Published online by Cambridge University Press: 29 January 2018
The nervous origin of paroxysmal tachycardia was stressed by many German-speaking authors (Hering, 1911; Rothberger and Winterberg, 1911a; Rothberger and Winterberg, 1911b; Schlesinger, 1906) at the beginning of the century. Thus Schlesinger (1906) pointed out that many patients who suffered from this disorder had neurasthenic or hysterical personalities. He postulated that there was a mechanism responsible for the attacks of tachycardia which could be set in motion by a stimulus in the nervous system. Somewhat later a French cardiologist (Gallavardin, 1922) described a type of paroxysmal tachycardia which he believed was of nervous origin. In more recent times Stokvis (1947) has given an account of a Jewish patient who was taught to think himself into an attack in order to avoid deportation by the German occupation authorities in Holland. There is some pharmacological support for the central origin of paroxysmal tachycardia. Thus Klein (1940) described a schizophrenic patient who when treated with pentamethylene tetrazol developed supraventricular paroxysmal tachycardia four minutes after the injection of the drug. He suggested that the delay between the injection and the onset of the attack indicated that the attack was due to an effect of the drug on the central nervous system. Several different workers (Evans, 1940; Peters and Penner, 1946) have claimed that intravenous injection of ergotamine tartrate will relieve an attack of supraventricular paroxysmal tachycardia within a few minutes. Rothlin and Cerletti (1949) have shown that the effect of adrenaline on the heart is not altered by ergot alkaloids, so that the effect of ergotamine in paroxysmal tachycardia cannot be due to an unopposed vagal effect and must therefore be due to a direct action on the brain centres which regulate cardiac activity.
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