The Influence of Cerebral Arterial Circle on Prominent Hypointense Vessel Signs in Patients With Internal Carotid Artery Occlusion

Background and PurposePrevious studies on the presence of asymmetrical prominent cortical and medullary vessel signs (APCV/APMV) and collateral circulation in patients with internal carotid artery occlusion internal carotid artery occlusion (ICAO) are rare, and the conclusions are inconsistent. Our study aimed to investigate the relationship between the presence of APCV/APMV and collateral circulation in patients with ICAO.MethodsPatients with acute ischemic stroke with ICAO were recruited in this study. All 74 patients were divided into two groups depending on the presence of APCV and APMV. The status of the cerebral arterial circle (CAC) was graded as poor or good. The poor CAC was defined as MCA was invisible. Severe stroke was defined as cerebral watershed infarction (CWI) or territorial infarction (TI). Clinical and radiological markers were compared between these two groups. Logistic regression was used to investigate the association between the APCV/APMV and clinical and radiological markers.ResultsA total of 74 patients with ICAO were enrolled. Forty-three patients (58.1%) presented with an APCV and APMV was found in 35 (47.2%) patients. Compared with patients with non-APCV, patients with APCV had a more severe stroke (P = 0.038) and had a significantly higher incidence of poor CAC (P = 0.022) than those with APCV. Patients with APMV had a more severe stroke (P = 0.001). Logistic regression showed that poor CAC was independently associated with APCV and severe stroke were independently associated with APMV.ConclusionsOur study demonstrates that poor CAC was independently associated with the presence of the APCV in patients with ICAO. Severe stroke was independently associated with the APMV.

Endovascular Treatment of Posterior Cerebral Artery Trunk Aneurysm: The Status Quo and Dilemma

The posterior cerebral artery (PCA) is an important artery that can be divided into four segments (P1-4): segments P1-2 are proximal segments, and segments P3-4 are distal segments. Various aneurysms can occur along the PCA trunk. True saccular aneurysms are rare, and most PCA trunk aneurysms are dissecting. Sometimes, the PCA trunk can give rise to flow-related aneurysms in association with high-flow arteriovenous shunt diseases or moyamoya disease and internal carotid artery occlusion. Some PCA trunk aneurysms require treatment, especially ruptured or large/giant aneurysms. Recently, endovascular treatment (EVT) has become the mainstream treatment for PCA trunk aneurysms, and it mainly involves reconstructive or deconstructive techniques. Traditional EVT includes selective coiling with/without stent or balloon assistance and parent artery occlusion (PAO). For proximal aneurysms, the PCA should be preserved. For distal aneurysms, PAO can be performed. However, during EVT, preservation of the PCA must naturally be the prime objective. Recently, flow-diverting stents have been used and are a revolutionary treatment for unruptured dissecting aneurysms of the PCA trunk. Despite the associated complications, EVT remains an effective method for treating PCA trunk aneurysms and can result in a good prognosis.

Retinal Degeneration in a Murine Model of Retinal Ischemia by Unilateral Common Carotid Artery Occlusion

Retinal degeneration is a progressive retinal damage in ocular vascular diseases. There are several reasons for this, such as occlusion of arteries or veins, diabetic retinopathy, or hereditary retinal diseases. To study pathological mechanisms of retinal degeneration, it is required to develop experimentally reproducible and clinically relevant models. In our previous studies, we developed a murine model of retinal hypoperfusion by unilateral common carotid artery occlusion (UCCAO) which mimics the pathophysiology of ocular ischemic syndrome (OIS) in humans, and described broad pathological mechanisms in the retina after UCCAO. However, there still remain missing pieces of the ocular pathologic process by UCCAO. In this study, we examined those unfound mechanisms. UCCAO was performed on adult mice. Ocular dysfunctions, histological deficits, and inflammation were examined after UCCAO, compared with sham-operated mice. Evaluation values were analyzed by electrophysiological, histological, and molecular biological methods. Eyelid drooping was permanently seen after UCCAO. Induction time point of acute reversible cataract under anesthesia was shortened. Retinal/visual dysfunctions were detected 2-4 weeks after UCCAO. Specifically, scotopic b-wave was more affected than a-wave, with the dysfunction of photopic b-wave. Impaired oscillatory potentials and visual evoked potential were constantly observed. Pathological Müller gliosis/inflammation was featured with NeuN-positive cell loss in the ganglion cell layer. Axial length, intraocular pressure, pupillary light reflex, and retinal pigment epithelium/choroidal thickness were not changed by UCCAO. A murine model of retinal ischemia by UCCAO can be useful for studying a series of degenerative process in the ischemic retina.

