Biomarkers of Coagulation and Inflammation in COVID-19-Associated Ischemic Stroke.

[Figure: see text].

Including Distal Motor Function within the NIHSS: Correlation with Motor Arm Function and IV rt-PA Treatment Response.

OBJECTIVES: The Distal Motor Function (DMF) sub-score of the NIH Stroke Scale (NIHSS) was measured in the NINDS rt-PA Stroke Trials but is currently not included in the NIHSS. The correlation of DMF with the NIHSS Motor Arm Function (MAF) sub-score, the effect of IV tPA treatment on DMF, and whether adding DMF changes the utility of the NIHSS have not been analyzed. MATERIALS AND METHODS: MAF and DMF sub-scores were retrieved from the original NINDS rt-PA Stroke Trials for both sides of the body at baseline, 2 hours, 24 hours, 7-10 days, and 3 months after IV tPA treatment. MAF and DMF scores were correlated using Spearman correlation. Clustering of DMF and MAF scores was determined using a Bentler Comparative Fit Index (CFI) to estimate variation in NIHSS when adding DMF. The effect of IV tPA on DMF and MAF was assessed using a linear model comparing changes in scores from baseline to 3 months. RESULTS: MAF and DMF were highly correlated (p < 0.0001) across all time points for both dichotomous and continuous data on both sides. Intravenous tPA accounted for 21% of the change in DMF (p < 0.014, R2 = 0.0157, N = 423) and 39% of the change in MAF (p < 0.093, R2 = 0.0125, N = 547) from 0 to 3 months. On adding DMF to NIHSS, CFI decreased from 0.98 to 0.80 and DMF clustered with MAF, indicating that addition of DMF is unlikely to produce any discrepancy to NIHSS. CONCLUSIONS: Including DMF to the NIHSS does not appear to be of additional value. After IV tPA treatment, proximal and distal motor function in upper extremity strongly correlate over time but greater improvement in MAF is noted. Further research is needed on the role of IV tPA on minor strokes with deficits of DMF.

Cerebral Hyperperfusion Syndrome After Carotid Revascularization and Acute Ischemic Stroke.

PURPOSE OF REVIEW: Cerebral hyperperfusion syndrome (CHS) is a rare but significant complication after carotid revascularization and is increasingly recognized after acute stroke treatments. In this review, we discuss the epidemiology and pathophysiology of CHS, clinical presentation including ipsilateral headache, seizures, and focal neurological deficits, and radiographic presentation. We propose preventive therapies with emphasis on acute stroke post-thrombectomy hyperperfusion. RECENT FINDINGS: CHS was first described after carotid revascularization but is now also reported in patients with acute ischemic stroke. Proposed criteria involve a combination of new clinical symptoms, radiographic evidence of hyperperfusion, and/or presence of intracerebral hemorrhage occurring within 30 days after the carotid or intracranial vessel manipulation. Strongest risk factors include reduced cerebral vasoreactivity, contralateral stenosis of ≥ 70%, post-procedure hypertension, and recent ipsilateral stroke. Pathophysiology is incompletely understood but is likely due to increase in cerebral blood flow and impaired cerebral autoregulation, particularly in the areas of disrupted blood-brain barrier, as well as baroreceptor dysfunction during carotid surgery. Strict blood pressure control pre-, during, and post-procedure is recommended, depending on the recanalization status of the vessel. However, there is no randomized data regarding the goal blood pressure to prevent cerebral hyperperfusion syndrome. With technical advances, carotid or intracranial vessel manipulation is increasingly common. CHS is a likely under-recognized and serious complication of carotid revascularization and intracranial thrombectomy. Awareness of and surveillance for CHS is important to reduce morbidity and mortality. Future research should focus on validation of proposed diagnostic criteria and determining optimal post-procedure hemodynamic management to prevent CHS.

Common carotid artery dissection: a case report and review of the literature.

