Reactive gliosis and neuroinflammation: prime suspects in the pathophysiology of post-acute neuroCOVID-19 syndrome

IntroductionAs the repercussions from the COVID-19 pandemic continue to unfold, an ever-expanding body of evidence suggests that infection also elicits pathophysiological manifestations within the central nervous system (CNS), known as neurological symptoms of post-acute sequelae of COVID infection (NeuroPASC). Although the neurological impairments and repercussions associated with NeuroPASC have been well described in the literature, its etiology remains to be fully characterized.ObjectivesThis mini-review explores the current literature that elucidates various mechanisms underlining NeuroPASC, its players, and regulators, leading to persistent neuroinflammation of affected individuals. Specifically, we provide some insights into the various roles played by microglial and astroglial cell reactivity in NeuroPASC and how these cell subsets potentially contribute to neurological impairment in response to the direct or indirect mechanisms of CNS injury.DiscussionA better understanding of the mechanisms and biomarkers associated with this maladaptive neuroimmune response will thus provide better diagnostic strategies for NeuroPASC and reveal new potential mechanisms for therapeutic intervention. Altogether, the elucidation of NeuroPASC pathogenesis will improve patient outcomes and mitigate the socioeconomic burden of this syndrome

Neurological manifestations of post-acute sequelae of COVID-19: which liquid biomarker should we use?

Long COVID syndrome, also known as post-acute sequelae of COVID-19 (PASC), is characterized by persistent symptoms lasting 3–12 weeks post SARS-CoV-2 infection. Patients suffering from PASC can display a myriad of symptoms that greatly diminish quality of life, the most frequent being neuropsychiatric. Thus, there is an eminent need to diagnose and treat PASC related neuropsychiatric manifestation (neuro-PASC). Evidence suggests that liquid biomarkers could potentially be used in the diagnosis and monitoring of patients. Undoubtedly, such biomarkers would greatly benefit clinicians in the management of patients; however, it remains unclear if these can be reliably used in this context. In this mini review, we highlight promising liquid (blood and cerebrospinal fluid) biomarkers, namely, neuronal injury biomarkers NfL, GFAP, and tau proteins as well as neuroinflammatory biomarkers IL-6, IL-10, TNF-α, and CPR associated with neuro-PASC and discuss their limitations in clinical applicability

Radiological markers of neurological manifestations of post-acute sequelae of SARS-CoV-2 infection: a mini-review

The neurological impact of COVID-19 is a rising concern among medical professionals, as patients continue to experience symptoms long after their recovery. This condition, known as neurological post-acute sequelae of COVID-19 (Neuro-PASC), can last for more than 12 weeks and includes symptoms such as attention disorders, brain fog, fatigue, and memory loss. However, researchers and health professionals face significant challenges in understanding how COVID-19 affects the brain, limiting the development of effective prevention and treatment strategies. In this mini-review, we provide readers with up-to-date information on the imaging techniques currently available for measuring the neurological impact of post-SARS-CoV-2 infection. Our search of PubMed and Google Scholar databases yielded 38 articles on various brain imaging techniques, including structural MRI (magnetic resonance imaging), functional MRI, diffusion MRI, susceptibility-weighted imaging, SPECT (single-photon emission computed tomography) imaging, and PET (positron emission tomography) imaging. We also discuss the optimal usage, limitations, and potential benefits of these techniques. Our findings show that various cerebral imaging techniques have been evaluated to identify a reliable marker for Neuro-PASC. For instance, 18F-FDG-PET/CT and functional MRI have demonstrated hypometabolism in cerebral regions that are directly linked to patient symptoms. Structural MRI studies have revealed different findings, such as infarcts, white matter atrophy, and changes in gray matter volumes. One SPECT imaging study noted frontal lobe hypometabolism, while diffusion MRI showed increased diffusivity in the limbic and olfactory cortical systems. The sequence SWI showed abnormalities primarily in white matter near the gray-white matter junction. A study on 18F-amyloid PET/CT found amyloid lesions in frontal and anterior cingulate cortex areas, and a study on arterial spin labeling (ASL) found hypoperfusion primarily in the frontal lobe. While accessibility and cost limit the widespread use of 18F-FDG-PET/CT scans and functional MRI, they seem to be the most promising techniques. SPECT, SWI sequence, and 18F-amyloid PET/CT require further investigation. Nevertheless, imaging remains a reliable tool for diagnosing Neuro-PASC and monitoring recovery

Phénotype associé aux duplications du gène APP (cohorte française)

BESANCON-BU Médecine pharmacie (250562102) / SudocSudocFranceF

Functional Neurological Symptom Disorder: A Diagnostic Algorithm

Functional neurological symptom disorder (FNSD) is a neuropsychiatric disorder characterized by the presence of neurological symptoms in the absence of any neurological abnormality that can be linked to a known pathology. Few studies have taken interest in this subject probably because of the heterogeneity of results. It is most often a diagnosis of exclusion which often means that patients undergo many tests and find themselves erring for a diagnosis with very little satisfaction of the outcomes. A reliable imagery pattern would therefore provide some relief and confirmation for both patients and clinicians. It could also facilitate acceptation of the diagnosis and reduce the societal cost associated with FNSD for the patient. The aim of this present study was to describe a clinicoradiological correspondence algorithm of FNSD using the PET scan and SPECT scan (PoSPs) and grant the clinician with a reliable tool to facilitate the diagnosis of FNSD. A systematic review according to the 2009 PRISMA criteria statement was used to guide the review. Our study included 3 of our own consenting patients who met the Diagnostic and Statistical Manual of Mental Disorders 5th edition criteria as well as 25 other patients from 7 different studies. Our results showed a hypoactivation with poor clinicoradiological correspondence and poor stability in time. This hypoactivation was mostly in the frontal lobe, which could explain some behavioral alterations. These findings oppose the ones found in organic pathologies and therefore should orient towards FNSD. In the light of these findings, we recommend the clinicians to perform two PoSPs, searching for clinicoradiological lack of correspondence and time stability using our algorithm

Executive and Attentional Disorders, Epilepsy and Porencephalic Cyst in Autosomal Recessive Cerebellar Ataxia Type 3 Due to <b><i>ANO10</i></b> Mutation

International audienceANO10 mutations have recently been reported in autosomal recessive cerebellar ataxia type 3 (ARCA3). The objective of this study was to describe the phenotype of 2 siblings with compound heterozygous ANO10 mutations and progressive cerebellar ataxia, epilepsy, and cognitive impairment. A porencephalic cyst was also described in one of them and a coenzyme Q10 deficiency in the other one

Cognitive Impairment Involving Social Cognition in SPG4 Hereditary Spastic Paraplegia

Objectives. To describe cognitive assessment including social cognition in SPG4 patients. Methods. We reported a series of nine patients with SPG4 mutation with an extensive neuropsychological examination including social cognition assessment. Results. None of our patients presented with mental retardation or dementia. All presented with mild cognitive impairment with a high frequency of attention deficit (100%), executive disorders (89%), and social cognition impairment (78%). An asymptomatic patient for motor skills presented with the same cognitive profile. No correlation was found in this small sample between cognitive impairment and motor impairment, age at disease onset, or disease duration. Conclusions. SPG4 phenotypes share some cognitive features of frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Cognitive disorders including executive disorders and social cognition impairment are frequent in SPG4 patients and might sometimes occur before motor disorders. Therefore, cognitive functions including social cognition should be systematically assessed in order to improve the clinical management of this population