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BACKGROUND Brugada syndrome is characterized by specific electrocardiographic changes predisposing individuals to ventricular arrhythmias and sudden cardiac death. Cases of coexisting Brugada syndrome and ischemic stroke are seldom documented, and an underlying pathophysiological link is yet unknown. This article presents a case in which a patient exhibited both Brugada syndrome patterns and an ischemic stroke, prompting a comprehensive literature review to explore the potential association between Brugada syndrome and ischemic stroke. CASE REPORT A 49-year-old man, previously healthy, was admitted to the hospital after being discovered unconscious at his workplace. Physical exam showed low oxygen saturation, fever, and abnormal neurological findings. Head computed tomography revealed a significant posterior circulation ischemic stroke. An electrocardiogram revealed Brugada syndrome type II initially, progressing to type III pattern. Despite efforts, the patient's condition rapidly deteriorated, leading to death within 24 hours. As far as we're aware, Brugada patterns following a posterior circulation ischemic stroke have only been documented in 1 other instance, in which the patient was also diagnosed with atrial fibrillation. CONCLUSIONS Both our literature review and the presented case indicate that Brugada patterns may coexist with and even be associated with ischemic stroke. More extensive research is required to shed light on this potential association. The question of whether Brugada syndrome is a precursor to or a result of ischemic stroke remains unanswered. We propose that patients with ischemic stroke should undergo an evaluation for electrocardiographic signs indicative of Brugada syndrome, particularly if no clear causes, like cardioembolism, are evident.

Introduction: Therapeutic plasma exchange (TPE) is commonly used as treatment of certain autoimmune neurological diseases (ANDs), and its main objective is the removal of pathogenic autoantibodies. Our aim was to describe the clinical profile and the experience with the usage of TPE in patients with ANDs at our institution., Methods: This is an observational retrospective study, including medical records of patients with diagnosis of ANDs who received TPE, between 2011 and 2018. Characteristics of TPE, such as number of cycles, type of replacement solution, and adverse effects, were evaluated. The modified Rankin Scale (mRS) was applied to measure the clinical response after the therapy., Results: 187 patients were included with the following diagnoses: myasthenia gravis (MG), n  = 70 (37%); Guillain-Barré syndrome (GBS), n  = 53 (28.3%), neuromyelitis optica spectrum disorders (NMOSD), n  = 35 (18.7%); chronic inflammatory demyelinating polyneuropathy (CIDP), n  = 23 (12.2%); and autoimmune encephalitis (AE), n  = 6 (3.2%). The most used types of replacement solution were albumin ( n  = 131, 70%) and succinylated gelatin ( n  = 45, 24%). All patients received a median of five cycles (IQR 5-5). Hypotension and hydroelectrolytic disorders were the main complications. After TPE, 99 patients (52.9%) showed improvement in the mRS scores and a statistical significance ( p < 0.05) was seen between the admission score and after TPE for every diagnosis except for CIDP., Conclusion: TPE has an adequate safety profile, and improvement in functionality in treated patients reflects its effectiveness., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2020 Ivana Nieto-Aristizábal et al.)

BACKGROUND Retinoid-induced myositis is a rare condition encountered in clinical practice. Its occurrence implies a diagnostic challenge due to the multiple causes associated with myopathic syndromes. The most common clinical presentation is generalized affection. Focal myositis is even less frequent and easily misdiagnosed as muscular disease of other etiology. CASE REPORT We describe a case of 45-year-old male with a history of nephrolithiasis and rosacea diagnosed by dermatology, who was management with isotretinoin 1 mg/kg per day in 2 doses with clinical improvement. Later, he presents muscle pain in the upper limbs with marked functional limitation associated by choluria, without muscular pains in other location; he had no history of using another medication. At his physical examination, vital signs were normal, with edema and pain in the bilateral bicipital region associated with limitation for flexion-extension of shoulders and elbows and high levels of creatine phosphokinase (CPK). He was transferred to the intensive care unit where he received fluid therapy because of the high risk of deterioration of renal function, very high CPK levels, and a history of obstructive uropathy. One year after this hospitalization, the cutaneous symptoms worsened and the patient voluntarily restarted isotretinoin and 5 months later he presented again with the same symptoms of the first episode. CONCLUSIONS Drug-induced myositis should be taken into consideration in the differential diagnosis of myopathic syndromes. Retinoids have the potential to cause varying degrees of myositis and their rapid identification could prevent major complications.