Acute disseminated encephalomyelitis following Tdap vaccination and bacterial meningoencephalitis.

INTRODUCTION: Association of Acute Disseminated Encephalomyelitis (ADEM) with both recent vaccination and viral infections is well described in current literature. However, the coincidence of ADEM and bacterial infections has been rarely documented. In this report, we present a case of ADEM which occurred after bacterial meningoencephalitis and prior vaccination against tetanus, diphtheria, and pertussis (Tdap). CASE PRESENTATION: A 62-year old woman was hospitalized with an upper respiratory tract infection three weeks after Tdap triple vaccination. A few days after admission, she became somnolent and developed meningism. Cerebrospinal fluid (CSF) analysis revealed pleocytosis and increased protein/lactate levels compatible with bacterial meningoencephalitis. The patient was treated with intravenous antibacterial triple therapy in combination with dexamethasone leading to a significant improvement of clinical symptoms and improvement of CSF parameters. Five days later, the patient's condition worsened again, and she developed aphasia and right-sided hemiparesis. A magnetic resonance imaging (MRI) scan revealed distinct fluid-attenuated inversion recovery sequence (FLAIR)-hyperintense lesions in both hemispheres. Following brain biopsy, the diagnosis of ADEM was made and methylprednisolone pulse therapy was initiated for five days leading to a nearly complete remission of symptoms. CONCLUSION: ADEM is a neurological syndrome which may be associated with bacterial infection of the central nervous system (CNS). We hypothesize that the preceding Tdap triple vaccination may have contributed to the development of ADEM.

[Tauopathies : From molecule to therapy]. / Tauopathien : Vom Molekül zur Therapie.

BACKGROUND: The microtubule-associated tau protein is the defining denominator of a group of neurodegenerative diseases termed tauopathies. OBJECTIVE: Provide a timely state of the art review on recent scientific advances in the field of tauopathies. MATERIAL AND METHODS: Systematic review of the literature from the past 10 years. RESULTS: Tau proteins are increasingly being recognized as a highly variable protein, underlying and defining a spectrum of molecularly defined diseases, with a clinical spectrum ranging from dementia to hypokinetic movement disorders. Genetic variation at the tau locus can trigger disease or modify disease risk. Tau protein alterations can damage nerve cells and propagate pathologies through the brain. Thus, tau proteins may serve both as a serological and imaging biomarker. Tau proteins also provide a broad spectrum of rational therapeutic interventions to prevent disease progression. This knowledge has led to modern clinical trials. CONCLUSION: The field of tauopathies is in a state of dynamic and rapid progress, requiring close interdisciplinary collaboration.