摘要:

&NA;Thirty adult Wistar rats underwent an extradural clip compression injury of 50g of force for 1 minute at T‐1. After injury, the animals were randomly separated into three groups: the control group received a saline infusion for the 2‐hour treatment period; the second group was given a blood transfusion over 2 hours titrated to maintain mean systemic arterial pressure (MSAP) at preinjury levels; and the third group received an intravenous bolus dose of naloxone (10 mg/kg), followed by a 2‐hour infusion of intravenous naloxone (2 mg/kg/minute). The rats were observed postoperatively for 15 weeks, during which their clinical recovery was measured weekly by the inclined plane technique. At 15 weeks, the spinal cords were removed and prepared for histological assessment. The blood pressure before, during, and immediately after injury did not differ statistically among the three groups. During the initial 2 hours after injury, blood transfusion produced a significant increase in MSAP (P<0.02) and hematocrit (P<0.001), but naloxone infusion did not result in a significant change in MSAP. Performance on the inclined plane at 15 weeks was 35.6 plusmn 6deg, 32.7 plusmn 4deg, and 36.1 plusmn 6deg for the control, transfusion, and naloxone groups, respectively, and no significant differences were found (P>0.05). Histological examination confirmed a consistent injury of moderate severity in all three groups with no major differences among groups. Thus, this study demonstrates no significant clinical benefit either from a blood transfusion to maintain MSAP or from naloxone given by bolus and infusion after an extradural clip compression injury of the rat spinal cord. In contrast to other studies of spinal cord injury, naloxone failed to improve MSAP and recovery, (Neurosurgery19:489‐494, 1986)

ISSN:0148-396X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

&NA;The parameters of hematoporphyrin‐derivative (HpD) photocytotoxicity of human glioma cells in cell culture were studied to determine the optimum wavelength and power density of light, to investigate the influence of tissue oxygenation, and to evaluate the role of singlet oxygen and free radicals in producing cell death. Cell survival curves demonstrated a relative killing efficiency of 12:1 for violet compared to red light. Eighty joules of red light were required to produce 100% cell kill at an HpD concentration of 10 b.nug/ml, a level of HpD that has been quantitated in biopsies from patients receiving HpD photoradiation therapy. No difference in cellular killing efficiency was observed for power densities of red light varying from 10 to 100 mW/cm2. Cytotoxicity was directly related to O2tension from 12 to 490 torr with a slight but consistent increase in cell kill at O2tensions from 7 to 12 torr. Cytotoxicity was effectively quenched by b.beta‐carotene, whereas mannitol had no effect, indicating that cytotoxicity is probably mediated via a mechanism involving singlet oxygen. This information may serve as a basis for more effective application of HpD photoradiation therapy and for designing protocols to study the efficacy of such therapy. (Neurosurgery19:495‐501, 1986)

ISSN:0148-396X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

&NA;Subarachnoid hemorrhage has a profound effect on cerebrovascular reactivity. The present study noted a progressive change in the sensitivity and reactivity of rabbit basilar artery to serotonin after experimentally induced hemorrhage. The basilar artery exhibited an initial diminished response to serotonin for periods up to 6 hours after hemorrhage, whereafter the vessel gradually became hyperresponsive. The hypersensitivity became maximal 36 hours after hemor‐rhage and then began to return to normal. Such early onset of serotonin hypersensitivity and reactivity after subarachnoid hemorrhage has not been previously reported. The level of tension developed, however, suggests that serotonin alone is unlikely to cause vasospasm. The strict differentiation of spasm into early and delayed components is questioned. (Neurosurgery19:502‐506; 1986)

