Epilepsy and other convulsive diseases : a study in neuro-dynamics and pathogenesis / by F.W. Langdon.

  • Langdon, Frank Warren, 1852-1933.
Date:
[1896]
Catalogue details

Licence: Public Domain Mark

Credit: Epilepsy and other convulsive diseases : a study in neuro-dynamics and pathogenesis / by F.W. Langdon. Source: Wellcome Collection.

Provider: This material has been provided by King’s College London. The original may be consulted at King’s College London.

    14/18 (page 12)
    citing an out-going “ motor ” discharge, which discharge is not inhibited. In other words cannot avail ilself of a proper number of “ shunting,” regulating or distributing mechanisms. The discharge being thus unrestrained by the proper inhibitory action, the phenomena of exhaus- tion naturally follow. Our attention is naturally directed at this point to the “ great pyramidal” neurons of the motor area of the cor- tex, generally conceded to be the mechanisms most di- rectly concerned in the initiation of voluntary move- ments. What are their connections—known or inferred ? and what bearing may they have on convulsive phenom- ena generally ? A hypothetical scheme of mechanisms (necessarily neurons or parts of neurons), probably required to pro- duce the simplest motor action under normal circum- stances is presented in Fig. 3. It is quite evident that hereditary or developmental defects, trauma, toxines and degenerative processes,—in short, all the recognized causes of epilepsy, would tend to fall with especial primary severity on the terminations of the neuron-processes, in accordance with the patholog- ical law that those portions of the neuron ramifications farthest from their source of nutrition (the neuron body) are the first to suffer from such causes as impair the vi- tality of the neuron body, or the neuron as a whole. The collateral processes, on account of their length, del- icacy and general direction, would be especially liable to damage of various degrees, the consequences of which must impair their “ conducting ” or functionating capac- ity, whatever that may be. Further, it would seem, from a dynamic standpoint, that the molecular play which we commonly call the “ nerve current ” must be productive of a certain “stress, tension, or pressure” in the axis- cylinder along which it passes. Should this stress attain undue proportions in any neuron, one of two events would seem likely to occur, namely : 1. A distribution to other areas, through contact with other neurons, which distribution may subserve purposes of memory, inhibi- tion, or “conservation of energy.” The most feasible route by which this “shunting ” might occur would ap- pear to be the “ collateral ” processes. (See Fig. 3). 2. Any failure in the efficiency of this supposed “ shunting ” process would be attended with undue ex- penditure of energy on lower centres, resulting in a con- vulsive action of the centre so over stimulated (see Fig.