26 research outputs found
High posterior cerebral artery flow predicts ischemia recurrence in patients with internal carotid artery occlusion
Recurrent stroke is a dreaded complication of symptomatic internal carotid artery occlusion (ICAO). Transcranial Duplex (TCD)-derived increased flow velocity in the ipsilateral posterior cerebral artery (PCA)-P2 segment indicates activated leptomeningeal collateral recruitment and hemodynamic impairment. Leptomeningeal collaterals are pial vascular connections between the anterior and posterior vascular territories. These secondary collateral routes are activated when primary collaterals via the Circle of Willis are insufficient. Our goal was to test the TCD parameter PCA-P2 flow for prediction of ipsilateral ischemia recurrence. We retrospectively analyzed clinical and ultrasound parameters in patients with ICAO. Together with clinical variables, we tested systolic PCA-P2 flow velocity as predictor of a recurrent ischemic event using logistic regression models. Of 111 patients, 13 showed a recurrent ischemic event within the same vascular territory. Increased flow in the ipsilateral PCA-P2 on transcranial ultrasound (median and interquartile range [IQR]: 60 cm/s [IQR 26] vs. 86 cm/s [IQR 41], p = <0.001), as well as previous transient ischemic attack (TIA) and low NIHSS were associated with ischemia recurrence. Combined into one model, accuracy of these parameters to predict recurrent ischemia was 89.2%. Our data suggest that in patients with symptomatic ICAO, flow increases in the ipsilateral PCA-P2 suggest intensified compensatory efforts when other collaterals are insufficient. Together with the clinical variables, this non-invasive and easily assessable duplex parameter detects ICAO patients at particular risk of recurrent ischemia
Management of aneurysmal subarachnoid hemorrhage patients with antiplatelet use before the initial hemorrhage: an international survey
INTRODUCTION
The case fatality in aneurysmal subarachnoid hemorrhage (aSAH) is 50% due to the initial hemorrhage or subsequent complications like aneurysmal rebleed or delayed cerebral ischemia (DCI). One factor that might influence the initial brain damage or subsequent complications is the use of antiplatelet medication before the initial hemorrhage. The goal of this survey was to assess the different management options of patients with aSAH with antiplatelet use before the initial hemorrhage.
MATERIAL AND METHODS
An anonymous survey of 11 multiple-choice questions about management of aSAH patients with antiplatelet use before the initial hemorrhage was distributed to the international panel of attendees of the European Association of Neurosurgical Societies (EANS) annual meeting in Venice, Italy at 1-5 October 2017.
RESULTS
A total of 258 (54%) completed surveys were returned. In about 80%, the departments of neurosurgery and neurology were responsible for acute management of aSAH patients, whereas in 15% the intensive care unit. Department guidelines were present in 32%. In 65%, the responders always stop the antiplatelet agent at admission and in 4.3% are thrombocytes always transfused. When a guideline is present, the neurospecialists consider thrombocyte transfusion more often (83% vs. 65% p=0.02).
CONCLUSION
Our survey among mainly European neurosurgeons show that there is a significant variability in the management of aSAH patients who have been using antiplatelets before the initial hemorrhage. These findings emphasize the importance of the development of evidence-based guidelines for management of patients with aSAH and antiplatelet use before the initial hemorrhage
Blood Oxygenation Level-Dependent Cerebrovascular Reactivity-Derived Steal Phenomenon May Indicate Tissue Reperfusion Failure After Successful Endovascular Thrombectomy
In acute ischemic stroke due to large-vessel occlusion (LVO), the clinical outcome after endovascular thrombectomy (EVT) is influenced by the extent of autoregulatory hemodynamic impairment, which can be derived from blood oxygenation level-dependent cerebrovascular reactivity (BOLD-CVR). BOLD-CVR imaging identifies brain areas influenced by hemodynamic steal. We sought to investigate the presence of steal phenomenon and its relationship to DWI lesions and clinical deficit in the acute phase of ischemic stroke following successful vessel recanalization.From the prospective longitudinal IMPreST (Interplay of Microcirculation and Plasticity after ischemic Stroke) cohort study, patients with acute ischemic unilateral LVO stroke of the anterior circulation with successful endovascular thrombectomy (EVT; mTICI scale ≥ 2b) and subsequent BOLD-CVR examination were included for this analysis. We analyzed the spatial correlation between brain areas exhibiting BOLD-CVR-associated steal phenomenon and DWI infarct lesion as well as the relationship between steal phenomenon and NIHSS score at hospital discharge.Included patients (n = 21) exhibited steal phenomenon to different extents, whereas there was only a partial spatial overlap with the DWI lesion (median 19%; IQR, 8-59). The volume of steal phenomenon outside the DWI lesion showed a positive correlation with overall DWI lesion volume and was a significant predictor for the NIHSS score at hospital discharge.Patients with acute ischemic unilateral LVO stroke exhibited hemodynamic steal identified by BOLD-CVR after successful EVT. Steal volume was associated with DWI infarct lesion size and with poor clinical outcome at hospital discharge. BOLD-CVR may further aid in better understanding persisting hemodynamic impairment following reperfusion therapy
Spatio-temporally resolved in situ transmission electron microscopy of the dynamics of nanostructured materials
Inventory of long and short term future needs of food chain users for future functions of internet
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Bilateral spontaneous regression of vestibular schwannoma in neurofibromatosis type 2: a case report
BACKGROUND Patients with neurofibromatosis type 2 and bilateral vestibular schwannoma (VS) are frequently treated surgically for any tumor progression, and often repeated surgery or radiation treatment is even considered. Some VS progression occurs without the development of new clinical symptoms, or it does not progress in size over many years, even in the absence of any specific treatment.
