If the patient is relaxed and a suitable dose has been injected, a good erection will occur within 10 minutes. Erectile dysfunction secondary to arterial disease may take several minutes longer to produce an erection.

Patients with neurogenic impotence may develop priapism with very low doses of papaverine but this should not be a deterrent to using adequate dosages. If the erection is unequivocally rigid and the penis cannot be buckled, vasculogenic impotence can be virtually eliminated and no further investigations are necessary.

If the erection is not rigid enough, a second dose may be employed at the same sitting. This is quite safe and systemic side effects are uncommon.

However, it must be emphasised that this should be performed in a hospital setting with full infrastructural back-up rather than in an office environment. Any curvature of the penis can be studied at the same time.

If the erection is still not rigid enough, vascular disease must be eliminated using more sophisticated tests. A Doppler study can be easily combined with the injection test. If an objective measurement of the erection is desired either for academic, medico-legal or psychotherapeutic purposes, a real-time Rigiscan monitoring may be", performed at the same session.

All patients MUST be monitored to, for the next several hours until the erection has subsided completely. Haematomas and swellings are extremely rare if a very fine needle is used and adequate pressure is applied on the puncture site. No erection must be allowed to last longer than 4 to 6 hours. Blood-letting, performed using an 18 or 19 gauge scalp vein set should decompress nearly all erections. Vasoconstrictor antidotes and shunt operations are almost never necessary.

2) The Rigiscan Test

The Rigiscan is the gold standard for NPTR (Nocturnal Penile Tumescence and Rigidity) measurement. It is the test of choice for non-invasive diagnosis.

It is especially suitable for anxious patients since it can be performed in the privacy of their own bedrooms. Its ability to objectively quantify erectile rigidity and establish physical normalcy makes it an important, reassurance-providing device to the patient with purely functional problems. It is also useful in medico-legal cases. Time and cost are two relative deterrents.

A Rigiscan tracing showing a good number of erectile episodes with rigidity levels of 80% or more and a duration of 20 minutes or more in a single episode almost effectively rules out serious vascular disease.

Arterial insufficiency and venous leaks can also be suspected on the basis of the Rigiscan graphs. Patients with purely arterial disease generally have low levels of maximum rigidity but of adequate duration.

Patients with predominant venous leakage will have varying rigidity levels depending on the severity of the leakage but the duration is almost always shortened. These patients must be evaluated using other means. The erectile response to vaso-active injection can be objectively studied by the concomitant application of the Rigiscan monitor. This is called a Real­time study.

3) Penile Ultrasound

A Doppler evaluation of the penile arteries is indicated if the «rectile response to the injection test is inadequate or if the patient's Rigiscan study is suggestive of arterial insufficiency. Pure arterial disease is relatively uncommon in the young patient unless there is congenital arterial dysplasia, premature arterial disease or trauma.

Ultrasonographic evaluation of the cavemosal arteries can be performed with varying degrees of sophistication once cavemosal smooth muscle has been effectively relaxed by vaso-active injection. A simple acoustic Doppler probe, which is inexpensive and portable, emits auditory signals which can effectively eliminate gross cavernosa! arterial disease. Duplex Doppler and Colour Doppler studies can help visualisation of the cavemosal arteries and measurement of flow.

They can also hint at the presence of venous disease. But while these are useful for quantifying penile arterial flow and help diagnose abnormalities in the main cavernosal arteries, they cannot altogether eliminate arterial insufficiency because of their inability to image the microvasculature. Thus, a normal arterial study does not eliminate arterial disease. This is important to bear in mind.

The DICC is an useful haemodynamic test for the diagnosis of CVOD (Corporal Veno-Occlusive Dysfunction). In its simplest form, two cannulae are inserted into the corpora cavernosa after smooth muscle relaxation has been achieved with a vaso-active injection. One cannula is connected to a pressure transducer; the other conducts saline or radio-opaque contrast solution at controlled flow rates through an adjustable flow pump. Pressures are measured after injection and 30 seconds after a pressure of 150 mm Hg has been induced. Flow rates are measured in order to induce erection and attain ISO mm Hg, to maintain erection at 150 mm Hg, and to maintain mean arterial pressure (MAP) - generally 80-90 mm Hg. The study is then repeated at a pressure setting of 90 mm Hg. The Cavernosal Artery Systolic Occlusion Pressure (CASOP) is also measured at the sametime using a Doppler device. These are also the only universally accepted standards for DICC evaluation. There are some centres that perform an 8 or 9 track multi-phasic DICC. Radiologic visualisation of leaking penile veins (cavernosography) is performed at the same sitting in many centres. Such radiologic studies are useful only if site-specific, selective ligation is planned as a surgical option.

5) Neurologic Evaluation

Nonselective beta blockers like propranolol cross tine blood brain barrier and inhibit central brain receptor, producing sedation or depression which may lead to loss of libido.

INCREASED LIBIDO

A variety of drugs have been reported to increase libido. The mechanisms of drug action in increasing sexual drive are diverse; the antidepressants may act primarily byVrelieving depression or they may share central catcholaminergic properties with other drugs causing hypersexual behaviour such as sympathomimetics, dopaminergic agents, amphetamines and cocaine. Hormones with sexual effects, like testosterone or anabolic steroids, may increase libido in men.

