-occlusive dysfunction
may result from ( Rajfer et al.,1988 ) The presence or development of
large venous channels draining the corpora cavernosa, Degenerative changes
(Peyronie’s disease, old age, and diabetes) or traumatic injury to the tunica
albuginea (penile fracture) resulting in inadequate compression of the
subtunical and emissary veins (Metz et al., 1983), Insufficient
trabecular smooth muscle relaxation, causing inadequate sinusoidal expansion
and insufficient compression of the subtunical venules which may occur in an
anxious individual with excessive adrenergic tone or in a patient with inadequate
neurotransmitter release and Acquired
venous shunts-arising from operative correction of priapism – causing persistent
glans/cavernosum or cavernosum/spongiosum shunting (Christ et al., 1990),
Structural alterations in the fibroelastic components of the trabeculae,
cavernous smooth muscle, and endothelium may result in venous leak (Lue, 1989).
iv)
Drug induce
Anti
hypertensives like beta blockers, thiazide diuretics, methaldopa. Non selective
beta –adrenergic blocking drugs may cause erectile dysfunction by potentiating
α-1 adrenergic activity in the penis ((Melman and Relman, 1999). Thiazide
diuretic have been reported to cause erectile dysfunction by an unknown
mechanism. Antidepressant like amitriptyline, doxepin and anti psychotics like phenothazine,
haloperidol, benzisoxazole (Risperidone) also cause ED. Anti androgens like
gonadotropine releasing hormone agonist, Estrogen containing medication, cimetidine
( at a very high dose) ( (Melman and Relman, 1999), ketoconazole, spiranolactone.
spiranolactone act by decreasing libido
and gynacomastia as well as causing erectile dysfunction. Cimetidine, a
histamine – H2 receptor antagonist, has been reported to decrease
libido and cause erectile dysfunction; it acts as an anti androgen and cause
hyperprolactinemia (Melman and Relman, 1999). Other recreational drugs that
cause ED include Alcohol abuse, cigarette smoking and heroin. Anti arrhythmic
drugs like disopyramide and digoxine has also been reported (Montague et al.,
1996).
v) Systemic diseases
Diabetic
mellitus is a
complex disease that affects many organ systems through the effects of
chronically elevated plasma glucose, which causes damage at the microvascular
level. The common pathway that leads to diabetes-induced microvascular damage
is the generation and impaired clearance of oxygen-derived free radicals
resulting to oxidative stress, which leads to production of a class of
compounds termed advanced glycation end products (AGEs). AGEs are a
heterogeneous group of products formed by non-enzymatic Maillard reactions
between a protein’s primary amino group and carbohydrate-derived aldehyde
groups. AGEs bind with a receptor, which
mediates binding of AGEs to endothelial cells, thereby inhibiting
endothelial-mediated smooth muscle relaxation via a nitric oxide pathway (Cartledge
et al., 2001) The end result of this
molecular cascade is impaired vasodilatation in any microvascular area, ranging
from coronary vasculature to the retina to the penis (Yamagishi et al., 2003). Other
systemic diseases include chronic renal failure, coronary heart disease,
mutifactorial neuronal and vascular dysfunction (El-sakka et al., 2004).
vi) Age
Sexual
function progressively decline as men age. The latent period between sexual
stimulation and erection increase, erection are less turgid, ejaculation is
less forceful, ejaculatory volume decrease,
the refractory period between erections lengthens and a decrease in
serum testosterone concentration (Virag et al., 1984), ( Corona et al.,
2004).
vii) Priapism
Priapism is a
clinical state in which there is persistent usually painful penile erection
often in the absence of erotic psychic stimuli or a condition in which erection
fail to subside despite orgasm. This is a urological emergency resulting from
the disturbance of the normal regulator mechanism controlling penile erection
and flaccidity. Men at risk of developing priapism are patients with erectile
dysfunction undergoing intracavernous form of therapy, sickle cell disease
(SCD) patients, cocaine and marijuana users, psychiatry patients and accident
victims (Adeyokunnu et al., 1981 and Pautler et al., 2001).
Figure 2.3. Pathogenesis of
priapism, endothelial nitric –oxide synthase (eNOS), phosphodiesterase (PDE), transforming
growth factor (TGF), postaglandin 1 (PG1), nitric–oxide (NO), (Culley et
al., 2009).
There are two
types of priapism, called low-flow and high-flow priapism. High-flow priapism
is relatively rare, in high-flow priapism there is a continuous high flow of
oxygen rich blood through the penis. High-flow priapism does not cause
long-term damage to the penis. In low-flow priapism the drainage of blood from
the penis is impaired. The glans (head) of the penis typically remains soft and
uninvolved by the process, while the shaft of the penis is filled with blood
that is starved of oxygen. Prolonged low-flow priapism leads to scarring and
fibrosis of the erectile tissue and permanent erectile dysfunction (McDonald
and Santucci, 2004).
In Nigeria,
identified SCD as the most common aetiological factor of priapism in our
environment, which accounted for 87.5% of cases (Adetayo et al., 1994
and Pautler et al., 2001). In the Eastern Nigeria,
SCD was second to a local aphrodisiac as the most common cause of priapism,
which indicates a slight regional difference in the commonest cause of priapism
among Nigerians (Aghaji, 2000).