Neurosurgery
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Changes in ventilatory rate affect arterial blood pH and PCO2 within seconds to minutes, but the corresponding acute changes for cerebrospinal fluid (CSF) pH and PCO2 have been as well documented. Using our previously-described swine model of brain retraction ischemia, we examined changes in arterial and CSF pH and PCO2 with acute changes in ventilation in four animals. Newly developed fluorescent dye technology permitted near-instantaneous recording of CSF pH and PCO2 during acute hyperventilation (end-tidal PCO2 of 20 mm Hg) and acute hypoventilation (end-tidal PCO2 of 50 mm Hg). ⋯ Changes in pH and PCO2 with hyperventilation and hypoventilation occurred rapidly in both arterial blood and CSF. Steady-state values were reached within 15 minutes for hypoventilation, and 30 minutes for hyperventilation. The correlation between arterial and CSF values for both pH and PCO2 at 5, 15, 30, and 60 minutes were all very highly significant (P < 0.001) except for arterial and CSF PCO2 at 5 minutes (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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Percutaneous compression of the trigeminal ganglion, which is currently being used for the control of trigeminal neuralgia, induces marked intraoperative elevations of the systemic blood pressure and heart rate changes, which may increase the risk of cardiovascular complications. We have analyzed the characteristics of the arterial hypertensive response and the cardiac rhythm changes induced by percutaneous compression of the trigeminal ganglion in 42 consecutive, unselected patients undergoing operations for essential trigeminal neuralgia under three different regimens of anesthesia. The first 22 patients (Group 1) underwent operations under brief general anesthesia without endotracheal intubation. ⋯ By contrast, patients of Group 3, who had local anesthetic blockade of Meckel's cave before ganglion compression, did not develop tachycardia or extrasystoles. Foramen ovale puncture elicited marked elevations of the systemic blood pressure in all patients. Ganglion compression further increased blood pressure, except in patients of Group 3, who had local anesthetic blockade of Meckel's cave.(ABSTRACT TRUNCATED AT 250 WORDS)
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Randomized Controlled Trial Clinical Trial
The effect of hypothermia on the incidence of delayed traumatic intracerebral hemorrhage.
Hypothermia has been shown to cause coagulation abnormalities, primarily related to platelet dysfunction. We reviewed coagulation function and the incidence of delayed traumatic intracerebral hemorrhage in a series of 36 patients with severe head injuries (Glasgow Coma Scale 3-7) enrolled in a prospective, randomized, clinical trial of therapeutic moderate hypothermia. Patients were randomized to a normothermic group (n = 16) or to a group cooled to 32 to 33 degrees C within 6 hours of injury (n = 20). ⋯ Three patients in the hypothermic group and one in the normothermic group developed thrombocytopenia (a platelet count of less than 100,000). There were no significant differences between the two groups in the incidence of delayed traumatic intracerebral hemorrhage, in measured coagulopathy, or in the mean values of measured coagulation parameters. Although the possibility of a hypothermia-induced coagulopathy has not yet been excluded, the short-term use of hypothermia does not appear to increase the risk for intracranial hemorrhagic complications in head injuries.
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The authors report the results of a retrospective review, between January 1986 and December 1991, of the results of early surgery and intrathecal thrombolytic therapy in 111 patients with aneurysmal subarachnoid hemorrhage. Effects on clot lysis, angiographic and symptomatic vasospasm, cerebral infarction, and clinical outcome were compared in 60 patients treated with urokinase (UK) 60,000 IU/d for 7 days (UK group), 22 patients treated with 0.042 to 1 mg tissue plasminogen activator (tPA) every 6 to 8 hours for 5 days (tPA group), and 29 patients who did not receive treatment with either thrombolytic agent (no-treatment group). The no-treatment group consisted of all patients treated before July 1986 and of patients in whom thrombolytic therapy was attempted but failed to start or in whom the therapy was not used intentionally because of small subarachnoid clot. ⋯ Meningitis was suspected in 16 patients of the UK group. However, in this relatively small retrospective series, there were no differences among the three groups in overall outcome at 3 months. This study indicates that postoperative intrathecal thrombolytic therapies, especially with less than 4 mg/d of tPA, are effective in lysing subarachnoid clot and preventing vasospasm and infarction safely.
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We examined the expression of fibroblast growth factor receptor-1 (FGFR-1), namely FLG, in tissues of 18 human gliomas, 10 human meningiomas, 3 human metastatic brain tumors, and 2 normal human brains by means of immunohistochemistry. All tissues were positively stained for FGFR-1. Primary brain tumors were more abundantly immunoreactive than normal brain tissues (Mann-Whitney U test, P < 0.05). ⋯ The expression level of FGFR-1 of tumor cells increased in correlation with that of endothelial cells in glioma tissues (Spearman's test, P < 0.001). We previously reported that basic FGF is produced in more than 90% of human glioma and meningioma tissues. Together with these data, it is suggested that basic FGF is involved in autonomous cell growth and tumorigenesis of gliomas and meningiomas as an autocrine growth factor in vivo.