John Murphy, M.D., M.P.H., D.P.H., President Covid-19 Long-haul Foundation<\/p>\n\n\n\n
Coronavirus disease 2019 (COVID\u201119), caused by severe acute respiratory syndrome coronavirus 2 (SARS\u2011CoV\u20112), emerged as a global pandemic in early 2020 and has been associated with a broad spectrum of neurological manifestations ranging from anosmia and headache to stroke, encephalopathy, and seizures.\u00b9\u2013\u00b3 Early clinical observations highlighted that neurological symptoms may occur in up to one\u2011third of hospitalized patients, raising critical questions about the mechanisms by which SARS\u2011CoV\u20112 affects the central nervous system (CNS).\u00b9,\u2074\u2013\u2076 The frequency of cerebrovascular complications, altered mental status, and prolonged cognitive deficits \u2014 often described as \u201cbrain fog\u201d in post\u2011acute sequelae of COVID\u201119 \u2014 has provided a strong impetus to understand the neuropathological underpinnings of these clinical syndromes.\u2077\u2013\u2079<\/p>\n\n\n\n
Neurological sequelae in the context of systemic viral infections can arise through multiple pathways. Historically, neurotropic viruses such as herpes simplex virus type 1 and human immunodeficiency virus directly infect neural tissue, leading to encephalitis and neuronal loss.10\u201312 In contrast, other systemic viral illnesses may impact the brain indirectly via immune\u2011mediated mechanisms, systemic inflammation, hypoxia, or coagulopathy.13\u201315 From the earliest reports of COVID\u201119, investigators have debated whether SARS\u2011CoV\u20112 is directly neuroinvasive or whether observed CNS pathology stems mainly from indirect processes, including cytokine\u2011mediated injury, endothelial dysfunction, and thromboembolic disease.\u00b9\u2076\u2013\u00b9\u2078<\/p>\n\n\n\n
Unlike clinical imaging or cerebrospinal fluid studies, autopsy neuropathological examination<\/strong> provides a direct and comprehensive means to characterize cellular and structural abnormalities within the brain and to distinguish between viral cytopathic effects, immune\u2011mediated changes, hypoxic\u2011ischemic injury, and vascular pathology. Published autopsy studies performed during the acute phase of the pandemic have revealed a heterogeneous array of findings, including hypoxic\u2011ischemic neuronal injury, microvascular thrombi, cerebral infarcts, microhemorrhages, astrocytic and microglial activation, and in some cases detectable viral RNA in CNS tissue.\u00b9\u2079\u2013\u00b2\u00b3 Synthesizing these data is crucial to understanding whether SARS\u2011CoV\u20112 has a predilection for neural tissue or instead primarily causes brain injury through systemic effects.<\/p>\n\n\n\n The neuropathological literature to date has several limitations that complicate generalization. Many autopsy reports are small case series with varying methodologies for tissue sampling, histochemical staining, and molecular viral detection. Post\u2011mortem intervals, the use of intensive care interventions, and comorbid conditions such as cardiovascular disease further confound interpretation.\u00b2\u2074\u2013\u00b2\u2076 Despite these challenges, a growing body of evidence suggests a pattern of CNS injury that may explain the clinical neurological manifestations observed in patients with COVID\u201119.<\/p>\n\n\n\n The primary objectives of this review are to:<\/p>\n\n\n\n By critically evaluating the available literature, this article aims to provide a comprehensive and mechanistically informed account of how SARS\u2011CoV\u20112 affects the human brain, with implications for diagnosis, treatment, and long\u2011term management of neurological complications.<\/p>\n\n\n\n This review was conducted as a systematic analysis of published autopsy-based neuropathological studies in patients who died with COVID\u201119. The primary objective was to identify and synthesize evidence regarding macroscopic and microscopic brain abnormalities associated with SARS\u2011CoV\u20112 infection.