Barton7272. Barton LM, Duval EJ, Stroberg E, Ghosh S, Mukhopadhyay S. COVID-19 autopsies, Oklahoma, USA. Am J Clin Pathol. 2020;153:725-33. 73. Bulfamante G, Chiumello D, Canevini MP, Priori A, Mazzanti M, Centanni S, et al. First ultrastructural autoptic findings of SARS -Cov-2 in olfactory pathways and brainstem. Minerva Anestesiol. 2020;86:678-9. 74. Menter T, Haslbauer JD, Nienhold R, Savic S, Hopfer H, Deigendesch N, et al. Postmortem examination of COVID-19 patients reveals diffuse alveolar damage with severe capillary congestion and variegated findings in lungs and other organs suggesting vascular dysfunction. Histopathology. 2020;77:198-209. 75. Puelles VG, Lütgehetmann M, Lindenmeyer MT, Sperhake JP, Wong MN, Allweiss L, et al. Multiorgan and renal tropism of SARS-CoV-2. N Engl J Med. 2020;383:590-2. 76. Schaller T, Hirschbühl K, Burkhardt K, Braun G, Trepel M, Märkl B, et al. Postmortem examination of patients with COVID-19. JAMA. 2020;323:2518-20. 77. Skok K, Stelzl E, Trauner M, Kessler HH, Lax SF. Post-mortem viral dynamics and tropism in COVID-19 patients in correlation with organ damage. Virchows Arch. 2020 Aug 20;1-11. doi: http://10.1007/s00428-020-02903-8. Online ahead of print. http://10.1007/s00428-020-02903-8...
78. Suess C, Hausmann R. Gross and histopathological pulmonary findings in a COVID-19 associated death during self-isolation. Int J Legal Med. 2020;134:1285-90. |
n=2, 2 ♀, age 42 and 77 |
Obesity, hypertension, deep vein thrombosis, splenectomy, pancreatitis, myotonic dystrophy |
NR |
H&E |
The study found no gross abnormalities in the CNS of either patient, including no abnormalities in brain weight. |
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The study did not investigate any further into the effects of COVID-19 on the CNS. |
Bradley61
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n=14, 8 ♀ and 6 ♂, age ± 73.5 |
Arterial hypertension, hyperlipidemia, type II DM, obesity, OSA, heart failure, atrial fibrillation, CAD, CKD, COPD, renal disease, osteoporosis, aortic stenosis, breast cancer |
All |
H&E |
Of the 14 patients, only six had brain examinations.Intraparenchymal hemorrhage was observed in one patient, while scattered punctate subarachnoid hemorrhages and punctate microhemorrhages in the brainstem were observed in another. |
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The other four patients showed no diagnostic alternations in the brain. |
Bulfamante73
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n=1, ♂, age 54 |
NR |
Olfactory nerve, gyrus rectus, and brainstem |
Ultrastructural analysis |
Severe and widespread tissue damage was observed in the neurons, glia, nerve axons, and myelin sheath. The damage from the olfactory nerve to the gyrus rectus, and to the brainstem was less severe. Various particles referable to virions of SARS-CoV-2 were observed. |
Conklin62
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n=16, 5 ♀/11 ♂, age ± 63.5 |
NR |
Cerebral and cerebellar white and grey matter |
H&E, MRI, RT-qPCR |
Eleven of 16 patients had lesions, with eight having > 10 lesions. |
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Of these eight patients, four had lesions involving the corpus callosum, and the other four had lesions involving subcortical and deep white matter. |
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Uncal and tonsillar herniation, diffuse discoloration of the grey-white matter junction, and numerous punctuate hemorrhages were found. Significant loss of axon and myelin was also noted. |
Coolen58
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n=19, 14 ♀ and 5 ♂, age ± 77.0 |
Hypertension, cardiac disorders, CKD, DM, COPD |
All |
MRI |
Parenchymal brain MRI abnormalities were documented in four of the 19 patients. Abnormalities included sub-cortical macro-and micro-hemorrhages, swelling induced by supratentorial white matter changes, and hazy hyperintensity in the MRI. |
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DIC was the predicted cause of one hemorrhage while the second remains unclear. Four separate decedents had asymmetric olfactory bulbs. Finally, no changes were found in the brainstem expect for a capillary telangiectasia in one patient. |
Jaunmuktane68
