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1.
J Neuropathol Exp Neurol ; 81(12): 988-995, 2022 Nov 16.
Article in English | MEDLINE | ID: covidwho-2077800

ABSTRACT

The brain of a 58-year-old woman was included as a civilian control in an ongoing autopsy study of military traumatic brain injury (TBI). The woman died due to a polysubstance drug overdose, with Coronavirus Disease 2019 (COVID-19) serving as a contributing factor. Immunohistochemical stains for ß-amyloid (Aß), routinely performed for the TBI study, revealed numerous, unusual neocortical Aß deposits. We investigated the autopsied brains of 10 additional young patients (<60 years old) who died of COVID-19, and found similar Aß deposits in all, using two different Aß antibodies across three different medical centers. The deposits failed to stain with Thioflavin-S. To investigate whether or not these deposits formed uniquely to COVID-19, we applied Aß immunostains to the autopsied brains of COVID-19-negative adults who died with acute respiratory distress syndrome and infants with severe cardiac anomalies, and also biopsy samples from patients with subacute cerebral infarcts. Cortical Aß deposits were also found in these cases, suggesting a link to hypoxia. The fate of these deposits and their effects on function are unknown, but it is possible that they contribute to the neurocognitive sequelae observed in some COVID-19 patients. Our findings may also have broader implications concerning hypoxia and its role in Aß deposition in the brain.


Subject(s)
Alzheimer Disease , Brain Injuries, Traumatic , COVID-19 , Neocortex , Humans , Adult , Female , Middle Aged , Neocortex/pathology , COVID-19/complications , Amyloid beta-Peptides/metabolism , Brain/pathology , Brain Injuries, Traumatic/pathology , Hypoxia/pathology , Alzheimer Disease/pathology
2.
Psychiatr Clin North Am ; 45(4): 625-637, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-2076620

ABSTRACT

Severe acute respiratory syndrome coronavirus 2, the novel coronavirus responsible for the coronavirus disease (COVID-19), affects the brain. Neurologic and neuropsychiatric symptoms may manifest in the acute and post-acute phases of illness. The vulnerability of the brain with aging further increases the burden of disease in the elderly, who are at the highest risk of complications and death from COVID-19. The mechanisms underlying the effects of COVID-19 on the brain are not fully known. Emerging evidence vis-à-vis pathogenesis and etiologies of COVID-19 brain effects is promising and may pave the way for future research and development of interventions.


Subject(s)
COVID-19 , Humans , Aged , Brain/pathology , Aging
3.
Cells ; 11(19)2022 10 04.
Article in English | MEDLINE | ID: covidwho-2065731

ABSTRACT

Here, we aim to describe COVID-19 pathology across different tissues to clarify the disease's pathophysiology. Lungs, kidneys, hearts, and brains from nine COVID-19 autopsies were compared by using antibodies against SARS-CoV-2, macrophages-microglia, T-lymphocytes, B-lymphocytes, and activated platelets. Alzheimer's Disease pathology was also assessed. PCR techniques were used to verify the presence of viral RNA. COVID-19 cases had a short clinical course (0-32 days) and their mean age was 77.4 y/o. Hypoxic changes and inflammatory infiltrates were present across all tissues. The lymphocytic component in the lungs and kidneys was predominant over that of other tissues (p < 0.001), with a significantly greater presence of T-lymphocytes in the lungs (p = 0.020), which showed the greatest presence of viral antigens. The heart showed scant SARS-CoV-2 traces in the endothelium-endocardium, foci of activated macrophages, and rare lymphocytes. The brain showed scarce SARS-CoV-2 traces, prominent microglial activation, and rare lymphocytes. The pons exhibited the highest microglial activation (p = 0.017). Microthrombosis was significantly higher in COVID-19 lungs (p = 0.023) compared with controls. The most characteristic pathological features of COVID-19 were an abundance of T-lymphocytes and microthrombosis in the lung and relevant microglial hyperactivation in the brainstem. This study suggests that the long-term sequelae of COVID-19 derive from persistent inflammation, rather than persistent viral replication.


