Inflammation after injury of the central nervous system (CNS) is increasingly viewed as a therapeutic target. However, comparative studies in different CNS compartments are sparse. To date only few studies based on immunohistochemical data and all referring to mechanical injury have directly compared inflammation in different CNS compartments.These studies revealed that inflammation is more pronounced in spinal cord than in brain. Therefore, it is unclear whether concepts and treatments established in the cerebral cortex can be transferred to spinal cord lesions and vice versa or whether immunological treatments must be adapted to different CNS compartments. By use of

Background COVID-19 pandemic caused a decline in stroke care in several countries. The objective was to describe lockdown stroke care in a tertiary stroke center in Düsseldorf, Germany near Heinsberg, a German hot spot for COVID-19 in spring 2020. Methods In a retrospective, observational, single-center study, we compared all patients treated in our emergency department (ED), patients seen by a neurologist in the ED, ED patients suffering from ischemic and hemorrhagic strokes and transient ischemic attacks (TIAs) as well as stroke patients admitted to our stroke unit during lockdown in spring 2020 (16 March 2020–12 April 2020) to those cared for during the same period in 2019 and lockdown light in fall 2020 (2 November – 29 November 2020). Results In spring 2020 lockdown the mean number of patients admitted to our ED dropped by 37.4%, seen by a neurologist by 35.6%, ED stroke patients by 19.2% and number of patients admitted to our stroke unit by 10% compared to the same period in 2019. In fall lockdown light 2020 effects were comparable but less pronounced. Thrombolysis rate was stable during spring and fall lockdown, however, endovascular treatment (EVT) rate declined by 58% in spring lockdown and by 51% in fall lockdown compared to the period in 2019. Conclusions Our study indicates a profound reduction of overall ED patients, neurological ED patients and EVT during COVID-19 pandemic caused lockdowns. Planning for pandemic scenarios should include access to effective emergency therapies.

Background Typically defined as a thromboinflammatory disease, ischemic stroke features early and delayed inflammatory responses, which determine the extent of ischemia‐related brain damage. T and natural killer cells have been implicated in neuronal cytotoxicity and inflammation, but the precise mechanisms of immune cell‐mediated stroke progression remain poorly understood. The activating immunoreceptor NKG2D is expressed on both natural killer and T cells and may be critically involved. Methods and Results An anti‐NKG2D blocking antibody alleviated stroke outcome in terms of infarct volume and functional deficits, coinciding with reduced immune cell infiltration into the brain and improved survival in the animal model of cerebral ischemia. Using transgenic knockout models devoid of certain immune cell types and immunodeficient mice supplemented with different immune cell subsets, we dissected the functional contribution of NKG2D signaling by different NKG2D‐expressing cells in stroke pathophysiology. The observed effect of NKG2D signaling in stroke progression was shown to be predominantly mediated by natural killer and CD8 + T cells. Transfer of T cells with monovariant T‐cell receptors into immunodeficient mice with and without pharmacological blockade of NKG2D revealed activation of CD8 + T cells irrespective of antigen specificity. Detection of the NKG2D receptor and its ligands in brain samples of patients with stroke strengthens the relevance of preclinical observations in human disease. Conclusions Our findings provide a mechanistic insight into NKG2D‐dependent natural killer– and T‐cell–mediated effects in stroke pathophysiology.

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