Articles: brain-injuries.
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Acta Neurochir. Suppl. · Jan 2000
Continuous assessment of cerebral autoregulation--clinical verification of the method in head injured patients.
Previously, using transcranial Doppler ultrasonography, we investigated whether the hemodynamic response to spontaneous variations in cerebral perfusion pressure (CPP) provides reliable information about cerebral autoregulatory reserve. In the present study we have verified this method in 166 patients after head trauma. Waveforms of intracranial pressure (ICP), arterial pressure and transcranial Doppler flow velocity (FV) were captured daily over 0.5-2.0 hour periods. ⋯ Mx depended on outcome following head injury stronger than the Glasgow Coma Score on admission (ANOVA, F values 18 and 15 respectively; N = 166). In patients who died, cerebral autoregulation was disturbed during the first two days following injury. These results indicate an important role for the continuous monitoring of autoregulation following head trauma.
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Acta Neurochir. Suppl. · Jan 2000
The role of decompressive craniectomy in the treatment of uncontrollable post-traumatic intracranial hypertension.
The benefit of decompressive craniectomy for the treatment of uncontrolled post-traumatic intracranial hypertension seems to be encouraging if medical management fails. We present our experience in 22 cases of cerebral edema due to head trauma. The edema alone was rarely the direct consequence of head trauma. ⋯ In our series 41% of patients had a good recovery, 18% a severe disability, 23% a vegetative state and 18% died. The findings showed that the bony decompression must be performed early before the situation becomes irreversible. We suggest that if intracranial pressure values remain greater than 30 mmHg with cerebral perfusion pressure below 70 mmHg, despite vigorous anti-edema therapy, decompressive craniectomy should be considered.
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Recent studies have suggested a role of connective tissue growth factor (CTGF) in repair processes of the skin as well as in various types of fibrotic disease. However, a function of this molecule in central nervous system (CNS) repair has not been demonstrated yet. ⋯ Interestingly, increased expression of this mitogen was accompanied by elevated levels of the extracellular matrix molecule fibronectin, which is a known target of CTGF action. Therefore, our data indicate a novel function of CTGF in postlesional restructuring of the hippocampus, where it possibly participates in glial scar formation.
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Neurol. Med. Chir. (Tokyo) · Jan 2000
Changes in local cerebral blood flow, glucose utilization, and mitochondrial function following traumatic brain injury in rats.
The pathophysiology of secondary brain damage following experimental traumatic brain injury was investigated by measuring local cerebral blood flow (lCBF), local cerebral glucose utilization (lCGU), and activity of succinate dehydrogenase (SDH), which is a mitochondrial enzyme of the tricarboxylic acid cycle, in the rat brain after moderate lateral fluid percussion injury. Measurements used autoradiography for lCBF and lCGU with [14C]iodoantipyrine and [14C]2-deoxyglucose, respectively. Regional SDH activity was determined using quantitative imaging of formazan produced from 2,3,5-triphenyl tetrazolium chloride by SDH. lCBF decreased at 1 hour after injury and was significantly lower than the preinjury level in almost all regions of both hemispheres at 6 and 24 hours, and remained low at 2 weeks. lCGU increased 1 hour after injury but was significantly decreased at 6 and 24 hours, and at 2 weeks in most regions of both hemispheres. ⋯ Necrosis in the injured cortex and reduction of the number of neurons in the ipsilateral hippocampus were observed 2 weeks after injury. The present study showed that a decrease in lCBF and mitochondrial dysfunction occur with glucose hypermetabolism around 1 hour after lateral fluid percussion injury, and that lCBF, lCGU, and mitochondrial function all deteriorate after 6 hours. This suggests that lCBF and cellular metabolism may change dynamically during the several hours following traumatic brain injury, and afterwards neuronal damage may result in an irreversible change in the areas with depressed glucose hypermetabolism in the early period after injury in combination with mitochondrial dysfunction.
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Acta Neurochir. Suppl. · Jan 2000
The use of decompressive craniectomy for the management of severe head injuries.
The aim of Neurosurgical care is to minimise the secondary brain damage that occurs after a severe head injury. This includes the evacuation of an intracranial space occupying haematoma, the reduction of intracranial volume, external ventricular drainage with hydrocephalus, and conservative therapy to reduce intracranial pressure (ICP) and to maintain tissue oxygen p(ti)O2. When conservative treatment fails, a decompressive craniectomy might be successful in lowering ICP. ⋯ The prognosis after decompression depends on clinical signs and symptoms on admission, patients' age and the existence of major extracranial injuries. Our guidelines for decompressive craniectomy after failure of conservative intervention and evacuation of space occupying hematomas included: a patient's age below 50 years without multiple trauma or a patient's age below 30 years in the presence of major extracranial injuries; severe brain swelling on CT scan (primary brainstem injuries were excluded). In 8 patients conservative 1TU treatment had failed.