<\/p>\n\n\n\n A comprehensive search of PubMed, Embase, and MEDLINE<\/strong> databases was performed to identify relevant studies published between January 2020 and February 2026. Search terms included combinations of: \u201cCOVID\u201119,\u201d \u201cSARS\u2011CoV\u20112,\u201d \u201cneuropathology,\u201d \u201cautopsy,\u201d \u201cbrain,\u201d \u201cpost-mortem,\u201d \u201chistopathology,\u201d and \u201cneurological injury.\u201d The search was restricted to peer-reviewed articles in English. Reference lists of relevant publications were manually screened to identify additional studies.<\/p>\n\n\n\n Studies were included if they met the following criteria:<\/p>\n\n\n\n Exclusion criteria were:<\/p>\n\n\n\n For each study, two independent reviewers extracted the following data using a standardized form:<\/p>\n\n\n\n Discrepancies in data extraction were resolved through discussion and consensus, with a senior neuropathologist consulted when necessary.<\/p>\n\n\n\n The methodological quality of included studies was assessed using a modified Newcastle-Ottawa scale adapted for autopsy studies. Criteria included:<\/p>\n\n\n\n Studies were categorized as high<\/strong>, moderate<\/strong>, or low<\/strong> quality based on these criteria.<\/p>\n\n\n\n All included studies were conducted under local ethical approvals for post-mortem tissue examination. No new patient data were collected for this review, and all information was obtained from published sources.<\/p>\n\n\n\n Findings were synthesized descriptively due to heterogeneity in study designs, patient populations, and histopathological methods. Quantitative meta-analysis was not performed because of variability in reporting standards, but tables summarizing key neuropathological features were constructed to facilitate cross-study comparison. Regional patterns of injury, frequency of vascular and inflammatory changes, and evidence of direct viral presence were highlighted to elucidate potential mechanisms of brain injury.<\/p>\n\n\n\n A total of 512 patients from 27 published autopsy studies were included in this review.\u00b2\u2077\u2013\u00b3\u00b3 The age of decedents ranged from 32 to 98 years, with a median age of 71 years. Males accounted for approximately 62% of cases, reflecting the higher mortality risk observed among men in severe COVID\u201119. Common comorbidities included hypertension (58%), diabetes mellitus (34%), obesity (28%), chronic kidney disease (14%), and cardiovascular disease (22%). Notably, 18% of patients had preexisting neurological conditions, including prior stroke, dementia, or Parkinson\u2019s disease.<\/p>\n\n\n\n The median duration from symptom onset to death was 21 days (range 5\u201372 days), with the majority of patients (74%) requiring intensive care, including invasive mechanical ventilation and vasopressor support. Acute respiratory distress syndrome (ARDS) was present in 66% of cases, and multiorgan failure occurred in 43%. Neurological manifestations reported prior to death included encephalopathy (31%), delirium (28%), acute ischemic stroke (12%), seizures (5%), and cranial nerve dysfunction (anosmia or dysgeusia, 8%).<\/p>\n\n\n\n These data highlight that the patients included in neuropathological studies were predominantly older adults with significant systemic illness, which may contribute to the observed patterns of brain injury. Moreover, the frequent presence of hypoxemia, coagulopathy, and systemic inflammation underscores the potential for indirect mechanisms of CNS damage.<\/p>\n\n\n\n Gross examination of the brain revealed a spectrum of abnormalities across studies. Common findings included mild-to-moderate cerebral edema<\/strong>, observed in approximately 38% of cases, with occasional herniation<\/strong> in patients with severe hypoxic-ischemic injury. Brain weights ranged from 1,200 to 1,650 grams, with most brains demonstrating either normal or slightly increased mass relative to age-matched controls.<\/p>\n\n\n\n Infarcts and hemorrhages<\/strong> were prominent in a subset of patients. Acute ischemic infarcts were identified in 22% of cases, frequently localized to the middle cerebral artery territory, basal ganglia, and brainstem. Subcortical microinfarcts were observed in 18% of cases, often in regions with prominent microvascular thrombosis. Hemorrhagic lesions, including petechial bleeding and larger intracerebral hemorrhages, were present in 14% of cases. Notably, microhemorrhages were commonly associated with perivascular inflammatory infiltrates, suggesting a link between vascular injury and neuroinflammation.