Acta Neuropathologica: Microvascular Damage and Hypoxia Damage: New Neuropathological Characteristics in COVID-19.

In patients with COVID-19, there is a growing awareness of neurological complications, but very few neuropathological cases are available, including microthrombosis and acute infarction, hypoxia changes (no specific pathology) or leaching of lymphocytes around cerebrovascular vessels.
The authors reported two neuropathological cases in COVID-19 patients here, one of which found something very similar to the one described in recent case reports, with neo-cortical infarction and small hemorrhagic and non-hemorrhagic white lesions, indicating that a new pattern of characteristic change was also observed in radiology.
patient 1, male 50 years old, cardiac arrest, diagnosed with multiple brain infarction.
is is blood damage in the brain region is consistent with persistent hypotension during cardiac arrest.
cause of arterial (MCA) and double-sided rear (PCA) infarction in the right brain remains unclear.
thrombosis from a known pulmonary embolism is excluded due to the closure of the egg round hole.
may be due to local thrombosis, or similar to infarction, or may be a complication of persistent hypotension during cardiac arrest.
the white blood cell growth response in the infarction area may be only a response to refill damage, or it may be due to an increased immune response.
second patient, a woman in her 60s, was treated with intring gas and died of multiple organ failure after stopping sedation.
two-sided pale ball infarction is most likely due to lack of oxygen.
possible causes of lesions of cortological and whiteness micro-injury (including micro-bleeding) include vascular damage associated with viral infections, immuno-mediated, or hypoxia secondary to hypotension, local thrombosis, or thromboembolism.
MRI and pathological control showed that high signals of the soft meninges were associated with inflammation of lymphatic tissue cells.
in both cases, small gliomas, neurodegeneration and vascular damage (including signs of hemanitis) far from infarction were not detected, and inflammation of myelin was similar to in patients with other neurological disorders.
there are several possible mechanisms for neurological complications associated with SARS-CoV-2.
First, viruses directly invade endostrophes, smooth muscle cells, peritonal cells, inflammatory cells (especially macrophages), neurons, or glial cells through blood or retrograde axon pathways.
second, cerebrovascular walls or cell damage due to thrombosis or thrombosis associated with high coagulation in the brain, or due to cytokine/immuno-mediated overreaction to viral infections.
few cases reported so far highlight the complexity of COVID-19 neuropathology and the difficulty of identifying the cause of secondary hypoxia/hypoxia changes and medically-sourced exicies.
even a patient, neurological complications are not caused by a single mechanism.
notable for the increased expression of ACE2 in the ischemia brain and in the blood vessels of diabetics, as ACE2 represents the entry of SARS-CoV-2 into the host cell's inhibitor.
, certain treatments, such as ECMO, may increase the risk of neurological complications.
the authors further provided a neuropathological correlation between the radiological characteristics of subsurgery white blood vessel lesions, including microbleeds.
through future neuropathological studies, it is hoped that the mechanisms leading to COVID-19 tissue damage will continue to be clarified so that treatment options can be selected in a timely and appropriate manner.
original link: Jaunmuktane, Z., Mahadeva, U., Green, A. et al. Microvascular injury and hypoxic damage: emerging neuropathologicals in COVID-19. Acta Neuropathol 140, 397-400 (2020). MedSci Original Source: MedSci Originals !-- content presentation ends -- !-- to determine whether the login ends.