Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2016
Effects of Brain Temperature on Cerebrovascular Autoregulation During the Acute Stage of Severe Traumatic Brain Injury.
The pressure reactivity index (PRx) is calculated as a moving correlation coefficient between intracranial pressure (ICP) and mean arterial blood pressure (MABP), and this analytical value is viewed as reflecting a vasomotor response to MABP variability. At present, the factors influencing the PRx value during the acute stage of traumatic brain injury (TBI) are not known. We observed significant cases where changes in the calculated value of PRx seemed to be influenced by changes in brain temperature during the course of acute stage TBI. ⋯ During the hypothermic condition, the mean value of PRx was -0.019; however, after gradual rewarming, the value of PRx increased drastically, and the mean value during the rewarming period, when the brain temperature exceeded 35 °C, was 0.331. Similarly, in another case where the patient underwent therapeutic brain hypothermia, the PRx showed a mean value of -0.038 during the hypothermic condition, and a mean value of 0.052 during the rewarming period. In both cases, a trend toward a negative correlation between ICP and MABP during brain hypothermia shifted to a positive correlation upon rewarming.
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Acta Neurochir. Suppl. · Jan 2016
Effects of Low-Dose Unfractionated Heparin Pretreatment on Early Brain Injury after Subarachnoid Hemorrhage in Mice.
Heparin is a pleiotropic drug that antagonizes many pathophysiological mechanisms. In this study, we evaluated whether heparin prevents early brain injury (EBI) after subarachnoid hemorrhage (SAH) in mice. SAH was induced by endovascular perforation in mice randomly assigned to sham-operated (n = 8), SAH + vehicle (n = 12), SAH + 10 U heparin pretreatment (n = 11), and SAH + 30 U heparin pretreatment (n = 14) groups. ⋯ Low-dose heparin pretreatment improved neurobehavioral function, and decreased brain edema in the ipsilateral cerebral hemisphere to the perforation side. High-dose heparin had a tendency for increased SAH, which obscured the neuroprotective effects by heparin. Low-dose heparin pretreatment may decrease the development of post-SAH EBI.
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Acta Neurochir. Suppl. · Jan 2016
Intrahospital Transfer of Patients with Traumatic Brain Injury: Increase in Intracranial Pressure.
To assess the dynamic of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and dynamic pressure reactivity index (PRx) during intrahospital transport. ⋯ Intrahospital transport of patients with TBI may lead to a significant increase in ICP, dynamic PRx, and decreased CPP. The results suppose that the decision to perform brain CT in comatose patients with TBI should be carefully considered by clinicians.
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Acta Neurochir. Suppl. · Jan 2016
CSF Lumbar Drainage: A Safe Surgical Option in Refractory Intracranial Hypertension Associated with Acute Posttraumatic External Hydrocephalus.
External lumbar drainage (ELD) of cerebrospinal fluid (CSF) in posttraumatic refractory intracranial hypertension (ICHT) is controversial. We report our experience of ELD in ICHT associated with acute disturbance of CSF flow within subarachnoid spaces (SASs). ⋯ Acute traumatic external hydrocephalus may explain some of the specific situations of secondary increased ICP, with a "normal" CT scan, that is refractory to medical treatment. In these situations, lumbar drainage should be considered to be a safe, minimally invasive, and effective surgical option.
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Research suggests that early brain injury following subarachnoid hemorrhage (SAH) is a primary therapeutic target, and early SAH-induced basal ganglia injury is not well studied. The present study examined basal ganglia injury in a rat model of SAH. Adult male Sprague-Dawley rats (n = 78) weighing 275-300 g underwent endovascular perforation to mimic aneurysmal SAH. ⋯ Basal ganglia neuronal injury was also determined by examining the levels of dopamine- and cAMP-regulated phosphoprotein, Mr 32 kDa (DARPP-32). We found that rats with hydrocephalus had more severe basal ganglia injury with greater DARPP-32 depletion (DARPP-32/beta-actin: 0.38 ± 0.32 vs. 0.86 ± 0.45 in rats without hydrocephalus and 1.10 ± 0.28 in sham, p < 0.05). In conclusion, SAH resulted in severe basal ganglia damage, which is associated with hydrocephalus development.