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autonomic reflex, sympathetic hyper-reflexia, mass reflex and the neurovegetative syndrome [1,11,12].A clear understanding of the pathophysiology of autonomic dysreflexia allows an appreciation of the precipitants, clinical features and potential sequelae of this condition. After stimulation, the afferent nerves from the bladder (S2-4) pass to the dorsal grey matter of the spinal cord where they synapse with interneurones. Most of these nerves then ascend in the lateral spinothalamic tract and dorsal columns (ascending long tracts) to the brain. However, some interneurones reflexively excite preganglionic sympathetic neurones of the splanchnic sympathetic outflow, between T5 and L2 [13], resulting in arteriolar vasoconstriction, pelvic visceral contractions and pilomotor spasms.In a neurologically intact patient higher centres ordinarily inhibit these sympathetic effects by baroreceptor control. Specifically, these receptors in the carotid sinus and aortic arch sense the increase in blood pressure caused by arteriolar vasoconstriction. Messages are relayed to the vasomotor centre in the medulla by afferents, via the glossopharyngeal and vagus nerves. Blood pressure is normalized by a compensatory vasodilatation of the splanchnic bed.In cases of SCI above the level of the sympathetic outflow the long tracts are disconnected and the inhibitory pathways are unable to reach the splanchnic bed, below the cord lesion. The continued presence of the nociceptive stimulus, with the unchecked sympathetic activity, and vasoconstriction below the level of the cord injury, leads to persistent hypertension. A vicious cycle of sympathetic overactivity ensues, which may be catastrophic unless the underlying cause is immediately and appropriately removed. EPIDEMIOLOGYAs survival rates from SCI have improved a large population of patients have become vulnerable to autonomic dysreflexia. Overall, it has been estimated that up to 85% of patients with SCI will have symptoms of this condition [14][15][16][17][18][19][20]. The incidence of autonomic dysreflexia in women is 60%, whilst 46% of men are affected, and there is a greater prevalence in patients with injuries to the cervical spine (60%) than to the thoracic spine, which is affected in 20% of cases [18]. Autonomic dysreflexia has been reported in both complete and incomplete lesions of the spinal cord, although the symptoms are milder in patients with the latter [1,21].

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autonomic reflex, sympathetic hyper-reflexia, mass reflex and the neurovegetative syndrome [1,11,12].A clear understanding of the pathophysiology of autonomic dysreflexia allows an appreciation of the precipitants, clinical features and potential sequelae of this condition. After stimulation, the afferent nerves from the bladder (S2-4) pass to the dorsal grey matter of the spinal cord where they synapse with interneurones. Most of these nerves then ascend in the lateral spinothalamic tract and dorsal columns (ascending long tracts) to the brain. However, some interneurones reflexively excite preganglionic sympathetic neurones of the splanchnic sympathetic outflow, between T5 and L2 [13], resulting in arteriolar vasoconstriction, pelvic visceral contractions and pilomotor spasms.In a neurologically intact patient higher centres ordinarily inhibit these sympathetic effects by baroreceptor control. Specifically, these receptors in the carotid sinus and aortic arch sense the increase in blood pressure caused by arteriolar vasoconstriction. Messages are relayed to the vasomotor centre in the medulla by afferents, via the glossopharyngeal and vagus nerves. Blood pressure is normalized by a compensatory vasodilatation of the splanchnic bed.In cases of SCI above the level of the sympathetic outflow the long tracts are disconnected and the inhibitory pathways are unable to reach the splanchnic bed, below the cord lesion. The continued presence of the nociceptive stimulus, with the unchecked sympathetic activity, and vasoconstriction below the level of the cord injury, leads to persistent hypertension. A vicious cycle of sympathetic overactivity ensues, which may be catastrophic unless the underlying cause is immediately and appropriately removed. EPIDEMIOLOGYAs survival rates from SCI have improved a large population of patients have become vulnerable to autonomic dysreflexia. Overall, it has been estimated that up to 85% of patients with SCI will have symptoms of this condition [14][15][16][17][18][19][20]. The incidence of autonomic dysreflexia in women is 60%, whilst 46% of men are affected, and there is a greater prevalence in patients with injuries to the cervical spine (60%) than to the thoracic spine, which is affected in 20% of cases [18]. Autonomic dysreflexia has been reported in both complete and incomplete lesions of the spinal cord, although the symptoms are milder in patients with the latter [1,21].

Study design: Retrospective analysis. Objectives: To evaluate the safety and efficacy of polydimethylsiloxane (PDS, Macroplastiquet) submucosal injections, in the treatment of male genuine stress urinary incontinence secondary to spinal cord injury (SCI). Setting: London Spinal Injuries Unit, Stanmore, UK and Institute of Urology and Nephrology, London, UK. Patients and methods: A retrospective analysis identified 14 patients treated with PDS for stress urinary incontinence secondary to SCI between 1997 and 2001. A single surgeon at a specialist spinal injuries unit managed all patients. A total of 13 patients had suffered a traumatic SCI (T11:n ¼ 2; T12:n ¼ 5; L1:n ¼ 5; L2:n ¼ 1), while one developed stress incontinence after spinal surgery. The mean age was 41 years (range 26-69 years) and the mean duration of injury was 9.6 years (range 1.5-48 years). The preoperative investigations included video cystometrogram (VCMG) confirming the presence of urodynamically proven stress incontinence without evidence of urge incontinence. Complete cure was defined as a cessation of pad usage with no evidence of leakage on VCMG. Incomplete cure with improvement was defined as a 450% reduction in the number of pads used, with incontinence present on VCMG. Results: The follow-up ranged from 12 to 58 months (mean 34.7 months). Five patients (36%) reported complete success, confirmed by VCMG. Three patients (21%) reported improvement with 450% reduction in the use of pads. The procedure failed completely in six patients (43%). No immediate or late complications were noted with the procedure. Conclusions: The use of PDS is a safe and minimally invasive treatment for genuine stress urinary incontinence in males following SCI with a stable compliant bladder. We achieved complete cure in 36% of our patients with confirmation on VCMG. A further 21% reported greater than 50% reduction in usage of pads; however, on VCMG stress incontinence was demonstrated in these patients. We suggest that PDS can be used as the first line of treatment in this difficult group of patients with complex problems.