摘要:

Between 1968 and 1988, 2298 head-injured patients of all grades of severity were registered in the data bank of a single clinic. The majority of patients were admitted to a community hospital and transferred later to the neurosurgical clinic. The data included mechanism of injury and clinical status at admission, including the level of consciousness according to the Glasgow Coma Score (GCS) before and after resuscitation. After admission, nearly all patients below a score of 8 were intubated and treated with controlled ventilation until the patient awakened, died, or had remained in a steady state for ∼3 weeks. Assessment of the final outcome was made according to the Glasgow Outcome Scale (GOS) both at discharge and again after the patient's status was stabilized. The results show a stable yearly outcome during the 21 years of recording but a significantly improved good recovery and mortality rate when compared with our previous results. Outcome was significantly correlated to age and type and severity of lesion, as judged by the postresuscitation GCS. The outcome of the 1264 most severely injured, comatose patients (GCS <9) shows a good recovery rate of 55%, a severely disabled rate of 14%, a vegetative rate of 7%, and a mortality rate of 24%. We attribute these results, which compare favorably with others, to prompt airway control and controlled ventilation in unconscious patients.

ISSN:0898-4921    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

We used the biphasic electroencephalographic (EEG) response to increasing concentrations of thiopental to measure regional brain responses to thiopental. Eight patients with cortical parietal brain tumors, 3.3 (SD 1.3) cm in diameter, and eight control patients with lung cancer and normal brain computed tomography scans received thiopental by infusion (50–75 mg/min) until burst suppression (50% isoelectric activity) on the EEG occurred. Infusion lasted 10.7 (SD 2.4) min, and the average dose of thiopental administered was 810 (SD 170) mg [11.2 (SD 1.9) mg/kg]. During infusion the EEG was continuously recorded from the F3, F4, P3, and P4 electrodes. On-line power spectral analysis was performed, and data were saved for later analysis. Four EEG parameters [log β (15–30 Hz) power, percent β power, spectral edge 95% and spectral edge 70%] were plotted against calculated brain concentration of thiopental [using an assumed plasma-effect site rate constant (ke0) of 0.58] for each individual. Three points were measured on each curve (50% upslope, peak, and zero intercept) to quantitate the EEG response. Statistical comparisons were performed between the following sets of data: EEG response at electrode closest to brain tumor versus electrode farthest from tumor (in the same patient); and electrodes closest to brain tumors (parietal P3 and P4) versus same electrode pair in control patients (patients with thoracic tumors) using analysis. No differences were found in any comparison. Thus, the presence of a brain tumor does not affect the response of the brain in this region to thiopental as measured using EEG.

ISSN:0898-4921    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Patients receiving anticonvulsants are resistant to nondepolanzing muscle relaxants (NDMR). This study examines the effect of plasma anticonvulsant levels on pipecuronium-induced neuromuscular blockade. Twenty adult patients scheduled for neurosurgery were assigned to one of two groups. Group 0 (G0) consisted of 10 patients not on anticonvulsant therapy; group 1 (G1) included 10 patients treated either with phenytoin or carbamazepine. G1 patients were further divided into Glu (n = 4) and Glw (n = 6) subgroups, according to the plasma anticonvulsant level measured the day before surgery—under (G1u) or within (G1w) the therapeutic range. Neuromuscular transmission was monitored with a Biometer International A/S Accelograph. Anesthesia was induced and maintained using propofol and sufentanil. After calibration of the accelograph, a bolus of pipecuronium 0.08 mg/kg was given IV. The time from pipecuronium injection to the peak reduction of T1 was taken as the onset time. The time in min from pipecuronium injection to recovery of T1 % (first accelograph response/baseline response) × 100 and TR % (fourth accelograph response/first accelograph response) × 100 were recorded at 25, 50, and 75% of baseline. The recovery index (RI) was taken as the time from 25 to 75% recovery of the baseline response. The onset time was not different in G0 (203 ± 60.4 s), G1 (230.5 ± 79.3 s), and G1u (181.8 ± 60.4 s) but prolonged in G1w (279.2 ± 67.7 s). The recovery times of T1 and TR to 25, 50, and 75% of baseline were significantly shorter in G1, G1u, and G1w than in G0 but not different between G1u and G1w. RI was significantly shorter in G1 (35 ± 14.6 min) than in G0 (65.6 ± 23.1 min) but did not differ between G1u (37 ± 17 min) and G1w (32.5 ± 12.7 min). In conclusion, patients treated with carbamazepine or phenytoin exhibit some resistance to pipecuronium blockade. That resistance results in a significantly accelerated recovery from paralysis and a prolonged onset time. The onset time prolongation is only observed in patients whose plasma anticonvulsant level is in the therapeutic range, but the accelerated recovery appears whatever the plasma level of the anticonvulsant.