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n=2, 1 ♀ and 1 ♂, age 50 and 60 |
Asthma, DM, hypertension |
All |
CD3, CD34, CD68, MRI, SMI31, SMI94 |
Patient 1 was found to suffer from multifocal brain infarcts. The MCA and PCA infarcts were likely caused by local thrombosis or hypertension. |
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The second patient, who died from multiorgan failure, suffered from cortical and white matter microlesions likely caused by vascular injury, immune-mediated, or hypoxia. |
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CD68 highlights many more lesions than MRI or microscopic examination. CD34 showed blood vessels within some white matter microlesions. SMI31 revealed swollen axons in neurofilament staining, but SMI94 showed no demyelination. |
Lacy63
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n=1 ♀, age 58 |
Type 2 DM, obesity, HLD, mild intermittent asthma, chronic lower extremity swelling with ulceration |
Brain |
Gross examination and H&E |
The brain (1,221 g) presented hydrocephalus ex-vacuo.The frontal horns measured 2.8 cm at the level of the temporal poles. |
Lax64
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n=11, 8 ♂ and 3 ♀, age ± 80.5 |
Arterial hypertension,DM type 2, ischemic stroke, dementia, pulmonary embolism |
Brain |
Dissection |
A brain autopsy was performed in only one patient, showing atrophy and arteriosclerotic changes but no acute alterations. |
Menter74
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n=21, 17 ♂ and 4 ♀, age ± 76.0 |
HTN, obesity, CVD, DM, chronic neurological condition, COPD, malignancy, CLD, CKD, immunosuppression |
Brain |
H&E |
A small number of RNA copies of the virus were found in the brain.Brain analysis revealed no inflammatory infiltrates or neuronal necrosis. Three of the four brains examined presented mild hypoxic injury. |
Nunes Duarte-Neto69
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n=10, 5 ♀ and 5 ♂, age 69 (33-83) |
Systemic arterial hypertension, DM, chronic cardiopathy, COPD, renal disease, neoplasia |
NR |
Hematoxylin, H&E, MIA-US, and qRT-PCR |
Reactive gliosis in the brain was found in eight out of nine autopsies. Other findings included neuronal satellitosis, small vessel disease, and perivascular hemorrhages. Alterations to the cerebral cortex, potentially caused by the viral infection, were also found. |
Paniz-Mondolfi60
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n=1, ♂, age 74 |
Parkinson’s disease |
Frontal lobes |
CRP, D-dimer level, ferritin, RT-PCR, TEM |
The postmortem sample indicated viral particles in the frontal lobe. Individual and small vesicles of pleomorphic viral-like particles were present. Transcellular |
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Penetration of the active pathogen through the brain microvascular endothelial cells was recorded. |
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Neural cell bodies demonstrated distended cytoplasmic vacuoles with enveloped viral particles and centers of electron density. The presence of SARS-CoV-2 was later confirmed through RT-PCR. |
Puelles75
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n=22, 16 ♀ and 6 ♂, age ± 75.9 |
Cardiovascular condition, respiratory condition, brain disorder, CKD, metabolic condition |
NR |
RT-PCR |
The highest levels of SARS-CoV-2 copies per cell were found in the respiratory system, although lower levels were discovered in the brain and other organs.PCR confirmed the presence of SARS-CoV-2 in the brains of eight/21 patients. The study suggests that brain tropism increases with the number of preexisting conditions. The findings indicate that COVID-19 has broad organotropism. |
Reichard57
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n=1, ♂, age 71 |
CAD |
Frontal lobes and corpus callosum |
H&E, LFB, GFAP, and PAS |
The postmortem brain sample presented mild brain swelling and hemorrhagic lesions disseminated throughout the cerebral hemispheric white matter. |
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There were foci of intraparenchymal blood in the white matter, with macrophages on the periphery of the lesions. |
