Earlier German and Scandinavian studies on postural tachycardia syndrome (PoTS)

The concept of postural tachycardia syndrome (PoTS), characterized by excessive orthostatic tachycardia and various asthenic symptoms, including general fatigue, dizziness, headache etc., was proposed in the 1990s in North America. However, there are numerous descriptions of PoTS in earlier German, Scandinavian and Japanese literature. To provide a better understanding for the concept, we made a historical review on PoTS. In Germany, von Noorden (1893) observed that vagal neurosis, attacks of bradycardia, arrhythmia and nausea in persons with hysterical character, were caused by a centrally-mediated increase in vagal activity. Vagal neurosis corresponds to the present neurally mediated syncope (NMS), which was first referred to as vasovagal attack in English literature in 1913. Rosenbach (1897) claimed that attacks of vagal neurosis were usually preceded by tachycardia, which was not simply explained by increased vagal activity. This is considered the first description of the coexistence of NMS and PoTS. Von Bergmann (1936) used the term of vegetative stigmatization to refer to all cases of autonomic imbalance, stating that both vagal and sympathetic activities were increased. Autonomic failure, in which both vagal and sympathetic activities were decreased, had not been widely recognized at that age. In Sweden, Bjure and Laurell (1927) defined asthenic symptoms of autonomic imbalance as arterial orthostatic anemia (AOA). They measured heart rate and cardiac output in AOA cases in the supine position, the free erect position, and the erect position with the lower body immersed in water. Heart rate increased and cardiac output decreased in the free erect position, but immersion in water prevented these cardiovascular changes, as well as the appearance of asthenic symptoms. Bjure and Laurell concluded that the primary cause of AOA was excessive blood pooling in the lower part of the body. Akesson (1936) showed sympathetic overactivity in AOA, suggesting a primary lesion within venous structures. The concept of AOA was then introduced in Germany, where it was renamed orthostatic dysregulation. In his animal experiments, Mellander (1960) demonstrated that low-grade sympathetic stimulation induced venous constriction rather than arterial constriction to prevent blood pooling in vein, while high-grade sympathetic stimulation provoked strong arterial constriction to translocate blood from arteries to veins, resulting in venous pooling. In consideration of these historical studies, we hypothesize that PoTS is caused by autonomic imbalance of central origin, which likely induces venous pooling through an excessive unloading of the cardiopulmonary baroreflex.