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1.
Ann Neurol ; 91(3): 367-379, 2022 03.
Article in English | MEDLINE | ID: covidwho-1636023

ABSTRACT

OBJECTIVE: The purpose of this study was to describe cerebrovascular, neuropathic, and autonomic features of post-acute sequelae of coronavirus disease 2019 ((COVID-19) PASC). METHODS: This retrospective study evaluated consecutive patients with chronic fatigue, brain fog, and orthostatic intolerance consistent with PASC. Controls included patients with postural tachycardia syndrome (POTS) and healthy participants. Analyzed data included surveys and autonomic (Valsalva maneuver, deep breathing, sudomotor, and tilt tests), cerebrovascular (cerebral blood flow velocity [CBFv] monitoring in middle cerebral artery), respiratory (capnography monitoring), and neuropathic (skin biopsies for assessment of small fiber neuropathy) testing and inflammatory/autoimmune markers. RESULTS: Nine patients with PASC were evaluated 0.8 ± 0.3 years after a mild COVID-19 infection, and were treated as home observations. Autonomic, pain, brain fog, fatigue, and dyspnea surveys were abnormal in PASC and POTS (n = 10), compared with controls (n = 15). Tilt table test reproduced the majority of PASC symptoms. Orthostatic CBFv declined in PASC (-20.0 ± 13.4%) and POTS (-20.3 ± 15.1%), compared with controls (-3.0 ± 7.5%, p = 0.001) and was independent of end-tidal carbon dioxide in PASC, but caused by hyperventilation in POTS. Reduced orthostatic CBFv in PASC included both subjects without (n = 6) and with (n = 3) orthostatic tachycardia. Dysautonomia was frequent (100% in both PASC and POTS) but was milder in PASC (p = 0.002). PASC and POTS cohorts diverged in frequency of small fiber neuropathy (89% vs 60%) but not in inflammatory markers (67% vs 70%). Supine and orthostatic hypocapnia was observed in PASC. INTERPRETATION: PASC following mild COVID-19 infection is associated with multisystem involvement including: (1) cerebrovascular dysregulation with persistent cerebral arteriolar vasoconstriction; (2) small fiber neuropathy and related dysautonomia; (3) respiratory dysregulation; and (4) chronic inflammation. ANN NEUROL 2022;91:367-379.


Subject(s)
Blood Pressure/physiology , COVID-19/complications , Cerebrovascular Circulation/physiology , Heart Rate/physiology , Inflammation Mediators/blood , Adult , COVID-19/blood , COVID-19/diagnosis , COVID-19/physiopathology , Fatigue/blood , Fatigue/diagnosis , Fatigue/physiopathology , Female , Humans , Male , Middle Aged , Orthostatic Intolerance/blood , Orthostatic Intolerance/diagnosis , Orthostatic Intolerance/physiopathology , Retrospective Studies
2.
J Clin Invest ; 131(8)2021 04 15.
Article in English | MEDLINE | ID: covidwho-1291498

ABSTRACT

BACKGROUNDThe coronavirus disease 2019 (COVID-19) rapidly progressed to a global pandemic. Although some patients totally recover from COVID-19 pneumonia, the disease's long-term effects on the brain still need to be explored.METHODSWe recruited 51 patients with 2 subtypes of COVID-19 (19 mild and 32 severe) with no specific neurological manifestations at the acute stage and no obvious lesions on the conventional MRI 3 months after discharge. Changes in gray matter morphometry, cerebral blood flow (CBF), and white matter (WM) microstructure were investigated using MRI. The relationship between brain imaging measurements and inflammation markers was further analyzed.RESULTSCompared with healthy controls, the decrease in cortical thickness/CBF and the changes in WM microstructure were more severe in patients with severe disease than in those with mild disease, especially in the frontal and limbic systems. Furthermore, changes in brain microstructure, CBF, and tract parameters were significantly correlated (P < 0.05) with the inflammatory markers C-reactive protein, procalcitonin, and interleukin 6.CONCLUSIONIndirect injury related to inflammatory storm may damage the brain, altering cerebral volume, CBF, and WM tracts. COVID-19-related hypoxemia and dysfunction of vascular endothelium may also contribute to neurological changes. The abnormalities in these brain areas need to be monitored during recovery, which could help clinicians understand the potential neurological sequelae of COVID-19.FUNDINGNatural Science Foundation of China.