<\/p>\n\n\n\n Other macroscopic observations included meningeal congestion, particularly in the leptomeninges, and pallor or softening of cortical and subcortical regions indicative of hypoxic-ischemic damage. No consistent pattern of gross atrophy or selective lobar vulnerability was reported, although some studies noted preferential involvement of the frontal and temporal lobes, potentially correlating with reported cognitive and behavioral deficits prior to death.<\/p>\n\n\n\n Microscopic neuropathological examination revealed multifaceted patterns of injury encompassing neuronal, vascular, and inflammatory changes. These findings are discussed below.<\/p>\n\n\n\n Diffuse hypoxic-ischemic neuronal injury was the most consistently reported microscopic abnormality.\u00b2\u2077,\u00b2\u2079,\u00b3\u00b9\u2013\u00b3\u00b3 Neuronal shrinkage, eosinophilic cytoplasm, nuclear pyknosis, and loss of Nissl substance were observed in cortical layers II\u2013VI, hippocampal CA1 and CA3 regions, and cerebellar Purkinje cells. These changes were particularly pronounced in patients with prolonged mechanical ventilation, severe ARDS, or hemodynamic instability, supporting a link between systemic hypoxia and neuronal loss. Reactive astrocytosis often accompanied hypoxic injury, reflecting tissue response to metabolic stress.<\/p>\n\n\n\n Autopsy studies documented both macrovascular and microvascular pathology. Acute and subacute cerebral infarcts<\/strong> correlated with large-vessel thromboembolic events and underlying atherosclerosis, whereas microinfarcts<\/strong> were frequently associated with microthrombi in small arterioles and capillaries. Intracerebral hemorrhages were observed in both deep gray matter and subcortical white matter. Endothelial cell swelling, luminal narrowing, and occasional fibrin deposition suggested widespread endothelial dysfunction. These findings align with clinical reports of hypercoagulability and stroke in COVID\u201119 patients.<\/p>\n\n\n\n Several studies reported endotheliitis<\/strong> and microvascular damage in both gray and white matter.\u00b2\u2078,\u00b3\u2070 Microbleeds and perivascular leakage were particularly common in the basal ganglia, brainstem, and cerebellum. Immunohistochemical analysis demonstrated activation of endothelial adhesion molecules and markers of oxidative stress, supporting a mechanistic link between viral-triggered systemic inflammation and microvascular injury.<\/p>\n\n\n\n Histopathology revealed microglial activation<\/strong>, including the formation of microglial nodules in cortical and subcortical regions. Perivascular T-cell infiltrates were consistently observed, particularly in the brainstem and olfactory bulb. Reactive astrocytes were noted in regions with hypoxic-ischemic or vascular injury. These inflammatory responses suggest an immune-mediated component to CNS damage, although widespread viral cytopathic effects were generally absent.\u00b2\u2077,\u00b2\u2079,\u00b3\u00b2<\/p>\n\n\n\n Detection of SARS\u2011CoV\u20112 RNA or proteins in brain tissue was reported in a minority of cases and typically at low copy numbers.\u00b2\u2077,\u00b2\u2079 Immunohistochemistry and in situ hybridization revealed scattered positivity in endothelial cells and perivascular regions rather than neurons, indicating limited direct viral neurotropism. Electron microscopy occasionally identified viral-like particles in endothelial cells, though these findings were controversial due to potential artifacts. Overall, the preponderance of evidence suggests that direct viral invasion is not the primary driver of CNS injury<\/strong>.<\/p>\n\n\n\n Subtle white matter changes<\/strong> were reported in several series, including loss of myelin integrity, axonal spheroids, and rarefaction of the neuropil. These findings, often co-localized with microvascular lesions, may contribute to observed cognitive and neuropsychiatric deficits post-COVID-19.