Ito Yasuo, Hasegawa Yasuhiro, Toda Kazukiyo, Nakahara Shinnosuke
Department of Orthopaedic Surgery, Kobe Red Cross Hospital, 5-6-22 Shimoyamatedori Chuo-ku, Kobe City 650-0011, Japan.
Spine J. 2002 Mar-Apr;2(2):101-6. doi: 10.1016/s1529-9430(01)00165-6.
In recent years there have been an increasing number of reports on surgical cases involving delayed neurological deficits caused by vertebral collapse after osteoporotic vertebral fracture.
We do not yet know which patients are most susceptible to delayed vertebral collapse and subsequent neurological deficits, or whether this pathological condition can be prevented or predicted. In this study, we investigated the mechanism of progression and radiographic features characteristic of this disease, and we report here the predictive or risk factors for delayed osteoporotic vertebral collapse.
Retrospectively, we investigated the pathogenesis and diagnosis of delayed vertebral collapse with neurological deficit resulting from osteoporosis.
A total of 28 patients (7 men and 21 women) with neurological deficits resulting from vertebral collapse caused by osteoporotic vertebral fractures were the subjects for this study.
Comparisons and investigations about clinical features and radiographic findings between the patient group of delayed vertebral collapse with neurological deficits and the group of osteoporotic spinal fracture with no neurological deficits.
The following factors were examined: the cause of injury; the length of time from injury, or the onset of pain, to the onset of neurological symptoms; radiographic findings obtained during the above period; the clinical course of vertebral fracture on plain X-ray films; time of appearance of the intravertebral cleft, and its localization and changes.
Six patients were hospitalized and prescribed a period of 2 weeks of bed rest followed by the fitting of a corset; seven outpatients were corseted but not prescribed bed rest; 15 patients were given medication only at an outpatient clinic. At radiography, intravertebral clefts were detected in 22 patients (79%) during the period from the appearance of pain to the onset of neurological deficit. In 14 patients (50%) who were radiographed every 1 to 2 weeks from the injury to the onset of neurological symptoms, the course of progression to collapse of the vertebral body could be observed.
Initial correct diagnosis and immobilization are important in preventing the delayed collapse with neurological deficit. The presence of an intravertebral cleft and instability of the affected vertebra represent risk factors for vertebral collapse with neurological deficit, requiring careful observation.
近年来,关于骨质疏松性椎体骨折后椎体塌陷导致延迟性神经功能缺损的手术病例报道越来越多。
我们尚不清楚哪些患者最易发生延迟性椎体塌陷及随后的神经功能缺损,也不清楚这种病理状况是否可以预防或预测。在本研究中,我们调查了该疾病的进展机制和影像学特征,并报告延迟性骨质疏松性椎体塌陷的预测因素或风险因素。
我们回顾性地研究了骨质疏松导致的伴有神经功能缺损的延迟性椎体塌陷的发病机制和诊断方法。
本研究的对象为28例因骨质疏松性椎体骨折导致椎体塌陷并伴有神经功能缺损的患者(7例男性,21例女性)。
对伴有神经功能缺损的延迟性椎体塌陷患者组与无神经功能缺损的骨质疏松性脊柱骨折患者组的临床特征和影像学表现进行比较和研究。
检查以下因素:损伤原因;从受伤或疼痛发作到神经症状发作的时间长度;上述期间获得的影像学表现;平片上椎体骨折的临床过程;椎体内裂隙出现的时间及其定位和变化。
6例患者住院并接受了为期2周的卧床休息,随后佩戴胸腰骶支具;7例门诊患者佩戴了支具但未被要求卧床休息;15例患者仅在门诊接受药物治疗。在影像学检查中,从疼痛出现到神经功能缺损发作期间,22例患者(79%)检测到椎体内裂隙存在。在从受伤到神经症状发作期间每1至2周进行一次影像学检查的14例患者(50%)中,可以观察到椎体进展至塌陷的过程。
初始正确诊断和固定对于预防伴有神经功能缺损的延迟性塌陷很重要。椎体内裂隙的存在和受累椎体的不稳定是伴有神经功能缺损的椎体塌陷的风险因素,需要仔细观察。