Cauda equina entrapment in a pseudomeningocele after lumbar Schwannoma extirpation

Incidental or intentional durotomy causing cerebrospinal fluid (CSF) leakage, leading to the formation of a pseudomeningocele is a known complication in spinal surgery. Herniation of nerve roots into such a pseudomeningocele is very rare, but can occur up to years after initial durotomy and has been described to cause permanent neurologic deficit. However, cauda equina fiber herniation and entrapment into a pseudomeningocele has not been reported before. Here, we present a case of symptomatic transdural cauda equina herniation and incarceration into a pseudomeningocele, 3 months after extirpation of a lumbar Schwannoma. A 59-year-old man, who previously underwent intradural Schwannoma extirpation presented 3 months after surgery with back pain, sciatica and loss of bladder filling sensation caused by cauda equina fiber entrapment into a defect in the wall of a pseudomeningocele, diagnosed with magnetic resonance imaging. On re-operation, the pseudomeningocele was resected and the herniated and entrapped cauda fibers were released and replaced intradurally. The dura defect was closed and the patient recovered completely. In conclusion, CSF leakage can cause neurological deficit up to years after durotomy by transdural nerve root herniation and subsequent entrapment. Clinicians should be aware of the possibility of this potentially devastating complication. The present case also underlines the importance of meticulous dura closure in spinal surgery

Gonadotropin-releasing hormone antagonist plus testosterone: a potential male contraceptive

No effective hormonal contraceptive has yet been devised for men. Through their suppressive effect on gonadotropin secretion, GnRH antagonists inhibit both testosterone (T) production and spermatogenesis in animals. Long term administration of an antagonist alone would result in androgen deficiency; this would cause unacceptable physiological and behavioral sequellae in men. Therefore, androgen replacement must be included in any GnRH antagonist regimen used in human male contraception. We tested the hypothesis that the combination of a GnRH antagonist plus T would suppress spermatogenesis in the male primate to azoospermic levels while maintaining normal serum T levels. We examined the effects of the GnRH antagonist Deterelix [N-Ac-DNal(2)1-DpCl-Phe2-DTrp3-DhArg(Et2)6 -DAla10-GnRH], alone and with simultaneous T replacement, on sperm production and serum T levels in adult male monkeys (n = 22). After 12 weeks of daily sc antagonist injection, all animals that received antagonist alone (n = 5) and those that 750 micrograms/kg.day antagonist plus T (n = 5) were azoospermic. After 16 weeks, four of five animals that received 250 micrograms/kg.day antagonist plus T became azoospermic. Control animals (n = 7) received daily injections of vehicle; sperm counts increased somewhat during the study period in that group. Castrate range T levels were achieved in animals receiving antagonist alone. T levels in the groups that received T supplementation and in the control group were in the normal male range throughout the treatment period. Sperm counts returned to the pretreatment range in all animals during the recovery period. We conclude that the combination of a GnRH antagonist plus T can induce azoospermia reversibly in this nonhuman primates species, and that a similar combination may be an effective contraceptive regimen in men. The GnRH antagonist alone may be an effective treatment for androgen-dependent neoplasia