Caleb Han, Spencer Waddle, Maria Garza, Larry T. Davis, Jarrod J. Eisma, Wesley T. Richerson, Matthew Fusco, Rohan Chitale, Chelsea Custer, Colin D. McKnight, Lori C. Jordan, Manus J. Donahue
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We extend this work to test the hypothesis that vascular reserve of the ChP is unrelated to intracranial vasculopathy.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>We performed hypercapnic reactivity (blood oxygenation level-dependent; echo time = 35 ms; spatial resolution = 3.5 × 3.5 × 3.5 mm, repetition time = 2000 ms) and catheter angiography assessments of ChP reserve capacity and vascular patency in moyamoya patients (<i>n</i> = 53) with and without prior surgical revascularization. Time regression analyses quantified maximum cerebrovascular reactivity and reactivity delay time in ChP and cortical flow territories of major intracranial vessels with steno-occlusion graded as <70%, 70%-99%, and occlusion using Warfarin-Aspirin-Symptomatic-Intracranial-Disease stenosis grading criteria. Analysis of variance (significance: two-sided Bonferroni-corrected <i>p</i> < .05) was applied to evaluate cortical and ChP reactivity, after accounting for end-tidal carbon dioxide change, for differing vasculopathy categories.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>In patients without prior revascularization, arterial vasculopathy was associated with reduced cortical reactivity and lengthened reactivity delay (<i>p</i> ≤ .01), as expected. Regardless of surgical history, the ChP reactivity metrics were not significantly related to the degree of proximal stenosis, consistent with ChP reactivity being largely preserved in this population.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>Findings are consistent with ChP reactivity in moyamoya not being dependent on observed vasculopathy. Future work may investigate the extent to which ChP hyperemia in chronic ischemia reflects circulating markers of glial or ischemic stress.</p>\n </section>\n </div>","PeriodicalId":16399,"journal":{"name":"Journal of Neuroimaging","volume":"34 1","pages":"152-162"},"PeriodicalIF":2.3000,"publicationDate":"2023-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jon.13161","citationCount":"0","resultStr":"{\"title\":\"Choroid plexus vascular reactivity in moyamoya: Implications for choroid plexus regulation in ischemic stress\",\"authors\":\"Caleb Han, Spencer Waddle, Maria Garza, Larry T. Davis, Jarrod J. Eisma, Wesley T. Richerson, Matthew Fusco, Rohan Chitale, Chelsea Custer, Colin D. McKnight, Lori C. Jordan, Manus J. Donahue\",\"doi\":\"10.1111/jon.13161\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Background and Purpose</h3>\\n \\n <p>Choroid plexus (ChP) hyperemia has been observed in patients with intracranial vasculopathy and to reduce following successful surgical revascularization. This observation may be attributable to impaired vascular reserve of the ChP or other factors, such as the ChP responding to circulating markers of stress. We extend this work to test the hypothesis that vascular reserve of the ChP is unrelated to intracranial vasculopathy.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods</h3>\\n \\n <p>We performed hypercapnic reactivity (blood oxygenation level-dependent; echo time = 35 ms; spatial resolution = 3.5 × 3.5 × 3.5 mm, repetition time = 2000 ms) and catheter angiography assessments of ChP reserve capacity and vascular patency in moyamoya patients (<i>n</i> = 53) with and without prior surgical revascularization. Time regression analyses quantified maximum cerebrovascular reactivity and reactivity delay time in ChP and cortical flow territories of major intracranial vessels with steno-occlusion graded as <70%, 70%-99%, and occlusion using Warfarin-Aspirin-Symptomatic-Intracranial-Disease stenosis grading criteria. Analysis of variance (significance: two-sided Bonferroni-corrected <i>p</i> < .05) was applied to evaluate cortical and ChP reactivity, after accounting for end-tidal carbon dioxide change, for differing vasculopathy categories.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>In patients without prior revascularization, arterial vasculopathy was associated with reduced cortical reactivity and lengthened reactivity delay (<i>p</i> ≤ .01), as expected. Regardless of surgical history, the ChP reactivity metrics were not significantly related to the degree of proximal stenosis, consistent with ChP reactivity being largely preserved in this population.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusions</h3>\\n \\n <p>Findings are consistent with ChP reactivity in moyamoya not being dependent on observed vasculopathy. 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Choroid plexus vascular reactivity in moyamoya: Implications for choroid plexus regulation in ischemic stress
Background and Purpose
Choroid plexus (ChP) hyperemia has been observed in patients with intracranial vasculopathy and to reduce following successful surgical revascularization. This observation may be attributable to impaired vascular reserve of the ChP or other factors, such as the ChP responding to circulating markers of stress. We extend this work to test the hypothesis that vascular reserve of the ChP is unrelated to intracranial vasculopathy.
Methods
We performed hypercapnic reactivity (blood oxygenation level-dependent; echo time = 35 ms; spatial resolution = 3.5 × 3.5 × 3.5 mm, repetition time = 2000 ms) and catheter angiography assessments of ChP reserve capacity and vascular patency in moyamoya patients (n = 53) with and without prior surgical revascularization. Time regression analyses quantified maximum cerebrovascular reactivity and reactivity delay time in ChP and cortical flow territories of major intracranial vessels with steno-occlusion graded as <70%, 70%-99%, and occlusion using Warfarin-Aspirin-Symptomatic-Intracranial-Disease stenosis grading criteria. Analysis of variance (significance: two-sided Bonferroni-corrected p < .05) was applied to evaluate cortical and ChP reactivity, after accounting for end-tidal carbon dioxide change, for differing vasculopathy categories.
Results
In patients without prior revascularization, arterial vasculopathy was associated with reduced cortical reactivity and lengthened reactivity delay (p ≤ .01), as expected. Regardless of surgical history, the ChP reactivity metrics were not significantly related to the degree of proximal stenosis, consistent with ChP reactivity being largely preserved in this population.
Conclusions
Findings are consistent with ChP reactivity in moyamoya not being dependent on observed vasculopathy. Future work may investigate the extent to which ChP hyperemia in chronic ischemia reflects circulating markers of glial or ischemic stress.
期刊介绍：
Start reading the Journal of Neuroimaging to learn the latest neurological imaging techniques. The peer-reviewed research is written in a practical clinical context, giving you the information you need on:
MRI
CT
Carotid Ultrasound and TCD
SPECT
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Endovascular Surgical Neuroradiology
Functional MRI
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and other new and upcoming neuroscientific modalities.The Journal of Neuroimaging addresses the full spectrum of human nervous system disease, including stroke, neoplasia, degenerating and demyelinating disease, epilepsy, tumors, lesions, infectious disease, cerebral vascular arterial diseases, toxic-metabolic disease, psychoses, dementias, heredo-familial disease, and trauma.Offering original research, review articles, case reports, neuroimaging CPCs, and evaluations of instruments and technology relevant to the nervous system, the Journal of Neuroimaging focuses on useful clinical developments and applications, tested techniques and interpretations, patient care, diagnostics, and therapeutics. Start reading today!
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