• Neuropathological Features of #Covid-19 | NEJM
    https://www.nejm.org/doi/10.1056/NEJMc2019373

    Pas de lésions cérébrales inflammatoires ou d’autres types de lésions pouvant être attribuées au #sars-cov2
    Présence du virus incertaine.

    In conclusion, histopathological examination of brain specimens obtained from 18 patients who died 0 to 32 days after the onset of symptoms of Covid-19 showed only hypoxic changes and did not show encephalitis or other specific brain changes referable to the virus. There was no cytoplasmic viral staining on immunohistochemical analysis. The virus was detected at low levels in 6 brain sections obtained from 5 patients; these levels were not consistently related to the interval from the onset of symptoms to death. Positive tests may have been due to in situ virions or viral RNA from blood.

    Neuropathology of patients with COVID-19 in Germany : a post-mortem case series - The Lancet Neurology
    https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30308-2/abstract

    Ici des lésions inflammatoires sont retrouvées et la présence du virus semble indiscutable mais ne semble pas augmenter les lésions

    43 patients were included in our study. Patients died in hospitals, nursing homes, or at home, and were aged between 51 years and 94 years (median 76 years [IQR 70–86]).

    We detected fresh territorial ischaemic lesions in six (14%) patients.

    37 (86%) patients had astrogliosis in all assessed regions.

    Activation of microglia and infiltration by cytotoxic T lymphocytes was most pronounced in the brainstem and cerebellum, and meningeal cytotoxic T lymphocyte infiltration was seen in 34 (79%) patients.

    SARS-CoV-2 could be detected in the brains of 21 (53%) of 40 examined patients, with SARS-CoV-2 viral proteins found in cranial nerves originating from the lower brainstem and in isolated cells of the brainstem. The presence of SARS-CoV-2 in the CNS was not associated with the severity of neuropathological changes.

    [...]

    In summary, our results show that SARS-CoV-2 RNA and proteins can be detected in the CNS. The brain shows mild neuropathological changes with pronounced neuroinflammation in the brainstem being the most common finding. However, the presence of SARS-CoV-2 in the CNS was not associated with the severity of neuropathological changes.16, 17 Careful neuropathological interpretation will be essential to disentangle which changes are attributable to SARS-CoV-2. All such changes must be mapped against neuropathological changes caused by pre-existing medical conditions often present in patients with COVID-19, as well as neuropathological changes caused by invasive treatments that are used in severe cases of COVID-19.35

  • COVID-19 related stroke in young individuals - The Lancet Neurology
    https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30272-6/fulltext

    Since then, this observation of COVID-19 related stroke in young patients has been supported by additional data from other centres worldwide. The mean patient age in several thrombectomy case series of COVID-19 (mean age of 52·8 years in a series from New York City [NY, USA],10
    mean age of 59·5 years in a series from Paris [France],11
    and mean age of 59·5 years in a combined series from New York City and Philadelphia [PA, USA]12
    ) is younger than the typical population having this procedure. Furthermore, in patients presenting with large vessel stroke during the pandemic, data from the Mount Sinai Health System in New York City confirm that patients who tested positive for SARS-CoV-2 were significantly younger, with a mean age of 59 years (SD 13), than patients who tested negative for SARS-CoV-2, who had a mean age of 74 years (SD 17),13
    mirroring the findings of the Paris group.11
    Patients with COVID-19 who had imaging confirmed stroke and were admitted to another large New York City medical centre were again found to be younger, with a mean age of 63 years (SD 17), than a control group of patients with stroke who tested negative for SARS-CoV-2 and had a mean age of 70 years (SD 18).3
    A case-control analysis of acute stroke protocol imaging from late March to early April, 2020, across a large New York City health system showed that, after adjusting for age, sex, and vascular risk factors, SAS-CoV-2 positivity was independently associated with stroke.

  • Neurological associations of COVID-19 - The Lancet Neurology
    https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30221-0/fulltext?dgcid=raven_jbs_etoc_email

    Background
    The COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is of a scale not seen since the 1918 influenza pandemic. Although the predominant clinical presentation is with respiratory disease, neurological manifestations are being recognised increasingly. On the basis of knowledge of other coronaviruses, especially those that caused the severe acute respiratory syndrome and Middle East respiratory syndrome epidemics, cases of CNS and peripheral nervous system disease caused by SARS-CoV-2 might be expected to be rare.
    Recent developments
    A growing number of case reports and series describe a wide array of neurological manifestations in 901 patients, but many have insufficient detail, reflecting the challenge of studying such patients. Encephalopathy has been reported for 93 patients in total, including 16 (7%) of 214 hospitalised patients with COVID-19 in Wuhan, China, and 40 (69%) of 58 patients in intensive care with COVID-19 in France. Encephalitis has been described in eight patients to date, and Guillain-Barré syndrome in 19 patients. SARS-CoV-2 has been detected in the CSF of some patients. Anosmia and ageusia are common, and can occur in the absence of other clinical features. Unexpectedly, acute cerebrovascular disease is also emerging as an important complication, with cohort studies reporting stroke in 2–6% of patients hospitalised with COVID-19. So far, 96 patients with stroke have been described, who frequently had vascular events in the context of a pro-inflammatory hypercoagulable state with elevated C-reactive protein, D-dimer, and ferritin.
    Where next?
    Careful clinical, diagnostic, and epidemiological studies are needed to help define the manifestations and burden of neurological disease caused by SARS-CoV-2. Precise case definitions must be used to distinguish non-specific complications of severe disease (eg, hypoxic encephalopathy and critical care neuropathy) from those caused directly or indirectly by the virus, including infectious, para-infectious, and post-infectious encephalitis, hypercoagulable states leading to stroke, and acute neuropathies such as Guillain-Barré syndrome. Recognition of neurological disease associated with SARS-CoV-2 in patients whose respiratory infection is mild or asymptomatic might prove challenging, especially if the primary COVID-19 illness occurred weeks earlier. The proportion of infections leading to neurological disease will probably remain small. However, these patients might be left with severe neurological sequelae. With so many people infected, the overall number of neurological patients, and their associated health burden and social and economic costs might be large. Health-care planners and policy makers must prepare for this eventuality, while the many ongoing studies investigating neurological associations increase our knowledge base.