Continuous Time-Domain Near-Infrared Spectroscopy During Endovascular Thrombectomy Enables Early Prediction of Post-Recanalization Cortical Infarct

medRxiv · 2026-04-29

Abstract Background Existing neuromonitoring tools lack the capability for continuous, intraoperative assessment of cerebral oxygenation and tissue viability during endovascular thrombectomy (EVT) of large vessel occlusion stroke. Time-domain near-infrared spectroscopy (TD-NIRS), an advanced non-invasive optical technique, may overcome this challenge. However, no study has yet investigated TD-NIRS’ feasibility as an intraoperative neuromonitoring tool during EVT and its capability in predicting post-recanalization infarct. Methods In this prospective observational study, eleven patients with middle cerebral artery or internal carotid artery occlusion were monitored during EVT using TD-NIRS. Absolute concentrations of oxyhemoglobin ([HbO 2 ]), deoxyhemoglobin ([HHb]), total hemoglobin ([tHb]), and tissue oxygen saturation (StO 2 ) on both hemispheres was derived using a scaled Monte Carlo approach. Patients were dichotomized into post-EVT cortical infarct and no infarct, and the Δ[HbO 2 ]/[HHb] pre- vs post-recanalization was assessed. Results Significant differences were observed in pre- vs post-recanalization [HbO 2 ] ( p =0.0068), [HHb] ( p =0.042), and StO 2 ( p =0.0020) on the affected hemisphere. The Δ[HbO 2 ]/[HHb] significantly differed between patients with and without post-EVT infarct ( p =0.0043). Logistic regression ( p =0.0041) and ROC (AUC=0.82) determined that Δ[HbO 2 ]/[HHb] reliably predicts post-EVT cortical infarct. Conclusions These results suggest TD-NIRS as a novel, adjunctive intraoperative neuromonitoring tool during EVT, with potential to predict post-EVT cortical infarct, guiding clinical management before/after thrombectomy. Graphical Abstract

Triple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles: Intracellular Aβ and Synaptic Dysfunction

Neuron · 2026-05-01

Continuous Time-Domain Near-Infrared Spectroscopy During Endovascular Thrombectomy Enables Early Prediction of Post-Recanalization Cortical Infarct Dataset

Mendeley Data · 2026-04-20

Eleven patients with occlusion of the middle cerebral artery and/or the internal carotid artery were monitored intraoperatively during endovascular thrombectomy using a time-domain near-infrared spectroscopy system (Hamamatsu's TRS-21). This dataset presents absolute concentrations of oxyhemoglobin ([HbO2]), deoxyhemoglobin ([HHb]), total hemoglobin ([tHb]), and tissue oxygen saturation (StO2) on both hemispheres of the brain, which were derived using a transport-rigorous scaled Monte Carlo approach. Demographics of the cohort, intraoperative vitals, and neuroimaging (computed tomography, magnetic resonance imaging, and fluoroscopy) are also presented for the cohort.

Predictive Value of Early Quantitative EEG Features in Critically Ill Moderate-severe Traumatic Brain Injury (TBI) Patient Prognostication (P12-7.008)

Neurology · 2025-04-07

To evaluate predictive performance of quantitative electroencephalogram (qEEG) features in predicting outcomes among moderate-severe traumatic brain injury (msTBI) patients.

What is the Philosophy of Neurology? Scoping Review and Defining the Discipline (P2-1.016)

Neurology · 2025-04-07

To chart a course for a new sub-discipline, the philosophy of neurology, informed by existing empirical literature in neurology with reciprocal influence for clinical care and philosophical topics.

Cerebrovascular alterations in a mouse model of late-onset Alzheimer’s disease

Neurophotonics · 2025-06-05 · 1 citations

SignificanceAlzheimer’s disease (AD) is an age-related neurodegenerative disorder with cerebrovascular alterations contributing to cognitive decline. Assessing cerebrovascular changes in mouse models that mimic the human condition of late-onset, sporadic AD is important for better human applicability.AimTo assess cerebrovascular changes in three mouse models: (1) 3xTg-AD; (2) the humanized amyloid-beta knock-in (hAβ-KI) mouse model of late-onset, sporadic AD; and (3) age-matched wild-type mice.ApproachWe measured resting-state cerebral blood flow (CBF) and neurovascular coupling (NVC) using laser speckle imaging (LSI) and performed ex vivo analyses of gene expression and cerebrovascular structure using bulk ribonucleic acid sequencing and confocal microscopy, respectively.ResultsOur study identifies specific cerebrovascular alterations in the hAβ-KI mouse model, including increased resting-state CBF, a shift toward smaller blood vessel diameters, impaired NVC, and transcriptomic changes related to metabolism and inflammation. Notably, we found that the increased resting-state CBF was primarily associated with female hAβ-KI mice.ConclusionsOur findings demonstrate that the hAβ-KI mouse model exhibits cerebrovascular alterations that warrant further investigation to uncover the underlying mechanisms. Expanding these studies could enhance our understanding of cerebrovascular alterations in AD and support the development of targeted therapeutic strategies.

