We present the case of a 67-year-old woman affected by hypertension and hypercholesterolemia. She had a history of alcoholism, anxiety disorder with panic attacks, and paroxysmal atrial fibrillation. Despite a previous transient ischemic attack and her thromboembolic risk (CHA 2 DS 2 -VASc score: 5), she had not been taking anticoagulants at home without a reasonable motivation. Moreover, around eighteen years prior, she had breast cancer and underwent surgical intervention, radiotherapy and several years of hormone-therapy. However, in the following years, she had pelvic bone metastasis needing multiple orthopaedic procedures.The patient was admitted to the Emergency Department with complaints of diarrhoea lasting one week and palpitations associated with dyspnoea in the last 24-hours.Laboratory tests showed severe hypokalaemia (2.8 meq/l), hypomagnesemia (0.4 mg/dl) and elevation, although not significant, of troponin I (0.09 ng/ml -NV ≤ 0.07).ECG showed atrial fibrillation with fast ventricular rate (140/min) and diffuse inverted T-wave, while echocardiography revealed a normal left ventricular function (EF ≈ 60%).A few hours after intravenous replacement of K + and Mg 2+ , the patient showed spontaneous restoration of sinus rhythm. However, suddenly, she became confused and developed generalized motor and non-motor seizures, causing aggravation of diarrhoea and electrolyte disorders. An urgent cerebral CT scan was performed, which excluded acute cerebral events.Contextually, the patient had severe hypotension (systolic blood pressure < 90 mmHg). A significant elevation of troponin I (34.9 ng/ ml) and lactates with low bicarbonates were detected. ECG was normal; however, the echocardiography revealed a severe left ventricular dysfunction (EF: ≈ 20%) due to akinesia of all basal segment and hyperkinesia of apex. Considering the clinical scenario and that regional wall motion abnormalities extended beyond a single epicardial vascular distribution, a basal Takotsubo syndrome (TTS) was hypothesized.After adequate refilling with bolus fluids and intravenous replacement of bicarbonates and electrolytes, the hemodynamic status improved.Simultaneously, in the following 48-hours neurologists tried multiplies oral and intravenous antiepileptics drugs (oxcarbazepine, levetiracetam, sodium valproate and phenytoin) without success, suggesting a non-convulsive status epilepticus, which was confirmed by electroencephalogram ( Fig. 1A). Finally, a deep sedation with propofol was induced and the patient was assisted by mechanical ventilation. In the following days, we assisted in the resolution of the cardiological and neurological states, and the patient was then extubated.