Spinal Cord and Brainstem Extensive Infarction: A Case with Rare Complication of COVID-19 Infection

A 15-year-old man was transferred to our hospital with a history of dyspnea with limb weakness for 8 days. Physical examination was notable for a blood pressure of 137/60 mmHg, a body temperature up to 39.2°C, and COVID-19 nucleic acid test positive. On coagulation panel, elevation of D-dimers (446.23 μg/l) was noted. The neurologic examination revealed the muscle tension of limbs was decreased symmetrically, without autonomous activity. Chest CT showed multiple patchy high-density under the pleura of both lungs Figure 1. MRI showed that the infarction foci were located in the medulla oblongata and cervical spinal cord, on which T2WI showed high signal, and the axial image showed typical 'owl eye sign' Figure 2. The patient was diagnosed as spinal cord and brainstem extensive infarction with COVID-19 infection, which was caused by the hypercoagulability of blood after COVID-19 infection. After 45 days treatment, the patient's lung infection was cured but still in paraplegia. The patient was transferred to the community hospital for rehabilitation treatment.Figure 1: Chest CT axial position; the arrow shows bilateral lung infectionFigure 2: MRI examination of cervical spinal cord and brain stem. The arrow shows the infarct area. Figures (a), (c), (d), and (e) show the examination on January 12, 2023, and Figure (b) shows the examination on January 30, 2023. Figure (a) and (b) were sagittal images of MRI T2WI, lesions located in medulla oblongata and cervical spinal cord, and high signal; Figure (c) is axial image of T2WI, showing lesions with high signal; Figure (d) is the axial DWI image of medulla oblongata, showing high signal; Figure (e) is the axial DWI image of the cervical spinal cord, showing high signalTo date, spinal cord infarction has been described in association with COVID-19 infection. The first case was reported by Eissa et al.1 Whether COVID-19 induces thrombosis directly or merely accentuates the hypercoagulable condition in predisposed individuals remains controversial.2 In our case, increased levels of fibrinogen and D-dimers reflect the hypercoagulable state as an underlying ischemic mechanism. MRI is the imaging modality of choice for spinal cord infarction; it can show T2 hyperintensities with associated spinal cord cytotoxic edema; these T2-weighted imaging changes, however, can take hours to days to develop, and its sensitivity is therefore low in the acute setting. Conversely, recent advances in DWI techniques of the spine applying a reduced field of view and high spatial resolution, combined with distortion reduction techniques and homogeneous fat saturation, allowed the identification of acute ischemic changes as a diffusion restriction-related signal in the small-sized spinal cord.3 Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship This work was supported by Chongqing Clinical Research Center of Imaging and Nuclear Medicine (CSTC2015YFPT-gcjsyjz × 0175) and Chongqing Clinical Key Specialty Construction Project. Conflicts of interest There are no conflicts of interest.