Subject(s)
COVID-19 , Thrombosis , Aged , Antigens, Viral , Brain/pathology , Humans , Kidney , Lung/pathology , Macrophages , RNA, Viral , SARS-CoV-2 , T-Lymphocytes , Thrombosis/pathology
4.
J Neurol Neurosurg Psychiatry ; 93(12): 1343-1348, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-2038335

ABSTRACT

BACKGROUND: To assess whether SARS-CoV-2 infection may affect the central nervous system, specifically neurons and glia cells, even without clinical neurological involvement. METHODS: In this single centre prospective study, serum levels of neurofilament light chain (sNfL) and glial fibrillar acidic protein (sGFAp) were assessed using SimoaTM assay Neurology 2-Plex B Assay Kit, in 148 hospitalised patients with COVID-19 without clinical neurological manifestations and compared them to 53 patients with interstitial pulmonary fibrosis (IPF) and 108 healthy controls (HCs). RESULTS: Age and sex-corrected sNfL levels were higher in patients with COVID-19 (median log10-sNfL 1.41; IQR 1.04-1.83) than patients with IPF (median log10-sNfL 1.18; IQR 0.98-1.38; p<0.001) and HCs (median log10-sNfL 0.89; IQR 0.72-1.14; p<0.001). Likewise, age and sex-corrected sGFAP levels were higher in patients with COVID-19 (median log10-sGFAP 2.26; IQR 2.02-2.53) in comparison with patients with IPF (median log10-sGFAP 2.15; IQR 1.94-2.30; p<0.001) and HCs (median log10-sGFAP 1.87; IQR 0.64-2.09; p<0.001). No significant difference was found between patients with HCs and IPF (p=0.388 for sNfL and p=0.251 for sGFAp). In patients with COVID-19, a prognostic model with mortality as dependent variable (26/148 patients died during hospitalisation) and sNfl, sGFAp and age as independent variables, showed an area under curve of 0.72 (95% CI 0.59 to 0.84; negative predictive value (NPV) (%):80,positive predictive value (PPV)(%): 84; p=0.0008). CONCLUSION: The results of our study suggest that neuronal and glial degeneration can occur in patients with COVID-19 regardless of overt clinical neurological manifestations. With age, levels of sNfl and GFAp can predict in-hospital COVID-19-associated mortality and might be useful to assess COVID-19 patient prognostic profile.


Subject(s)
Brain , COVID-19 , Neuroglia , Neurons , Humans , Biomarkers/blood , Brain/pathology , Brain/virology , COVID-19/mortality , COVID-19/pathology , Neurofilament Proteins/blood , Neuroglia/pathology , Neuroglia/virology , Neurons/pathology , Neurons/virology , Prospective Studies , SARS-CoV-2 , Male , Female , Prognosis
5.
Acta Biomed ; 93(S1): e20222140, 2022 06 29.
Article in English | MEDLINE | ID: covidwho-2002823

ABSTRACT

Different neurological complications associated with the severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection have been widely documented. Acute disseminated encephalomyelitis (ADEM) is a rare immune-mediated demyelinating disorder, described within the spectrum of neurological manifestations of COVID-19. Herein, we describe a case of adult-ADEM presenting with diplopia and slowly progressive ataxia developed one month after SARS-CoV-2 infection. Brain magnetic resonance imaging (MRI) revealed acute multifocal demyelinating lesions throughout the brain. Other possible etiologies have been ruled out. After treatment with high-dose steroids, we observed a progressive clinical and radiological improvement. A 4-months follow-up showed complete clinical recovery. Although extremely rare, ADEM could be associated to SARS-CoV-2 infection and should be considered in the differential diagnosis. Early recognition of this COVID-19 neurological complication, even in the absence of pulmonary involvement, is important to start a prompt immune-modulatory treatment and, consequently, ensure a good outcome.


