Dihydrolipoic acid enhances autophagy and alleviates neurological deficits after subarachnoid hemorrhage in rats

2021 ◽  
pp. 113752
Author(s):  
Keren Zhou ◽  
Budbazar Enkhjargal ◽  
Jun Mo ◽  
Tongyu Zhang ◽  
Qiquan Zhu ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Neurological Deficits ◽  
Dihydrolipoic Acid

scholarly journals TRAF3 mediates neuronal apoptosis in early brain injury following subarachnoid hemorrhage via targeting TAK1-dependent MAPKs and NF-κB pathways

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yan Zhou ◽  
Tao Tao ◽  
Guangjie Liu ◽  
Xuan Gao ◽  
Yongyue Gao ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Therapeutic Target ◽  
Cortical Neurons ◽  
Neuronal Apoptosis ◽  
Early Brain Injury ◽  
Neurological Deficits ◽  
Human Brain Tissue

AbstractNeuronal apoptosis has an important role in early brain injury (EBI) following subarachnoid hemorrhage (SAH). TRAF3 was reported as a promising therapeutic target for stroke management, which covered several neuronal apoptosis signaling cascades. Hence, the present study is aimed to determine whether downregulation of TRAF3 could be neuroprotective in SAH-induced EBI. An in vivo SAH model in mice was established by endovascular perforation. Meanwhile, primary cultured cortical neurons of mice treated with oxygen hemoglobin were applied to mimic SAH in vitro. Our results demonstrated that TRAF3 protein expression increased and expressed in neurons both in vivo and in vitro SAH models. TRAF3 siRNA reversed neuronal loss and improved neurological deficits in SAH mice, and reduced cell death in SAH primary neurons. Mechanistically, we found that TRAF3 directly binds to TAK1 and potentiates phosphorylation and activation of TAK1, which further enhances the activation of NF-κB and MAPKs pathways to induce neuronal apoptosis. Importantly, TRAF3 expression was elevated following SAH in human brain tissue and was mainly expressed in neurons. Taken together, our study demonstrates that TRAF3 is an upstream regulator of MAPKs and NF-κB pathways in SAH-induced EBI via its interaction with and activation of TAK1. Furthermore, the TRAF3 may serve as a novel therapeutic target in SAH-induced EBI.

Effects of subarachnoid hemorrhage on cerebral blood volume, blood flow, and oxygen utilization in humans

1977 ◽  
Vol 46 (4) ◽  
pp. 446-453 ◽  
Author(s):  
Robert L. Grubb ◽  
Marcus E. Raichle ◽  
John O. Eichling ◽  
Mokhtar H. Gado
Keyword(s):  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Blood Volume ◽  
Cerebral Vasospasm ◽  
Cerebral Blood Volume ◽  
Neurological Deficits ◽  
Regional Cerebral Blood ◽  
Oxygen Utilization ◽  
Ruptured Intracranial Aneurysm ◽  
Regional Cerebral Blood Volume

✓ Forty-five studies of regional cerebral blood volume (rCBV), regional cerebral blood flow (rCBF), and regional cerebral oxygen utilization (rCMRO2) were performed in 30 patients undergoing diagnostic cerebral angiography for evaluation of a subarachnoid hemorrhage due to a ruptured intracranial aneurysm. Tracer methods employing radioactive oxygen-15 were used to measure rCBV, rCBF, and rCMRO2. The patient studies were divided into groups based on their neurological status and the presence or absence of cerebral vasospasm. Subarachnoid hemorrhage, with and without vasospasm, produced significant decreases in CBF and CMRO2. In general, patients with more severe neurological deficits, and patients with more severe degrees of vasospasm, had a more marked depression of CBF and CMRO2. The most striking finding was a significant (p < 0.001) increase in CBV (to 58% above normal) in patients with severe neurological deficits associated with severe cerebral vasospasm. This large increase suggests that cerebral vasospasm consists of constriction of the large, radiographically visible extraparenchymal vessels accompanied by a massive dilation of intraparenchymal vessels.

scholarly journals Ruptured Bilateral Pericallosal Artery Aneurysm in Mirror Position: Case Report

2018 ◽  
Vol 37 (03) ◽  
pp. 263-266
Author(s):  
Lucas Meguins ◽  
Linoel Valsechi ◽  
Ronaldo Fernandes ◽  
Dionei Morais ◽  
Antonio Spotti
Keyword(s):  
Case Report ◽  
Subarachnoid Hemorrhage ◽  
External Ventricular Drain ◽  
Artery Aneurysm ◽  
Operative Management ◽  
Neurological Deficits ◽  
Pericallosal Artery ◽  
Digital Subtraction Arteriography ◽  
The Many ◽  
The Right