Subject(s)
COVID-19/diagnostic imaging , Cerebrovascular Circulation/physiology , SARS-CoV-2 , Aged , Brain/blood supply , Brain/diagnostic imaging , Brain/pathology , C-Reactive Protein/metabolism , COVID-19/epidemiology , COVID-19/physiopathology , Case-Control Studies , China/epidemiology , Diffusion Tensor Imaging , Echo-Planar Imaging , Female , Follow-Up Studies , Gray Matter/diagnostic imaging , Gray Matter/pathology , Humans , Imaging, Three-Dimensional , Inflammation Mediators/blood , Interleukin-6/blood , Male , Middle Aged , Neuroimaging , Pandemics , Procalcitonin/blood , Severity of Illness Index , Time Factors , White Matter/diagnostic imaging , White Matter/pathology
3.
J Clin Invest ; 131(8)2021 04 15.
Article in English | MEDLINE | ID: covidwho-1186424

ABSTRACT

BACKGROUNDThe coronavirus disease 2019 (COVID-19) rapidly progressed to a global pandemic. Although some patients totally recover from COVID-19 pneumonia, the disease's long-term effects on the brain still need to be explored.METHODSWe recruited 51 patients with 2 subtypes of COVID-19 (19 mild and 32 severe) with no specific neurological manifestations at the acute stage and no obvious lesions on the conventional MRI 3 months after discharge. Changes in gray matter morphometry, cerebral blood flow (CBF), and white matter (WM) microstructure were investigated using MRI. The relationship between brain imaging measurements and inflammation markers was further analyzed.RESULTSCompared with healthy controls, the decrease in cortical thickness/CBF and the changes in WM microstructure were more severe in patients with severe disease than in those with mild disease, especially in the frontal and limbic systems. Furthermore, changes in brain microstructure, CBF, and tract parameters were significantly correlated (P < 0.05) with the inflammatory markers C-reactive protein, procalcitonin, and interleukin 6.CONCLUSIONIndirect injury related to inflammatory storm may damage the brain, altering cerebral volume, CBF, and WM tracts. COVID-19-related hypoxemia and dysfunction of vascular endothelium may also contribute to neurological changes. The abnormalities in these brain areas need to be monitored during recovery, which could help clinicians understand the potential neurological sequelae of COVID-19.FUNDINGNatural Science Foundation of China.


Subject(s)
COVID-19/diagnostic imaging , Cerebrovascular Circulation/physiology , SARS-CoV-2 , Aged , Brain/blood supply , Brain/diagnostic imaging , Brain/pathology , C-Reactive Protein/metabolism , COVID-19/epidemiology , COVID-19/physiopathology , Case-Control Studies , China/epidemiology , Diffusion Tensor Imaging , Echo-Planar Imaging , Female , Follow-Up Studies , Gray Matter/diagnostic imaging , Gray Matter/pathology , Humans , Imaging, Three-Dimensional , Inflammation Mediators/blood , Interleukin-6/blood , Male , Middle Aged , Neuroimaging , Pandemics , Procalcitonin/blood , Severity of Illness Index , Time Factors , White Matter/diagnostic imaging , White Matter/pathology
4.
Curr Pain Headache Rep ; 25(3): 19, 2021 Feb 25.
Article in English | MEDLINE | ID: covidwho-1100995

ABSTRACT

PURPOSE OF REVIEW: This review provides an updated discussion on the clinical presentation, diagnosis and radiographic features, mechanisms, associations and epidemiology, treatment, and prognosis of posterior reversible encephalopathy syndrome (PRES). Headache is common in PRES, though headache associated with PRES was not identified as a separate entity in the 2018 International Classification of Headache Disorders. Here, we review the relevant literature and suggest criteria for consideration of its inclusion. RECENT FINDINGS: COVID-19 has been identified as a potential risk factor for PRES, with a prevalence of 1-4% in patients with SARS-CoV-2 infection undergoing neuroimaging, thus making a discussion of its identification and treatment particularly timely given the ongoing global pandemic at the time of this writing. PRES is a neuro-clinical syndrome with specific imaging findings. The clinical manifestations of PRES include headache, seizures, encephalopathy, visual disturbances, and focal neurologic deficits. Associations with PRES include renal failure, preeclampsia and eclampsia, autoimmune conditions, and immunosuppression. PRES is theorized to be a syndrome of disordered autoregulation and endothelial dysfunction resulting in preferential hyperperfusion of the posterior circulation. Treatment typically focuses on treating the underlying cause and removal of the offending agents.


Subject(s)
Endothelium/physiopathology , Headache/physiopathology , Posterior Leukoencephalopathy Syndrome/physiopathology , Seizures/physiopathology , Vision Disorders/physiopathology , Acute Chest Syndrome/epidemiology , Aminolevulinic Acid/analogs & derivatives , Anemia, Sickle Cell/epidemiology , Autoimmune Diseases/epidemiology , Blood-Brain Barrier/metabolism , Brain Edema/diagnostic imaging , Brain Edema/physiopathology , COVID-19/epidemiology , Cerebrovascular Circulation/physiology , Cytokines/metabolism , Eclampsia/epidemiology , Female , Homeostasis/physiology , Humans , Hypertension/physiopathology , Magnetic Resonance Imaging , Posterior Leukoencephalopathy Syndrome/diagnostic imaging , Posterior Leukoencephalopathy Syndrome/epidemiology , Posterior Leukoencephalopathy Syndrome/therapy , Pre-Eclampsia/epidemiology , Pregnancy , Prognosis , Renal Insufficiency/epidemiology , SARS-CoV-2 , Vasospasm, Intracranial/physiopathology
5.
Stroke ; 52(1): 260-270, 2021 01.
Article in English | MEDLINE | ID: covidwho-916325