ISSN:0898-4921    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

We describe a case of propylene glycol toxicity due to intravenous administration of etomidate for cerebral protection. A continuous etomidate infusion was titrated to burst suppression of the electroencephalogram during surgical resection of a large intracranial arteriovenous malformation. The etomidate formulation used (Amidate, Abbot) contains etomidate 2mg/ml in a 35% propylene glycol vehicle. A total of 5 g/kg of the solvent was given during 12 h. Adverse effects of propylene glycol were observed including hyperosmolality with an increased osmolal gap, hemolysis, hemoglobinuria, and metabolic acidosis. Normalization of these metabolic and ionic alterations occurred after 12 h of discontinuation of the infusion. The potential toxicity of the solvent should be considered during long-term administration of etomidate.

ISSN:0898-4921    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

MK-801, although more consistently neuroprotective in focal ischemia, has had more variable success in the management of global ischemia. This difference could be due to a vasoactive effect that would improve blood flow in focal ischemia but would not be operative in global ischemia. Therefore, a possible direct cerebrovascular effect of MK-801 was investigated in vitro in basilar arteries from 13 dogs and 16 guinea pigs. Two rings were obtained from each animal; in one the endothelium was removed and in the other the endothelium was maintained intact. Each ring was suspended in an organ bath and isometric tension was recorded. After half-maximal contractions with either KC1 or 5-hydroxytryptamine, a dose of MK-801 or the same volume of saline was added to the bath. MK-801 concentrations between 0.1 and 1.0 μMhad no effect on both canine and guinea pig basilar arteries with or without endothelium whereas concentrations 10–160 μMfurther contracted the arteries in an endothelium dependent fashion, with the exception of the KC1 precontracted endothelium intact canine artery. Higher concentrations of MK-801 tended to dilate the arteries and the dilation was endothelium independent. Thus, MK-801 has dose-dependent cerebral vascular effects and our results may explain some of the conflicting results of MK-801 on CBF.

ISSN:0898-4921    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Sedative doses of benzodiazepines, i.e., midazolam, can cause electroencephalography (EEG) activation, which is reversed by the benzodiazepine antagonist flumazenil. Hyperbaric oxygen (HBO) can cause acute cerebral toxicity with sensory and motor abnormalities, including seizures. Benzodiazepines are also administered for anxiolysis, sedation, and seizure prophylaxis to patients receiving HBO treatments. Because of possible interactions on monitored neuroelectric activity, we decided to evaluate the effects of midazolam on the EEG and cortical somatosensory evoked potentials (CEPs) in rats exposed to HBO, as well as to compare this to the effects of flumazenil. Thirty-six Sprague-Dawley rats were studied. Analog 2-channel and computerized EEG analysis (compressed spectral array with spectral edge, power spectrum, and power bands) and CEPs were monitored. Studies were divided into two phases. In phase 1, after baseline recordings, 16 rats were randomly assigned to receive midazolam, 0.1 mg · kg-1intravenously, then compression to 1,824 mm Hg of O2(n = 8), or 1,824 mm Hg of O2followed by the midazolam (n = 8). In phase 2, after baseline recordings, rats were randomly assigned to four (n = 5) groups: midazolam, 0.1 mg · kg-1intravenously, then compression to 1,824 mm Hg of O2; midazolam, then flumazenil, 0.05 mg · kg-1intravenously; compression, then midazolam; or flumazenil, then midazolam. Recordings of EEG and CEPs were compared by analysis of variance and the Student'sttest. In phase 1, midazolam first showed EEG activation in six (75%) rats, which was reversed by HBO. The HBO first activated the EEG in two rats (25%); midazolam then given had no effect. The CEPs were not altered. In phase 2, raw EEG activation was observed after midazolam alone, increasing power in high-frequency bands (p> 0.05), but not with flumazenil or HBO alone. Flumazenil and HBO both prevented new and attenuated existing EEG activation from midazolam. The CEPs were again unaffected. Although neither HBO nor flumazenil alone altered rat EEG activity, both HBO and flumazenil had similar effects in that both prevented and attenuated midazolam-induced EEG activation.

ISSN:0898-4921    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Nitrous oxide (N2O), 70%, in O2is often used as a control condition after surgical preparation in rodents undergoing neuroscience investigations. Concern has been expressed that this constitutes a stressful condition. Microdialysis was used in 15 rats to assess extracellular striatal dopamine concentrations during overnight soundproof isolation and on the following day after vascular cannulation and halothane excretion under N2O sedation with concomitant neuromuscular blockade. The overnight dialysate dopamine concentration was 22.8 ± 8.7 pg/40μl. Thirty minutes after stopping halothane, the dialysate concentration was 362.6 ± 91.6 pg/40μl during postsurgical N2O sedation. These data indicate that (a) compared to an unstressed baseline, significant brain dopamine effects occur with N2O sedation after surgery with halothane N2O anesthesia, and (b) baseline conditions can have a major effect on microdialysis data expressed as percentage of baseline.

ISSN:0898-4921    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0898-4921    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0898-4921    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0898-4921    

出版商:OVID    

年代:1995

数据来源: OVID