3D exoscopic versus microscopic superficial temporal artery to middle cerebral artery bypass surgery for moyamoya disease - a comparative series.

PURPOSE: Superficial temporal artery to middle cerebral artery (STA-MCA) direct bypass surgery is the most common surgical procedure to treat moyamoya disease (MMD). Here, we aim to compare the performance of the 3D exoscope in bypass surgery with the gold standard operative microscope. METHODS: All direct STA-MCA bypass procedures performed at a single university hospital for MMD between 2015 and 2023 were considered for inclusion. Data were retrospectively collected from patient files and surgical video material. From 2020 onwards, bypass procedures were exclusively performed using a digital three-dimensional exoscope as visualization device. Results were compared with a microsurgical bypass control group (2015-2019). The primary endpoint was defined as total duration of surgery, duration of completing the vascular anastomosis (ischemia time), bypass patency, number of stiches to perform the anastomosis, added stiches after leakage testing of the anastomosis and the Glasgow outcome scale (GOS) at last follow-up as secondary outcome parameter. RESULTS: A total of 16 consecutive moyamoya patients underwent 21 STA-MCA bypass procedures. Thereof, six patients were operated using a microscope and ten patients using an exoscope (ORBEYE® n = 1; AEOS® n = 9). Total duration of surgery was comparable between devices (microscope: 313 min. ± 116 vs. exoscope: 279 min. ± 42; p = 0.647). Ischemia time also proved similar between groups (microscope: 43 min. ± 19 vs. exoscope: 41 min. ± 7; p = 0.701). No differences were noted in bypass patency rates. The number of stiches per anastomosis was similar between visualization devices (microscope: 17 ± 4 vs. exoscope: 17 ± 2; p = 0.887). In contrast, more additional stiches were needed in microscopic anastomoses after leakage testing the bypass (p = 0.035). CONCLUSION: Taking into account the small sample size, end-to-side bypass surgery for moyamoya disease using a foot switch-operated 3D exoscope was not associated with more complications and led to comparable clinical and radiological results as microscopic bypass surgery.

Elevated concentrations of macrophage migration inhibitory factor in serum and cerebral microdialysate are associated with delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.

Objective: Inflammation is increasingly recognized to be involved in the pathophysiology of aneurysmal subarachnoid hemorrhage (aSAH) and may increase the susceptibility to delayed cerebral ischemia (DCI). Macrophage migration inhibitory factor (MIF) has been shown to be elevated in serum and cerebrospinal fluid (CSF) after aSAH. Here, we determined MIF levels in serum, CSF and cerebral microdialysate (MD) at different time-points after aSAH and evaluated their clinical implications. Methods: MIF levels were measured in serum, CSF and MD obtained from 30 aSAH patients during early (EPd1-4), critical (CPd5-15) and late (LPd16-21) phase after hemorrhage. For subgroup analyses, patients were stratified based on demographic and clinical data. Results: MIF levels in serum increased during CPd5-15 and decreased again during LPd16-21, while CSF levels showed little changes over time. MD levels peaked during EPd1-4, decreased during CPd5-15 and increased again during LPd16-21. Subgroup analyses revealed significantly higher serum levels in patients with aneurysms located in the anterior vs. posterior circulation during CPd5-15 (17.3 [15.1-21.1] vs. 10.0 [8.4-11.5] ng/ml, p = 0.009) and in patients with DCI vs. no DCI during CPd5-15 (17.9 [15.1-22.7] vs. 11.9 [8.9-15.9] ng/ml, p = 0.026) and LPd16-21 (17.4 [11.7-27.9] vs. 11.3 [9.2-12.2] ng/ml, p = 0.021). In addition, MIF levels in MD during CPd5-15 were significantly higher in patients with DCI vs. no DCI (3.6 [1.8-10.7] vs. 0.2 [0.1-0.7] ng/ml, p = 0.026), while CSF levels during the whole observation period were similar in all subgroups. Conclusion: Our findings in a small cohort of aSAH patients provide preliminary data on systemic, global cerebral and local cerebral MIF levels after aSAH and their clinical implications. Clinical trial registration: ClinicalTrials.gov, identifier: NCT02142166.

Posttraumatic subarachnoid hemorrhage related to concomitant carotid artery dissection and ruptured basilar trunk aneurysm: A case report and literature review.

BACKGROUND: Carotid artery dissections (CADs) are a relatively rare disorder, whereas intracranial aneurysms (IAs) form a common cerebrovascular pathology. Since both vascular entities share similar risk factors and associations with connective tissue and vascular disorders, a common pathogenesis has been suggested. Here, we present a case of the concomitant occurrence of a CAD and a ruptured basilar trunk aneurysm (BTA). In the discussion, we elaborate on both vascular entities and have reviewed the literature on their concomitant incidence and potential shared pathogenesis. CASE DESCRIPTION: We present a case of a 40-year-old female patient who was admitted to our hospital because of subarachnoid hemorrhage following a minor head trauma. Imaging revealed a BTA and unilateral extracranial dissection of the internal carotid artery. Despite coiling of the aneurysm, stenting of the dissection, and antithrombotic therapy, the patient died due to extensive cerebral ischemia sequelae. CONCLUSION: CAD and BTAs have both been associated with a vascular vulnerability but their concomitant occurrence has not been described previously. The previous studies have suggested an increased incidence of IAs in patients with a CAD and vice versa. However, the number of studies and reports on this mutual increased incidence is limited. Therefore, a shared pathogenesis seems rather speculative. In our case, we suggest that a posttraumatic CAD-induced hemodynamic alterations resulting in rupture of the saccular BTA.

