Journal of neurotrauma
-
Journal of neurotrauma · Aug 2010
Differential impact of temporary and permanent noise-induced hearing loss on neuronal cell density in the mouse central auditory pathway.
Although acoustic overstimulation has a major pathophysiological influence on the inner ear, central components of the auditory pathway can also be affected by noise-induced hearing loss (NIHL). The present study investigates the influence of a noise-induced temporary threshold shift (TTS) and/or permanent threshold shift (PTS) on neuronal cell densities in key structures of the central auditory pathway. Mice were noise-exposed (3 h, 5-20 kHz) at 115 dB sound pressure level (SPL) under anesthesia, and were investigated immediately (TTS group, n = 5) after the exposure, or 1 week later (PTS group, n = 6). ⋯ Cell density was significantly reduced in all investigated auditory structures at 1 week post-exposure (PTS group), except in layer II of the AI (VCN: -30% and DCN: -30% (high-frequency); -39% (low-frequency); ICC: -31%; MGBd: -31%; MGBm: -28%; MGBv: -31%; AI: -10 to 14%). Thus there were dramatic changes within the neuronal cytoarchitecture of the central auditory pathway following a single noise exposure. The present findings should help clinicians to better understand the complex psychoacoustic phenomena of NIHL.
-
Journal of neurotrauma · Aug 2010
Review Meta AnalysisSurvival after spinal cord injury: a systematic review.
Spinal cord injury (SCI) leading to neurological deficits produces long-term effects that persist over a lifetime. Survival analysis of patients with SCI, at individual and population level, is important for public health management and the assessment of treatment achievements. The current study evaluated survival following traumatic and non-traumatic SCI worldwide. ⋯ An increase in survival over time was found. However, the SMRs of individuals with SCI still exceed those of an age-matched non-disabled population, mainly due to secondary complications. Lower survival rates were observed in non-traumatic SCI compared with traumatic SCI.
-
Journal of neurotrauma · Aug 2010
BCL2 genotypes: functional and neurobehavioral outcomes after severe traumatic brain injury.
Traumatic brain injury (TBI) triggers a cascade of apoptotic-related events that include BCL2 expression, a pro-survival protein in the apoptosis pathway. The purpose of this study was to use tagging single nucleotide polymorphism (tSNP) genotypes to screen the BCL2 gene to determine if genetic variability in the BCL2 gene influences outcomes in 205 patients with severe TBI. Outcomes (Glasgow Outcome Scale [GOS], Disability Rating Scale [DRS], mortality, and Neurobehavioral Rating Scale-Revised [NRS-R]) were analyzed at 3, 6, 12, and 24 months. ⋯ The homozygous variant for rs949037 was associated with favorable outcomes (GOS p = 0.04; DRS p = 0.03), and the homozygous wild-type was associated with increased mortality at 3 months (p = 0.005; OR = 3.67; CI 1.08,12.49). The only finding that stood up to Bonferroni correction was rs17759659 for GOS. These data support the possibility that genetic variability for pro-survival proteins, particularly genetic variation in the BCL2 gene, impacts outcomes after severe TBI.
-
Journal of neurotrauma · Aug 2010
Spontaneous epileptiform activity in rat neocortex after controlled cortical impact injury.
A hallmark of severe traumatic brain injury (TBI) is the development of post-traumatic epilepsy (PTE). However, the mechanisms underlying PTE remain poorly understood. In this study, we used a controlled cortical impact (CCI) model in rats to examine post-traumatic changes in neocortical excitability. ⋯ The evoked discharges resembled those observed at week 1, but with longer burst durations. Spontaneous activity included prolonged, ictal-like discharges lasting up to 8-10 sec, and briefer interictal-like burst events (<1 sec). These results indicate that during the first 2 weeks following severe CCI injury, there is a progressive development of neocortical hyperexcitability that ultimately leads to spontaneous epileptiform firing, suggesting a rapid epileptogenic process.
-
Journal of neurotrauma · Aug 2010
Mild fluid percussion injury in mice produces evolving selective axonal pathology and cognitive deficits relevant to human brain injury.
Mild traumatic brain injury (TBI) accounts for up to 80% of clinical TBI and can result in cognitive impairment and white matter damage that may develop and persist over several years. Clinically relevant models of mild TBI for investigation of neurobiological changes and the development of therapeutic strategies are poorly developed. In this study we investigated the temporal profile of axonal and somal injury that may contribute to cognitive impairments in a mouse model of mild TBI. ⋯ At 4 and 6 weeks post-injury, axonal damage was evident in the external capsule, and was seen at 6 weeks in the dorsal thalamic nuclei. At 3 weeks post-injury, injured mice showed an impaired ability to learn the water maze task, suggesting injury-induced alterations in search strategy learning. The evolving localization of axonal damage points to ongoing degeneration after injury that is concomitant with a deficit in learning.