Articles: traumatic-brain-injuries.
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J Neurol Surg A Cent Eur Neurosurg · Mar 2016
Posttraumatic Hydrocephalus after Decompressive Craniectomy in 126 Patients with Severe Traumatic Brain Injury.
Severe traumatic brain injuries (TBIs) occur frequently. In some of these patients decompressive craniectomy (DC) must be performed. Posttraumatic hydrocephalus (PTH) can develop after TBI further damaging the brain. DC is considered to be one of the causes of PTH. This study defines the incidence of PTH in TBI patients who underwent DC and tries to determine associated factors. ⋯ Our study suggests that PTH development is multifactorial and shows that PTH is not that rare. We showed a correlation between craniectomy size and the incidence of PTH.
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Neurological research · Mar 2016
Traumatic brain injury accelerates kindling epileptogenesis in rats.
Traumatic brain injury (TBI) is a well-known cause of symptomatic epilepsy. In animal models of post-traumatic epilepsy (PTE), progression of trauma to epilepsy takes several weeks to months. Although this long process is similar to clinical PTE, it is costly and laborious. We used a combination of TBI and kindling as an accelerated animal model to develop epilepsy in much shorter period compared to that occurring in PTE. ⋯ Traumatic brain injury facilitates acquisition of epilepsy in both chemical and electrical kindling models. Combination of trauma and kindling can be considered as an inexpensive and time-saving animal model in PTE studies.
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A 40-year-old man suffered severe brain injury and received left side subdural hematoma evacuation with decompressive craniectomy. Intraoperative brain swelling had occurred during the surgery. ⋯ Secondary hematoma evacuation was performed and found a linear fracture near a bleeding meningeal artery. 2 days later CT scan showed cerebral infarction mainly in right posterior cerebral artery distribution. Early diagnosis by postoperative CT scan or other potential ways such as intraoperative sonography is important to prompt treatments and interrupt the pathophysiological chain of the serial attacks.
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Experimental neurology · Mar 2016
Alterations of functional properties of hippocampal networks following repetitive closed-head injury.
Traumatic brain injury (TBI) is the leading cause of death for persons under the age of 45. Military service members who have served on multiple combat deployments and contact-sport athletes are at particular risk of sustaining repetitive TBI (rTBI). Cognitive and behavioral deficits resulting from rTBI are well documented. ⋯ Moreover, the effect of 3× CHI on mIPSCs was opposite to that of the sIPSCs. Specifically, the frequency of the mIPSCs was decreased while the amplitudes were increased. These results are consistent with a mechanism in which repetitive closed-head injury affects CA1 hippocampal function by promoting a remodeling of excitatory and inhibitory synaptic inputs leading to impairment in hippocampal-dependent tasks.
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Ther Hypothermia Temp Manag · Mar 2016
Comprehensive Evaluation of Neuroprotection Achieved by Extended Selective Brain Cooling Therapy in a Rat Model of Penetrating Ballistic-Like Brain Injury.
Brain hypothermia has been considered as a promising alternative to whole-body hypothermia in treating acute neurological disease, for example, traumatic brain injury. Previously, we demonstrated that 2-hours selective brain cooling (SBC) effectively mitigated acute (≤24 hours postinjury) neurophysiological dysfunction induced by a penetrating ballistic-like brain injury (PBBI) in rats. This study evaluated neuroprotective effects of extended SBC (4 or 8 hours in duration) on sub-acute secondary injuries between 3 and 21 days postinjury (DPI). ⋯ The protective effects of SBC on delayed axonal injury (silver staining) were evident out to 14 DPI. In conclusion, the CCA cooling method of SBC produced neuroprotection measured across multiple domains that were evident days/weeks beyond the cooling duration and in the absence of overt adverse effects. These "proof-of-concept" results suggest that SBC may provide an attractive neuroprotective approach for clinical considerations.