Publications by authors named "Silvia Bozzetti"
Coronavirus disease 2019 (COVID-19), which is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains a global public health emergency. Although SARS-CoV-2 is primarily a respiratory pathogen, extra-respiratory organs, including the CNS, can also be affected. Neurologic symptoms have been observed not only during acute SARS-CoV-2 infection, but also at distance from respiratory disease, also known as long-COVID or neurological post-acute sequelae of COVID-19 (neuroPASC).
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- This study focuses on autoimmune encephalitis (AE), detailing its clinical findings, treatment options, and long-term effects, particularly related to epilepsy.
- Researchers examined 263 patients with new-onset seizures due to AE, noting that 63.5% had antineuronal antibodies, which influenced seizure types and treatment outcomes.
- Key findings suggest that early immunotherapy is crucial for better outcomes, but severe initial seizures are linked to a higher risk of developing chronic epilepsy.
The persistence of neurological symptoms after SARS-CoV-2 infection, as well as the presence of late axonal damage, is still unknown. We performed extensive systemic and neurological follow-up evaluations in 107 out of 193 consecutive patients admitted to the COVID-19 medical unit, University Hospital of Verona, Italy between March and June 2020. We analysed serum neurofilament light chain (NfL) levels in all cases including a subgroup (n = 29) of patients with available onset samples.
View Article and Find Full Text PDFSARS-CoV-2 survivors may report persistent symptoms that resemble myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). We explored (a) ME/CFS-like symptom prevalence and (b) whether axonal, inflammatory, and/or lung changes may contribute to ME/CFS-like symptoms in SARS-CoV-2 survivors through clinical, neuropsychiatric, neuropsychological, lung function assessment, and serum neurofilament light chain, an axonal damage biomarker. ME/CFS-like features were found in 27% of our sample.
View Article and Find Full Text PDFBackground: Recent findings indicated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-related neurological manifestations involve cytokine release syndrome along with endothelial activation, blood brain barrier dysfunction, and immune-mediated mechanisms. Very few studies have fully investigated the cerebrospinal fluid (CSF) correlates of SARS-CoV-2 encephalitis.
Methods: Patients with polymerase chain reaction (PCR)-confirmed SARS-CoV-2 infection and encephalitis (COV-Enc), encephalitis without SARS-CoV-2 infection (ENC), and healthy controls (HC) underwent an extended panel of CSF neuronal (neurofilament light chain [NfL], T-tau), glial (glial fibrillary acidic protein [GFAP], soluble triggering receptor expressed on myeloid cells 2 [sTREM2], chitinase-3-like protein 1 [YKL-40]) and inflammatory biomarkers (interleukin [IL]-1β, IL-6, Il-8, tumor necrosis factor [TNF] α, CXCL-13, and β2-microglobulin).
Epileptic seizures of suspected autoimmune origin: a multicentre retrospective study.
J Neurol Neurosurg Psychiatry
November 2020
Objective: To analyse autoantibody status in a well-defined European multicentre cohort of patients with epilepsy of unknown aetiology and to validate the recently proposed Antibody Prevalence in Epilepsy (APE2) and Response to ImmunoTherapy in Epilepsy (RITE2) scores.
Methods: We retrospectively collected clinical and paraclinical data of 92 patients referred to the Neurology Units of Verona and Salzburg between January 2014 and July 2019 with new-onset epilepsy, status epilepticus or chronic epilepsy of unknown aetiology. Fixed and live cell-based assays, tissue-based assays, immunoblot, and live rat hippocampal cell cultures were performed in paired serum/cerebrospinal fluid (CSF) to detect antineuronal and antiglial antibodies.
Nervous system: subclinical target of SARS-CoV-2 infection.
J Neurol Neurosurg Psychiatry
September 2020
Article Synopsis
- Diagnosing peripheral neuropathies is difficult, so this study examines the use of sural nerve biopsy and serum neurofilament light chain levels (NfL) as biomarkers for axonal damage.
- The study involved 82 patients, mostly older adults, revealing that neuropathy often starts slowly, primarily affects the lower limbs, and presents with more sensory than motor symptoms; various neuropathological patterns were identified.
- Although nerve biopsy provided a definitive diagnosis in some cases, there was a correlation between elevated serum NfL levels and active axonal degeneration, suggesting that NfL could be a valuable, accessible biomarker for these conditions.
Article Synopsis
- Emery Dreifuss muscular dystrophy (EDMD) is an inherited muscle disease that leads to early joint stiffness, gradual muscle weakness, and heart issues, caused by mutations in various genes, particularly the emerin gene for the X-linked form.
- A case study details a 40-year-old man who initially displayed symptoms at age 6 and was misdiagnosed with spinal muscular atrophy type 3 but later developed cardiac problems and severe muscle atrophy.
- Genetic testing revealed a new mutation in the emerin gene, enhancing the understanding of X-linked EDMD's clinical and genetic variations.
Fingolimod is a commonly used treatment for highly active relapsing-remitting multiple sclerosis (MS). We describe the case of a 50-year old man on fingolimod since 2011 who presented, in April 2017, with a voluminous swelling of the left tonsil. A left tonsillectomy was performed, and histological exam disclosed a papillary squamous cell carcinoma of the palatine tonsil, with an in situ hybridization positive for human papillomavirus (HPV)-16 DNA.
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