Brugada syndrome mainly affects men in the third and fourth decade of life. It presents with a typical electrocardiographic pattern, unmasked by sodium channel blocking drugs or hyperpyrexia. A 36–year–old young man, with no reported cardiovascular risk factors or family history of sudden death, had convulsions and loss of consciousness during hyperpyrexia, for which family members alerted the local emergency service. During transport to the hospital, the vital parameters and heart rhythm were normal, but, due to the onset of seizures, the patient was sedated, intubated and hospitalized in intensive care unit (ICU). The ECG performed at the entrance (in the course of hyperpyrexia) showed a dubious type 1 Brugada pattern (Figure 1). The echocardiogram (as well as the subsequent cardiac resonance) showed the absence of cardiac structural alterations. Prompt treatment of hyperpyrexia was recommended, the use of drugs listed on brugadadrugs.org was contraindicated and careful ECG monitoring was recommended. Non–sustained ventricular tachycardia was documented during the hospitalization in ICU. When the clinical picture stabilized with resumption of spontaneous breathing, the patient was transferred to our ICU for continuation of the diagnostic and therapeutic process (Figure 2). From the interview with the patient, a previous paroxysmal tachycardia from atrio–ventricular reentry emerged in antiarrhythmic prophylaxis for several years with Propafenone and subsequently treated with catheter ablation of the right lateral accessory path. Considering the lack of documentation of complex ventricular arrhythmias by the 118 during transport to the hospital and during the stay in the UTIC, the long antiarrhythmic therapy with sodium channel inhibitors, as well as the absence of a typical Brugada pattern during fever, we decide to perform a Flecainide test (2 mg / Kg in 10 ‘), negative result for Brugada type 1 pattern (Figure 2) In the following days, considering the absolute negativity of all the neuroradiological and EEG investigations, not having found the cause of the loss of consciousness during hyperpyrexia, we performed ajmaline test (1 mg / kg in 100 cc of SG5% in 10 ‘) with the identification of the diagnostic pattern type 1 (Figure 3). Finally, the implantation of a subcutaneous cardioverting defibrillator (S–ICD) was performed.