The diagnosis of diseases of the spinal cord.

  • Gowers, W. R. (William Richard), 1845-1915.
Date:
1880
Catalogue details

Licence: Public Domain Mark

Credit: The diagnosis of diseases of the spinal cord. Source: Wellcome Collection.

Provider: This material has been provided by The University of Leeds Library. The original may be consulted at The University of Leeds Library.

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    of the calf-muscles against a considerable resistance fas in standing for some time on tip-toe) is also broken into clonus. These are evidently the same phenomenon, the difference being that it cannot in health be excited by passive tension. For this to be effective a morbid reflex irritability is needful, such as only exists in disease. In morbid states, in which the myotatic irritability is exces- sive, the posture I have just described excites the clonus very readily; and the jerking legs of paraplegics as they sit must be familiar to you. In attempting to walk, also, the tension on the calf-muscles has the same effect, and the patient may be jerked violently by the spasm. It is probable that this reflex relation between tension and contractility of muscles is of the highest importance in their associated action, and that the reason why, in certain muscles, as those of the calf, these phenomena are more readily observed, is because in these, during the process of walking, at every step contraction succeeds tension, and so the reflex relation between the two has attained a higher degree of development. It is rare to get a distinct clonus in a child who has never walked, even in the pathological conditions in which in adults it would certainly be obtained. The excess of these myotatic contractions is especially related to degeneration in the lateral coluran of the cord (pyramidal tracts). It is seen in extreme degree, for instance, in lesions of the cord higher up, which cause descending degeneration in those columns. It is seen also in cases of hemiplegia with similar descending degeneration on the paralysed side. The excess is apparently not due to the simple loss of a cerebral influence. It does not, as a rule, occur immediately, but develoj)es gradually at the end of a week or ten days, i.e., after a time sufficient to allow the nutrition-changes of commencing degeneration to pass down the lateral (pyramidal) fibres to the neighbour- hood of the muscle-reflex centres. Over-action of these centres follows, and must be ascribed to the loss of some controlling influence. But the control cannot be exerted by the fibres themselves, or the over-action due directly