Subject(s)
COVID-19 , Encephalomyelitis, Acute Disseminated , Nervous System Diseases , Adult , Brain/pathology , COVID-19/complications , Encephalomyelitis, Acute Disseminated/complications , Encephalomyelitis, Acute Disseminated/diagnosis , Humans , Nervous System Diseases/complications , SARS-CoV-2
6.
Genome Med ; 14(1): 94, 2022 08 17.
Article in English | MEDLINE | ID: covidwho-1993378

ABSTRACT

The cerebrospinal fluid (CSF) features a unique immune cell composition and is in constant contact with the brain borders, thus permitting insights into the brain to diagnose and monitor diseases. Recently, the meninges, which are filled with CSF, were identified as a neuroimmunological interface, highlighting the potential of exploring central nervous system (CNS) immunity by studying CNS border compartments. Here, we summarize how single-cell transcriptomics of such border compartments advance our understanding of neurological diseases, the challenges that remain, and what opportunities novel multi-omic methods offer. Single-cell transcriptomics studies have detected cytotoxic CD4+ T cells and clonally expanded T and B cells in the CSF in the autoimmune disease multiple sclerosis; clonally expanded pathogenic CD8+ T cells were found in the CSF and in the brain adjacent to ß-amyloid plaques of dementia patients; in patients with brain metastases, CD8+ T cell clonotypes were shared between the brain parenchyma and the CSF and persisted after therapy. We also outline how novel multi-omic approaches permit the simultaneous measurements of gene expression, chromatin accessibility, and protein in the same cells, which remain to be explored in the CSF. This calls for multicenter initiatives to create single-cell atlases, posing challenges in integrating patients and modalities across centers. While high-dimensional analyses of CSF cells are challenging, they hold potential for personalized medicine by better resolving heterogeneous diseases and stratifying patients.


Subject(s)
CD8-Positive T-Lymphocytes , Multiple Sclerosis , Brain/pathology , Central Nervous System/pathology , Humans , Immunity , Multicenter Studies as Topic
7.
Proc Natl Acad Sci U S A ; 119(35): e2200960119, 2022 08 30.
Article in English | MEDLINE | ID: covidwho-1991765

ABSTRACT

Although increasing evidence confirms neuropsychiatric manifestations associated mainly with severe COVID-19 infection, long-term neuropsychiatric dysfunction (recently characterized as part of "long COVID-19" syndrome) has been frequently observed after mild infection. We show the spectrum of cerebral impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, ranging from long-term alterations in mildly infected individuals (orbitofrontal cortical atrophy, neurocognitive impairment, excessive fatigue and anxiety symptoms) to severe acute damage confirmed in brain tissue samples extracted from the orbitofrontal region (via endonasal transethmoidal access) from individuals who died of COVID-19. In an independent cohort of 26 individuals who died of COVID-19, we used histopathological signs of brain damage as a guide for possible SARS-CoV-2 brain infection and found that among the 5 individuals who exhibited those signs, all of them had genetic material of the virus in the brain. Brain tissue samples from these five patients also exhibited foci of SARS-CoV-2 infection and replication, particularly in astrocytes. Supporting the hypothesis of astrocyte infection, neural stem cell-derived human astrocytes in vitro are susceptible to SARS-CoV-2 infection through a noncanonical mechanism that involves spike-NRP1 interaction. SARS-CoV-2-infected astrocytes manifested changes in energy metabolism and in key proteins and metabolites used to fuel neurons, as well as in the biogenesis of neurotransmitters. Moreover, human astrocyte infection elicits a secretory phenotype that reduces neuronal viability. Our data support the model in which SARS-CoV-2 reaches the brain, infects astrocytes, and consequently, leads to neuronal death or dysfunction. These deregulated processes could contribute to the structural and functional alterations seen in the brains of COVID-19 patients.