Anesthetic Management for Spine Surgery in a Patient with Left Internal Carotid Artery Occlusion and Penetrating Aortic Ulcer: A Case Report

A key challenge of anesthesia is to provide patients with safe and optimized anesthetic management to improve prognosis and minimize mortality and morbidity. To this end, the anesthesiologist should comprehensively understand the patient’s physical status through pre-anesthetic assessment and carefully monitor the patient during surgery. Several types of novel patient-monitoring devices may be useful to achieve this purpose. We report a case of anesthetic management in a patient with left internal carotid artery occlusion and penetrating aortic ulcer.

Transient Hypoperfusion to Ischemic/Anoxic Spreading Depolarization is Related to Autoregulatory Failure in the Rat Cerebral Cortex

Background In ischemic stroke, cerebral autoregulation and neurovascular coupling may become impaired. The cerebral blood flow (CBF) response to spreading depolarization (SD) is governed by neurovascular coupling. SDs recur in the ischemic penumbra and reduce neuronal viability by the insufficiency of the CBF response. Autoregulatory failure and SD may coexist in acute brain injury. Here, we set out to explore the interplay between the impairment of cerebrovascular autoregulation, SD occurrence, and the evolution of the SD-coupled CBF response. Methods Incomplete global forebrain ischemia was created by bilateral common carotid artery occlusion in isoflurane-anesthetized rats, which induced ischemic SD (iSD). A subsequent SD was initiated 20–40 min later by transient anoxia SD (aSD), achieved by the withdrawal of oxygen from the anesthetic gas mixture for 4–5 min. SD occurrence was confirmed by the recording of direct current potential together with extracellular K+ concentration by intracortical microelectrodes. Changes in local CBF were acquired with laser Doppler flowmetry. Mean arterial blood pressure (MABP) was continuously measured via a catheter inserted into the left femoral artery. CBF and MABP were used to calculate an index of cerebrovascular autoregulation (rCBFx). In a representative imaging experiment, variation in transmembrane potential was visualized with a voltage-sensitive dye in the exposed parietal cortex, and CBF maps were generated with laser speckle contrast analysis. Results Ischemia induction and anoxia onset gave rise to iSD and aSD, respectively, albeit aSD occurred at a longer latency, and was superimposed on a gradual elevation of K+ concentration. iSD and aSD were accompanied by a transient drop of CBF (down to 11.9 ± 2.9 and 7.4 ± 3.6%, iSD and aSD), but distinctive features set the hypoperfusion transients apart. During iSD, rCBFx indicated intact autoregulation (rCBFx < 0.3). In contrast, aSD was superimposed on autoregulatory failure (rCBFx > 0.3) because CBF followed the decreasing MABP. CBF dropped 15–20 s after iSD, but the onset of hypoperfusion preceded aSD by almost 3 min. Taken together, the CBF response to iSD displayed typical features of spreading ischemia, whereas the transient CBF reduction with aSD appeared to be a passive decrease of CBF following the anoxia-related hypotension, leading to aSD. Conclusions We propose that the dysfunction of cerebrovascular autoregulation that occurs simultaneously with hypotension transients poses a substantial risk of SD occurrence and is not a consequence of SD. Under such circumstances, the evolving SD is not accompanied by any recognizable CBF response, which indicates a severely damaged neurovascular coupling.

Prevalence and Clinical Characteristics of Subclavian Steal Phenomenon/Syndrome in Patients with Acute Ischemic Stroke

There are no published clinical studies regarding the prevalence of subclavian steal among acute ischemic stroke patients. The aim of this study was to evaluate the prevalence and clinical significance of subclavian steal among a large number of consecutive ischemic stroke patients. Materials and methods: We reviewed the medical records of 2192 consecutive cases of acute ischemic stroke at a tertiary neurology clinic in Targu Mures, Romania, between 2018 and 2020. In total, 47 patients (2.2%) were diagnosed with subclavian steal phenomenon/syndrome. Results: Stroke patients with associated steal phenomenon were significantly younger (64.2 ± 11.1 versus 70.2 ± 12.8, p = 0.005) and predominantly male (68.1%). From among the 47 patients with subclavian steal phenomenon, nine (19.1%) presented stroke symptomatology in the vertebrobasilar territory. Overall, 83.3% of the stroke patients with associated steal phenomenon presented cerebral infarction and 16.7% presented TIA. There was no difference between groups regarding the affected vascular territory (VB versus carotid). Large artery atherosclerosis was more frequent in the stroke group with associated steal phenomenon (81.3% versus 43.5%, p = 0.0033). The NIHSS score at admission was higher in the patient group with associated steal phenomenon, but there was no difference in mRS at discharge. Associated carotid artery occlusion was more frequent in the stroke group with steal phenomenon (p < 0.01). Smoking and peripheral arteriopathy were more frequent in the patient group with associated steal phenomenon. Of the nine symptomatic patients, five underwent revascularization treatment. Conclusions: The prevalence of subclavian steal phenomenon among acute ischemic stroke patients was not higher than in other cohorts with heterogenous peripheral vascular pathologies. Similar to the general population, in acute ischemic stroke patients, the associated subclavian steal behaved like a benign hemodynamical condition, without severe consequences.