Risperidone was stopped immediately. He improved only slightly on this treatment, and was referred to the andrology department for shunting, which was performed the next day. A subsequent magnetic resonance imaging scan showed significant penile

ischaemia, which required surgery and the insertion of a penile implant 7 days later. After a medication-free period, risperidone was replaced with aripiprazole. He tolerated this well and was discharged from hospital. He reported no further episodes of priapism after despite discharge. On further questioning, Y admitted to one previous episode of priapism, which had occurred 3 days earlier and resolved spontaneously after 2 h. He denied any prior experience of priapism or Inhibitors,research,lifescience,medical any other erectile dysfunction. Apart Inhibitors,research,lifescience,medical from

taking antipsychotic medication, he had no risk selleck factors for priapism. He tested negative for sickle cell disease or trait and did not have any haematological disorder. He had never taken drugs for erectile dysfunction and had no history of illegal substance use such as cocaine or cannabis. He had no past or current medical history of note and was not on any medication with the exception of sodium valproate and risperidone. At home, he drank alcohol most days (beer) but rarely exceeded 2 units a day. Inhibitors,research,lifescience,medical He was a nonsmoker and had never had pelvic or genital trauma. Family history was unremarkable and he denied any drug allergy. Written informed consent was obtained from Y for this publication. Pathology In Inhibitors,research,lifescience,medical physiological erection, relaxation of the two corpora cavernosa allows increased arterial blood flow into the penis. This causes pressure on the veins that normally drain the penis, reducing venous outflow.

The two mechanisms combine to cause a temporary engorgement Inhibitors,research,lifescience,medical of blood in the penis and erection. Reversal of this process causes detumescence. Several neurotransmitters have been implicated in the regulation of this complex process both centrally and peripherally. At the level of the peripheral nervous system, relaxation of the penile muscles is mediated mostly by the parasympathetic system (via acetylcholine muscarinic receptors) and the GSK-3 release of nitric oxide from the endothelium of the bloods vessels that line the corpora cavernosa. Detumescence and flaccidity are mediated by the sympathetic system, which releases noradrenaline acting on α-adrenergic receptors to cause contraction of the penile vessels and smooth muscles, which in turn reduces blood flow into the penis [Andersohn et al. 2010; Andersson, 2001]. Two types of priapism have been identified: low flow (ischaemic) and high flow (nonischaemic). In low-flow priapism, there is prolonged failure of venous outflow, typically either because the draining veins become obstructed (for instance in sickle cell or other haematological disorders) or because the sympathetic system fails to initiate detumescence. Blood stasis leads to ischaemia and fibrosis if left untreated.