Subject(s)
Brain , COVID-19 , Central Nervous System Viral Diseases , SARS-CoV-2 , Astrocytes/pathology , Astrocytes/virology , Brain/pathology , Brain/virology , COVID-19/complications , COVID-19/pathology , Central Nervous System Viral Diseases/etiology , Central Nervous System Viral Diseases/pathology , Humans
8.
Int J Psychophysiol ; 172: 17-23, 2022 02.
Article in English | MEDLINE | ID: covidwho-1956176

ABSTRACT

Cognitive deficits in infants born preterm and infants at term with risk factors for brain damage are a common outcome. Attention deficits in preterm infants are related to the development of attention-deficit/hyperactivity disorder (ADHD), and therefore, there is a need for earlier evaluations and treatment procedures that are implemented before the presence of signs of ADHD. METHODS: We studied preterm (74%) and term infants with the Infant Scale of Selective Attention (ISSA, Escala de Evaluación de la Atención Selectiva (EEAS), in Spanish). This scale evaluates both visual- and auditory-orienting attention. Two groups participated, one with attention deficits (n = 26) and another with regular performance (n = 36). An early attention-stimulation program (EASP) was implemented in the infant group with attention deficits from three to eight months of age. All infants underwent magnetic resonance imaging (MRI), and visual and auditory evoked responses were assessed. RESULTS: All infants had prenatal and perinatal risk factors for brain damage and abnormal MRI findings, and the majority had abnormalities compatible with white matter injury. However, there were four infants with porencephalic cysts; 3 of them were in the treated group. At the beginning of the treatment, ISSA values showed differences between groups. These differences persisted for five months in the visual test and up to the sixth month in the auditory evaluation. Afterward, there were no significant differences, indicating that infants with attention deficits had satisfactorily responded to the treatment. CONCLUSIONS: The ISSA is helpful for the early evaluation of visual and auditory attention. Infants with attention deficits react well enough after six months of EASP.


Subject(s)
Attention Deficit Disorder with Hyperactivity , Brain Injuries , Attention Deficit Disorder with Hyperactivity/diagnosis , Attention Deficit Disorder with Hyperactivity/pathology , Attention Deficit Disorder with Hyperactivity/therapy , Brain/diagnostic imaging , Brain/pathology , Brain Injuries/pathology , Humans , Infant , Infant, Newborn , Infant, Premature/physiology , Magnetic Resonance Imaging/methods , Risk Factors
9.
Clin Neurol Neurosurg ; 220: 107367, 2022 09.
Article in English | MEDLINE | ID: covidwho-1926300

ABSTRACT

OBJECTIVES: Brain dural arteriovenous fistulas(bDAVFs) are anomalous connections between dural arteries and cerebral veins or sinuses. Cerebral venous thrombosis(CVT) often precedes or coincides with bDAVFs and is considered a risk factor for these vascular malformations. Recently, vaccine-induced thrombotic thrombocytopenia causing CVTs has been associated with COVID-19 vaccines. Concurrently with the start of massive vaccination in our region, we have observed a fivefold increase in the average incidence of bDAVFs. Our objective is to raise awareness of the potential involvement of COVID-19 vaccines in the pathogenesis of bDAVF. METHODS: A retrospective review of demographic, clinical, radiological, COVID-19 infection and vaccination data of patients diagnosed with bDAVFs between 2011 and 2021 was conducted. Patients were divided into two cohorts according to their belonging to pre- or post-COVID-19 vaccination times. Cohorts were compared for bDAVFs incidences and demographic and clinical features. RESULTS: Twenty-one bDAVFs were diagnosed between 2011 and 2021, 7 of which in 2021. The mean age was 57.7 years, and 62 % were males. All cases except one were treated; of them, 85 % exclusively managed with surgery. All treated cases were successfully occluded. The incidence in 2021 was significantly higher than that in the prevaccination period (1.72 vs 0.35/100,000/year;p = 0.036; 95 %Confidence Interval=0.09-2.66). Cohorts were not different in age, sex, hemorrhagic presentation, dural sinus thrombosis or presence of prothrombotic or cardiovascular risk factors. CONCLUSION: The significant increase in the incidence of bDAVF following general vaccination policies against COVID-19 observed in our region suggests a potential correlation between these two facts. Our findings need confirmation from larger cohorts and further pathogenic research.


