Cognitive Communicative Challenges in TBI: Assessment and Intervention in the Long Term

Author(s):  
Lori G. Cook ◽  
Roberta DePompei ◽  
Sandra B. Chapman

Neurocognitive stall is defined as a failure or lag in achieving later emerging cognitive milestones, representing an increasing “gap” in neurocognitive, social, and educational functioning after early brain injury (Chapman, 2006). This paper provides an overview of the subject in regard to pediatric traumatic brain injury (TBI), briefly discussing both ineffective and proactive methods for detecting and monitoring later emerging deficits associated with neurocognitive stall. The paper concludes with discussion of an emerging intervention to mitigate impairments in higher-order cognitive skills and enhance learning efficiency, including suggestions for use in rehabilitation settings and within school environments.

2014 ◽  
Vol 31 (7) ◽  
pp. 649-657 ◽  
Author(s):  
Nicholas P. Ryan ◽  
Vicki Anderson ◽  
Celia Godfrey ◽  
Miriam H. Beauchamp ◽  
Lee Coleman ◽  
...  

2017 ◽  
Vol 38 (1) ◽  
pp. 49-57 ◽  
Author(s):  
Anna H. Hung ◽  
Amy Cassedy ◽  
Hanna M. Schultz ◽  
Keith Owen Yeates ◽  
Hudson Gerry Taylor ◽  
...  

2007 ◽  
Vol 22 (1) ◽  
pp. 56-64 ◽  
Author(s):  
Lisa A. Brenner ◽  
Jeanne E. Dise-Lewis ◽  
Sarah K. Bartles ◽  
Susan E. OʼBrien ◽  
Matthew Godleski ◽  
...  

PM&R ◽  
2015 ◽  
Vol 7 ◽  
pp. S86-S86 ◽  
Author(s):  
Elana Katz ◽  
Beth Slomine ◽  
Stacy J. Suskauer

2021 ◽  
Author(s):  
Hattan Arif ◽  
Emily A Troyer ◽  
Jane S Paulsen ◽  
Florin Vaida ◽  
Elisabeth A. Wilde ◽  
...  

2014 ◽  
Vol 34 (10) ◽  
pp. 1637-1645 ◽  
Author(s):  
Amandine Jullienne ◽  
Jill M Roberts ◽  
Viorela Pop ◽  
M Paul Murphy ◽  
Elizabeth Head ◽  
...  

In our juvenile traumatic brain injury (jTBI) model, emergence of cognitive dysfunctions was observed up to 6 months after trauma. Here we hypothesize that early brain injury induces changes in the neurovascular unit (NVU) that would be associated with amyloid-beta (Aβ) accumulation. We investigated NVU changes for up to 6 months in a rat jTBI model, with a focus on the efflux protein P-glycoprotein (P-gp) and on the basement membrane proteins perlecan and fibronectin, all known to be involved in Aβ clearance. Rodent-Aβ staining is present and increased after jTBI around cerebral blood microvessels, and the diameter of those is decreased by 25% and 34% at 2 and 6 months, respectively, without significant angiogenesis. P-glycoprotein staining in endothelium is decreased by 22% and parallels an increase of perlecan and fibronectin staining around cerebral blood vessels. Altogether, these results strongly suggest that the emergence of long-term behavioral dysfunctions observed in rodent jTBI may be related to endothelial remodeling at the blood–brain barrier alongside vascular dysfunction and altered Aβ trafficking. This study shows that it is important to consider jTBI as a vascular disorder with long-term consequences on cognitive functions.


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