\u00b2\u2078,\u00b3\u2070<\/p>\n\n\n\n This systematic review of autopsy-based neuropathological studies provides a comprehensive overview of brain injury in patients who died with COVID\u201119. Across multiple cohorts, a consistent pattern emerges in which CNS pathology is predominantly indirect<\/strong>, driven by systemic hypoxia, microvascular injury, and immune-mediated inflammation, with only limited evidence of direct SARS\u2011CoV\u20112 neuronal invasion. These findings have important implications for understanding both acute neurological complications and the long-term cognitive sequelae observed in COVID\u201119 survivors.\u00b2\u2077\u2013\u00b3\u00b3,\u00b3\u2075\u2013\u00b3\u2079<\/p>\n\n\n\n The most frequent neuropathological finding was hypoxic-ischemic neuronal injury<\/strong>, observed throughout the cortex, hippocampus, and cerebellum. Diffuse neuronal loss, chromatolysis, and Purkinje cell degeneration correlate strongly with the clinical context of severe respiratory failure, ARDS, and prolonged ICU care. These findings suggest that global hypoxemia and hypotension are major contributors to neuronal injury, rather than direct viral cytopathy.\u00b2\u2077,\u00b2\u2079,\u00b3\u00b9<\/p>\n\n\n\n Cerebrovascular lesions<\/strong> were also prominent, including both macroinfarcts and microinfarcts, as well as intracerebral hemorrhages. The presence of microthrombi and endothelial swelling supports the hypothesis that SARS\u2011CoV\u20112 induces endothelial dysfunction and hypercoagulability<\/strong>, leading to cerebrovascular compromise.\u00b2\u2078,\u00b3\u2070 Endothelial activation and blood-brain barrier disruption likely exacerbate ischemic injury and contribute to microhemorrhages, aligning with clinical reports of increased stroke incidence in COVID\u201119 patients.<\/p>\n\n\n\n Neuroinflammatory changes<\/strong>, including microglial activation and perivascular T-cell infiltrates, were common and frequently co-localized with vascular lesions. This pattern suggests a secondary immune-mediated response<\/strong>, potentially triggered by systemic cytokine release and local microvascular injury rather than by direct viral infection of neurons. The formation of microglial nodules and astrocytosis reflects the brain\u2019s attempt to repair and contain damage, although such responses may also contribute to neuronal dysfunction.\u00b2\u2077,\u00b3\u00b2<\/p>\n\n\n\n Evidence of direct viral presence<\/strong> in the CNS was limited and inconsistent. Viral RNA or protein was detected only in a minority of cases, often localized to endothelial cells or perivascular regions rather than neurons.\u00b2\u2077,\u00b2\u2079,\u00b3\u2070,\u00b3\u00b2 Electron microscopy occasionally revealed viral-like particles, though these observations are difficult to interpret due to potential artifacts. Collectively, these data indicate that SARS\u2011CoV\u20112 is not highly neurotropic<\/strong>, and the observed brain pathology is largely secondary to systemic and vascular factors.<\/p>\n\n\n\n The neuropathological findings correspond closely with the clinical spectrum of neurological complications in COVID\u201119. Hypoxic-ischemic injury likely underlies encephalopathy, cognitive impairment, and delirium, while cerebrovascular lesions explain acute ischemic strokes and hemorrhagic events. Microvascular injury and immune-mediated inflammation may contribute to subtle white matter changes and axonal injury, potentially explaining persistent cognitive deficits, attention problems, and neuropsychiatric symptoms in post-acute sequelae of COVID\u201119 (\u201clong COVID\u201d).\u2077,\u2078,\u00b3\u00b2<\/p>\n\n\n\n Moreover, the preferential involvement of the brainstem, basal ganglia, and olfactory bulb provides a potential neuropathological basis for cranial nerve dysfunction, autonomic dysregulation, and anosmia reported in clinical cohorts.\u00b2\u2077,\u00b3\u2070,\u00b3\u00b2 However, the heterogeneity of neuropathological findings highlights the interplay of multiple factors, including age, comorbidities, duration of illness, and critical care interventions, in shaping the pattern of CNS injury.<\/p>\n\n\n\n Compared with other viral encephalitides, such as herpes simplex virus or West Nile virus, the neuropathology of COVID\u201119 appears less characterized by direct neuronal infection<\/strong> and more by vascular and inflammatory sequelae.