Journal of neurotrauma
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Journal of neurotrauma · Aug 2010
Resting cerebral blood flow alterations in chronic traumatic brain injury: an arterial spin labeling perfusion FMRI study.
Non-invasive measurement of resting state cerebral blood flow (CBF) may reflect alterations of brain structure and function after traumatic brain injury (TBI). However, previous imaging studies of resting state brain in chronic TBI have been limited by several factors, including measurement in relative rather than absolute units, use of crude spatial registration methods, exclusion of subjects with substantial focal lesions, and exposure to ionizing radiation, which limits repeated assessments. This study aimed to overcome those obstacles by measuring absolute CBF with an arterial spin labeling perfusion fMRI technique, and using an image preprocessing protocol that is optimized for brains with mixed diffuse and focal injuries characteristic of moderate and severe TBI. ⋯ Hypoperfusion in superior and middle frontal cortices, in contrast, was associated with focal lesions. These results suggest that structural lesions, both focal and diffuse, are the main contributors to the absolute CBF alterations seen in chronic TBI, and that CBF may serve as a tool to assess functioning neuronal volume. We also speculate that resting reductions in posterior cingulate perfusion may reflect alterations in the default-mode network, and may contribute to the attentional deficits common in TBI.
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Journal of neurotrauma · Aug 2010
Hypothermia prior to decompression: buying time for treatment of acute spinal cord injury.
Human spinal cord injury (SCI) is usually accompanied by persistent cord compression. Experimental data demonstrate that compression of the traumatized cord results in rapid neurological decline over hours. Undertaking decompression in humans within this time frame has proved impractical, with the time to surgery in studies of urgent decompression averaging between 10 and 24 h. ⋯ The hypothermia-treated group regained weight-supported locomotion (Basso-Beattie-Bresnahan [BBB] locomotor assessment score 9.5 +/- 0.9), while the normothermic group remained severely paraparetic (BBB score 5.3 +/- 0.6; p
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Journal of neurotrauma · Aug 2010
High blood glucose does not adversely affect outcome in moderately brain-injured rodents.
In a number of clinical studies researchers have reported that acute hyperglycemia is associated with increased mortality and worsened neurological outcome in patients with traumatic brain injury (TBI). In contrast, it has been demonstrated that intensive insulin therapy to lower blood glucose can lead to an increased frequency of hypoglycemic episodes and poor outcome. Consistent with this, experimental and clinical studies have shown that TBI causes a "metabolic crisis" in the injured brain, suggesting that a reduction in glucose availability may exacerbate brain damage. ⋯ We find that the presence of persistent STZ-induced hyperglycemia results in a reduction of brain edema. Insulin therapy to reduce blood glucose reverses this beneficial effect of hyperglycemia. Taken together, our results indicate that an acute increase in blood glucose levels may not be harmful, and that intervention with insulin therapy to lower blood glucose levels in TBI patients may increase secondary brain damage.
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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.
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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.