Dwyer F C
Clin Orthop Relat Res. 1975 Jan-Feb(106):254-75. doi: 10.1097/00003086-197501000-00038.
Notable historical aspects relating to the etiology and treatment of pes cavus have been critically examined. The characteristic features of the deformity are described and an explanation offered for the mechanism of their production. Although its etiology remains uncertain, a study of the literature and a great deal of clinical material has established certain well supported conclusions regarding the etiology and pathology of the condition. Certain aspects of cerebral palsy serve to strengthen impressions of earlier authors that the primary center of origin of pes cavus lies somewhere in the central nervous system. Localized foci of partial damage lying adjacent to tracts of nerve cells more seriously affected by a neurological disease could emit irritating stimuli capable of producing degrees of over-action of the invertor muscles varying from obvious spasm to clinically undetectable increase in muscle tone. Biral or other factors which stop short at creating nothing more than such a focus of irration could explain the insidious onset of the deformity in the idiopathic group. Over-action of invertor muscles for one reason or another, including ischemia, is almost certainly responsible for initiating the deformity, though primary contracture of the plantar fascia could possibly do so. With the appearance of supination of the heel, the calcanean tendon becomes an active invertor adding its force to that of the plantar fascia to produce structural varus of the calcaneum. Contracture of the plantar fascia and supination of the heel are regarded as features of major importance. Correction of the latter can be achieved more effectively by suitable osteotomy than by subtaloid fusion, which is regarded with great disfavor. Conservative treatment consists of exercises and shoe appliances. Surgical correction is based on calcanean osteotomy and plantar fasciotomy supplemented where necessary by suitable tendon transplantations, correction of clawing of the toes, and tarsal or metatarsal wedge resections. Preservation of the midtarsal subtaloid joint complex is essential. With the heel correctly aligned the degree of improvement to be expected in the forefoot deformity is such that any structural operation on it should be deferred until a fair period of walking has been tried.
对与高弓足病因及治疗相关的显著历史方面进行了批判性审视。描述了该畸形的特征，并对其产生机制进行了解释。尽管其病因仍不确定，但对文献及大量临床资料的研究已就该病症的病因及病理得出了一些有充分依据的结论。脑性瘫痪的某些方面强化了早期作者的观点，即高弓足的主要起源中心位于中枢神经系统的某个部位。与受神经系统疾病影响更严重的神经细胞束相邻的局部部分损伤灶可能会发出刺激性信号，从而导致内翻肌出现不同程度的过度活动，从明显的痉挛到临床上难以察觉的肌张力增加。双侧或其他仅造成这种刺激灶的因素可以解释特发性组中畸形的隐匿性发作。无论出于何种原因，包括局部缺血，内翻肌的过度活动几乎肯定是引发畸形的原因，尽管足底筋膜的原发性挛缩也可能导致畸形。随着足跟内翻的出现，跟腱成为一个活跃的内翻肌，其力量与足底筋膜的力量相加，导致跟骨结构内翻。足底筋膜挛缩和足跟内翻被视为至关重要的特征。通过合适的截骨术比通过距下关节融合术能更有效地矫正后者，而距下关节融合术备受诟病。保守治疗包括锻炼和鞋具矫正。手术矫正基于跟骨截骨术和足底筋膜切开术，必要时辅以合适的肌腱移植、矫正爪形趾以及跗骨或跖骨楔形切除术。保留中跗距下关节复合体至关重要。当足跟正确对线后，预计前足畸形的改善程度使得在尝试了一段合理的行走时间之前，对其进行任何结构性手术都应推迟。
