scholarly journals Oxidative stress in subarachnoid haemorrhage: significance in acute brain injury and vasospasm

Author(s):  
R. E. Ayer ◽  
J. H. Zhang
2021 ◽  
Author(s):  
Jia Xu Lim ◽  
Yuan Guang Lim ◽  
A Aravin Kumar ◽  
Tien Meng Cheong ◽  
Julian Xinguang Han ◽  
...  

Abstract IntroductionAneurysmal subarachnoid haemorrhage (aSAH) is a condition with significant morbidity and mortality. In the context of acute brain injury, frailty, sarcopaenia and osteopaenia have become increasing concerns. Multiple indices have been devised in various surgical specialties to predict outcome and guide management. In this study, we examined whether such markers have relevance towards outcomes from acute brain conditions, such as aSAH. MethodsAn observational study in a tertiary neurosurgical unit on 51 consecutive patients with ruptured aSAH was performed. We compared various frailty indices (modified frailty index 11, and 5, and the National Surgical Quality Improvement Program score [NSQIP]), temporalis (TMT) and zygoma thickness (markers of sarcopaenia and osteopaenia), against traditional markers (age, World Federation of Neurological Surgery and modified Fisher scale [MFS]) for aSAH outcomes. ResultsTMT was the best performing marker in our cohort with an AUC of 0.82, Somers’ D statistic of 0.63 and Tau statistic 0.25. Of the frailty scores, the NSQIP performed the best (AUC 0.69, Somer’s D 0.40, Tau 0.16), at levels comparable to traditional markers of aSAH, such as MFS (AUC 0.68, Somer’s D 0.43, Tau 0.17). After multivariate analysis, patients with TMT ≥5.5mm (defined as non-frail), were less likely to experience complications (OR 0.20 [0.06 – 0.069], p = 0.011), and had a larger proportion of favourable mRS on discharge (95.0% vs. 58.1%, p = 0.024) and at 3-months (95.0% vs. 64.5%, p = 0.048). However, the gap between unfavourable and favourable mRS was insignificant at the comparison of 1-year outcomes. ConclusionTMT, as a marker of sarcopaenia, correlated well with the presenting status, and outcomes of aSAH. Frailty, as defined by NSQIP, performed at levels equivalent to aSAH scores of clinical relevance, suggesting that, in patients presenting with acute brain injury, both non-neurological and neurological factors were complementary in the determination of eventual clinical outcomes. Further validation of these markers, in addition to exploration of other relevant frailty indices, may help to better prognosticate aSAH outcomes and allow for a precision medicine approach to decision making and optimization of best outcomes Trial registrationNot applicable


2014 ◽  
Vol 2 ◽  
pp. 396-399 ◽  
Author(s):  
DJ Albers ◽  
J Claassen ◽  
M Schmidt ◽  
G Hripcsak

Therapy ◽  
2006 ◽  
Vol 3 (3) ◽  
pp. 399-405
Author(s):  
Elham Hadidi ◽  
Mojtaba Mojtahedzadeh ◽  
Mohammad Hassan Paknejad ◽  
Shekoufeh Nikfar ◽  
Mohammad Jafar Zamani ◽  
...  

2014 ◽  
Vol 21 (10) ◽  
pp. 1201-1211 ◽  
Author(s):  
Ana Rodriguez-Rodriguez ◽  
Juan Egea-Guerrero ◽  
Francisco Murillo-Cabezas ◽  
Antonio Carrillo-Vico

2018 ◽  
Vol 17 (9) ◽  
pp. 689-695 ◽  
Author(s):  
Nidhi Khatri ◽  
Manisha Thakur ◽  
Vikas Pareek ◽  
Sandeep Kumar ◽  
Sunil Sharma ◽  
...  

Background & Objective: Traumatic Brain Injury (TBI) is one of the major causes of mortality and morbidity worldwide. It represents mild, moderate and severe effects of physical assault to brain which may cause sequential, primary or secondary ramifications. Primary injury can be due to the first physical hit, blow or jolt to one of the brain compartments. The primary injury is then followed by secondary injury which leads to biochemical, cellular, and physiological changes like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and generation of oxidative stress. Apart from this, there is also an immediate increase in glutamate at the synapses following severe TBI. Excessive glutamate at synapses in turn activates corresponding NMDA and AMPA receptors that facilitate excessive calcium influx into the neuronal cells. This leads to the generation of oxidative stress which further leads to mitochondrial dysfunction, lipid peroxidation and oxidation of proteins and DNA. As a consequence, neuronal cell death takes place and ultimately people start facing some serious disabilies. Conclusion: In the present review we provide extensive overview of the role of reactive oxygen species (ROS)-induced oxidative stress and its fatal effects on brain after TBI.


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