On the degeneration of the neurone / [Sir F.W. Mott].

  • Mott, F. W. (Frederick Walker), 1853-1926
Date:
1900
Catalogue details

Licence: In copyright

Credit: On the degeneration of the neurone / [Sir F.W. Mott]. Source: Wellcome Collection.

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    resistance to the passage of the impulses in the physiological junction of the upper and lower neurones, or in the protoplasm of the cell-body ? According to the neurone theory it would be at the junction. A stimulus which is insufficient to rise into consciousness may, by repetition, lead to summation, and the opening up of a path (Bahnung) by breaking down resistance; thus Urban t- schitch has shown that very weak sounds, at first not audible, become so by repetition. This effect can be explained by the stimulus opening up the path to the auditory perceptive centre. The same effect can be produced by an effort of the will and concentration of attention, by which the auditory perceptive centre becomes more excitable. That an excitation may spread over the whole nervous system is not to be wondered at when we consider the length of some of the projection system neurones ; for example, the posterior spinal sensory neurones, which have their cells of origin in the first sacral ganglion, extend from the nape of the neck to the sole of the foot. The central projection of the T-shaped process gives off a branch, which extends in the column of Goll the whole length of the spinal axis, and the peripheral portion as a sensory fibre extends to the sole of the foot. It is probable, therefore, that the central projection establishes connexions by delicate collaterals with the grey matter of the whole spinal axis. The reason why excitations do not spread is probably dependent upon the condition of the bio-chemical stability of the neurones. In strychnia and tetanus poisoning the most localised peripheral excitation will cause general muscular spasm; in both toxic conditions the spread is probably due to a bio-chemical change in the protoplasm of the spinal motor neurones to be referred to later, whereby the excitability is greatly increased, and a slight impulse is sufficient to fulminate the whole system of motor neurones. In epilepsy and other paroxysmal neuroses and psychoses it is possible that some altered condition of the blood associated with an inherited bio-chemical instability of certain groups, systems, or com- munities of neurones may act as a fulminating agent. In neuralgia and local hyperaesthesia the slightest general or distant local irritation suffices to produce pain; thus coughing, the vibration of a passing train, or a slamming door may produce pain by the stimulation of the hyper-excitable neurones.