Journal of neurotrauma
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Journal of neurotrauma · Jan 2011
A longitudinal proton magnetic resonance spectroscopy study of mild traumatic brain injury.
Despite the prevalence and impact of mild traumatic brain injury (mTBI), common clinical assessment methods for mTBI have insufficient sensitivity and specificity. Moreover, few researchers have attempted to document underlying changes in physiology as a function of recovery from mTBI. Proton magnetic resonance spectroscopy (¹H-MRS) was used to assess neurometabolite concentrations in a supraventricular tissue slab in 30 individuals with semi-acute mTBI, and 30 sex-, age-, and education-matched controls. ⋯ In addition, 17 mTBI patients (57%) returned for a follow-up evaluation (mean = 120 days post-injury). A significant group × time interaction indicated recovery in the mTBI group for gray matter Glx, and trends toward recovery in white matter Cre and Glx. An estimate of premorbid intelligence predicted the magnitude of neurometabolite normalization over the follow-up interval for the mTBI group, indicating that biological factors underlying intelligence may also be associated with more rapid recovery.
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Journal of neurotrauma · Jan 2011
Phenylephrine infusion prevents impairment of ATP- and calcium-sensitive potassium channel-mediated cerebrovasodilation after brain injury in female, but aggravates impairment in male, piglets through modulation of ERK MAPK upregulation.
Traumatic brain injury (TBI) contributes to morbidity in children and boys, and hypotension worsens outcome. Extracellular signal-related kinase (ERK) mitogen-activated protein kinase (MAPK) is upregulated more in males and reduces cerebral blood flow (CBF) after fluid percussion injury (FPI). Increased cerebral perfusion pressure (CPP) via phenylephrine (Phe) sex-dependently improves impairment of the cerebral autoregulation seen after FPI through modulation of ERK MAPK upregulation, which is aggravated in males, but is blocked in females. ⋯ Co-administration of U 0126, an ERK antagonist, and Phe fully restored dilation to cromakalim, calcitonin gene-related peptide (CGRP), and NS 1619, in males after FPI. These data indicate that Phe sex-dependently prevents impairment of Katp and Kca channel-mediated cerebrovasodilation after FPI in females, but aggravates impairment in males, through modulation of ERK MAPK upregulation. Since autoregulation of CBF is dependent on intact functioning of potassium channels, these data suggest a role for sex-dependent mechanisms in the treatment of cerebral autoregulation impairment after pediatric TBI.
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Journal of neurotrauma · Jan 2011
Post-traumatic seizures exacerbate histopathological damage after fluid-percussion brain injury.
The purpose of this study was to investigate the effects of an induced period of post-traumatic epilepsy (PTE) on the histopathological damage caused by traumatic brain injury (TBI). Male Sprague Dawley rats were given a moderate parasagittal fluid-percussion brain injury (1.9-2.1 atm) or sham surgery. At 2 weeks after surgery, seizures were induced by administration of a GABA(A) receptor antagonist, pentylenetetrazole (PTZ, 30 mg/kg). ⋯ In addition, the TBI-PTZ rats showed less NeuN-immunoreactive cells within the ipsilateral parietal cerebral cortex (p < 0.05) and there was a trend for decreased hippocampal CA3 neurons in TBI-PTZ rats compared with TBI-saline or sham-operated rats. These results demonstrate that an induced period of post-traumatic seizures significantly exacerbates the structural damage caused by TBI. These findings emphasize the need to control seizures after TBI to limit even further damage to the injured brain.
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Journal of neurotrauma · Jan 2011
Rotational acceleration closed head flexion trauma generates more extensive diffuse brain injury than extension trauma.
Our aim was to investigate if seemingly identical head and neck trauma would generate differing types of brain damage. We experimentally evaluated induced brain injuries immediately after trauma exposure, and at 1 week post-injury. Anesthetized rabbits were exposed once to a sagittal rotational acceleration head and neck injury at either a high or a low load level, using either flexion or extension. ⋯ The diffuse brain injury seen after a low-level flexion trauma was equal to or more extensive than that seen after a high-level extension trauma. A low-level extension trauma induced only minor histopathological abnormalities. We conclude that a sagittal rotational acceleration trauma of the head and neck induced diffuse brain injury, and that flexion caused more extensive damage than extension at the same applied load.
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Journal of neurotrauma · Jan 2011
Electrocortical pathology in a rat model of penetrating ballistic-like brain injury.
Traumatic brain injury (TBI) causes severe disruption of cerebral electrical activity and electroencephalography (EEG) is emerging as a standard tool to monitor TBI patients in the acute period of risk for secondary injuries. However, animal studies of EEG pathology in the context of TBI are surprisingly sparse, largely because of the lack of real-time continuous EEG (cEEG) monitoring in animal TBI models. Here, we performed long-term EEG monitoring to study nonconvulsive seizures (NCS), periodic epileptiform discharges (PED), and EEG power spectra following three injury severity levels in a rat model of penetrating ballistic-like brain injury (PBBI). ⋯ In contrast, decreases in higher frequency power (i.e., 30-35 Hz) remained depressed throughout 14 days. This is the first long-term cEEG study of the acute injury phase in a rat model of severe TBI, demonstrating common occurrences of clinically observed electrocortical pathology, such as NCS, PED, and cortical slowing. These EEG pathologies may serve as critical care biomarkers of brain injury, and offer clinically relevant metrics for studying acute therapeutic interventions.