I enjoyed immensely studying the latest, in a series, review by Y-Hassan, published on-line ahead of print on October 17, 2013 in the Journal in which he argues persuasively about the pathophysiology of Takotsubo syndrome (TTS) being a central-nervous system mediated local sympathetic neuronal disruption, leading to damage of both myocytes and distal ramifications of the sympathetic nerves, a short of cardiac “chemical neuritis/myocarditis”. Although the pathophysiology of TTS is still elusive, it appears that great progress is being made in the past 2 years, and that intense interaction among workers will accelerate our quest to elucidate the causes of this mysterious disease. It is in this spirit that I beg the author to respond to some comments/inquiries about his fine review: 1) Although reference is made about descriptions of TTS going back to 1967, there is the work of Cannon in 1942 that preceded more recent descriptions of this pathology, as discussed by Samuels, whose work the author quotes . 2) In this reference the issue about an autonomic parasympathetic participation is made, and I wonder what the author feels about it. 3) Microcirculation dysfunction most probably is a late epiphenomenon of TTS, and thus the occasionally persisting ST-segment elevations need an explanation; does the author feel that they are neurally induced phenomena (question mechanism), or causally due to “nonischemic dyskinesis” similar to the one seen in chronic myocardial infarction, as this author has suggested . 4) Although the arguments about left ventricular outflow obstruction (LVOT) are well supported, there is always a possibility that very early in the process, patients with TTS have much higher rates of dynamic LVOT obstruction; right ventricular involvement in this scenario might have been preceded by right ventricular out flow obstruction. 5) In the same vein, it is possible that blood catecholamine levels are much higher early in the process, than the ones detected in patients with TTS at the hospital, considering their short half-life . 5) It is refressing to read the author’s comment about the coexistence of acute coronary syndromes and TTS, with the former precipitating the latter, which this author believes to be frequent; does this call for change in the currently used criteria of TTS?