Journal of neurotrauma
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Journal of neurotrauma · Feb 2014
A follow-up study of neurometabolic alterations in female concussed athletes.
Athletes who sustain a concussion demonstrate a variety of symptoms and neuropsychological alterations that could be brought on by neurometabolic abnormalities. However, no study has yet investigated these aspects in female athletes using magnetic resonance spectroscopy. The present study investigated the neurometabolic and -psychological effects of a concussion in the acute (7-10 days postinjury) and chronic (6 months postinjury) phases after injury. ⋯ Concussed athletes showed neurometabolic impairment in prefrontal and motor cortices characterized by a pathological increase of glutamine/glutamate and creatine (Cr) only in the chronic phase. Also, a significant decrease in N-acetyl-aspartate/Cr ratio was observed in control athletes at the second time point. Concussed female athletes showed acute cognitive alterations and higher severity of symptoms that do not appear to be underlied by neurometabolic abnormalities, which are only present in the chronic postinjury phase.
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Journal of neurotrauma · Feb 2014
Acute Alcohol Intoxication Prolongs Neuroinflammation without Exacerbating Neurobehavioral Dysfunction Following Mild Traumatic Brain Injury.
Traumatic brain injury (TBI) represents a leading cause of death and disability among young persons with ∼1.7 million reported cases in the United States annually. Although acute alcohol intoxication (AAI) is frequently present at the time of TBI, conflicting animal and clinical reports have failed to establish whether AAI significantly impacts short-term outcomes after TBI. The objective of this study was to determine whether AAI at the time of TBI aggravates neurobehavioral outcomes and neuroinflammatory sequelae post-TBI. ⋯ TBI induced a transient upregulation of cortical interleukin (IL)-6 and monocyte chemotactic protein (MCP)-1 mRNA expression at 6 h, which was resolved at 24 h. AAI did not modulate the inflammatory response at 6 h but prevented resolution of inflammation (IL-1, IL-6, tumor necrosis factor-α, and MCP-1 expression) at 24 h post-TBI. AAI at the time of TBI did not delay the recovery of neurological and neurobehavioral function but prevented the resolution of neuroinflammation post-TBI.
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Journal of neurotrauma · Feb 2014
Review Meta AnalysisOlfactory dysfunction in pediatric traumatic brain injury: A systematic review.
The neuropsychological outcomes of pediatric traumatic brain injury (TBI) have received increasing study over the past 20 years and are currently well delineated in the research literature. One outcome that has received little attention is that of olfactory dysfunction after pediatric TBI. This is despite literature indicating that anosmia and olfactory dysfunction are common after adult TBI and are likely to be linked to severity of injury, neuropathology, and executive dysfunction. ⋯ The studies found were limited by methodological weaknesses, variability in measures, small sample size, and difficulty of comparison across cohorts studied. Despite this, they reported consistent findings of anosmia and olfactory dysfunction in their TBI cohorts and identified a dose-response relationship between severity of injury and olfactory dysfunction. The results of the studies are discussed in terms of relevant findings, limitations, and areas requiring further exploration.
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Journal of neurotrauma · Feb 2014
ReviewThe Presence and Role of Iron in Mild Traumatic Brain Injury: An Imaging Perspective.
Mild traumatic brain injury (mTBI), although often presenting without the gross structural abnormalities seen in more severe forms of brain trauma, can nonetheless result in lingering cognitive and behavioral problems along with subtle alterations in brain structure and function. Repeated injuries are associated with brain atrophy and dementia in the form of chronic traumatic encephalopathy (CTE). The mechanisms underlying these dysfunctions are poorly understood. ⋯ In addition, there is evidence that iron may contribute to pathology after mTBI through a number of mechanisms, including generation of reactive oxygen species (ROS), exacerbation of oxidative stress from other sources, and encouragement of tau phosphorylation and the formation of neurofibrillary tangles. Finally, recent animal studies suggest that iron may serve as a therapeutic target in mitigating the effects of mTBI. However, research on the presence and role of iron in mTBI and CTE is still relatively sparse, and further work is necessary to elucidate issues such as the sources of increased iron and the chain of secondary injury.
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Journal of neurotrauma · Feb 2014
Functionally-detected cognitive impairment in high school football players without clinically-diagnosed concussion.
Head trauma and concussion in football players have recently received considerable media attention. Postmortem evidence suggests that accrual of damage to the brain may occur with repeated blows to the head, even when the individual blows fail to produce clinical symptoms. There is an urgent need for improved detection and characterization of head trauma to reduce future injury risk and promote development of new therapies. ⋯ This new category was associated with significantly higher numbers of head collision events to the top-front of the head, directly above the DLPFC. The discovery of this new category suggests that more players are suffering neurological injury than are currently being detected using traditional concussion-assessment tools. These individuals are unlikely to undergo clinical evaluation, and thus may continue to participate in football-related activities, even when changes in brain physiology (and potential brain damage) are present, which will increase the risk of future neurological injury.