Subject(s)
COVID-19 , Central Nervous System Vascular Malformations , Brain/pathology , COVID-19/epidemiology , COVID-19 Vaccines , Central Nervous System Vascular Malformations/surgery , Cerebral Angiography , Female , Humans , Male , Middle Aged
10.
Eur Neuropsychopharmacol ; 61: 71-77, 2022 08.
Article in English | MEDLINE | ID: covidwho-1914353

ABSTRACT

SARS-CoV-2 is a novel coronavirus that mainly affects the respiratory system. However, clinical manifestations such as neurological symptoms, psychopathological outcomes and brain alterations suggest brain involvement during SARS-CoV-2 infection. Depressive symptoms and cerebral white matter hypodensities/hyperintensities (WMH) have been widely reported in COVID-19 survivors and have been shown to persist after recovery from infection. At the same time viral Infections, including COVID-19, have been shown to lead to oxidative stress. Glutathione (GSH) is the main antioxidant in the brain and reduced GSH levels have been implicated both in COVID-19 and depression. We therefore hypothesise that reduced GSH levels may be associated with depressive symptoms and WMH in COVID-19 survivors. Forty-nine participants (age 18-70) surviving COVID-19 underwent magnetic resonance imaging to measure WMH and brain GSH levels in the ACC, blood sampling to measure systemic inflammation and psychopathological assessment for depressive symptoms. ACC concentrations of GSH inversely associated with both depression scores and the number and volume of WMH. The volume of WMH also positively associated with depressive symptomatology. Finally, systemic inflammation negatively predicted GSH concentration in ACC. In conclusion, we observed overlapping associations of GSH levels in ACC, WMH and severity of depression in COVID-19 survivors, and confirmed the central role of systemic inflammation, thus warranting interest for further study of oxidative stress and antioxidants in the post-acute COVID-19 syndrome.


Subject(s)
COVID-19 , White Matter , Adolescent , Adult , Aged , Brain/diagnostic imaging , Brain/pathology , COVID-19/complications , Depression/diagnostic imaging , Glutathione , Gyrus Cinguli/diagnostic imaging , Humans , Inflammation , Magnetic Resonance Imaging , Middle Aged , SARS-CoV-2 , Survivors , White Matter/diagnostic imaging , White Matter/pathology , Young Adult
12.
Brain ; 145(9): 3203-3213, 2022 09 14.
Article in English | MEDLINE | ID: covidwho-1890882

ABSTRACT

While neuropathological examinations in patients who died from COVID-19 revealed inflammatory changes in cerebral white matter, cerebral MRI frequently fails to detect abnormalities even in the presence of neurological symptoms. Application of multi-compartment diffusion microstructure imaging (DMI), that detects even small volume shifts between the compartments (intra-axonal, extra-axonal and free water/CSF) of a white matter model, is a promising approach to overcome this discrepancy. In this monocentric prospective study, a cohort of 20 COVID-19 inpatients (57.3 ± 17.1 years) with neurological symptoms (e.g. delirium, cranial nerve palsies) and cognitive impairments measured by the Montreal Cognitive Assessment (MoCA test; 22.4 ± 4.9; 70% below the cut-off value <26/30 points) underwent DMI in the subacute stage of the disease (29.3 ± 14.8 days after positive PCR). A comparison of whole-brain white matter DMI parameters with a matched healthy control group (n = 35) revealed a volume shift from the intra- and extra-axonal space into the free water fraction (V-CSF). This widespread COVID-related V-CSF increase affected the entire supratentorial white matter with maxima in frontal and parietal regions. Streamline-wise comparisons between COVID-19 patients and controls further revealed a network of most affected white matter fibres connecting widespread cortical regions in all cerebral lobes. The magnitude of these white matter changes (V-CSF) was associated with cognitive impairment measured by the MoCA test (r = -0.64, P = 0.006) but not with olfactory performance (r = 0.29, P = 0.12). Furthermore, a non-significant trend for an association between V-CSF and interleukin-6 emerged (r = 0.48, P = 0.068), a prominent marker of the COVID-19 related inflammatory response. In 14/20 patients who also received cerebral 18F-FDG PET, V-CSF increase was associated with the expression of the previously defined COVID-19-related metabolic spatial covariance pattern (r = 0.57; P = 0.039). In addition, the frontoparietal-dominant pattern of neocortical glucose hypometabolism matched well to the frontal and parietal focus of V-CSF increase. In summary, DMI in subacute COVID-19 patients revealed widespread volume shifts compatible with vasogenic oedema, affecting various supratentorial white matter tracts. These changes were associated with cognitive impairment and COVID-19 related changes in 18F-FDG PET imaging.


