Acta neurochirurgica. Supplement
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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
Pressure reactivity index correlates with metabolic dysfunction in a porcine model of intracerebral hemorrhage.
We correlated oxygen, flow, and pressure indices of cerebrovascular reactivity (CR) with extracellular cerebral metabolite concentrations in a porcine model of intracerebral hemorrhage (ICH). ⋯ We found evidence for impaired CR in a porcine model of ICH. The findings suggest that, among other parameters of CR, positive PRx coefficients have the highest significance and could be associated with microdialysis alterations during hypoxic events.
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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.