Retinal Vessel Responses to Flicker Stimulation Are Impaired in Ca v 2.3-Deficient Mice-An in-vivo Evaluation Using Retinal Vessel Analysis (RVA).

Objective: Metabolic demand increases with neuronal activity and adequate energy supply is ensured by neurovascular coupling (NVC). Impairments of NVC have been reported in the context of several diseases and may correlate with disease severity and outcome. Voltage-gated Ca2+-channels (VGCCs) are involved in the regulation of vasomotor tone. In the present study, we compared arterial and venous responses to flicker stimulation in Cav2.3-competent (Cav2.3[+/+]) and -deficient (Cav2.3[-/-]) mice using retinal vessel analysis. Methods: The mice were anesthetized and the pupil of one eye was dilated by application of a mydriaticum. An adapted prototype of retinal vessel analyzer was used to perform dynamic retinal vessel analysis. Arterial and venous responses were quantified in terms of the area under the curve (AUCart/AUCven) during flicker application, mean maximum dilation (mMDart/mMDven) and time to maximum dilation (tMDart/tMDven) during the flicker, dilation at flicker cessation (DFCart/DFCven), mean maximum constriction (mMCart/mMCven), time to maximum constriction (tMCart/tMCven) after the flicker and reactive magnitude (RMart/RMven). Results: A total of 33 retinal scans were conducted in 22 Cav2.3[+/+] and 11 Cav2.3[-/-] mice. Cav2.3[-/-] mice were characterized by attenuated and partially reversed arterial and venous responses, as reflected in significantly lower AUCart (p = 0.031) and AUCven (p = 0.047), a trend toward reduced DFCart (p = 0.100), DFCven (p = 0.100), mMDven (p = 0.075), and RMart (p = 0.090) and a trend toward increased tMDart (p = 0.096). Conclusion: To our knowledge, this is the first study using a novel, non-invasive analysis technique to document impairment of retinal vessel responses in VGCC-deficient mice. We propose that Cav2.3 channels could be involved in NVC and may contribute to the impairment of vasomotor responses under pathophysiological conditions.

Two out of three of octogenarians benefitted from delayed resection of spinal meningiomas.

BACKGROUND: Can elderly patients with thoracic meningioma and severe paraparesis benefit from delayed surgery? CASE DESCRIPTION: Two out of three octogenarians with severe preoperative paraparesis (all wheelchair-bound) were able to walk again following delayed (60-120 days from onset of deficit) surgical resection of thoracic spinal meningiomas. CONCLUSION: Two out of three octogenarians with thoracic meningiomas causing severe paraparesis benefitted from the delayed (i.e. from 60 to 289 days) surgical resection of their tumors.

Assessment and Imaging of the Cerebrovascular Glycocalyx.

The glycocalyx is a gel-like layer lining the luminal surface of the endothelium. The glycocalyx exerts an important barrier role because it prevents exposure of plasma components to the endothelial surface. Disruption of the glycocalyx by local inflammation or ischemia results in decreased glycocalyx thickness which is associated with a number of vascular diseases. The cerebrovascular glycocalyx has sparsely been studied, but is of great interest because of its potential role in cerebrovascular disease. In this review, we describe all existing techniques to visualize the glycocalyx and designate techniques that may be suitable for studying the cerebrovascular glycocalyx. A total of seven imaging techniques are discussed thoroughly, including transmission electron microscopy, intravital microscopy, micro-particle image velocimetry, confocal laser scanning microscopy, two-photon laser scanning microscopy, orthogonal polarization spectral imaging and sidestream dark field/oblique imaging. Measurement of serum concentrations of glycocalyx-specific constituents is another method for glycocalyx analysis. Also, we have reviewed the methods of glycocalyx analysis by using these imaging techniques. So far, the cerebrovascular glycocalyx has only been studied in vitro. However, other cerebral microcirculatory properties have been studied in vivo. This suggests that the cerebrovascular glycocalyx can be studied in vivo by using some of the described techniques, when specific software is subjoined to the analysis. In conclusion, we have summarized techniques available for glycocalyx assessment, and explained the significance and technical possibilities regarding cerebrovascular glycocalyx visualization. Cerebrovascular glycocalyx assessment would add valuable information to our understanding of the pathophysiology of cerebrovascular disease. Moreover, as a part of the blood-brain barrier, more knowledge on the cerebrovascular glycocalyx may lead to better understanding of neurodegenerative conditions that are caused by a compromised blood-brain barrier including Alzheimer`s disease, vascular dementia, multiple sclerosis and epilepsy.