Subject(s)
COVID-19 , White Matter , Brain/diagnostic imaging , Brain/pathology , COVID-19/complications , Edema , Fluorodeoxyglucose F18 , Humans , Prospective Studies , Water , White Matter/diagnostic imaging , White Matter/pathology
13.
Neurol Neurochir Pol ; 56(2): 118-130, 2022.
Article in English | MEDLINE | ID: covidwho-1887304

ABSTRACT

INTRODUCTION: Neuropathological brain and spinal cord post mortem examination is a distinct procedure that still plays an important role in modern medicine. In front of increasing amounts of clinical and genetic data, together with important developments in the field of neuroimaging, the Polish Association of Neuropathologists have updated their recommendations regarding central nervous system (CNS) examination. These guidelines are aimed at neuropathologists, pathologists and clinicians. AIM OF THE STUDY: Presentation of the outlined recommendations as their goal is to improve the quality, informativity, and cost effectiveness of CNS post mortem examinations. A comprehensive study of the literature was conducted to provide a clinical background of neuropathological autopsy. There are numerous open questions in neuroscience, and new strategies are required to foster research in CNS diseases. These include the challenge of organizing brain banks tasked with managing and protecting detailed multidisciplinary information about their resources. Complex neuropathological analyses of post mortem series are also important to assess the effectiveness of diagnostics and therapy, identify environmental impact on the development of neurological disorders, and improve public health policy. The recommendations outline the need for collaboration between multiple specialists to establish the proper diagnosis and to broaden knowledge of neurological disorders.


Subject(s)
Central Nervous System Diseases , Neuropathology , Autopsy/methods , Brain/pathology , Central Nervous System Diseases/pathology , Humans , Neuroimaging
14.
Emerg Microbes Infect ; 11(1): 1572-1585, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-1873822

ABSTRACT

Cryptococcal meningoencephalitis (CM) is emerging as an infection in HIV/AIDS patients shifted from primarily ART-naive to ART-experienced individuals, as well as patients with COVID-19 and immunocompetent hosts. This fungal infection is mainly caused by the opportunistic human pathogen Cryptococcus neoformans. Brain or central nervous system (CNS) dissemination is the deadliest process for this disease; however, mechanisms underlying this process have yet to be elucidated. Moreover, illustrations of clinically relevant responses in cryptococcosis are currently limited due to the low availability of clinical samples. In this study, to explore the clinically relevant responses during C. neoformans infection, macaque and mouse infection models were employed and miRNA-mRNA transcriptomes were performed and combined, which revealed cytoskeleton, a major feature of HIV/AIDS patients, was a centric pathway regulated in both infection models. Notably, assays of clinical immune cells confirmed an enhanced macrophage "Trojan Horse" in patients with HIV/AIDS, which could be shut down by cytoskeleton inhibitors. Furthermore, myocilin, encoded by MYOC, was found to be a novel enhancer for the macrophage "Trojan Horse," and an enhanced fungal burden was achieved in the brains of MYOC-transgenic mice. Taken together, the findings from this study reveal fundamental roles of the cytoskeleton and MYOC in fungal CNS dissemination, which not only helps to understand the high prevalence of CM in HIV/AIDS but also facilitates the development of novel therapeutics for meningoencephalitis caused by C. neoformans and other pathogenic microorganisms.


