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Background: The term rapidly progressive dementia (RPD) describes a disorder with rapid progression which leads to a major cognitive decline in less than 1 or 2 years. Neurosyphilis is an infectious cause of RPD and it is classified clinically into early and late forms. The latter affect the brain and spinal cord parenchyma. The objective of this report is to present a case of RPD caused by neurosyphilis. Clinical case: 55-year-old man, with no past medical history, who in July 2022 had a clinical presentation of aggressiveness, irritability, lability, difficulty in performing simple activities, amnesia, hallucinations, delusions, abulia, low responsiveness, all of which affected his independence and quality of life. Initially, it was treated as schizophrenia with no signs of improvement and clinical deterioration. When atypical data and rapid progression were evident at patient's consultation in January 2023, there was a suspicion of the presence of RPD, highlighting positive VDRL and IgM-IgG anti-Treponema pallidum antibodies in cerebrospinal fluid (CSF). Computed tomography (CT) and magnetic resonance imaging (MRI) showed global cortical atrophy, predominantly frontal. Treatment with ceftriaxone was started for 14 days, with clinical improvement observed in the MOCA test from 13/30 to 23/30. Conclusions: The etiological identification of RPD is a clinical challenge due to the wide variety of causes, which is why it is important a specific diagnostic approach and a timely treatment in order to avoid the progression of potentially reversible causes. [ABSTRACT FROM AUTHOR]

Background: Anti-GQ1B syndrome includes a group of diseases characterized by antibody-mediated polyneuropathy. Guillain Barre syndrome (GBS) and the Miller-Fisher syndrome (MFS) have been related to COVID-19 vaccine application. Clinic case: 48-year-old man, with history of Pfizer-BioNTech vaccination against COVID-19, 5 days prior to the symptoms, who assisted to the Emergency room with blurred vision and diplopia; adding dysarthria, facial diplegia and left upper limb weakness after 48 hours. In his first evaluation it was found ophthalmoplegia, facial diplegia, decreased gag reflex, weakness of thoracic limbs, bilateral trapezius muscle and areflexia. Serum studies and nuclear magnetic resonance of the brain were performed without alterations. It was complemented with IgG anti-ganglioside GQ1b antibodies with a positive result. Once the diagnosis was confirmed, treatment was started with immunoglobulin calculated at 2 g per kg for 5 days. The patient was discharged once the immunoglobulin was administered with evaluation at 2 months without ataxia, ophthalmoplegia, areflexia and weakness. Conclusions: Following the documented reports of GBS and its variants secondary to vaccination, neurological side effects have been catalogued as being of great importance. Therefore, the reported case can be used as a point of reference to consider this clinical spectrum as a differential diagnosis in patients with post-vaccination neurological symptomatology. [ABSTRACT FROM AUTHOR]