Rozhold O, Andrs M, Vojácek K
Research Institute of Higher Nervous Activity, Palacký University, Olomouc, Czechoslovakia.
Acta Univ Palacki Olomuc Fac Med. 1990;125:197-207.
Samples of paravertebral muscles were obtained from the lesion sites of forty patients operated on for recurrent lumboischiadic syndrome of discogenic etiology. None of the specimens was physiological. All of them were pathologically altered in various grades of involvement. The histopathological changes were highly varied. The findings included muscle fibre atrophy of a nonspecific type, neurogenic atrophy of typical fascicular distribution. Apart from atrophic fibres there were hypertrophic ones either at the same time or in connection with another histopathological process. Changes of myopathic nature were also present with rounded up muscle fibres and shift of nuclei from the subsarcolemnic spaces into the centre of the muscle fibre, multiplication of the connective tissue and vicarious growth of adipose tissue. The visible neuromuscular spindles contained thickened connective tissue capsules and atrophied intrafusal fibres. The present authors' conclusion of their interpretation of these histopathological changes is that they are not produced by one but by a whole set of factors. What results is a cyclic nature of the changes, when it is hard to decide whether we are facing a primary cause or its sequela. The regular company of discopathies are repeated microtraumas during recurrent paravertebral contractures and spinal blocks. A not negligible part can be played also by primary muscle diseases affecting, among others, back muscles, e.g. progressive muscular dystrophy of Duchenne's and Becker's type, various myopathies, nonspecific myositis and paravertebral polymyositis, and other rheumatological involvement. These muscular diseases with disturbed proprioception causing unphysiological posture and loading the spine can share in the origin degenerative processes on intervertebral disks.
从40例因椎间盘源性病因导致复发性腰坐骨神经综合征而接受手术的患者病变部位获取椎旁肌样本。所有样本均非生理性的。它们都有不同程度的病理改变。组织病理学变化差异很大。研究结果包括非特异性类型的肌纤维萎缩、典型束状分布的神经源性萎缩。除了萎缩的纤维外，同时或与其他组织病理学过程相关还存在肥大的纤维。还存在肌病性改变，表现为肌纤维变圆，细胞核从肌膜下间隙移至肌纤维中心，结缔组织增生和脂肪组织的替代生长。可见的神经肌肉纺锤体包含增厚的结缔组织囊和萎缩的梭内纤维。作者对这些组织病理学变化的解释结论是，它们不是由单一因素而是由一整套因素引起的。结果是这些变化具有循环性，很难确定我们面对的是原发性病因还是其后果。椎间盘疾病常见的伴随情况是复发性椎旁挛缩和脊柱阻滞期间反复出现的微创伤。原发性肌肉疾病，如杜兴氏和贝克氏型进行性肌营养不良、各种肌病、非特异性肌炎和椎旁多肌炎以及其他风湿性病变，也可能起不可忽视的作用。这些伴有本体感觉障碍、导致非生理性姿势并给脊柱增加负荷的肌肉疾病，可能参与椎间盘退变过程的起源。