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Reactive astrocytes were observed in the white matter. At the same time, APP immunostaining showed swollen and damaged axons on the periphery of the hemorrhagic foci. |
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The brain sample also presented the loss of myelin and positive macrophages. |
Remmelink59
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n=17, 12 ♂ and 5 ♀, age ± 72.0 |
Arterial hypertension, DM, cerebrovascular disease, CAD, cancer |
Frontal lobe |
H&E, RT-PCR |
A brain autopsy was performed on eleven patients, with SARS-CoV-2 RNA detected in nine. |
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The post-mortem analysis found cerebral hemorrhage or hemorrhagic suffusion, focal ischemic necrosis, edema and/or vascular congestion, and diffuse or focal spongiosis.No evidence of viral encephalitis or vasculitis, isolated neuronal necrosis, or perivascular lymphocytic infiltration was found. |
Schaller76
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n=10 ,7 ♀ and 3 ♂, mean age 79 (64-90) |
Arterial hypertension, arteriosclerosis, atrial fibrillation, CKD, COPD, DM, obesity, hypothyroidism, adenocarcinoma - lung, CAD, CML, CLL, cardiomyopathy, fatty liver disease, dementia, HCM, hyperthyroidism |
NR |
H&E |
Postmortem examination of 10 patients showed no morphologically detectable pathology in the brain. No evidence was found of encephalitis or central nervous vasculitis. |
Skok77
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n=28, 17 ♂ and 11 ♀, age ± 82.9 |
NR |
Lateral ventricles and corpus callosum |
qPCR |
No viral RNA was found in brain tissue or CSF samples.No brain autopsy was performed. |
Solomon67
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n=18, 14 ♂ and 4 ♀, age ± 62.0 |
DM, HTN, CVD, HLD, CKD, prior stroke, dementia, treated anaplastic astrocytoma |
Frontal and occipital lobe, olfactory bulb, cingulate gyrus, corpus callosum, hippocampus, BG, thalamus, cerebellum, midbrain, pons, and medulla |
H&E, CD45, RT-PCR (qRT-PCR) for the SARS-CoV-2 |
All 18 patients had acute hypoxic-ischemic damage in the cerebrum and cerebellum and were SARS-CoV-2-positive in the frontal/olfactory medulla.A loss of neurons was detected in the cerebral cortex, hippocampus, and cerebellar Purkinje cell layer. |
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Eight out of 18 patients presented mild arteriolosclerosis, three had chronic infarcts, five had moderate arteriolosclerosis, four presented pathological features of Alzheimer’s disease, two showed pathological features of Lewy body disease, four had Alzheimer’s type II astrocytosis, three had focal leptomeningeal chronic inflammation, one had a recurrent or residual anaplastic astrocytoma, and one had a single microglial nodule. |
Suess & Hausmann78
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n=1, ♂, age 59 |
Hypertension, type II DM |
NR |
CD-68, H&E, PAS, and TTF-1 |
The autopsy of the subject, whose coronavirus infection was confirmed by a pharyngeal swab test, found no abnormalities in brain weight and no major lesions. |
von Weyhern66
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n=6, 4 ♂ and 2 ♀, age ± 69.0 |
HTN, COPD, CRF, PHT, PAD, CAD, atrial fibrillation, alcohol abuse |
Hippocampus, neocortex, cerebellum, and brainstem nuclei |
H&E, LFB, and IHC |
Brain examination revealed localized perivascular and interstitial encephalitis with neuronal cell loss and axon degeneration in the dorsal motor nuclei of the vagus nerve, CNV, nucleus tractus solitarii, dorsal raphe nuclei, and fasciculus longitudinalis medialis, but no territorial infarctions. |
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Petechial bleeding was observed in four of the six patients. |
Wichmann65
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n=12, 9 ♀ and 3 ♂, age ± 73.0 |
CAD, arterial hypertension, obesity, type 2 DM, atrial fibrillation, asthma, CKD, Parkinson’s, COPD, dementia, epilepsy, granulomatous pneumopathy, NSCLC, PAD, trisomy 21, ulcerative colitis |
NR |
AE1/AE3, and H&E |
Four patients had detectable viral RNA in the brain. The authors suspected that one patient had septic encephalomalacia, although confirmation is pending brain dissection. Another patient was found to have below average brain weight. |