Abstract Reverse–Tako–tsubo (r–TTC) is a rare variant of Tako–tsubo syndrome (TTC). TTC is characterized by transient and reversible left ventricular systolic dysfunction, for which an emotional or physical stressful trigger can usually be identified. Clinically, it mimics an acute myocardial infarction, with elevation of myocardial cytonecrosis enzymes and no obstractive coronary artery stenosis. On imaging, r–TTC is characterized by hypokinesia of the mid–basal regions associated with hyperkinesia of the apical region that resolves spontaneously. Case report: 78–year–old female affected by cerebral atrophy, leukoencephalopathy, cognitive impairment, behavior disorders. Reported episode of loss of consciousness lasting several minutes, associated with spontaneously resolving tremors and left hemisome hyposthenia. When she arrived in the emergency room, the haematological tests found high troponin values. On CT brain without contrast, no evidence of alterations of the encephalic tissues referable to acute lesions, but it showed of diffuse supratentorial leukoaraiosis and widening of the cerebrospinal fluid spaces on an atrophic basis. The neurological evaluation excludes the presence of a seizure. The electrocardiogram showed diffuse negative T waves and QTc 636 ms. The coronary angiography didn’t show significant coronary arteries stenosis and the ventriculography showed normal ventricular dimensions with total akinesia of the mid segments and normokinesia of the apical region with an ejection fraction of 50%. With these findings a diagnosis of mid left ventricular Tako–tsubo (r–TTC) was made. Transthoracic color Doppler echocardiography confirmed the alterations of the left ventricular kinetics observed by ventriculography. Conclusions compared to CTT, r–TTC is associated with a lower decline in global systolic function and, as reported in the literature, there is a greater connection to neurological insults as triggering factors, such as episodes of aneurysmal subarachnoid hemorrhage, brain surgery, ischemic stroke seizures and traumatic brain injury. The underlying mechanisms are still unknown, a crucial role in catecholamine–induced cardiotoxicity, coronary microvascular dysfunction or coronary vasospasm and/or estrogen deficiency is hypothesized.