Context: Guillain-Barré syndrome is a polyradiculoneuropathy of heterogeneous manifestations, necessarily presenting progressive appendicular weakness of variable intensity associated with reduction or abolition of deep reflexes. One of its variants is known as Miller Fisher Syndrome (MFS), characterized by ophthalmoparesis, ataxy and areflexia. It usually has, by etiology, immunomediated reactions induced by acute infections, including HIV. Objectives: This report aims to describe a case of MFS with concomitants HIV infection, attended in a tertiary hospital in northern Paraná and compared it with the literature. [1,7] Case report: A 27-year-old white male patient who presented binocular diplopia, dysarthria, dysphagia, generalized hypotonia, myasfasciculations, sensory ataxia and arreflexia, with a score on the Medical Research Council (MRC) muscle strength scale of 54 points. Treatment with empirical intravenous human immunoglobulina ( IVIG ) was performed pending the result of serologies for etiological screening. He was discharged after eleven days of hospitalization with partial symptomatic improvement and results indicative of acute HIV infection. We compared this case with those described in the published literature Discussion: We compared this case with those described in the published literature and given the low incidence found in the literature of patients with the stage of HIV viremia and the opening of the picture of SMF, the concrete pathophysiology itself is still unknown. The mechanism, however, in which the literature proposes in two theories: (1) an autoimmune action against myelin due to abnormal immunoregulation by HIV; (2) direct action of neurotropic strains of HIV-1. [2.3] Our literature review shows that since 1995, cases of associated guillain barré syndrome have already been reported in the course of HIV viremia. Treatment with immunoglobulin at a dose of 400mg / kg / day for 5 days was done and the symptoms improved. [1,4,6,7] Conclusion: It is exposed, then, a case of HIV-induced MFS whose relationship has consistency, temporality, biological plausibility, coherence and analogy compatible with current literature.

Background: Infection with SARS-CoV-2 can cause COVID-19, which mainly affects the respiratory system. However, neurological complications are frequent, including the group of acquired immune-mediated demyelinating neuropathies (NDAI), including Miller-Fisher syndrome (SMF), characterized by the triad of ophthalmoparesis, ataxia and areflexia. Infection with C. jejuni is the main precipitant of NDAI, but viruses are also related. Objectives: This report aims to describe a case of SMF with concomitant SARS-CoV-2 infection, seen at a tertiary hospital in Northern Paraná and to compare it with the literature. Design and setting: case report of a patient at the hospital neurology service of the Evangelical Hospital, Londrina, Paraná, Brazil. Methods: Report a case of SMF right after confirmation of COVID-19 seen at a tertiary hospital in Northern Paraná and compare it with the literature. Results: Male, 70 years old, white, evolved with progressive and symmetrical crural paraparesis 17 days after confirmation of COVID-19. Upon admission, he presented ataxia, paraesthesia, and crural myotactic areflexia with no signs of pyramidal release, and a score on the Medical Research Council (MRC) muscle strength scale of 58 points. Analysis of CSF with albumin-cytological dissociation. Treatment was performed with intravenous human immunoglobulin (IVIG) and discharged after six days of hospitalization with partial symptomatic improvement. We compared this case with those described in the published literature. Not found Brazilian case published to date. Conclusion: Rare case report of SMF by SARS-CoV-2. The relationship has consistency, temporality, biological plausibility, coherence and analogy compatible with the current literature. Studies with a higher level of evidence are needed to determine the strength of such an association.

Introduction: Ramsay Hunt Syndrome, a rare clinical entity, is caused by the reactivation of the varicella zoster virus, which results in inflammation of the geniculate ganglion of the facial nerve. Characterized by the triad: ipsilateral facial paralysis, otalgia and herpetic vesicles in the external ear. Due to the broad symptomatology, which encompasses atypical symptoms and present in several other pathologies, it is often underdiagnosed. Case report: A 62-year-old woman admitted to Hospital Evangélico de Londrina due to paresthesia in the left hemiface, associated with vertigo and severe headache. On physical examination, peripheral facial paralysis on the left and vesicles on the palate and left external ear were observed. AVC protocol exams were requested (normal) and liquor was collected (clear, colorless appearance, 92% lymphocytes). New serologies and magnetic resonance imaging of the skull with contrast were requested. Prescribed acyclovir, prednisone, eye drops and ocular occlusion. The patient evolved with maintenance of headache and otalgia. Prednisone was replaced by intravenous dexamethasone, gabapentin and topical lidocaine were added, and other medications were maintained. Non-reactive requested serologies. Analysis of the herpes simplex virus by polymerase chain reaction > 30. In view of the data, a diagnosis of viral meningitis due to herpes associated with Ramsay Hunt syndrome was diagnosed. Maintained treatment, patient evolved with improvement of the condition. Conclusion: Based on the clinical correlation and unfavorable prognosis, the importance of early identification and treatment lies in order to reduce the time of active disease and neural damage, avoiding possible complications.