More pronounced hemodynamic alterations in patients with brain arteriovenous malformation-associated epilepsy.

OBJECTIVE: Epileptic seizures in patients with brain arteriovenous malformations (bAVMs) may be caused by hemodynamic alterations due to the complex angioarchitecture of bAVMs. In particular, an arterial steal phenomenon and venous outflow disruption may play an etiological role in seizure development but remain challenging to demonstrate quantitatively. Blood oxygenation level-dependent (BOLD) cerebrovascular reactivity (CVR) imaging is an emerging technique that can measure both arterial steal phenomenon (as a paradoxical BOLD signal decrease during a vasodilatory stimulus) and impaired perinidal BOLD-CVR (which has been found in the presence of venous congestion on conventional angiography in bAVM patients with epilepsy). By applying this innovative BOLD-CVR technique, the aim is to better study CVR patterns and their correlation with morphological features on conventional angiography in patients with bAVM with and without epilepsy. METHODS: Twenty-two patients with unruptured and previously untreated bAVMs (8 with and 14 without epilepsy) were included in this case-control study. Quantitative CVR measurements were derived from BOLD functional MRI volumes using a novel standardized and precise hypercapnic stimulus (i.e., % BOLD/mm Hg CO2). In addition, 22 matched healthy controls underwent an identical BOLD-CVR study. Evaluation of venous congestion was performed on conventional angiography for all patients with bAVM. RESULTS: Patients with bAVM-associated epilepsy showed impaired whole-brain BOLD-CVR compared to those in the nonepilepsy group, even after correction for AVM volume and AVM grade (epilepsy vs nonepilepsy group: 0.17 ± 0.07 vs 0.25 ± 0.07, p = 0.04). A BOLD-CVR-derived arterial steal phenomenon was observed in 2 patients with epilepsy (25%). Venous congestion was noted in 3 patients with epilepsy (38%) and in 1 patient without epilepsy (7%; p = 0.08). CONCLUSIONS: These data suggest that whole-brain CVR impairment, and more pronounced hemodynamic alterations (i.e., arterial steal phenomenon and venous outflow restriction), may be more present in patients with bAVM-associated epilepsy. The association of impaired BOLD-CVR and bAVM-associated epilepsy will need further investigation in a larger patient cohort.

Flow augmentation STA-MCA bypass evaluation for patients with acute stroke and unilateral large vessel occlusion: a proposal for an urgent bypass flowchart.

OBJECTIVE: Endovascular recanalization trials have shown a positive impact on the preservation of ischemic penumbra in patients with acute large vessel occlusion (LVO). The concept of penumbra salvation can be extended to surgical revascularization with bypass in highly selected patients. For selecting these patients, the authors propose a flowchart based on multimodal MRI. METHODS: All patients with acute stroke and persisting internal carotid artery (ICA) or M1 occlusion after intravenous lysis or mechanical thrombectomy undergo advanced neuroimaging in a time window of 72 hours after stroke onset including perfusion MRI, blood oxygenation level-dependent functional MRI to evaluate cerebrovascular reactivity (BOLD-CVR), and noninvasive optimal vessel analysis (NOVA) quantitative MRA to assess collateral circulation. RESULTS: Symptomatic patients exhibiting persistent hemodynamic impairment and insufficient collateral circulation could benefit from bypass surgery. According to the flowchart, a bypass is considered for patients 1) with low or moderate neurological impairment (National Institutes of Health Stroke Scale score 1-15, modified Rankin Scale score ≤ 3), 2) without large or malignant stroke, 3) without intracranial hemorrhage, 4) with MR perfusion/diffusion mismatch > 120%, 5) with paradoxical BOLD-CVR in the occluded vascular territory, and 6) with insufficient collateral circulation. CONCLUSIONS: The proposed flowchart is based on the patient's clinical condition and multimodal MR neuroimaging and aims to select patients with acute stroke due to LVO and persistent inadequate collateral flow, who could benefit from urgent bypass.

Leptomeningeal collateral activation indicates severely impaired cerebrovascular reserve capacity in patients with symptomatic unilateral carotid artery occlusion.

For patients with symptomatic unilateral internal carotid artery (ICA) occlusion, impaired cerebrovascular reactivity (CVR) indicates increased stroke risk. Here, the role of collateral activation remains a matter of debate, whereas angio-anatomical collateral abundancy does not necessarily imply sufficient compensatory flow provided. We aimed to further elucidate the role of collateral activation in the presence of impaired CVR. From a prospective database, 62 patients with symptomatic unilateral ICA occlusion underwent blood oxygenation-level dependent (BOLD) fMRI CVR imaging and a transcranial Doppler (TCD) investigation for primary and secondary collateral activation. Descriptive statistic and multivariate analysis were used to evaluate the relationship between BOLD-CVR values and collateral activation. Patients with activated secondary collaterals exhibited more impaired BOLD-CVR values of the ipsilateral hemisphere (p = 0.02). Specifically, activation of leptomeningeal collaterals showed severely impaired ipsilateral hemisphere BOLD-CVR values when compared to activation of ophthalmic collaterals (0.05 ± 0.09 vs. 0.12 ± 0.04, p = 0.005). Moreover, the prediction analysis showed leptomeningeal collateral activation as a strong independent predictor for ipsilateral hemispheric BOLD-CVR. In our study, ipsilateral leptomeningeal collateral activation is the sole collateral pathway associated with severely impaired BOLD-CVR in patients with symptomatic unilateral ICA occlusion.