Subject(s)
COVID-19 , Cryptococcosis , Cryptococcus neoformans , HIV Infections , Meningoencephalitis , MicroRNAs , Animals , Brain/pathology , Cryptococcosis/microbiology , Cryptococcus neoformans/genetics , Disease Models, Animal , Humans , Macaca , Meningoencephalitis/microbiology , Mice , MicroRNAs/genetics , Transcriptome
15.
Am J Case Rep ; 23: e934955, 2022 May 24.
Article in English | MEDLINE | ID: covidwho-1863323

ABSTRACT

BACKGROUND The SARS-CoV-2 viral infection is associated with respiratory and multi-organ systemic disease. It has been shown to affect the central nervous system and produce varied neurological symptoms, including ischemic strokes, seizures, and encephalitis. Neurological manifestations of this viral infection are thought to be due to neurotropic reactions on the central nervous system or post-infectious immune-mediated damage. This report presents a case of bilateral tremor of the upper limbs more than 6 weeks after a diagnosis of COVID-19, with confirmed volumetric brain loss shown by follow-up brain magnetic resonance imaging (MRI) combined with 3-dimensional volumetric NeuroQuant image analysis. CASE REPORT We report a case of new-onset tremors in a 62-year-old man after SARS-CoV-2 infection. MRI of the brain was performed shortly after the onset of tremors, and a follow-up MRI after 2 months showed evidence of rapid parenchymal volume, loss of midbrain substance, and increased cerebrospinal fluid volume within 2 months of the initial examination. CONCLUSIONS This case report shows central neurological effects of COVID-19, which can be evaluated by quantitative volumetric MRI analysis, although further studies are warranted to determine how this type of brain imaging can be used to evaluate the effects of SARS-CoV-2 infection over time.


Subject(s)
COVID-19 , Brain/diagnostic imaging , Brain/pathology , Humans , Male , Middle Aged , SARS-CoV-2 , Tremor/etiology , Tremor/pathology , Upper Extremity
16.
Pract Neurol ; 22(3): 228-230, 2022 Jun.
Article in English | MEDLINE | ID: covidwho-1854394

ABSTRACT

A 73-year-old woman developed cognitive decline over 1 year. MR scan of the brain showed a focal asymmetrical leukoencephalopathy involving the right frontal, temporal, parietal and occipital lobes. Extensive laboratory investigations found no cause but brain biopsy identified amyloid-beta-related angiitis (ABRA), a potentially treatable cause of rapid-onset dementia. We gave intravenous methylprednisolone and then two courses of intravenous cyclophosphamide, after which her cognitive skills gradually but significantly improved over several months.


Subject(s)
Dementia , Vasculitis , Aged , Amyloid beta-Peptides/metabolism , Biopsy , Brain/pathology , Dementia/complications , Dementia/diagnostic imaging , Dementia/drug therapy , Female , Humans , Vasculitis/pathology
17.
Indian J Pathol Microbiol ; 65(Supplement): S146-S152, 2022 May.
Article in English | MEDLINE | ID: covidwho-1847488

ABSTRACT

The COVID-19 pandemic has placed global health care systems under unprecedented strain but has, at the same time, provided a unique opportunity for pathologists to turn autopsy findings into directly actionable insights into patient care. The current data on the neuropathology of COVID-19 remains preliminary and is limited by the lack of suitable controls, but certain tentative conclusions can be drawn. SARS-CoV-2 can infect multiple cell types in the central nervous system and does so in a subset of patients, although the clinical significance of direct infections remains in the central nervous system (CNS) and the peripheral nervous system (PNS) infections remains unclear. The best-described neuropathological manifestations of COVID-19 in the brain are variable patterns of neuroinflammation and vascular injury, although again, it remains unclear to what degree these findings are specifically due to COVID-19. There is also intriguing preliminary data to suggest a complex relationship between COVID-19 and neurodegeneration, with certain alleles that increase AD risk also increasing the risk of severe COVID-19, and conversely, the possibility that COVID-19 may increase the risk of neurodegenerative disease. The neuropathology of so-called "long-COVID" and the potential effects of COVID-19, or critical illness in general, on neurodegenerative disease remains unclear. There is thus an urgent need for long-term cohort studies of COVID-19 survivors, including brain donation, particularly in elderly patients, with careful recruitment of controls with similar non-COVID inflammatory illnesses.


