Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Apr 1997
Intact cerebral blood flow reactivity during remifentanil/nitrous oxide anesthesia.
Remifentanil hydrochloride is a new opioid rapidly metabolized by blood and tissue esterases. The swift degradation accounts for the elimination half-life (t1/2 beta) of < 10 min. An anesthetic agent allowing more rapid postoperative assessment of the neurosurgical patient would be beneficial. ⋯ Electroencephalographic monitoring showed a spectral edge frequency of 26 +/- 1 Hz before induction, 25 +/- 1 Hz during maintenance of the remifentanil/N2O anesthetic (0.32 +/- 0.15 microgram/kg/ min), 24 +/- 1 Hz during hypocapnic CBF determination, and 24 +/- 2 Hz during normocapnic CBF determination. At the completion of the procedure, the patients responded to commands within 3.6 +/- 2.5 min and were extubated 7.2 +/- 4.5 min after the remifentanil/N2O was discontinued. In conclusion, absolute CBF values during remifentanil/N2O are similar to previously reported CBF values during fentanyl/N2O and isoflurane/N2O anesthesia, and cerebrovascular reactivity to CO2 remains intact.
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J Neurosurg Anesthesiol · Apr 1997
Case Reports Comparative StudySensitivity to vecuronium after botulinum toxin administration.
When used to treat focal dystonias, botulinum toxin may cause a transient impairment of neuromuscular transmission in muscles distant from those injected. These systemic effects are not clinically evident, but should not be ignored when patients are exposed to other drugs or conditions that also impair neuromuscular transmission. ⋯ Compared with that observed in 24 individuals who were free from neuromuscular problems, the patient's sensitivity to vecuronium was low 90 days after the seventh treatment with toxin and normal 8 days after the ninth. The possibility is considered that repeated treatments with the toxin may cause continuous remodeling of neuromuscular junctions and may cause the patient to develop some tolerance to the action of neuromuscular blockers.
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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.