| Object: To provide basis for the congenital clubfoot on etiology, pathology, clinical efficacy, and therapeutic evaluation, by ways of neural electrophysiology, pathological examination, immunohistochemistry and ultrastructural observation.Method: The KEYPOINT evoked potential meter was applied to 248 cases of CCF (338 feet), and the MCV, SCV, and wave amplitude were recorded. The data were analyzed in statistical methods combined with the clinical findings. The pathological examinations of gastrocnemius, long flexor muscle of thumb, and musculus abductor pollicis longus, were given to 38 cases of unilateral CCF who had an adromia of gastrocnemius preoperatively and underwent operations. The located and quantitative expression of Neuronal Nitric Oxide Synthase (nNOS) and synaptophysin (Syn) were used to observe pathological changes. Tertiary ramulus of nervus suralis in lengths of 0.3-0.5cm were received beneath external malleolus during operations as well for transmission electron microscope observation. The samples of control group were calf muscles received from 18 cases of other operation on legs, who did not have neuromuscular diseases. The data of two group were analyzed in statistical method.Result: Conduction disorder of motor nerve was detected in 216 cases (291 feet), about 86.1% of all the cases. Conduction disorder of sensory nerve was also found in 181 cases (252 feet), 74.6% of the whole sample. Prolongations of latency, decline or deficiency of wave amplitude were found. According to statistical approach of Mantel-Haenzsel, abnormal index of motor nerve in all types of CCF were different, which got statistical significance (χ~2=32.31 ,P<0.01). The abnormal index of sensory nerve also showed statistical difference (χ~2=16.37 ,P<0.0 1 ).The effectiveness of nonoperative therapy were different(χ~2=134.30 ,P<0.0 1) . The expression of nNOS and Syn in the way of immunohistochemistry staining in the sarolemma of CCF was obviously decreased than that in control group.Expression was varied in different muscles of CCF.It was significantly lower in gastrocnemius, musculus abductor pollicis longus, and long flexor muscle of thumb. Muscular atrophy was found in foot muscles of CCF using HE staining. Adipose hyperplasia,small angular fiber and spliting fiber were also found. The different is detected by Fisher's Ex act test( P<0.05) . According to transmission electron microscope, vacuolation, hyperplasia of myelin, segmental demyelination,and denaturation of neuraxon were detected in nervus suralis of 38 CCF. Conclusion: Neural electrophysiology examination can reflect the conduction disturbance and degree of pathological change in CCF objectively. The relevance analysis of malformation degree, conduction abnorrnality, and therapeutic effect suggested that the more severe the malformation was, the more obvious the abnormity of electrophysiology was. The treatment effect and evaluation became worse as well when the malformation degree were more severe. Immunohistochemistry test showed a significantly decreased expression of nNOS in the sarolemma of CCF than that in control group, and the decrease was correlated to atrophy of muscle fiber. The abnormal expression of of nNOS suggests that muscular imbalance may play an important role in the muscle and nerve pathology of CCF. Observation on ultrastructure of nervus suralis may suggest indirectly that motor nerves have the similar ultrastructure, which contributed to the neuromuscular theory of CCF. It provided guidance for choice of therapeutic schedule and long-term therapeutic evaluation. |
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