Decavel P, Bonniaud V, Joassin R, Pérennou D
Service de rééducation neurologique, centre hospitalier universitaire de Dijon, 23, rue Gaffarel, 21079 Dijon cedex, France.
Ann Readapt Med Phys. 2007 Apr;50(3):174-8. doi: 10.1016/j.annrmp.2006.12.003. Epub 2007 Jan 17.
Bladder dysfunction is common in the acute phase of decompression sickness and often precedes motor disorders. Few studies have reported the persistence of urinary problems, and no prior reports describe a neurogenic bladder in the primary presentation of decompression sickness.
We report the case of a 21-year-old female scuba diver with no medical history. After two successive deep dives, dysbaric myelitis developed. The risk factors were foramen ovale and history of diving. The patient initially showed tetraparesia, which was quickly followed by paraparesia with urinary retention. Treatment consisted of recompression with high concentrations of inspired oxygen, aspirin administration and continuous drainage by an indwelling catheter. No lesion was found on 2 sessions of magnetic resonance imaging (MRI) (cerebral and spinal), and somatosensory-evoked potentials were normal. Motor-evoked potential onset latencies were delayed. Neuro-urodynamic investigations revealed detrusor sphincter dysynergia and detrusor overactivity. On quick, complete motor recovery, the patient returned to work and continued with sports (except scuba diving). A year later, she still had urinary and faecal urgencies which were not completely resolved with medication and altered her quality of life.
Half of the cases of neurological decompression involve dysbaric myelitis. Venous ischemia is the most likely cause. Foramen ovale is an important risk factor, but the pathophysiology is obscure. Bladder problems, common in the acute phase of decompression sickness, may be the primary presentation, and may be prolonged.
膀胱功能障碍在减压病急性期很常见,且常先于运动障碍出现。很少有研究报道过泌尿系统问题的持续存在,此前也没有关于减压病首发时出现神经源性膀胱的报道。
我们报告一例21岁无病史的女性潜水员病例。在连续两次深度潜水后,发生了减压性脊髓炎。危险因素为卵圆孔未闭和潜水史。患者最初表现为四肢轻瘫,随后很快出现截瘫并伴有尿潴留。治疗包括高压氧再压缩、给予阿司匹林以及通过留置导尿管持续引流。两次磁共振成像(MRI)(脑部和脊髓)检查均未发现病变,体感诱发电位正常。运动诱发电位起始潜伏期延迟。神经尿动力学检查显示逼尿肌括约肌协同失调和逼尿肌过度活动。在运动快速完全恢复后,患者重返工作岗位并继续从事运动(除潜水外)。一年后,她仍有尿急和便急症状,药物治疗未能完全缓解,影响了她的生活质量。
半数神经系统减压病例涉及减压性脊髓炎。静脉缺血是最可能的病因。卵圆孔未闭是一个重要危险因素,但病理生理机制尚不清楚。膀胱问题在减压病急性期很常见,可能是首发表现,且可能会持续存在。