Background and objectives:COVID-19 related inflammation, endothelial dysfunction and coagulopathy may increase the bleeding risk and lower efficacy of revascularization treatments in patients with acute ischemic stroke. We aimed to evaluate the safety and outcomes of revascularization treatments in patients with acute ischemic stroke and COVID-19.Methods:Retrospective multicenter cohort study of consecutive patients with acute ischemic stroke receiving intravenous thrombolysis (IVT) and/or endovascular treatment (EVT) between March 2020 and June 2021, tested for SARS-CoV-2 infection. With a doubly-robust model combining propensity score weighting and multivariate regression, we studied the association of COVID-19 with intracranial bleeding complications and clinical outcomes. Subgroup analyses were performed according to treatment groups (IVT-only and EVT).Results:Of a total of 15128 included patients from 105 centers, 853 (5.6%) were diagnosed with COVID-19. 5848 (38.7%) patients received IVT-only, and 9280 (61.3%) EVT (with or without IVT). Patients with COVID-19 had a higher rate of symptomatic intracerebral hemorrhage (SICH) (adjusted odds ratio [OR] 1.53; 95% CI 1.16–2.01), symptomatic subarachnoid hemorrhage (SSAH) (OR 1.80; 95% CI 1.20–2.69), SICH and/or SSAH combined (OR 1.56; 95% CI 1.23–1.99), 24-hour (OR 2.47; 95% CI 1.58–3.86) and 3-month mortality (OR 1.88; 95% CI 1.52–2.33).COVID-19 patients also had an unfavorable shift in the distribution of the modified Rankin score at 3 months (OR 1.42; 95% CI 1.26–1.60).Discussion:Patients with acute ischemic stroke and COVID-19 showed higher rates of intracranial bleeding complications and worse clinical outcomes after revascularization treatments than contemporaneous non-COVID-19 treated patients. Current available data does not allow direct conclusions to be drawn on the effectiveness of revascularization treatments in COVID-19 patients, or to establish different treatment recommendations in this subgroup of patients with ischemic stroke. Our findings can be taken into consideration for treatment decisions, patient monitoring and establishing prognosis.

Background Lewis-Sumner Syndrome (LSS) is considered an asymmetric sensory-motor variant of Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), mostly affecting the limbs distally, with electrophysiological evidence of multifocal motor conduction blocks. Cranial nerve involvement is present in a minority. Various well-known infectious agents, directly or via the host’s immune responses, may trigger or exacerbate acute and chronic peripheral neuropathies, which may manifest clinically through a multitude of signs and symptoms. Case presentation We present the case of a 57-year-old male with Lewis-Sumner Syndrome, whose clinical course was quite stable over many years. He developed severe hyperacute relapse of his neuropathic disease in the context of active pneumonia due to influenza A (H1N1) virus infection. During this exacerbation, besides the obvious worsening of the previous asymmetric limb involvement, the patient also manifested left peripheral facial palsy and dysphagia that rapidly evolved over minutes, mimicking a stroke. The patient also showed rapid recovery, with marked improvement of the acute neuropathic dysfunction, immediately after initiation of treatment with oseltamivir. Our hypothesis is that the direct modulation of Na + ion channel activity in the host’s peripheral nerve cell by H1N1 viral proteins could cause acute and potentially reversible dysfunction in the conduction of nerve action potentials. Direct viral neuritis could also have been the cause. Immunomodulatory agents, namely IVIg, were not administered due to the swift clinical improvement noticed in the following days. Conclusions We aim to raise awareness of the possibility of atypical neurological presentations of viral infections, especially relevant in the context of the pandemic the world is now facing.

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