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In earlier parts of this survey we have attempted to describe in broad outline the clinical progress of a series of rather more than 300 consecutive cases of spina bifida cystica first seen between 1949 and 1958 (Doran and Guthkelch, 1961), to indicate some considerations that seem important in deciding when to repair the spinal defect (Guthkelch, 1962a), and to demonstrate a previously undescribed seasonal variation in births of infants with spina bifida (Guthkelch, 1962b). The present communication is concerned with a more detailed examination of the neurological findings in these cases, for this is one aspect of the study of spina bifida cystica which seems to have received less attention than perhaps it deserves, most writers confining themselves to general statements, such as that there is always 'definite paralysis ' in rachischisis (myelocoele) and so on; Warkany (1960), indeed, complained that nowhere in the literature was it definitely stated whether or not neural conduction ever occurs through such a lesion. MacNab (1957) has said that 93 % of cases of 'myelomeningocoele ' show 'clinical evidence of paralysis', presumably implying that in 7 % there is no neurological deficit, but his classification of spina bifida cystica excludes all cases of rachischisis in which there is no true sacculation, and although he notes that there are some cases in which the neural element 'forms part of the sac wall at its fundus, giving rise to the clinical appearance of ulceration... (and others in which)... true skin is separated from the lesion by a large fibro-fatty mass of tissue' he does not distinguish between the neurological findings in the two varieties. Consequently MacNab's work does not explicitly answer the point raised by Warkany, for it could have happened that those of MacNab's cases which were neurologically intact were the ones in which the cord was not exposed on the surface of the body and which to Warkany would not be cases of myelocoele. Laurence (1960a and b) analysed a series of 407 cases of spina bifida with respect to neurological deficit. He does not
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Doran et al. (1963) studied this question.
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