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Results for “Diffuse Axonal Injury”

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At least 163 records · Page 9Linked to original sources
PubMed2005

Catalase activity and thiobarbituric acid reactive substances (TBARS) production in a rat model of diffuse axonal injury. Effect of gadolinium and amiloride.

This study evaluated the effect of mechanogated membrane ion channel blockers on brain catalase (CAT) activity and thiobarbituric acid reactive substances (TBARS) production after traumatic brain injury (TBI). A weight drop trauma model was used. Controls were sham-operated and received no weight drop. Gadolinium (GAD) or amiloride (AMI) were administered to control and experimental rats (30 min after TBI). Brain CAT activity and TBARS production were measured. When blood vessels were washed out with saline perfusion brain CAT activity significantly increased up to 6 h after trauma, decreasing significantly by 24 h; GAD or AMI administration preserved CAT activity 24 h after TBI. TBARS production increased after trauma, this effect being significantly reversed by GAD or AMI administration. GAD significantly decreased TBARS production in control animals. Mechanogated membrane ion channels may be involved in the genesis of the ionic disruption leading to oxidative stress and other secondary injury processes in head trauma.

Amiloride↗
PubMed2002

Expression of interleukin-6 messenger RNA in a rat model of diffuse axonal injury.

Having demonstrated a transcranial gradient of the cytokine interleukin-6 (IL-6) in patients with either traumatic brain injury or spontaneous subarachnoid haemorrhage we have employed in situ hybridisation for IL-6 messenger RNA (mRNA) to determine the site of this IL-6 production within the central nervous system (CNS). A rodent weight drop model of traumatic brain injury was used. IL-6 mRNA levels in brains were determined 6 h after injury. Sham animals had normal constitutive expression for IL6 mRNA. In traumatised animals an intense area of IL-6 mRNA labelling was found below the hippocampus. Cells strongly expressing IL-6 mRNA were also seen in the dentate gyrus. This inflammatory cytokine is clearly implicated in the response to CNS injury, but whether this response is neuroprotective or pathological is uncertain.

Animals↗
PubMed1999

Diffuse axonal injury in a rugby player.

Sections of the cerebrum, cerebellum, and brain stem of a rugby player who died 15 hours after being tackled were stained using an immunoperoxidase technique to detect beta-amyloid protein. The sections of the pons showed axonal spheroids in the base, and those of the cerebellum showed axonal spheroids in deep white matter. The findings demonstrated axonal injury following a fall from the victim's height in a team sporting event.

Adult↗
PubMed1993

The use of antibodies targeted against the neurofilament subunits for the detection of diffuse axonal injury in humans.

Axonal injury is a common feature of human traumatic brain injury. Typically, damaged axons cannot be recognized unless a patient survives the injury by at least 10-12 hours (h). Limitations associated with the use of the traditional silver methods have been linked with this inability to recognize early posttraumatic reactive axonal change. Recently, we reported that antibodies targeting the neurofilament subunits proved useful in recognizing early traumatically induced axonal change in traumatically brain-injured animals. Accordingly, in the present communication, we employed antibodies to detect at the light microscopic level the 68 kD Nf-L and 170-200 kD Nf-H neurofilament subunits in head-injured patients who survived the traumatic event for periods ranging from 6 h to 59 days. Antibodies targeting all of the above-described subunits revealed a progression of reactive axonal change. Antibodies to the 68 kD subunit proved most useful, as they were not complicated by concomitant immunoreactivity in surrounding nuclei and/or dendritic and somatic elements. These immunocytochemical strategies revealed, at 6 h postinjury, focally swollen axons which appeared intact. By 12 h, this focal swelling had progressed to disconnection, with the immunoreactive swelling undergoing further expansion over 1 week postinjury. These findings demonstrate the utility of the previously described immunocytochemical strategies for detecting reactive axonal change in brain-injured humans, particularly in the early posttraumatic course. More importantly, these methods also demonstrate in humans that reactive axonal change is not necessarily caused by traumatically induced tearing.

Accidental Falls↗
PubMed2002

Saccade sequences as markers for cerebral dysfunction following mild closed head injury.

Diffuse axonal injury caused by mild closed head injury (CHI) is likely to affect the neural networks concerned with the planning and execution of sequences of memory-guided saccades. Thirty subjects with mild CHI and thirty controls were tested on 2- and 3-step sequences of memory-guided saccades. CHI subjects showed more directional errors, larger position errors, and hypermetria of primary saccades and final eye position. No deficits were seen in temporal accuracy (timing and rhythm). These results suggest that computerized tests of saccade sequences can provide sensitive markers of cerebral dysfunction after mild CHI.

Adolescent↗