An 87-year-old man (weight 80.9 kg, height 1.79 m and BMI 25.3 kg/m2) presented with a syncope and fall at the emergency department. Upon arrival (at 4 p.m.) he was well oriented; BP (seated) was 168/59 mmHg with a regular pulse at 65/min (auscultatory). He had dyspnea (respiratory rate 15/min) with an arterial O2 saturation of 89 % (98 % after oxygen administration). His mouth mucosa was dry and he had bilateral pulmonary stasis, but no jugular tumescence. There was a slight degree of peripheral pitting edema and he had a urethral catheter. The neurologic examination was repeatedly normal; his MMSE score was 25/30. His basic ADL (Katz-scale) was 8/24; the instrumental ADL score (Lawton) was 15/27. He was mobile with a four-wheel walker under supervision from his wife. He was a previous smoker and admitted drinking three alcohol consumptions per day on average. His non-fasting glycemia was 107 mg/dL (fasting reference values 70–100 mg/dL) and follow-up revealed neither hyper- nor hypoglycemia; his hemoglobinemia was 12.6 g/dL (reference values: 13.0- 16.5 g/dL). OH had been documented since approximately three years, with a systolic BP varying between 73 and 93 mmHg. An orthostatic test, two years before the present admission, had shown a BP of 184/111 mmHg and a heart rate (HR) of 73/min. in supine position. After standing one minute, BP was 98/70 mmHg and pulse rate 85/min; after three minutes 99/71 mmHg and 82/min.; after five minutes 98/63 mmHg and 78/min. He presented almost weekly syncopes and falls, mainly occurring after meals or physical effort. Convulsions, lasting ± 30 seconds, had been observed once. His medical history mentioned atrial fibrillation (with periods of slow ventricular response), bronchiectasis, colon diverticulosis, urge incontinence and urine retention, treated by trans-urethral catheter, and bilateral hip prosthesis for osteoporotic fractures after falls. Three months earlier, during a hospitalization for OH (86/53 mmHg), a discrete rigidity of the right arm and a slight bilateral tremor of the hands had been noted, suggesting an essential tremor or a beginning PD. It had been concluded that he suffered from severe OH, mainly due to sodium and fluid deficit, resulting in cerebral hypoperfusion. Several investigations had already been completed recently. A transthoracic cardiac ultrasound examination had shown no signs of cardiac amyloidosis, and a primary adrenal cortical failure was excluded. His medication upon arrival consisted of rivaroxaban 15 mg q.d., amiodarone 200 mg q.d., bumetanide 1 mg q.d., spironolactone 25 mg q.d., fludrocortisone 0.1 mg b.i.d., finasteride 5 mg q.d., folic acid 4 mg q.d., calcium carbonate 1000 mg q.d., cholecalciferol 800 IE q.d., zolendronate 5 mg i.v. once a year, and paracetamol 1 g if necessary. He had been advised to wear elastic stockings, rise slowly, apply a mild anti-Trendelenburg position during the night, avoid large meals, and drink sufficiently. Upon admission to the geriatric ward amiodarone and finasteride were stopped. He developed a pneumonia, empirically treated with piperacilline and tazobactam. This treatment was successful, but he developed heart failure, necessitating fludrocortisone to be stopped. A CT scan of the brain showed slight cortico-subcortical and cerebellar atrophy, and some small lacunar infarctions in the basal ganglia. An EEG was normal. Given the history of syncopes, hypotension, and bradycardia, the cardiologist advised a coronaroangiography that showed only a moderate stenosis at two sites. An ultrasound examination of the neck showed no arterial stenosis, but revealed a multinodular thyroid goiter (thyroid hormone levels were found to be normal). An electromyography showed signs of length-dependent chronic axonal sensory-motoric polyneuropathy. He had a calculated MDRD of 40ml/min, with normal renal ultrasound examination and no signs of renal artery stenosis. Continuous ECG registration confirmed a regular sinus rhythm with an average frequency of 52/min, (33–61/min) and a second degree A-V block Mobitz type II. Placing of a pacemaker normalized the heart rhythm, but syncopes and daytime OH persisted. 24-hours BP registration revealed a reversal of the day-night rhythm with hypotension during the day and hypertension during the night (see Fig. ). The daytime average systolic, diastolic, and mean arterial pressures (StDev) were respectively 98 (33.7), 59 (19.2), and 72 (24.0) mm Hg; during the night these values were respectively 147 (17.0), 85 (8.8), and 106 (11.4) mm Hg. Trying to control the BP, bumetanide and spironolactone were stopped, and fludrocortisone (0.5 mg) was given in the morning and captopril (12.5 mg) in the evening. With this treatment, BP values varied between 80 and 180 mmHg with a tendency for improvement towards the end of his hospitalization that continued afterwards. A PET brain scan showed no arguments for Lewy body disease. An 18 FDG PET CT brain scan demonstrated cerebellar hypometabolism, arguing in favour of MSA. Due to the 2020 Covid 19 pandemic, we could not realize a follow-up 24 h BP registration. However, the patient reported a clear improvement with a significant reduction of symptomatic events.