Introduction Pericallosal artery (PA) aneurysms represent 2 to 9% of all intracranial aneurysms, and their management remains difficult. Objective The aim of the present study is to describe the case of an adult woman with subarachnoid hemorrhage and bilateral PA aneurysm in mirror position. Case Report A 46-year-old woman was referred to our institution 20 days after a sudden severe headache. She informed that she was treating her arterial hypertension irregularly, and consumed ∼ 20 cigarettes/day. The patient was neurologically intact at admission. A non-contrast computed tomography (CT) on the first day of the onset of the symptoms revealed hydrocephaly and subarachnoid hemorrhage (Fisher III). An angio-CT/digital subtraction arteriography showed bilateral PA aneurysms in mirror position. The patient was successfully treated with surgery via the right interhemispheric approach (because the surgeon is right-handed); the surgeon performed the proximal control with temporary clipping, and introduced an external ventricular drain at the end of the surgery. The patient was discharged on the fourth postoperative day without any additional neurological deficits or ventricular shunts. Conclusion Ruptured PA aneurysm is a surgically challenging aneurysm due to the many anatomical nuances and risk of rebleeding. However, the operative management of ruptured bilateral PA aneurysms is feasible and effective.

scholarly journals Vasospasm as the sole cause of cerebral ischemia: how strong is the evidence?

2006 ◽  
Vol 21 (3) ◽  
pp. 1-7 ◽  
Author(s):  
Sherman C. Stein ◽  
Joshua M. Levine ◽  
Seema Nagpal ◽  
Peter D. LeRoux
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Potential Role ◽  
Review Literature ◽  
Neurological Deficits ◽  
Therapeutic Approaches ◽  
Large Arteries ◽  
Novel Therapeutic

✓ The authors review literature that challenges the view that vasospasm involving large arteries is the exclusive cause of delayed ischemic neurological deficits (DINDs) following subarachnoid hemorrhage. They discuss alternative mechanisms and review the evidence supporting a potential role for thromboembolism. They conclude that vasospasm and thromboembolism play interrelated and additive roles in the development of DINDs, and that this interaction provides opportunities for novel therapeutic approaches.

Positron Emission Tomographic Cerebral Perfusion Disturbances and Transcranial Doppler Findings among Patients with Neurological Deterioration after Subarachnoid Hemorrhage

Neurosurgery ◽  
2003 ◽  
Vol 52 (5) ◽  
pp. 1017-1024 ◽  
Author(s):  
Pawan S. Minhas ◽  
David K. Menon ◽  
Piotr Smielewski ◽  
Marek Czosnyka ◽  
Peter J. Kirkpatrick ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Carotid Artery ◽  
Cerebral Perfusion ◽  
Internal Carotid ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Neurological Deficits ◽  
Positron Emission Tomographic ◽  
Positron Emission ◽  
Arterial Vasospasm ◽  
The Mean

Abstract OBJECTIVE After aneurysmal subarachnoid hemorrhage, approximately 30% of patients experience delayed neurological deficits, related in part to arterial vasospasm and dysautoregulation. Transcranial Doppler (TCD) ultrasonography is commonly used to noninvasively detect arterial vasospasm. We studied cerebral perfusion patterns and associated TCD indices for 25 patients who developed clinical signs of delayed neurological deficits. METHODS Patients were treated in a neurosurgical intensive care unit and were studied if they exhibited delayed focal or global neurological deterioration. Positron emission tomographic cerebral blood flow (CBF) studies and TCD studies measuring the mean flow velocity (FV) of the middle cerebral artery and the middle cerebral artery FV/internal carotid artery FV ratio (with the internal carotid artery FV being measured extracranially at the cranial base) were performed. Glasgow Outcome Scale scores were assessed at 6 months. RESULTS A markedly heterogeneous pattern of CBF distribution was observed, with hyperemia, normal CBF values, and reduced flow being observed among patients with delayed neurological deficits. TCD indices were not indicative of the cerebral perfusion findings. The mean CBF value was slightly lower for patients who did not survive (32.3 ml/100 g/min), compared with those who did survive (36.0 ml/100 g/min, P= 0.05). CONCLUSION Among patients who developed delayed neurological deficits after aneurysmal subarachnoid hemorrhage, a wide range of cerebral perfusion disturbances was observed, calling into question the traditional concept of large-vessel vasospasm. Commonly used TCD indices do not reflect cerebral perfusion values.

Use of the Extracranial-Intracranial Arterial Bypass in the Management of Refractory Vasospasm: A Case Report

Neurosurgery ◽  
1985 ◽  
Vol 17 (3) ◽  
pp. 474-479 ◽  
Author(s):  
Jacob Rosenstein ◽  
Hunt H. Batjer ◽  
Duke S. Samson
Keyword(s):  
Case Report ◽  
Subarachnoid Hemorrhage ◽  
Arterial Hypertension ◽  
Volume Expansion ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Morbidity And Mortality ◽  
Neurological Deficits ◽  
Collateral Flow ◽  
Intravascular Volume ◽  
Arterial Vasospasm

Abstract Cerebral arterial vasospasm after aneurysmal subarachnoid hemorrhage remains one of the major causes of morbidity and mortality in patients surviving the initial hemorrhage. Once established, no known method has been shown to reverse this process in humans. Although intravascular volume expansion and induced arterial hypertension have been shown to be effective in the reversal of neurological deficits secondary to vasospasm, a large proportion of patients remain refractory to these methods. We report one such case successfully managed by the estalishment of an extracranial-intracranial anastomosis in an attempt to augment collateral flow.