ABSTRACT

BACKGROUND AND PURPOSE: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is associated with an increased rate of cerebrovascular events including ischemic stroke and intracerebral hemorrhage. The mechanisms underlying cerebral endothelial susceptibility and response to SARS-CoV-2 are unknown yet critical to understanding the association of SARS-CoV-2 infection with cerebrovascular events. METHODS: Endothelial cells were isolated from human brain and analyzed by RNA sequencing. Human umbilical vein and human brain microvascular cells were used in both monolayer culture and endothelialized within a 3-dimensional printed vascular model of the middle cerebral artery. Gene expression levels were measured by quantitative polymerase chain reaction and direct RNA hybridization. Recombinant SARS-CoV-2 S protein and S protein-containing liposomes were used to measure endothelial binding by immunocytochemistry. RESULTS: ACE2 (angiotensin-converting enzyme-2) mRNA levels were low in human brain and monolayer endothelial cell culture. Within the 3-dimensional printed vascular model, ACE2 gene expression and protein levels were progressively increased by vessel size and flow rates. SARS-CoV-2 S protein-containing liposomes were detected in human umbilical vein endothelial cells and human brain microvascular endothelial cells in 3-dimensional middle cerebral artery models but not in monolayer culture consistent with flow dependency of ACE2 expression. Binding of SARS-CoV-2 S protein triggered 83 unique genes in human brain endothelial cells including upregulation of complement component C3. CONCLUSIONS: Brain endothelial cells are susceptible to direct SARS-CoV-2 infection through flow-dependent expression of ACE2. Viral S protein binding triggers a unique gene expression profile in brain endothelia that may explain the association of SARS-CoV-2 infection with cerebrovascular events.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/virology , Endothelial Cells/virology , SARS-CoV-2/metabolism , Spike Glycoprotein, Coronavirus/metabolism , Transcriptome , Brain/metabolism , Brain/virology , COVID-19/metabolism , Cells, Cultured , Cerebrovascular Circulation/physiology , Endothelial Cells/metabolism , Humans , Models, Anatomic , Stress, Mechanical
6.
Turk J Med Sci ; 51(2): 435-439, 2021 04 30.
Article in English | MEDLINE | ID: covidwho-836298

ABSTRACT

Background/aim: Coronavirus 2019 disease (Covid-19) was first seen in December 2019 and afterwards it became pandemic. Several systemic involvements have been reported in Covid-19 patients. In this study, it was aimed to investigate the cerebrovascular hemodynamics in patients with Covid-19. Materials and methods: The sample of this study included 20 patients hospitalized in our clinic diagnosed with Covid-19 via PCR modality and 20 healthy volunteers of similar age and sex. Bilateral middle cerebral arteries were investigated with transcranial Doppler ultrasonography. Basal cerebral blood flow velocities and vasomotor reactivity rates were determined and statistically compared. Results: When patient and control groups were compared, the mean blood flow velocity was found to be higher in Covid-19 patients than in the healthy volunteers and it was statistically significant (P = 0.00). The mean vasomotor reactivity rates values were found to be lower in the Covid-19 group than the healthy group and was also statistically significant (P = 0.00). Conclusion: An increase in basal cerebral blood velocity and a decrease in vasomotor reactivity rates in patients with Covid-19 can be considered as an indicator of dysfunction of cerebral hemodynamics in the central nervous system and this can be evaluated as a result of endothelial dysfunction.


Subject(s)
Blood Flow Velocity/physiology , COVID-19/physiopathology , Cerebrovascular Circulation/physiology , Hemodynamics/physiology , Middle Cerebral Artery/physiopathology , Vasomotor System/physiopathology , Adult , Aged , Aged, 80 and over , COVID-19/diagnostic imaging , Case-Control Studies , Female , Humans , Male , Middle Aged , Middle Cerebral Artery/diagnostic imaging , SARS-CoV-2 , Ultrasonography, Doppler, Transcranial , Vasomotor System/diagnostic imaging , Young Adult
7.
Neuroepidemiology ; 54(5): 370-374, 2020.
Article in English | MEDLINE | ID: covidwho-713643

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) causes the coronavirus disease 2019 (COVID-19). It quickly became pandemic, and so did a new concern about COVID-19 infections increasing the risk for cerebrovascular diseases. There is an association between COVID-19 illness in people and acute stroke. Several chemical, mechanical, and/or inflammatory central nervous system pathologies are proposed to explain how this viral infection might induce acute cerebrovascular disease. Timely available evaluation and/or intervention is imperative for patients with concerns about acute cerebrovascular issues.


Subject(s)
Betacoronavirus , Brain/virology , Cerebrovascular Circulation/physiology , Coronavirus Infections/complications , Pneumonia, Viral/complications , Stroke/etiology , Stroke/virology , Betacoronavirus/metabolism , Brain/metabolism , Brain Ischemia/etiology , Brain Ischemia/metabolism , Brain Ischemia/virology , COVID-19 , Coronavirus Infections/metabolism , Humans , Pandemics , Pneumonia, Viral/metabolism , SARS-CoV-2 , Stroke/metabolism
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