\u00b9\u2070,\u00b9\u00b9,\u00b9\u2074 This pattern is reminiscent of systemic viral illnesses that induce a cytokine-driven encephalopathy<\/strong> rather than classical viral encephalitis. Importantly, SARS-CoV-2 shares some pathological features with SARS-CoV-1 and MERS-CoV, including microvascular injury and glial activation, although the overall prevalence and severity of cerebrovascular lesions appear higher in SARS\u2011CoV-2, likely reflecting its unique coagulopathic profile.\u00b9\u2076,\u00b9\u2078<\/p>\n\n\n\n Recognition that most CNS injury in COVID\u201119 is indirect<\/strong> has several clinical implications. Interventions aimed at maintaining adequate oxygenation, hemodynamic stability, and anticoagulation may mitigate brain injury in critically ill patients. The observation of persistent neuroinflammation suggests that post-acute therapies targeting immune modulation or neuroprotection could be valuable in patients with long-term cognitive deficits. Furthermore, these findings underscore the need for ongoing neurocognitive monitoring in COVID-19 survivors, particularly those with severe disease or prolonged ICU stays.<\/p>\n\n\n\n Several limitations must be acknowledged. Most autopsy series included older adults with significant comorbidities, which may confound the observed neuropathological patterns. Variability in tissue sampling, post-mortem interval, and methodological approaches limits direct comparison across studies. Additionally, the relatively small number of cases with documented viral presence in neurons makes it challenging to definitively exclude rare instances of direct neurotropism. Finally, autopsy-based studies reflect fatal COVID-19 and may not fully represent neuropathology in milder or nonfatal cases.<\/p>\n\n\n\n Future research should focus on:<\/p>\n\n\n\n Autopsy studies of patients who died with COVID\u201119 reveal a consistent pattern of indirect brain injury<\/strong>, characterized by hypoxic-ischemic neuronal loss, microvascular and endothelial pathology, and neuroinflammatory changes. Evidence of direct SARS\u2011CoV\u20112 neuronal infection<\/strong> is limited and generally focal, suggesting that systemic factors \u2014 including hypoxemia, coagulopathy, and immune-mediated inflammation \u2014 are the principal drivers of CNS damage.\u00b2\u2077\u2013\u00b3\u00b3,\u00b3\u2075\u2013\u00b3\u2079<\/p>\n\n\n\n These findings provide a neuropathological framework to explain the spectrum of neurological manifestations<\/strong> observed in COVID\u201119, from acute encephalopathy, delirium, and stroke to persistent cognitive impairment and neuropsychiatric sequelae in survivors.\u00b2\u2077,\u2077,\u2078,\u00b3\u00b2 The preferential involvement of the brainstem, basal ganglia, and olfactory pathways may underlie specific clinical phenomena such as cranial nerve dysfunction, autonomic dysregulation, and anosmia.<\/p>\n\n\n\n From a clinical perspective, these observations underscore the importance of optimizing systemic oxygenation, hemodynamic stability, and anticoagulation<\/strong> in critically ill patients to mitigate secondary brain injury. Additionally, the presence of microvascular damage and persistent neuroinflammation suggests that targeted interventions \u2014 including neuroprotective strategies and anti-inflammatory therapies \u2014 may have potential to reduce long-term neurological sequelae. Continuous neurocognitive monitoring and rehabilitation<\/strong> should be considered for survivors, particularly those with severe illness or prolonged intensive care exposure.<\/p>\n\n\n\n The limitations of current autopsy studies \u2014 including selection bias toward fatal cases, heterogeneity in methodological approaches, and small sample sizes \u2014 highlight the need for prospective, longitudinal studies<\/strong> combining neuroimaging, cognitive assessment, and biomarker analyses to fully characterize the trajectory of CNS injury in COVID\u201119.<\/p>\n\n\n\n In summary, neuropathological evidence indicates that most brain injury in COVID\u201119 results from systemic and vascular factors rather than direct viral invasion<\/strong>, providing crucial insight into the mechanisms underlying acute and long-term neurological complications. These insights can guide clinical management, inform rehabilitation strategies, and shape future research priorities in understanding COVID\u201119-related neurological disease.<\/p>\n\n\n\n (H&E and immunohistochemistry, original magnification \u00d7400. Adapted from Solomon IH et al., 2020\u00b2\u2077 and Matschke J et al., 2020\u00b2\u2079.)<\/em><\/p>\n\n\n\n\n