CASE DESCRIPTION We report now a 61-year-old male patient with neurofibromatosis type 2 presenting with bilateral VS. In a long-term follow-up, both had increased in size but also showed bilateral spontaneous regression during an 11-year follow-up period with a "watch and wait" strategy.
CONCLUSIONS We emphasize conservative treatment ("watch and wait") in older patients even with long-term tumor progression without significant compression related clinical symptoms
Author response: BOLD cerebrovascular reactivity as a novel marker for crossed cerebellar diaschisis
We kindly thank Drs. Reidler and Kunz for their insightful comments regarding our article.1  The main objective was to study blood oxygen level–dependent cerebrovascular reactivity (BOLD-CVR) for crossed cerebellar diaschisis (CCD) detection. In this regard, worse clinical outcome in the CCD(+) group should indeed be interpreted with caution. Ideally, this association needs to be further investigated in a uniform stroke cohort with sequential follow-up studies.
We deliberately did not comment on supratentorial stroke volume because it is an inexact measurement and does not say anything about the infarct location.2 Besides, the concept that stroke volume is highly associated with the presence of CCD in the acute phase remains debatable, as the studies mentioned in the readers' comment appeared to be in disagreement.3,4 Nevertheless, we agree that stroke location would be a better variable for an adjusted analysis.
The statement made by Drs. Reidler and Kunz about “inferior cerebrovascular response indicating more severe supratentorial lesions”  is, however, erroneous. We have only shown the presence of more impaired supratentorial BOLD-CVR in the CCD(+) group. This finding has led us to believe that hemodynamic alterations may also cause CCD rather than a functional disruption alone. In general, BOLD imaging enables investigations on resting-state functional connectivity and the influence of CCD-induced altered metabolism in patients with stroke.
Gebrauch von Plättchenhemmer vor stattgehabten Subarachnoidalblutung - internationale Umfrage über das Management und aktuelle Praxis
Investigating the Association of Wallerian degeneration and diaschisis after ischemic stroke with BOLD cerebrovascular reactivity
Introduction: Wallerian degeneration and diaschisis are considered separate remote entities following ischemic stroke. They may, however, share common neurophysiological denominators, since they are both related to disruption of fiber tracts and brain atrophy over time. Therefore, with advanced multimodal neuroimaging, we investigate Wallerian degeneration and its association with diaschisis.
Methods: In order to determine different characteristics of Wallerian degeneration, we conducted examinations on seventeen patients with chronic unilateral ischemic stroke and persisting large vessel occlusion, conducting high-resolution anatomical magnetic resonance imaging (MRI) and blood oxygenation-level dependent cerebrovascular reactivity (BOLD-CVR) tests, as well as Diamox (O)-HO-PET hemodynamic examinations. Wallerian degeneration was determined using a cerebral peduncle asymmetry index (% difference of volume of ipsilateral and contralateral cerebral peduncle) of more than two standard deviations away from the average of age-matched, healthy subjects (Here a cerebral peduncle asymmetry index > 11%). Diaschisis was derived from BOLD-CVR to assess the presence of ipsilateral thalamus diaschisis and/or crossed cerebellar diaschisis.
Results: Wallerian degeneration, found in 8 (47%) subjects, had a strong association with ipsilateral thalamic volume reduction (r = 0.60) and corticospinal-tract involvement of stroke (p < 0.001). It was also associated with ipsilateral thalamic diaschisis (p = 0.021), No cerebral peduncular hemodynamic differences were found in patients with Wallerian degeneration. In particular, no CBF decrease or BOLD-CVR impairment was found.
Conclusion: We show a strong association between Wallerian degeneration and ipsilateral thalamic diaschisis, indicating a structural pathophysiological relationship