scholarly journals Biomechanics of Traumatic Brain Injury: Influences of the Morphologic Heterogeneities of the Cerebral Cortex

2008 ◽  
Vol 36 (7) ◽  
pp. 1203-1215 ◽  
Author(s):  
R.J.H. Cloots ◽  
H.M.T. Gervaise ◽  
J.A.W. van Dommelen ◽  
M.G.D. Geers
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury

Development of a de novo arteriovenous malformation after severe traumatic brain injury

2014 ◽  
Vol 14 (4) ◽  
pp. 418-420 ◽  
Author(s):  
Brandon A. Miller ◽  
David I. Bass ◽  
Joshua J. Chern
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Arteriovenous Malformation ◽  
Severe Traumatic Brain Injury ◽  
Arteriovenous Malformations ◽  
De Novo ◽  
First Report ◽  
Congenital Lesions

Arteriovenous malformations (AVMs) are typically considered congenital lesions, although there is growing evidence for de novo formation of these lesions as well. The authors present the case of an AVM in the same cerebral cortex that had been affected by a severe traumatic brain injury (TBI) more than 6 years earlier. To the best of the authors' knowledge, this is the first report attributing the formation of an AVM directly to TBI.

Temporal Lobe Syndromes

2020 ◽  
pp. 122-135
Author(s):  
Arpit Parmar ◽  
G. S. Kaloiya ◽  
Harsimarpreet Kaur
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Middle Cerebral Artery ◽  
Temporal Lobe ◽  
Cerebral Artery ◽  
Left Temporal Lobe ◽  
Temporal Lobes ◽  
Functional Aspects ◽  
The Common

Temporal lobes are one of the four major lobes of the cerebral cortex and perform a complex array of interrelated functions. They play an important role in various day-to-day functioning. The common pathologies leading to isolated temporal lobe dysfunction are infarction (of the middle cerebral artery), hemorrhage, seizures, tumors, encephalitis, and traumatic brain injury. Temporal lobe syndromes include a wide array of various neurological (Kluver-Bucy syndrome, Geschwind Gastaut syndrome, etc.), elementary (e.g., vertiginous syndromes, hallucinations, etc.), neuropsychiatric (e.g., anxiety, agitation, aggression, etc.), and cognitive (e.g., Korsakoff amnesia, cortical deafness, etc.) disorders. The presentation depends on a multitude of factors including involvement of dominant or non-dominant lobe. Left temporal lobe involvement usually leads to various forms of aphasia while right side involvement leads to more covert and varied syndromes. In this chapter, the authors discuss the anatomy of the temporal lobe, its functional aspects, and various syndromes of temporal lobe dysfunction.

Increased expression of ferritin in cerebral cortex after human traumatic brain injury

2012 ◽  
Vol 34 (7) ◽  
pp. 1173-1180 ◽  
Author(s):  
Huan-Dong Liu ◽  
Wei Li ◽  
Zhen-Rui Chen ◽  
Meng-Liang Zhou ◽  
Zong Zhuang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury

scholarly journals Multiple Sites of Vasopressin Synthesis in the Injured Brain

2010 ◽  
Vol 31 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Brian J Zink ◽  
Adam Chodobski
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Impact Model ◽  
Proinflammatory Mediators ◽  
Injured Brain ◽  
Pathophysiological Role ◽  
Cerebrovascular Endothelium ◽  
Vasopressin Synthesis

Previous studies have indicated that the primary targets for vasopressin actions on the injured brain are the cerebrovascular endothelium and astrocytes, and that vasopressin amplifies the posttraumatic production of proinflammatory mediators. Here, the controlled cortical impact model of traumatic brain injury in rats was used to identify the sources of vasopressin in the injured brain. Injury increased vasopressin synthesis in the hypothalamus and cerebral cortex adjacent to the posttraumatic lesion. In the cortex, vasopressin was predominantly produced by activated microglia/macrophages, and, to a lesser extent, by the cerebrovascular endothelium. These data further support the pathophysiological role of vasopressin in brain injury.

Expression of the NLRP3 Inflammasome in Cerebral Cortex After Traumatic Brain Injury in a Rat Model

2013 ◽  
Vol 38 (10) ◽  
pp. 2072-2083 ◽  
Author(s):  
Huan-Dong Liu ◽  
Wei Li ◽  
Zhen-Rui Chen ◽  
Yang-Chun Hu ◽  
Ding-Ding Zhang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Rat Model ◽  
Nlrp3 Inflammasome

scholarly journals Interactome and reciprocal activation of pathways in topical mesenchymal stem cells and the recipient cerebral cortex following traumatic brain injury

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Ping K. Lam ◽  
Kevin K. W. Wang ◽  
Anthony W. I. Lo ◽  
Cindy S. W. Tong ◽  
Don W. C. Ching ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cerebral Cortex ◽  
Brain Injury

Activation of JAK2/STAT pathway in cerebral cortex after experimental traumatic brain injury of rats

2011 ◽  
Vol 498 (2) ◽  
pp. 147-152 ◽  
Author(s):  
Jin-bing Zhao ◽  
Yang Zhang ◽  
Guang-zhao Li ◽  
Xing-fen Su ◽  
Chun-hua Hang
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Experimental Traumatic Brain Injury ◽  
Stat Pathway
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