Delayed neurological deficits detected by an ischemic pattern in the extracellular cerebral metabolites in patients with aneurysmal subarachnoid hemorrhage

2004 ◽  
Vol 100 (1) ◽  
pp. 8-15 ◽  
Author(s):  
Jane Skjøth-Rasmussen ◽  
Mette Schulz ◽  
Soren Risom Kristensen ◽  
Per Bjerre
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Metabolism ◽  
Brain Infarction ◽  
Neurological Deficits ◽  
Parent Artery ◽  
Glycerol Concentration ◽  
Microdialysis Probe ◽  
Content Type ◽  
Fine Print

Object. In the treatment of patients with aneurysmal subarachnoid hemorrhage (SAH), early occlusion of the aneurysm is necessary as well as monitoring and treatment of complications following the primary bleeding episode. Monitoring with microdialysis has been studied for its ability to indicate and predict the occurrence of delayed ischemic neurological deficits (DINDs) in patients with SAH. Methods. In 42 patients with aneurysmal SAH microdialysis monitoring of metabolites was performed using a 0.3-µl/minute perfusion flow over several days, and the results were correlated to clinical events and to brain infarction observed on computerized tomography scans. The microdialysis probe was inserted into the territory of the parent artery of the aneurysm. The authors defined an ischemic pattern as increases in the lactate/glucose (L/G) and lactate/pyruvate (L/P) ratios that were greater than 20% followed by a 20% increase in glycerol concentration. This ischemic pattern was found in 17 of 18 patients who experienced a DIND and in three of 24 patients who did not experience a delayed clinical deterioration. The ischemic pattern preceded the occurrence of a DIND by a mean interval of 11 hours. Maximum L/G and L/P ratios did not correlate with the presence of DIND or outcome, and there was no association between the glycerol level and subsequent brain infarction. Conclusions. Microdialysis monitoring of the cerebral metabolism in patients with SAH may predict with high sensitivity and specificity the occurrence of a DIND. Whether an earlier diagnosis results in better treatment of DINDs and, therefore, in overall better outcomes remains to be proven, as it is linked to an efficacious treatment of cerebral vasospasm.

Correlation Among Systemic Inflammatory Parameter, Occurrence of Delayed Neurological Deficits, and Outcome After Aneurysmal Subarachnoid Hemorrhage

Neurosurgery ◽  
2012 ◽  
Vol 72 (3) ◽  
pp. 367-375 ◽  
Author(s):  
Carl Muroi ◽  
Michael Hugelshofer ◽  
Martin Seule ◽  
Ilhan Tastan ◽  
Masayuki Fujioka ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Confidence Interval ◽  
Early Phase ◽  
Odds Ratio ◽  
Time Course ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Unfavorable Outcome ◽  
Neurological Deficits ◽  
Inflammatory Parameters ◽  
Leukocyte Counts

Abstract BACKGROUND: The role and impact of systemic inflammatory response after aneurysmal subarachnoid hemorrhage remain to be elucidated. OBJECTIVE: To assess the time course and correlation of systemic inflammatory parameters with outcome and the occurrence of delayed ischemic neurological deficits (DINDs) after subarachnoid hemorrhage. METHODS: Besides the baseline characteristics, daily interleukin-6 (IL-6), procalcitonin, C-reactive protein levels, and leukocyte counts were prospectively measured until day 14 after subarachnoid hemorrhage. Occurrence of infectious complications and application of therapeutic hypothermia were assessed as confounding factors. The primary end point was outcome after 3 months, assessed by Glasgow Outcome Scale; the secondary end point was the occurrence of DINDs. RESULTS: During a 3-year period, a total of 138 patients were included. All inflammatory parameters measured were higher in patients with unfavorable outcome (Glasgow Outcome Scale score, 1-3). After adjustment for confounding factors, elevated IL-6 and leukocyte counts remained significant risk factors for unfavorable outcome. The odds ratio for log IL-6 was 4.07 (95% confidence interval, 1.18 to 14.03; P = .03) and for leukocyte counts was 1.24 (95% confidence interval, 1.06-1.46, P = .008). The analysis of the time course established that IL-6 was the only significantly elevated parameter in the early phase in patients with unfavorable outcome. Higher IL-6 levels in the early phase (days 3-7) were associated with the occurrence of DINDs. The adjusted odds ratio for log IL-6 was 4.03 (95% confidence interval, 1.21-13.40; P = .02). CONCLUSION: Higher IL-6 levels are associated with worse clinical outcome and the occurrence of DINDs. Because IL-6 levels were significantly elevated in the early phase, they might be a useful parameter to monitor.

Sign in / Sign up

Export Citation Format

Share Document