Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2000
Evidence for lactate uptake after rat fluid percussion brain injury.
Traumatic brain injury (TBI) places enormous early energy demand on brain tissue to reinstate normal ionic balance. Glucose declines and lactate increases after TBI as demonstrated in clinical and lab studies, suggesting increased glycolysis. This led us to hypothesize that high extracellular fluid (ECF) lactate may be beneficial after TBI. We measured cerebral dialysate lactate and glucose, and arterial lactate and glucose, before & after rat Fluid Percussion Injury (FPI) (2.06 +/- 0.13 atm) with and without i.v. lactate infusion (100 mM x 4.5 hours) to test the hypotheses that arterial lactate determines ECF lactate. 14C-lactate autoradiography was also performed, to demonstrate whether lactate is taken up by traumatized brain. ⋯ Dialysate lactate was always significantly higher than arterial. After lactate infusion, both the dialysate and the arterial lactate were significantly increased (P < 0.0001). Dialysate lactate increased within 10 min. following FPI, with significantly higher values in the lactate infusion group (82% higher with lactate infusion after FPI). Dialysate glucose fell following FPI, with a more severe decline in the saline group (129% lower), suggesting lactate infusion preserves or "spares" glucose in ECF. In our autoradiographic study, i.v. 14C-lactate accumulated at the injury site, with levels 2-4 times higher than in contralateral cortex. In conclusion, arterial lactate augmentation thus increases brain dialysate lactate and results in less reduction in ECF glucose, after FPI. Infused lactate accumulates at the injury site, where metabolism is probably the greatest.
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Acta Neurochir. Suppl. · Jan 2000
The effects of dopamine on edema formation in two models of traumatic brain injury.
The risk of vasopressors worsening cerebral edema has been raised. Previously we have reported that dopamine was able to restore cerebral blood flow in a model of monotonically rising intracranial pressure. In this study the effects of dopamine on cortical contusion and diffuse injury with secondary insult are examined. ⋯ Dopamine however significantly worsened edema in ipsilateral and contralateral hippocampus and both temporal cortices. ADC remained unchanged except in the contralateral hippocampus where both water content and ADC rose with dopamine suggesting precipitation of a vasogenic edema. In this study dopamine clearly worsened edema formation in two models of traumatic brain injury, and we conclude that there may be analogous clinical situations; therefore pressors should not be considered a 'blanket' therapy for all patients with a low cerebral perfusion pressure.
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Acta Neurochir. Suppl. · Jan 2000
Assessment of 2-chloroadenosine treatment after experimental traumatic brain injury in the rat using arterial spin-labeled MRI: a preliminary report.
Adenosine is a putative endogenous neuroprotectant. Its action at A1 receptors mitigates excitotoxicity while action at A2 receptors increases cerebral blood flow (CBF). We hypothesized that cerebral injection of the adenosine analog, 2-chloroadenosine, would decrease swelling and increase CBF early after experimental traumatic brain injury (TBI). ⋯ In normal rats, injection of 0.3 nmole of 2-chloroadenosine did not increase CBF, but the higher dosage of 6 nmole dramatically increased hemispheric CBF by 1.5-2.0-fold. The effect of local injection of 2-chloroadenosine at a dose of 0.3 nmole after experimental TBI on Tlobs presumably represents a reduction in post-traumatic edema. This reduction in edema, along with the augmentation of CBF seen in normal rats at higher dosage (6 nmole), supports a role for adenosine in neuroprotection following TBI.
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Acta Neurochir. Suppl. · Jan 1999
System analysis of patient management during the pre- and early clinical phase in severe head injury.
Head injury with or without polytrauma is the most important cause of death and severe morbidity in an age bracket of up to 45 years. Two major factors are determining its outcome, the extent and nature of the primary irreversible brain injury, and the subsequently developing manifestations of secondary brain damage, which in principle can be prevented by the management procedures and therapeutical interventions. Therefore, a better outcome from severe head injury depends exclusively on a higher efficiency of the management and treatment in order to inhibit secondary brain damage. ⋯ The data flow during the investigation was maintained among others by regular conferences of the Study Group including the crew of documentation assistants at regular intervals. The presently reported phase-1 study was concluded in October 1997. It is followed by a phase-2 study with the attempt to collect prehospital- and early clinical management and care data in the catchment area on an epidemiological basis. (ABSTRACT TRUNCATED)
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Acta Neurochir. Suppl. · Jan 1999
ReviewA combined transorbital-transclinoid and transsylvian approach to carotid-ophthalmic aneurysms without retraction of the brain.
A series of 138 patients with 143 carotid-ophthalmic aneurysms (COAs) have been treated by direct surgical approach over the past 15 years. In 5 cases the COAs were bilateral and in 15 cases either one or more aneurysms were associated with a COA. Of the 143 COAs, 87 were small, 41 large and 15 were giant. ⋯ The latter approach provides ample space for proximal and distal control of the internal carotid artery (ICA) and makes it possible to deal with demanding large/giant COAs safely. In the series presented, there was no case of premature rupture of the aneurysm. Moreover, since we started using the described approach to COAs, retraction of the brain has not been necessary, regardless of the size of the aneurysm.