A. Dingwall-Fordyce
1906 BMJ (Clinical Research Edition)  
When the patient came under my care I was at first inclined to think she was suffering from epilepsy-and this opinion I based on her history-namely, that fourteen months before she had s'uddenly fallen in a fit, to which succeeded four' others the same day; and that up to the day of admission to hospital she. had had recurrence of fits. I accordingly gave her a course of treatment by the bromides, and had her under close observation. In a short time, however, I saw that' the more likely
more » ... n between the fits and the slow pulse lay in the direction of the cardiac arrhythmia being the direct cause of the fits. Later on I could foretell by two or three seconds that a fit was imminent, and I was able to observe that the fits were not due to simply the infrequency of the pulse, for they did not occur even while the pulse-rate was as slow as 18 to 20 in the minute, but that they were sure to occur when arrhythmia occurred and when pauses of 8 to 10 to 15 seconds were, noticed. It was the more prolonged cessation of circulation, and presumably the cerebral anaemia rather than venous stasis, which caused the syncopal and convulsive attacks. That cerebral anaemia is a cause of convulsion is well known and daily verified, and the experimental work of Kussmaul and Tenner, by inducing cerebral anaemia and causing epileptic convulsions, is still uncontroverted. For a full account of this subject in relation to arrhythmia I would againi refer to the work of Dr. Alfred Webster. The conclusion he arrived at after analysing the clinical features of 13 cases of slow pulse and epileptiform attacks, and after making many hundreds of observations and pulse tracings on his own case-included in the 13-seems to commend itself as the true explanation.; " Our own experience," he writes, i "tends to show a slow pulse, 18 to 24 in the minute, with even a moderate degree of irregularity, is not associated with convulsions. For, example, a pulse-rate of' 20 in the minute, which, means an asphyxial state of 3 seconds each, or even a pulse-rate of 12, which equals 5 seconds in each pause, is not enough, so long as it is fairly regular; lbut whln the pulse is irregular, then convulsions will be induced." Accepting these conclusions--to which many recorded cases of "sheart-block" conform-I would say, therefore, the arrhythmia, and not simply the bradycardia, should be looked upon as the causal factor in the production of the convulsions. When, however, we look for the cause of the arrhythmia we must acknowledge we are not much nearer its discovery, as the only point of agreement between various observers, on the Continent and America as well as in this country, seems to be the absence of any gross lesion by which the symptoms of Stokes-Adams syndrome might be accounted for, if we except arterio-sclerosis of the basilar artery and the circle of Willis, and of the vessels of the medulla. Granting these pathological changes to be the cause, how are they applicable in such a case as that of Mrs. MIN.? I shall not, therefore, take up more of your time in discussing the many theories propounded to explain it, and in recording my case-devoid, as it unfortunately is, of the results of a post-mortem examination-I am sadly conscious I have added little to the etiology, and nothing to the pathology, of the condition. But if I have awakened an interest in the clinical record of a very unusual and rare case, and if the full details of its course to a fatal termination may stimulate others to a clearer conception, and the unravelling of the mysteries attending bradycardia, I shall feel my claim upon your patience and time has not been unwarranted nor misplaced.
doi:10.1136/bmj.1.2365.971 fatcat:qzwrhkau5ng4jab5x6r7xmpvmq