Search results for "Traumatic Brain Injury"

2017

Danger associated molecular patterns (DAMPs) are released by damaged cells and trigger neuroinflammation through activation of non-specific pattern recognition receptors (PRRs), e.g. Toll-like receptors (TLRs). Since the role of TLR 2 and 4 after traumatic brain injury (TBI) is still unclear, we examined the outcome and the expression of proinflammatory mediators after experimental TBI in Tlr2/4 / and wild-type (WT) mice. Tlr2/4 / and wild-type mice were subjected to controlled cortical injury and contusion volume and brain edema formation were assessed 24 h thereafter. Expression of inflammatory markers in brain tissue was measured by quantitative PCR 15 min, 3, 6, 12, and 24 h after contr…

Neurostimulation and Reach-to-Grasp Function Recovery Following Acquired Brain Injury: Insight From Pre-clinical Rodent Models and Human Applications.

2020

Reach-to-grasp is an evolutionarily conserved motor function that is adversely impacted following stroke and traumatic brain injury (TBI). Non-invasive brain stimulation (NIBS) methods, such as transcranial magnetic stimulation and transcranial direct current stimulation, are promising tools that could enhance functional recovery of reach-to-grasp post-brain injury. Though the rodent literature provides a causal understanding of post-injury recovery mechanisms, it has had a limited impact on NIBS protocols in human research. The high degree of homology in reach-to-grasp circuitry between humans and rodents further implies that the application of NIBS to brain injury could be better informed…

Anatomy and physiology of cisternostomy

2016

Cisternostomy is defined as opening the basal cisterns to atmospheric pressure. This technique helps to reduce the intracranial pressure in severe head trauma as well as other conditions when the so-called sudden “brain swelling” troubles the surgeon. We elaborated the surgical anatomy of this procedure as well as the proposed physiology of how cisternostomy works. This novel technique may change the current trends in neurosurgery.

2017

Neuronal degeneration following traumatic brain injury (TBI) leads to intracellular accumulation of dysfunctional proteins and organelles. Autophagy may serve to facilitate degradation to overcome protein debris load and therefore be an important pro-survival factor. On the contrary, clearing may serve as pro-death factor by removal of essential or required proteins involved in pro-survival cascades. Sequestosome 1 (SQSTM1/p62) is a main regulator of the autophagic pathway that directs ubiquinated cargoes to autophagosomes for degradation. We show that SQSTM1 protein levels are suppressed 24 h and by trend 5 days after trauma. In line with these data the expression of Sqstm1 mRNA is reduced…

Is erythropoietin a worthy candidate for traumatic brain injury or are we heading the wrong way?

2016

Traumatic brain injury (TBI) is a leading cause of death and disability in the modern society. Although primary prevention is the only strategy that can counteract the primary brain damage, numerous preclinical studies have been accumulated in order to find therapeutic strategies against the secondary damage. In this scenario erythropoietin (EPO) has been shown to be a promising candidate as neuroprotective agent. A recent clinical trial, however, has shown that EPO has not an overall effect on outcomes following TBI thus renewing old concerns.  However, the results of a prespecified sensitivity analysis indicate that the effect of EPO on mortality remains still unclear. In the light of the…

Supporting recovery from brain injury

2018

The beauty and intricacy of the human brain is unfortunately also mirrored by its vulnerability. Damage to the brain is typically permanent. Because cells of the adult brain, apart from rare exceptions, no longer divide, there is essentially no regrowth of damaged brain tissue. Acquired brain injury in the majority of cases occurs directly through traumatic events such as an accident involving a blow to the head or indirectly through interruption of the blood supply, namely a stroke. Brain injury is a major burden, with an estimated 1.7 million people in the United States suffering a traumatic brain injury and nearly 800,000 Americans suffering a stroke each year ( 1 , 2 ). However, current…

Can mild cognitive impairment be stabilized by showering brain mitochondria with laser photons?

2019

There is now substantial evidence that cerebral blood flow (CBF) declines with age. From age 20 to 60, CBF is estimated to dip about 16% and continues to drop at a rate of 0.4%/year. This CBF dip will slowly reduce oxygen/glucose delivery to brain thus lowering ATP energy production needed by brain cells to perform normal activities. Reduced ATP production from mitochondrial loss or damage in the wear-and-tear of aging worsens when vascular risk factors (VRF) to Alzheimer's disease develop that can accelerate both age-decline CBF and mitochondrial deficiency to a level where mild cognitive impairment (MCI) develops. To date, no pharmacological or any other treatment has been successful in r…

Changing paradigm in mild traumatic brain injury research

2016

Multifaceted Mechanisms of WY-14643 to Stabilize the Blood-Brain Barrier in a Model of Traumatic Brain Injury

2017

The blood-brain barrier (BBB) is damaged during ischemic insults such as traumatic brain injury or stroke. This contributes to vasogenic edema formation and deteriorate disease outcomes. Enormous efforts are pursued to understand underlying mechanisms of ischemic insults and develop novel therapeutic strategies. In the present study the effects of PPARα agonist WY-14643 were investigated to prevent BBB breakdown and reduce edema formation. WY-14643 inhibited barrier damage in a mouse BBB in vitro model of traumatic brain injury based on oxygen/glucose deprivation in a concentration dependent manner. This was linked to changes of the localization of tight junction proteins. Furthermore, WY-1…

The psychometric measures to assess aggressive dimension following traumatic brain injury: A review.

2021

Abstract Background: higher level of aggression and antisocial behavior are frequent following head trauma, due to specific brain alterations. Many tests are used to assess this aspect. A descriptive review was conducted on the main tests used to detect the appearance of aggressive dimensions following traumatic brain injury. Review summary: we searched on PubMed and Web of Science databases and screening references of included studies and review articles for additional citations. From initial 723 publications, only 7 met our search criteria. Findings showed that various psychometric tools are used to assess aggressiveness and its subdomains, following head trauma. Conclusions: further inve…