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A 79-year-old man presented to the emergency room with sudden onset of dysarthria followed by coma. Eight months before admission, he had undergone C1-C2 posterior fusion. Brain MRI showed multiple posterior circulation infarcts. He experienced resolution of symptoms after intravenous thrombolysis. CT angiography revealed the irregularity of the V3 segment of the right vertebral artery where the cervical screw contacted. Although the dual antiplatelet therapy with aspirin and clopidogrel had been started, he developed severe consciousness disturbance, quadriplegia, and decerebrate posturing to painful stimuli on the 24th hospital day. His eyes were fixed in the midline. Diffusionweighted imaging revealed a subtle hyperintense lesion in the pons, and MR angiography showed basilar artery occlusion. He underwent mechanical thrombectomy. Complete recanalization was achieved on the second attempt using a stent retriever, and the patient s condition recovered to pretreatment level. Heparin and cilostazol were started after the discontinuation of aspirin and clopidogrel. On the 52nd hospital day, the right vertebral artery sacrifice with coil embolization was performed to prevent recurrences. Cerebral infarction could occur as a long-term complication of C1-C2 posterior fusion. A vertebral artery injury at the site of cervical screw contact could be one of the causes of the complication. Endovascular parent artery occlusion should be considered in ischemic stroke patients who have vertebral artery legions after cervical spine surgery.

Background: It is unclear whether biomarkers of cardiac dysfunction are associated with cryptogenic stroke (CS). Methods: We retrospectively evaluated consecutive ischemic stroke patients. Patients underwent transthoracic echocardiography to evaluate left atrial diameter and the peak transmitral filling velocity/mean mitral annular velocity during early diastole (E/e’). Patent foramen ovale (PFO) and left atrial appendage flow velocity were evaluated by transesophageal echocardiography. We compared clinical characteristics and biomarkers of cardiac dysfunction (brain natriuretic peptide [BNP], left atrial diameter, E/e’, and left atrial appendage flow velocity) between CS or CS without large PFO and other causative stroke subtypes. Results: Among 1,514 patients with ischemic stroke, 264 patients were classified as having CS. Of these, transesophageal echocardiography revealed 27/158 (17%) large PFOs. In comparison, for the noncardioembolic stroke group, which consisted of large artery and small vessel subtypes, patients with CS without large PFO had higher log10 BNP (adjusted OR 2.70; 95% CI 1.92–3.78; p < 0.001), higher log10 E/e’ (3.41; 1.21–13.15; p = 0.019), and lower left atrial appendage flow velocity (0.98; 0.97–1.00; p = 0.031). Left atrial diameter was similar for noncardioembolic stroke and CS without large PFO (p = 0.380). Cutoff values of BNP, E/e’, and left atrial appendage flow velocity capable of distinguishing CS without large PFO from noncardioembolic stroke were 65.0 pg/mL (sensitivity 55.3%; specificity 70.9%), 13.0 (45.5%; 68.0%), and 46.0 cm/s (37.1%; 87.5%), respectively. Conclusion: Patients with CS without large PFO could have biomarkers of cardiac dysfunction.

A 25-year-old woman was admitted to our hospital due to tonic convulsion with severe headache after having experienced symptoms of nausea and vomiting for a month. Brain MRI showed extensive symmetrical lesions in the cortical and subcortical areas of parieto-occipital lobes and basal ganglia, consistent with typical characteristics of posterior reversible encephalopathy syndrome (PRES). Furthermore, some residual lesions in the left side of dorsal medulla oblongata and central area of the cervical spinal cord along with the presence of serum anti-aquaporin-4 antibody yielded the diagnosis of neuromyelitis optica spectrum disorder (NMOSD). We herein discuss the mechanism by which PRES may occur together with NMOSD.