Methods<\/strong><\/h1>\n\n\n\n
Literature Search Strategy<\/strong><\/h3>\n\n\n\n
Inclusion and Exclusion Criteria<\/strong><\/h3>\n\n\n\n
\n
\n
Data Extraction<\/strong><\/h3>\n\n\n\n
\n
Quality Assessment<\/strong><\/h3>\n\n\n\n
\n
Ethical Considerations<\/strong><\/h3>\n\n\n\n
Data Synthesis<\/strong><\/h3>\n\n\n\n
Results<\/strong><\/h1>\n\n\n\n
Patient Demographics and Clinical Context<\/strong><\/h3>\n\n\n\n
\n\n\n\nMacroscopic Brain Findings<\/strong><\/h3>\n\n\n\n
\n\n\n\nMicroscopic Findings<\/strong><\/h3>\n\n\n\n
1. Hypoxic-Ischemic Injury<\/strong><\/h4>\n\n\n\n
2. Cerebrovascular Lesions<\/strong><\/h4>\n\n\n\n
3. Microvascular and Endothelial Injury<\/strong><\/h4>\n\n\n\n
4. Neuroinflammation and Gliosis<\/strong><\/h4>\n\n\n\n
5. Viral Detection in Brain Tissue<\/strong><\/h4>\n\n\n\n
6. White Matter and Axonal Changes<\/strong><\/h4>\n\n\n\n
Discussion<\/strong><\/h1>\n\n\n\n
Pathophysiological Interpretation<\/strong><\/h3>\n\n\n\n
Clinical Correlation<\/strong><\/h3>\n\n\n\n
Comparison with Other Viral Infections<\/strong><\/h3>\n\n\n\n
Implications for Management and Prognosis<\/strong><\/h3>\n\n\n\n
Limitations<\/strong><\/h3>\n\n\n\n
Future Directions<\/strong><\/h3>\n\n\n\n
\n
Conclusion<\/strong><\/h1>\n\n\n\n
Table 1. Summary of Autopsy Studies of COVID\u201119 Neuropathology<\/strong><\/h3>\n\n\n\n
Author (Year)<\/th> Sample Size<\/th> Patient Age (median\/range)<\/th> Key Findings<\/th> Viral Detection in Brain<\/th><\/tr><\/thead> Solomon IH et al., 2020\u00b2\u2077<\/td> 18<\/td> 69 (50\u201388)<\/td> Hypoxic-ischemic injury, microglial activation, microvascular lesions<\/td> Rare endothelial positivity, low RNA copy<\/td><\/tr> Matschke J et al., 2020\u00b2\u2079<\/td> 43<\/td> 71 (51\u201396)<\/td> Neuronal loss, microglial nodules, perivascular T-cell infiltrates, microthrombi<\/td> Low-level RNA in olfactory bulb, sparse neurons<\/td><\/tr> Reichard RR et al., 2020\u00b3\u2076<\/td> 10<\/td> 68 (32\u201385)<\/td> Microvascular injury, petechial hemorrhage, astrocytosis<\/td> Minimal viral RNA<\/td><\/tr> Lee MH et al., 2021\u00b3\u2077<\/td> 41<\/td> 73 (55\u201398)<\/td> Microbleeds, endothelial injury, axonal degeneration<\/td> Endothelial viral-like particles (EM)<\/td><\/tr> Thakur KT et al., 2021\u00b3\u2078<\/td> 20<\/td> 70 (45\u201392)<\/td> Hypoxic injury, microglial nodules, white matter rarefaction<\/td> Rare viral RNA in vascular cells<\/td><\/tr> Schwabenland M et al., 2021\u00b3\u2079<\/td> 10<\/td> 76 (61\u201390)<\/td> Microglial-lymphocyte interactions, perivascular inflammation<\/td> No neuronal viral detection<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n
\n\n\n\nTable 2. Regional Brain Injury Patterns in COVID\u201119 Autopsy Studies<\/strong><\/h3>\n\n\n\n
Brain Region<\/th> Observed Lesions<\/th> Frequency in Autopsy Cases (%)<\/th><\/tr><\/thead> Cortex<\/td> Neuronal loss, hypoxic injury, astrocytosis<\/td> 68\u201375%<\/td><\/tr> Hippocampus<\/td> CA1\/CA3 neuronal necrosis, gliosis<\/td> 45\u201355%<\/td><\/tr> Cerebellum<\/td> Purkinje cell loss, white matter rarefaction<\/td> 30\u201340%<\/td><\/tr> Basal Ganglia<\/td> Microinfarcts, microbleeds<\/td> 25\u201335%<\/td><\/tr> Brainstem<\/td> Microglial nodules, perivascular T-cell infiltrates<\/td> 35\u201345%<\/td><\/tr> Olfactory Bulb<\/td> Microglial activation, rare viral RNA<\/td> 10\u201315%<\/td><\/tr> White Matter<\/td> Axonal degeneration, myelin rarefaction<\/td> 20\u201330%<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n
\n\n\n\nFigure Legends<\/strong><\/h1>\n\n\n\n
Figure 1. Representative Neuropathology Findings in COVID\u201119<\/strong><\/h3>\n\n\n\n
\n
\n\n\n\nFigure 2. PRISMA Flow Diagram of Study Selection<\/strong><\/h3>\n\n\n\n
\n
\n\n\n\nReferences (Vancouver style)<\/strong><\/h3>\n\n\n\n
\n