Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2006
Decompressive craniectomy for severe head injury in patients with major extracranial injuries.
Neurosurgical therapy aims to minimize secondary brain damage after a severe head injury. This includes the evacuation of intracranial space-occupying hematomas, the reduction of intracranial volumes, external ventricular drainage, and aggressive therapy in order to influence increased intracranial pressure (ICP) and decreased P(ti)O2. ⋯ The prognosis after decompression depends on the clinical signs and symptoms at admission, patient age, and the existence of major extracranial injuries. Our guidelines for decompressive craniectomy after failure of conservative interventions and evacuation of space-occupying hematomas include: patient age below 50 years without multiple trauma, patient age below 30 years in the presence of major extracranial injuries, severe brain swelling on CT scan, exclusion of a primary brainstem lesion or injury, and intervention before irreversible brain stem damage.
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Acta Neurochir. Suppl. · Jan 2006
Controlled Clinical TrialPharmacological brain cooling with indomethacin in acute hemorrhagic stroke: antiinflammatory cytokines and antioxidative effects.
We evaluated the effects of a novel pharmacological brain cooling (PBC) method with indomethacin (IND), a nonselective cyclooxygenase inhibitor, without the use of cooling blankets in patients with hemorrhagic stroke. Forty-six patients with hemorrhagic stroke (subarachnoid hemorrhage; n = 35, intracerebral hemorrhage; n = 11) were enrolled in this study. Brain temperature was measured directly with a temperature sensor. ⋯ CSF IL-1beta and serum bilirubin levels were suppressed in treated patients. IND has several beneficial effects on damaged brain tissues (anticytokine, free radical scavenger, antiprostaglandin effects, etc.) and prevents initial and secondary brain damage. PBC treatment for hemorrhagic stroke in patients appears to yield favorable results by acting as an antiinflammatory cytokine and reducing oxidative stress.
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Acta Neurochir. Suppl. · Jan 2006
Clinical TrialUse of ICM+ software for on-line analysis of intracranial and arterial pressures in head-injured patients.
To summarize our experience from the first 2 years of use of the ICM+ software in our Neurocritical Care Unit (NCCU). ⋯ The new version of ICM+ software proved to be useful clinically in the NCCU. It allows continuous monitoring of pressure reactivity and exploratory analysis of factors implicating intracranial hypertension.
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Acta Neurochir. Suppl. · Jan 2006
Delayed profound local brain hypothermia markedly reduces interleukin-1beta gene expression and vasogenic edema development in a porcine model of intracerebral hemorrhage.
White matter (lobar) intracerebral hemorrhage (ICH) can cause edema-related deaths and life-long morbidity. In our porcine model, ICH induces oxidative stress, acute interstitial and delayed vasogenic edema, and up-regulates interleukin-1beta (IL-1beta), a proinflammatory cytokine-linked to blood-brain barrier (BBB) opening. In brain injury models, hypothermia reduces inflammatory cytokine production and protects the BBB. ⋯ We froze brains in situ at 16 hours after ICH induction, sampled perihematomal white matter, extracted RNA, and performed real-time RT-PCR. Local brain cooling markedly reduced both IL-1beta RNA levels and vasogenic edema. These robust results support the potential for local brain cooling to protect the BBB and reduce injury after ICH.
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Acta Neurochir. Suppl. · Jan 2006
Controlled Clinical TrialChanges in coagulative and fibrinolytic activities in patients with intracranial hemorrhage.
To investigate whether any changes occur in the coagulative/fibrinolytic cascade in patients with subarachnoid hemorrhage (SAH) or hypertensive intracerebral hemorrhage (HICH). ⋯ Both coagulative and fibrinolytic activities were altered after the onset of SAH. These results demonstrate that the coagulative/fibrinolytic cascade might be activated via different mechanisms in different types of stroke. It remains unclear, however, whether a significant alteration of the fibrinolytic cascade in patients with ROSC-SAH might be a nonspecific phenomenon attributable to the reperfusion after collapse.