Journal of neurotrauma
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Journal of neurotrauma · Sep 2002
Cerebral blood flow at one year after controlled cortical impact in rats: assessment by magnetic resonance imaging.
Progressive tissue loss and delayed cognitive deficits are seen in rats during the initial year after experimental traumatic brain injury (TBI). As much as 10% of parenchymal volume is lost even in the contralateral hemisphere by 1 year after controlled cortical impact (CCI) in rats. Progressive declines in cerebral blood flow (CBF) are also associated with advanced age and neurodegenerative diseases. ⋯ We conclude that, at 1 year after CCI, CBF is reduced in anatomic structures at or near the impact site, including injured cortex and hippocampus, and this translates into a reduction in hemispheric CBF. However, despite both significant occult tissue loss ipsilateral and contralateral to the injury and delayed cognitive deficits, widespread reductions in CBF are not observed. This suggests the possibility of remodeling or repackaging of the brain that preserves CBF outside of the cystic lesion.
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Journal of neurotrauma · Sep 2002
Case Reports Comparative StudyArachnoid cyst is a risk factor for chronic subdural hematoma in juveniles: twelve cases of chronic subdural hematoma associated with arachnoid cyst.
Chronic subdural hematoma (CSDH) tends to occur in elderly patients with a history of mild head injury at a few months prior to the onset of symptoms. Intracranial arachnoid cyst is believed to be congenital and sometimes becomes symptomatic in pediatric patients. These two distinct clinical entities sporadically occur in the same young patient. ⋯ Hematoma evacuation is adequate at first operation. If the preoperative symptoms persist, additional arachnoid cyst surgery should be considered. The present results also suggest that CSDH formation may be preceded by subdural hygroma caused by the rupture of arachnoid cyst.
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Journal of neurotrauma · Sep 2002
Cationic liposome-mediated GDNF gene transfer after spinal cord injury.
Glial cell line-derived neurotrophic factor (GDNF) has been shown to protect cranial and spinal motoneurons, which suggests potential uses of GDNF in the treatment of spinal cord injury (SCI) and motor neuron disease. We examined neuroprotective effect of cationic liposome-mediated GDNF gene transfer in vivo on axonal regeneration and locomotor function recovery after SCI in adult rats. The mixture of DC-Chol liposomes and recombinant plasmid pEGFP-GDNF cDNA was injected after SCI. ⋯ The locomotion function of hindlimbs of rats was evaluated using inclined plane test and BBB locomotor scores. The locomotion functional scores in GDNF group were higher than that in control group within 1-4 weeks after SCI (p < 0.05). These data demonstrate that in vivo transfer of GDNF cDNA can promote axonal regeneration and enhance locomotion functional recovery, suggesting that cationic liposome-mediated delivery of GDNF cDNA may be a practical gene transfer method for traumatic SCI treatment.