Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Apr 1997
Case ReportsHyperalgesia induced by high-dose intrathecal sufentanil in neuropathic pain.
The patient had lower lumbar arachnoiditis as part of a failed back surgery syndrome. Two years after discectomy, she still suffered from left lumbosciatic pain despite various invasive treatments. Psychologic impairment could be excluded. ⋯ Increasing the dose to 50 mg daily could only be supported for 3 h. Sufentanil was stopped and saline started, after which the evoked hyperalgesia disappeared. It is concluded that relatively high doses of sufentanil may induce hyperalgesia in patients with arachnoiditis and neuropathic pain.
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J Neurosurg Anesthesiol · Apr 1997
Comparative StudyFurosemide decreases cerebrospinal fluid formation during desflurane anesthesia in rabbits.
Previous studies suggest that desflurane may increase cerebrospinal fluid (CSF) formation rate (Vf) and volume, particularly during conditions of hypocapnia combined with elevated CSF pressure. The present study was designed to determine whether treatments routinely used in patients during anesthesia for neurological surgery would decrease Vf during desflurane anesthesia in rabbits. Three groups of six rabbits each were examined at four experimental conditions. ⋯ During the combination of desflurane, hypocapnia, and elevated CSF pressure, furosemide decreased Vf to 3.2 +/- 1.7 microliters.min-1, mannitol increased plasma osmolality and decreased plasma sodium concentration, and fentanyl decreased heart rate and increased plasma potassium concentration. Values for Ra and brain water content did not differ between groups. Of the four treatments examined, only furosemide decreased Vf during the combination of desflurane, hypocapnia, and elevated CSF pressure.
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J Neurosurg Anesthesiol · Apr 1997
Effects of normo- and hypocapnic nitrous-oxide-inhalation on cerebral blood flow velocity in patients with brain tumors.
Nitrous oxide (N2O) use during anesthesia for intracranial procedures has been a subject of controversy in the past. To date, the isolated influence of N2O on mean cerebral blood flow velocity in the middle cerebral artery (VMCA) has not been investigated during hypocapnia in patients with brain tumors. We compared VMCA during normocapnic (ETCO2: 40 mm Hg) and hypnocapnic (ETCO2: 25 mm Hg) inhalation of air and 50% nitrous oxide in oxygen N2O/O2 in eight patients with unilateral brain tumors on both the tumor side and the healthy side. ⋯ Mean VMCA increased during normocapnic inhalation of N2O/O2 (tumor side: 86 +/- 16 cm sec-1; healthy side: 74 +/- 17 cm sec-1) when compared with air (tumor side: 72 +/- 18 cm sec-1; healthy side: 62 +/- 14 cm sec-1, p < 0.01), whereas during hyperventilation VMCA decreased on both sides (p < 0.001). Mean VMCA values were quite similar during hypocapnic inhalation of 50% N2O/O2 (tumor side: 50 +/- 12 cm sec-1; healthy side: 45 +/- 13 cm sec-1) and air (tumor side: 51 +/- 14 cm sec-1; healthy side: 45 +/- 12 cm sec-1). The data of our study suggest that in patients with cerebral tumors the N2O-induced increase in mean VMCA can be completely reversed by hyperventilation.
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J Neurosurg Anesthesiol · Apr 1997
Case ReportsCerebral oximetry during circulatory arrest for aneurysm surgery.
A patient underwent surgical clipping of a complex giant intracranial carotid aneurysm with the aid of extracorporeal circulation and complete hypothermic circulatory arrest. During the entire procedure, cerebrovascular oxygen saturation (ScO2) was spectroscopically measured. The patient experienced circulatory arrest for 34 min; for 15 of the 34 min ScO2 was < 34% (minimum 32%). The patient tolerated the procedure without new neurological deficit, thus demonstrating that the previously suggested "critical" level of 35% ScO2 is not absolute.
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J Neurosurg Anesthesiol · Apr 1997
Comparative StudyThe influence of acute and chronic alcohol treatment on brain edema, cerebral infarct volume and neurological outcome following experimental head trauma in rats.
The aim of this study was to determine the influence of acute and chronic ethanol treatment on neurological outcome following head trauma in rats. Eight-two Sprague-Dawley rats were divided into 10 groups. Four groups received sham head trauma (surgical incision of the scalp but no trauma) and were treated with (A) nothing, (B) chronic ethanol (6% ethanol in drinking water for 40 days), (C) acute ethanol 1.5 g/kg, intraperitoneally (IP) and (D) acute ethanol 3 g/kg IP. ⋯ Specific gravity was also lower in the acute ethanol-treated groups compared with no ethanol, chronic ethanol, and acute ethanol plus ketamine groups (p < 0.03). Based on these observations, we conclude that in this rat head trauma model acute ethanol treatment increases mortality, neurological deficit, hemorrhagic necrosis volume, and brain edema. On the other hand, chronic ethanol treatment has no apparent effect and ketamine treatment does not counteract the effect of acute ethanol treatment.