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when the vagi are irritated, the action of the heart is rendered slower, and may be even temporarily arrested.*

When the sympathetic cardiac supply is irritated, the action of the heart is for a time accelerated, and when the same supply is enfeebled the action is rendered slower. Thus we can induce intermittent action of the heart in inferior animals, pigeons and rabbits, by the simple process of causing deep narcotism with chloroform or chloride of amyl. When either of these agents is carefully administered so that it may cause deep sleep, although there may be in the early stages of narcotism very marked irregularity of the heart, there will be no intermittency until the last degree or stage of sleep has been attained. The brain may be narcotised until all its functions cease, the spinal centres may in like manner be temporarily extinguished, the voluntary muscles may be utterly paralysed, and yet there may be regular though slow action of the heart. At last there is heard, as the prelude to death, if the narcotism be continued, the intermittent action, precisely as it is detected in the human subject in those who suffer from intermittent stroke.

Falling back on our knowledge of the nervous mechanism of the heart, we ask again, Where is the seat of the nervous lesion that causes intermittent action, and what is the nature of the lesion? It might be irritation of the pneumogastric in some part of its course, for irritation of the pneumogastric would cause slow action of the heart, and might momentarily stop action. It might be failure of power of the sympathetic cardiac supply, or of the true cardiac centres, for exhaustion of supply from the sympathetic and cardiac ganglia would create failure and cripple action. From all the evidence I have before me, I am led now to the view that the cause is failure of the sympathetic supply to the heart. As this view is corrective of the view I first advanced, in which the cerebral origin of the disorder was indicated, it is right I should briefly explain the reasons for such modification of opinion. The reasons are as follow :

* In the volume of the “Journal of Anatomy and Physiology for May, 1869, the reader will find an admirable paper on the Function of the Pneumogastrio Nerves, and the Motion of the Heart, by Professor Rutherford, of King's College. The paper defines, more clearly and perfectly than any I have read, the nervous supply and nervous mechanism of the heart.

(1) A larger experience of the disorder has failed altogether to lead me to connect the phenomenon of intermittent action with any other symptom of cerebral lesion : such as paralysis of motion or sensation, convulsion, chorea, cranial pain, or any special symptom pointing to cerebral complication. I look over the records of the last fifty cases I have seen, and I find not a symptom of certain cerebral or spinal lesion. It seems to me almost impossible to assume that if the cause of the interruption of the heart were cerebral or spinal—if for instance there were disease implicating the pneumogastric at its origin—there could be persistency of the one symptom, and no sign of any other symptom of a cerebral nature.

(2) If the symptom were due to irritation of the pneumogastric in some part of its wandering course away from its origin, there would be afforded some very distinct evidence of the fact. There would be symptoms of pain or of nausea, or of disturbance of the stomach, whenever there was disturbance of the heart. But on referring to actual facts, I find no indication whatever of any such necessary connection of symptoms. I infer, therefore, that in cases of intermittent pulse the pneumogastric is, as a rule, quiescent.

(3) The symptom of intermittent pulse does not appear to me to be dependent upon irritation and exaltation of function of nerve. In all I have seen of it it has been connected with failure of nervous power, and with failure of the heart, not because the heart is arrested by any overruling force, but because it is not supported by a proper and efficient force.

(4) The evidence derivable from experiment with narcotics seems to me conclusive against the cerebral origin of the symptom, for it is not in the stage of general muscular excitement, when the pneumogastric clearly is under excitation, that the symptom is demonstrated, but at the stage when the cerebrum is practically dead, when the muscles which are under cerebral and spinal influence are dead, and when nothing lives except the cardiac ganglia, and their reserve, the sympathetic cardiac ganglia.

(5) Further, the same experiment differentiates between the action of the sympathetic cardiac ganglia, and the true cardiac ganglia; for when the sympathetic fails in function, and intermittent action is developed, the cardiac centres still sustain a feeble action, even when all other nervous communication is cut off. Hence the failure does not lie in the true cardiac centres.

(6) The last reason for a modification of view respecting the seat of nervous lesion in cases of intermittency of the pulse, is the strength of the proposition that the centres of the great ganglionic system are either the distinct centres of the emotional faculties, or that there is a direct connection between the sensorial organs and the sympathetic, so that emotions received through the senses are at once transmitted to the organic centres. It was demonstrated many years ago by the distinguished physiologist, Dr. Wilson Philip, that the ganglionic system can be excited to action through the sensorial organs without exciting the muscles called voluntary; and that when an impression which excites us involuntarily is received by the senses, it must pass through the involuntary nervous system to the involuntary muscles. Thus, change in the centres of the involuntary nervous chain may be excited by what is called mental impression, and central function may be destroyed as easily by such an impression as by a physical injury.

I look at the diagram of the organic nervous system, and see there depicted the emotional brain. If we could put the organic

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