Myasthenia gravis / by Charles S. Myers.

  • Charles Samuel Myers
Date:
1902?]
Catalogue details

Licence: In copyright

Credit: Myasthenia gravis / by Charles S. Myers. Source: Wellcome Collection.

    19/46 page 321
    tetanising stimulations, the negative variation produced by each stimulation is never followed by a period of ‘ restful ’ positive change. One negative variation follows uninterruptedly on another. There is no break to allow of anabolic reorganisation in the nervous tissue. Instead of remaining constant, as in normal nerve, the negative variations quickly diminish in intensity until, finally, the electric excitability of the nerve is destroyed. In the face of this result it is difficult to explain the second of Watts EdeiTs experiments quoted above, so long as we assume that excitability and conductivity of nerve are dependent on the associated electrical changes. I can only suggest that expecting exhaustion,, rather -than exhaustibility, of nerve, he did not stimulate his nerve for sufficient time to prove his case. But indeed the whole subject of protoveratrine-poisoning requires working out afresh. What seems to be definitely elucidated is its remarkable effect on the metabolism of nerve fibres: whether it has also a direct action on muscle or end plates may be held unproven. That it has a general effect on nerve fibres is also supported by certain of Watts Eden’s experiments which go to prove a paralytic effect on sensory nerves. Lauder Brunton Cash, and others have investigated the action of ammonium salts on the muscle-nerve preparation. Lauder Brunton states that “ when a muscle has been poisoned by some ammonium salts, a single stimula¬ tion applied to the nerve causes a strong contraction like that of an unpoisoned muscle; but a second stimulus has sometimes little or no action, and when the muscle is stimulated directly it soon becomes exhausted.” He adds that this paralysing action of ammonium salts, though usually ascribed to their effect on motor nerves, appears to be due to a disturbance of the relation between muscle and nerve,—by which he probably suggests a poisoning of the end plate. When we attempt to apply what little knowledge we possess of these drugs to the explanation of myasthenic phenomena, we are met at the threshold with several difficulties. We have to remember that it is impossible to argue from electrically produced muscular actions to those volitionally produced. In his case of myasthenia gravis Murri (2^) showed that the fatigue produced by electric stimulation had no effect on the activity of immediately following volitional contractions, and vice versd ; but this was not confirmed by Goldflam Murri found,, moreover, that the bodily movements of his patient were completely exhaustible by repeated electric stimulation of the nerves, but were incompletely exhaustible by the will. In the second place,, excitability and conductivity of nerve tissue are by no means inter¬ dependent properties. It is well known that at the start of re¬ generation after a nerve lesion a volitional impulse may produce a contraction in the muscles innervated, while the nerve at the point of regeneration is still inexcitable by electric stimuli. These and other difficulties beset us in the application of experimental knowledge to^ the clinical problems of neurology.
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