Antipsychotic Practice Patterns and Clinical Outcomes in Moderate-to-severe TBI (P10-7.005)

Neurology · 2025-04-07

In this study, we sought to assess the pattern of antipsychotics used for moderate-severe TBI (msTBI) and their relationship to functional outcomes.

Inflammation and Neurological Outcomes in Cardiac Arrest – a Narrative Review of Serum Biomarker Investigations

Journal of Intensive Care Medicine · 2025-07-13 · 2 citations

BACKGROUND: Hypoxic-ischemic brain injury (HIBI) is a significant cause of disability following cardiac arrest (CA). Activation of the inflammatory cascade is central to HIBI pathophysiology and drives post-cardiac arrest syndrome (PCAS), which can induce further secondary brain injury. Although numerous studies have described this mechanism in preclinical models, translating this knowledge to therapeutic targets and neurological outcomes in humans is variable and incomplete. The impact of inflammation on the neurovascular unit, comprising neurons, astroglia, and capillary endothelium, may play a significant role in outcomes but is poorly understood in humans. OBJECTIVE: This narrative review explores studies examining PCAS, inflammation, and neurological outcomes in adult CA and classifies them into interrelated pathomechanisms. METHODS: We searched multiple databases using a search string constructed from core concepts, including inflammation, CA, neurovascular unit components, and neurologic outcomes. We screened abstracts published from database conception until July 2024 and excluded animal/in-vitro studies, unrelated topics, duplicates, foreign language articles, reviews/commentaries, studies without neurological outcomes, and case studies. RESULTS: The biomarkers studied fit into three general domains: reperfusion-induced oxidative stress, local and systemic inflammatory response, and coagulopathy associated with endothelial injury. Numerous markers were associated with neurological outcomes after CA, but few demonstrated a strong association in multivariate analysis. Few clinical trials of therapies for CA have studied impacts on the inflammatory cascade or have targeted inflammatory components. Associations between inflammation reduction and neurological outcomes are variable. However, various limitations reduce the applicability of these trials. CONCLUSIONS: Inflammatory mechanisms in PCAS may hold the key to secondary brain injury and warrant larger, more systematic studies to establish therapeutic targets to improve neurological outcomes.

Abstract 4369129: Essential Role of KCNQ5 (Kv7.5) Potassium Channels in Vascular Reactivity and Adrenergic Signaling

Circulation · 2025-11-03

Introduction/Background: Vascular tone dysregulation is central to cardiovascular pathophysiology. KCNQ (Kv7) potassium channels, primarily heteromeric KCNQ4/5 channels, regulate smooth muscle membrane potential and contractility, yet the specific role of the KCNQ5 subunit in vascular reactivity remains underexplored. The absence of KCNQ5-specific tools has limited mechanistic understanding, particularly regarding receptor-mediated signaling in distinct vascular beds. Research Questions/Hypothesis: We hypothesized that KCNQ5 plays a critical, region-specific role in vascular contractility and receptor-mediated relaxation, particularly to adrenergic stimuli. We aimed to determine whether genetic deletion of KCNQ5 disrupts vasoreactivity and arterial signaling dynamics. Methods/Approach: We generated a CRISPR-based germline KCNQ5 knockout ( Kcnq5 -/- ) rat line. Using in vivo multimodal monitoring (cardiac and brain hemodynamics), ex vivo myography of mesenteric and cerebral arteries, and in vitro electrophysiology of Xenopus oocytes expressing KCNQ4/5/KCNE4 complexes, we analyzed vascular responses to pharmacologic and physiologic stimuli including adrenergic agonists, KCNQ modulators, and the botanical KCNQ5 isoform-selective vasorelaxant aloperine. Results/Data: Kcnq5 -/- rats displayed blunted heart rate, cerebral blood flow, and vasoregulatory responses to hypercapnia and isoflurane, and impaired cerebral vasodilation to aloperine. In contrast, cerebral artery segments mounted in a wire myograph displayed preserved function. In mesenteric artery segments studied using wire myography, deletion of KCNQ5 did not affect basal tone or luminal diameter but impaired relaxation responses to the Kv7 channel opener ML213, aloperine, and the β-adrenergic agonist isoprenaline. Constriction to the α 1 -adrenergic agonist methoxamine was enhanced and showed reduced sensitivity to linopirdine, highlighting KCNQ5’s key role in regulating adrenergic vasoconstriction. Cellular electrophysiology studies delineated PKA/PKC sensitivity of KCNQ5-containing channels. Conclusions: KCNQ5 is essential for receptor-mediated signaling in specific vascular beds. Its deletion enhances α 1 -adrenergic constriction and impairs β-adrenergic and botanical-induced vasorelaxation, highlighting its important functional role. These findings identify KCNQ5 as a key component of Kv7 channel architecture and vasoregulation, which likely varies across vascular beds.