Common carotid artery dissection (CCAD) is a rare and poorly characterized cause of ischemic stroke. We describe a case of multiple cerebral infarcts in a patient with CCAD initially detected by carotid duplex ultrasonography, and review the literature on CCAD. A Medline search from 1960 to the present for cases of CCAD yielded 46 cases. We extracted demographic data, anatomical location, symptoms, neurosonography, neuroradiology, pathological findings, treatment, and outcomes. The mean age of the patients was 48.8 ± 15.8 years (range, 19-89 years). With our patient, our search found 20 cases of spontaneous CCAD, 11 cases of traumatic CCAD, 4 cases of iatrogenic CCAD, and 12 cases of CCAD associated with aortic arch dissection. The most common presenting neurologic symptoms of CCAD were hemiparesis, decreased consciousness, headache/neck pain, aphasia, and monocular field deficit. The most frequently reported neurosonographic findings included a double lumen, mural thrombus, intraluminal hyperechoic/isoechoic lesion, and intimal flap. Most cases of CCAD were subsequently confirmed with conventional angiography, computed tomography angiography, or magnetic resonance angiography. Treatment differed based on etiology; anticoagulation was used most commonly for spontaneous CCAD, and surgical repair was most often done for traumatic and aortic dissection-associated CCAD. Prognosis was generally good; the majority of patients achieved complete clinical recovery, but 3 died. Our findings indicate that carotid Doppler is a widely accessible, rapid, and noninvasive technique for diagnosing CCAD. Our case and literature review further characterizes the diverse etiologies, clinical course, and radiographic features of CCAD.

Cross-Sectional Retrospective Study to Identify Clinical and Radiographic Features Associated With VZV Reactivation in Cryptogenic Stroke Patients With CSF Testing.

Background and Purpose: A large proportion of ischemic stroke patients lack a definitive stroke etiology despite extensive diagnostic testing. Varicella-Zoster Virus (VZV) can directly invade blood vessels causing vasculitis and may be associated with cryptogenic stroke (CS). Methods: We conducted a retrospective cross-sectional study of CS patients tested for VZV. The following were considered evidence of VZV reactivation (VZV+): positive CSF VZV PCR, anti-VZV IgM in CSF, or anti-VZV IgG CSF/serum ratio of 1:10 or higher. We describe the cohort, report VZV+ proportion with 95% confidence intervals (CI) determined with the Wald method, and compare patient groups using standard statistical tests. Results: A total of 72 CS patients met full study inclusion criteria. Most of the patients were <65 years old, had few traditional vascular risk factors, and had multifocal infarcts. Mean age was 49 years (SD ±13) and 47% were women. A total of 14 patients (19.4%; CI: 11.4-30.8%) had evidence of CNS VZV reactivation. There was no difference in evaluated demographic or radiographic features between those with versus without evidence of VZV reactivation. History of ischemic stroke in the past year (11/14 vs 25/43, P<.05) and hypertension (13/14 vs 35/58 and P<.05) were associated with VZV+. Conclusion: We found a high proportion of CNS VZV reactivation in a cross-sectional cohort of CS patients selected for CSF testing. Testing for VZV might be reasonable in CS patients who are young, have multifocal infarcts, or had an ischemic stroke within the past year, but additional research is needed.

Bilateral internal carotid artery dissection in the postpartum period.

BACKGROUND: Bilateral internal carotid artery dissection is a rare event associated with pregnancy, especially in a patient without any predisposing risk factors. CASE: A 34-year-old woman presented with postpartum unilateral weakness, headaches, and blurry vision 14 days after vaginal delivery. Radiologic imaging revealed bilateral cervical internal carotid artery dissections and cerebral infarctions. She was treated with anticoagulation and showed radiographic and clinical improvement. CONCLUSION: The pathophysiology of cervical artery dissection appears multifactorial, with evidence suggesting environmental and genetic contributions. Intimal injury related to the Valsalva maneuver during labor as well as hemodynamic and hormonal changes related to pregnancy are presumed causes of peripartum spontaneous carotid artery dissection. Antithrombotic therapy for at least 3 to 6 months after dissection and follow-up neuroimaging are suggested.