In laboratory animals, increased sexual behaviour can be induced by altering catecholamine metabolism through increasing synthesis with L-dopa, or decreasing degradation with a monoamine oxidase B inhibitor, deprenyl. Amphetamine, a catecholamine releasing agent and cocaine, a catecholamine uptake inhibitor increases sexual behaviour in rats and libido in men following acute administration.

The theory of dopaminergic receptor involvement is further supported by the observations of increased libido in patients being treated with dopamine agonist, e.g. apomorphine, pergolide and dopamine reuptake inhibitors, e.g. nomifensine and bupropion. 20-30% of patients with parkinsonism treated with levodopa report change in sexual activity including increased libido. Bromocriptine, a selective dopamine-2 agonist, may augment sexual behaviour in man. It is well established that hyperprolactinaemic states secondary to pituitary microadenomas, renal failure and other states are associated with diminished libido which is not alleviated by testosterone replacement but is reversed by bromocriptine therapy. Prolactin released by the pituitary lactotropin is under trophic inhibition by the catecholamine dopamine, therefore, the dopamine agonist bromocriptine will lower prolactin concentration and can restore gonadotropin secretion and gonadal function.

ERECTILE DYSFUNCTION

Most cases of priapism are due to venous outflow obstruction but occasional cases are due to abnormal increase in arterial flow and vasodilators like hydralazine; papaverine may induce priapism by such a mechanism. Delay in treatment may lead to thickening and oedema of corpora cavernosa and result in impotence. In addition to stopping the offending drug, the treatment of drug induced priapism, as for all cases, is to remove the stagnant blood from corpora cavernosa. In the early phases, aspiration of corpora cavernosa and irrigation with saline may be all that is needed but priapism of long duration requires that a shunt procedure be carried out. Medications that havebeen used to reverse priapism include alpha adrenergic compounds like phenylephrine, ephedrine, norepinephrine injected in corpora cavernosum after penile aspiration.

forward in the process of ejaculation. As in the case of behavioural and erectile phases, dopaminergic and sertotonergic modulate the central component of ejaculatory reflex while alpha adrenergic stimulation is implicated in seminal emission and bladder neck closure. Role of cholinergic nervous system in the process of ejaculation is not clear.

NO OR DELAYED EJACULATION

Agents that decrease dopaminergic activity increase ejaculatory latency and reduce ejaculatory capacity. One of the postulated mechanisms of ejaculatory failure caused by antipsychotic agents may be the central effects of these agents in decreasing dopaminergic activity.

A number of commonly prescribed antidepressants including imipramine, amitriptyline and isocarboxazid are associated with ejaculatory failure. These agents block the reuptake of 5-HT and increase serotonin levels. Sertraline and fluoxetine are selective 5-HT uptake inhibitors and produce delayed ejaculation. Interestingly these effects of antidepressants (both tricyclic and MAO inhibitors) can be reversed by administration of cyproheptadine, a drug with antiserotonergic properties.

Pharmacological agents that deplete functional pools of catecholamines or have alpha-1 adrenergic antagonist activity predictably impair emission, ejaculation, and the experience of orgasm. The agents that diminish presynaptic norepinephrine release include reserpine, methyldopa, guanethidine. Agents with significant alpha-1 adrenergic antagonist activity include antihypertensive agents like phenoxybenzamine, phentolamine, prazosin, labetalol, psychotropic agents like chlorpromazine, thioridazine, trifluoperazine, phenelzine, amitriptyline and clomipramine.

RETROGRADE EJACULATION

During the process of ejaculation, there is reflex closure of the internal urethral sphincter which prevents retrograde ejaculation and this is mediated predominantly by alpha-1 adrenergic nervous system.

Drags that possess alpha-1 adrenergic antagonist properties can cause retrograde ejaculation and these agents include all the drugs mentioned in the previous section. Sympathomimetic agents such as pseudoephedrine, ephedrine, and phenylpropanolamine have been used to treat retrograde ejaculation.

MISCELLANEOUS EJACULATORY DISORDERS

Spontaneous ejaculation has been described to occur in patients being treated with trifluoperazine, thiothixene and mazindol and pergolide, while painful ejaculation has been reported in patients being treated with clomipramine, haloperidol, imipramine, protriptyline, thioridazine and trifluoperazine.

DISORDERS OF ORGASM

Orgasm in man consists of a pleasurable sensation associated with emission and ejaculation but orgasm can occur independent of ejaculation. It results from cerebral processing of afferent stimuli from the dorsal and pudendal nerves. Orgasm in women consists of a pleasurable sensation that usually begins at the clitoris and rapidly spreads throughout the pelvis and is marked by simultaneous rhythmic muscular contractions of the uterus, outer third of vagina and the anal sphincter.

Disorders of orgasm can occur both in men and women but are frequently described in literature in women.

Psychotropic drugs have often been associated with anorgasmia (inability to have orgasm) and the offending agents include selective serotonin reuptake inhibitors (SSRI) like fluoxetine, paraxetine and sertraline, MAO inhibitors like phenelzine, isocarboxazid and tranylcypromine, tricyclic antidepressants like clomipramine and major tranquilizer like thioridazine.