Subject(s)
COVID-19 , Neurodegenerative Diseases , Aged , Brain/pathology , Humans , Neurodegenerative Diseases/pathology , Pandemics , SARS-CoV-2
18.
J Med Virol ; 94(6): 2860-2869, 2022 06.
Article in English | MEDLINE | ID: covidwho-1813544

ABSTRACT

Progressive multifocal leukoencephalopathy (PML), a demyelinating disease of the brain, caused by the John Cunningham virus (JCV) is usually seen in patients who are immunocompromised. Here, we describe a case of an immunocompetent patient diagnosed with PML and a comprehensive literature review. A 64-year-old Caucasian male presented with acute worsening of progressive neurological decline with difficulty in vision and reading. Based on history, examination, cerebrospinal fluid markers, histopathology, and magnetic resonance imaging brain at the time of presentation diagnosed the patient with PML in a setting of no immunosuppression disorder. The patient was started on Pelfilgrastim with significant systematic improvement. In our literature review, it was seen that the average age of symptom presentation was 57.5 with predominance in males. Most of the patients presented with progressive neurological deficits with symptomology ranging from mild confusion, aphasia, anxiety to sensory disturbances with numbness, hemiparesis, and hemianopsia. Out of the 21 cases, patients responded to mirtazapine and intravenous pulse methylprednisolone (IVMP). The mortality rate was close to 50% with 11 fatal cases and 10 nonfatal cases. Our case and literature review demonstrate the possibility that PML may very rarely occur in patients that are immunocompetent. Furthermore, our review showed that patients responded well to mirtazapine and IVMP. We also want to highlight that the mortality rate was lower in this review and was only compared to mortality in PML associated with immunocompromised status.


Subject(s)
JC Virus , Leukoencephalopathy, Progressive Multifocal , Brain/diagnostic imaging , Brain/pathology , Humans , Leukoencephalopathy, Progressive Multifocal/diagnostic imaging , Leukoencephalopathy, Progressive Multifocal/drug therapy , Magnetic Resonance Imaging/adverse effects , Male , Middle Aged , Mirtazapine/therapeutic use
20.
J Neuroradiol ; 49(6): 428-430, 2022 Nov.
Article in English | MEDLINE | ID: covidwho-1768429

ABSTRACT

BACKGROUND: Various neurological sequalae have been described following COVID-19 vaccination. Here we describe the first case of untreated post COVID-19 vaccine encephalitis with spontaneous resolution of contrast enhancing hyperintensities on MRI concomitant with clinical improvement. CASE PRESENTATION: A 59-year-old woman presented with a two-day history of unsteady gait, incoordination, visual symptoms, and lethargy. She had received AZD1222 (AstraZeneca) and mRNA-1273 (Moderna) COVID-19 vaccines at 3 months and 12 days, respectively, before presentation. Brain MRI showed no abnormality on the non-enhanced sequences, but numerous enhancing lesions in the cerebral cortex, deep grey matter, brainstem, and cerebellum. Treatment was expectant, the patient improved clinically over 10 days, and repeat MRI showed near complete resolution of the imaging abnormality. CONCLUSIONS: We describe neurological deterioration 12 days after a second dose of COVID-19 vaccine. There was no evidence of edema or demyelinating lesions in the brain on MRI, but there was extensive contrast-enhancement indicating loss of blood-brain barrier (BBB) integrity. This provides a potential in vivo, clinical-imaging correlate of the post-mortem evidence that SARS-CoV-2 spike protein may induce loss of BBB permeability. While this adds to the list of rare adverse neurological reactions to COVID-19 vaccination, the benefits of receiving the vaccine far outweigh these risks.


Subject(s)
COVID-19 Vaccines , COVID-19 , Female , Humans , Middle Aged , COVID-19 Vaccines/adverse effects , COVID-19/prevention & control , SARS-CoV-2 , ChAdOx1 nCoV-19 , Magnetic Resonance Imaging , Vaccination , Brain/diagnostic imaging , Brain/pathology
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