Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2012
Comparing brain tissue oxygen measurements and derived autoregulation parameters from different probes (Licox vs. Raumedic).
We investigated two commercially available probes for measurement of the partial pressure of brain tissue oxygen (PbrO2) and calculation of the index of brain tissue oxygen pressure reactivity (ORx) in 7 patients after aneurysmal subarachnoid hemorrhage (SAH). Simultaneous monitoring of PbrO2 using the Licox(®) probe and the multiparameter Raumedic probe (Neurovent PTO(®)), measuring PbrO2, intracranial pressure (ICP) and brain temperature (Neurovent PTO) was performed for a median of 9 days (range 7-17 days). Both probes provided stable monitoring throughout the desired period. ⋯ There was a difference in the measurement of PbrO2 of -2.73 ± 10.1 mmHg (Licox - Raumedic). The difference in the two values for the calculated ORx was far smaller (0.03 ± 0.31; Licox - Raumedic) and the correlation coefficient higher than for both values of PbrO2 (0.76 for ORx vs. 0.56 for PbrO2). The calculation of the autoregulation parameter ORx seemed more independent of the measurement process than the measurement of PbrO2 itself and signifies the potential clinical importance of this parameter.
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Acta Neurochir. Suppl. · Jan 2012
Cerebrospinal fluid lactate concentration after withdrawal of metabolic suppressive therapy in subarachnoid hemorrhage.
Hyperglycolysis is a known phenomenon after severe subarachnoid hemorrhage (SAH) and after brain injury. It is characterized by decreased oxidative metabolism and relatively increased anaerobic glycolysis. Metabolic suppressive therapy reduces the cerebral metabolic rate of oxygen (CMRO(2)) and the cerebral metabolic rate of glucose (CMRGluc). ⋯ In 56% of patients an increase in CSF lactate (mean: 3.2 ± 0.9 mmol/L) after withdrawal of metabolic suppressive therapy was observed. Mean Glasgow Outcome Score (GOS) was lower in patients with an increase in CSF lactate concentration (>0.5 mmol/L) after withdrawal of metabolic suppressive therapy (p = 0.095). In 88% of patients who died during the first 30 days after SAH, a CSF lactate elevation of more than 0.5 mmol/L after withdrawal of metabolic suppressive therapy was found (p = 0.071).
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Acta Neurochir. Suppl. · Jan 2012
Quantification of normal CSF flow through the aqueduct using PC-cine MRI at 3T.
Quantification of cerebrospinal fluid (CSF) flow through the cerebral aqueduct is of paramount importance in patients with hydrocephalus. The purpose of this study was to evaluate the normal CSF flow measurements at three different anatomical levels of the aqueduct utilizing 3-Tesla (3 T) magnetic resonance imaging. ⋯ CSF peak positive velocity, peak negative velocity, and mean flow through the aqueduct were calculated in 22 young healthy volunteers performed at 3 T. Our measurements did not show significant difference compared with the reported measurements obtained at 1.5 T. Slight differences were observed in the CSF hydrodynamic measurements, depending on the anatomical level of the aqueduct; however, they did not vary significantly.
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Acta Neurochir. Suppl. · Jan 2012
Spontaneous cortical spreading depression and intracranial pressure following acute subdural hematoma in a rat.
Acute subdural hemorrhage (ASDH) is a frequent and devastating consequence of traumatic brain injury. Tissue damage develops rapidly and makes treatment even more difficult. Management of increased intracranial pressure (ICP) due to extravasated blood volume and brain swelling is often insufficient to control all adverse effects of ASDH. ⋯ Tissue impedance increased by around 203% of baseline during subdural infusion of 300 μl of autologous, venous blood and dropped back to baseline within 22 min. Fifty-six minutes after the start of ASDH a cluster of four short-lasting (3-3.5 min; 140-160% of baseline) IMP increases started that reflected spontaneous CSDs. This pattern presumes that CSD occurs early after ASDH and therefore may contribute to the rapid lesion development in this disease.
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Acta Neurochir. Suppl. · Jan 2012
Development of an experimental model to study the pathophysiology of cerebral salt wasting following subarachnoid hemorrhage.
Hyponatremia is frequent following cranial -neurosurgery or acute brain injury like subarachnoid hemorrhage (SAH), and increases mortality by 30%. The patho-physiology is not understood nor does a causal therapy exist. Since clinical trials are potentially dangerous in this very ill population, we examined whether an established rat model allows studying cerebral salt wasting (CSW) following SAH. ⋯ Neither SAH(mild) (100 μL), the injection of hemolyzed blood (100 μL) or hypertonic saline (200 μL) replicated the effect. The immediate release of ADH (32.23 ± 34.87 pg/mL) following SAH(severe) normalized over the next few days. We conclude that first, the rat model of SAH is suitable for studying CSW, second the increase in intracranial pressure generates the delayed hyponatremia, and third, the ADH release does not mediate natriuresis.