scholarly journals Faculty Opinions recommendation of A lack of amyloid beta plaques despite persistent accumulation of amyloid beta in axons of long-term survivors of traumatic brain injury.

2008 ◽  
Author(s):  
George Perry
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Amyloid Beta ◽  
Long Term Survivors

Cognitive strategy usage in long-term survivors of severe traumatic brain injury with persisting impulsive aggression

2002 ◽  
Vol 32 (4) ◽  
pp. 639-647 ◽  
Author(s):  
Kevin W Greve ◽  
Jeff Love ◽  
Elisabeth Sherwin ◽  
Matthew S Stanford ◽  
Charles Mathias ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Cognitive Strategy ◽  
Impulsive Aggression ◽  
Long Term Survivors

scholarly journals Juvenile Traumatic Brain Injury Induces Long-Term Perivascular Matrix Changes Alongside Amyloid-Beta Accumulation

2014 ◽  
Vol 34 (10) ◽  
pp. 1637-1645 ◽  
Author(s):  
Amandine Jullienne ◽  
Jill M Roberts ◽  
Viorela Pop ◽  
M Paul Murphy ◽  
Elizabeth Head ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Amyloid Beta ◽  
Vascular Dysfunction ◽  
Neurovascular Unit ◽  
Early Brain Injury ◽  
Glycoprotein P ◽  
P Glycoprotein ◽  
Blood Microvessels

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.

Changes in White Matter in Long-Term Survivors of Severe Non-Missile Traumatic Brain Injury: A Computational Analysis of Magnetic Resonance Images

2005 ◽  
Vol 22 (1) ◽  
pp. 76-82 ◽  
Author(s):  
Francesco Tomaiuolo ◽  
Keith J. Worsley ◽  
Jason Lerch ◽  
Margherita Di Paola ◽  
Giovanni A. Carlesimo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Magnetic Resonance ◽  
Computational Analysis ◽  
Magnetic Resonance Images ◽  
Long Term Survivors

scholarly journals A Lack of Amyloid β Plaques Despite Persistent Accumulation of Amyloid β in Axons of Long-Term Survivors of Traumatic Brain Injury

2009 ◽  
Vol 19 (2) ◽  
pp. 214-223 ◽  
Author(s):  
Xiao-Han Chen ◽  
Victoria E. Johnson ◽  
Kunihiro Uryu ◽  
John Q. Trojanowski ◽  
Douglas H. Smith
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Amyloid Β ◽  
Long Term Survivors

Antiepileptic Drugs for Preventing Seizures Following Acute Traumatic Brain Injury

2012 ◽  
Vol 2 (2) ◽  
pp. 1-5
Author(s):  
Amy Price
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Antiepileptic Drugs ◽  
Late Onset ◽  
Pooled Data ◽  
Cognitive Behavioural ◽  
Acute Traumatic Brain Injury ◽  
Long Term Survivors ◽  
Overall Mortality

The work was done to explore the effectiveness of prophylactic antiepileptic drugs for acute traumatic brain injury and assess risk: benefit ratios. The author asked if this intervention helped sort-term survivors avoid seizures after injury and assessed the influence of such medication on death and disability which result in seizures in long term survivors of TBI. Finally, the work assessed the benefits given potential adverse reactions to these drugs. The author found that using anti-epileptic drugs in the early stages after traumatic brain injury does decrease seizures. This review found that anti-epileptic drugs were effective for decreasing seizures in the first week after a TBI. Available pooled data failed to demonstrate reductions in overall mortality, late onset seizures, or the development of persistent vegetative states. However, the conclusions are limited by the scarcity of clear data collected to investigate cognitive/behavioural, neurological, or hematopoietic adverse effects thought to result from the anti seizure medications.

Traumatic Brain Injury: A Trauma Surgeon's Perspective

2012 ◽  
Vol 22 (3) ◽  
pp. 82-89
Author(s):  
Oscar D. Guillamondegui
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Multidisciplinary Approach ◽  
Trauma Team ◽  
The United States ◽  
Long Term Outcomes ◽  
Term Care ◽  
Injured Brain ◽  
The Moment

Traumatic brain injury (TBI) is a serious epidemic in the United States. It affects patients of all ages, race, and socioeconomic status (SES). The current care of these patients typically manifests after sequelae have been identified after discharge from the hospital, long after the inciting event. The purpose of this article is to introduce the concept of identification and management of the TBI patient from the moment of injury through long-term care as a multidisciplinary approach. By promoting an awareness of the issues that develop around the acutely injured brain and linking them to long-term outcomes, the trauma team can initiate care early to alter the effect on the patient, family, and community. Hopefully, by describing the care afforded at a trauma center and by a multidisciplinary team, we can bring a better understanding to the armamentarium of methods utilized to treat the difficult population of TBI patients.

Prosodic Impairment Associated With Traumatic Brain Injury

2009 ◽  
Vol 19 (3) ◽  
pp. 97-102
Author(s):  
Billy Irwin
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Detailed Analysis ◽  
Acoustic Characteristics ◽  
Individual Variations

Abstract Purpose: This article discusses impaired prosody production subsequent to traumatic brain injury (TBI). Prosody may affect naturalness and intelligibility of speech significantly, often for the long term, and TBI may result in a variety of impairments. Method: Intonation, rate, and stress production are discussed in terms of the perceptual, physiological, and acoustic characteristics associated with TBI. Results and Conclusions: All aspects of prosodic production are susceptible to the effects of damage resulting from TBI. There are commonly associated prosodic impairments; however, individual variations in specific aspects of prosody require detailed analysis.

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