ISSN:0148-396X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

&NA;The cerebrospinal fluid pulse pressure (CSFPP) has found application as a measure of intracranial elastance. However, CSFPP is also dependent on the magnitude of the pulsatile variation in cerebral blood volume (ΔVb), The purpose of the present study was to assess the effect on ΔVbof changes in systemic arterial pressure (SAP) and arterial carbon dioxide tension (PaCO2) as well as elevation of intracranial pressure (ICP). Therefore, ΔVbwas computed from the electromagnetically measured flow profile in the vertebral artery of the dog on the assumption of a nonpulsatile cerebral venous outflow. During arterial hypotension, ΔVbwas increased due to a shift of flow from diastole to systole, whereas mean flow was not affected. The reverse phenomenon was observed when SAP was raised. Changes in PaCO2had little effect on pulsatile blood flow. The changes in total blood flow that occurred were evenly distributed over the cardiac cycle. Consequently, ΔVbwas not significantly affected, although CSFPP was considerably changed. When ICP was raised, a breakpoint pressure was observed above which cerebral blood flow (CBF) decreased and CSFPP and ΔVbincreased. This contradiction was explained by the finding of a decrease in diastolic flow, causing the fall in CBF, whereas systolic flow relative to mean flow was increased, resulting in an increased ΔVb. The underlying mechanisms of the pulsatile flow changes are extensively discussed. It is argued that the arterial inflow profile is largely determined by the compliance of the inflow section of the cerebral vascular bed. Vascular compliance is significantly altered by changes in SAP and ICP because they affect the transmural pressure of the vessels, whereas this is not the case during changes in PaCO2. (Neurosurgery19:507‐522, 1986)

ISSN:0148-396X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

&NA;Abnormalities of coagulation and fibrinolysis in 12 head‐injured patients were studied in early (within 24 hours of onset) and late (10th to 17th day after onset) stages.agr2Plasmin inhibitor (agr2PI), antithrombin III (ATIII), and fibrinopeptide A (FPA) and Bb.beta15‐42 (FPBb.beta) were measured in particular, in addition to the usual tests (platelet count (PLT), prothrombin time (PT), partial thromboplastin time, fibrinogen, and fibrin/fibrinogen degradation products (FDP)).agr2PI was abnormally lower, and FPA and FPBb.betawere much higher; fibrinogen and ATIII were moderately lower in the early stage than in the late stage in 6 head‐injured patients with postoperative intracranial hemorrhage.agr2PI, ATIII, and fibrinogen were moderately lower and FPA was moderately higher in the early stage than in the late stage in 6 head‐injured patients without postoperative intracranial hemorrhage. PLT and fibrinogen were lower,agr2PI was much lower, and FPA was much higher in the 6 patients with postoperative intracranial hemorrhage than in the 6 patients without postoperative intracranial hemorrhage. One patient with acute epidural and subdural hematomas had recurrent postoperative intracerebral hematoma twice. This recurrent hemorrhage was due to disseminated intravascular coagulation (DIC) caused by primary brain damage and was associated with extremely high FPA and FPBb.betalevels and abnormally lowagr2PI and PLT. Fresh‐frozen plasma and intravenous low‐dose heparin were administered after the two recurrent hemorrhages, after which FPA and FPBb.betanormalized immediately, although other screening tests showed only gradual improvement. Abnormalities of coagulation and fibrinolysis have been noted frequently in severe head injury and related to postoperative and/or recurrent intracranial hemorrhage. FPA and FPBb.betaare sensitive indicators of these abnormalities and may help evaluate the effect of treatment of DIC in severe head injury, (Neurosurgery19:523‐531, 1986)

ISSN:0148-396X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

&NA;Thirty patients suffering from minor head injury were examined with auditory brain stem responses (ABR), neuropsy‐chological tests for assessment of higher nervous functions, and a questionnaire on postconcussional symptoms. Comparison of the 6 patients with altered ABR with the other 24 showed no statistical difference in either the number of long‐lasting postconcussional symptoms or the scores on neuropsychological tests. Subclinical brain stem involvement as shown by ABR does not seem to correlate with impaired mental function or symptoms of the postconcussion syndrome. This greatly limits the use of ABR in forensic medicine. (Neurosurgery19:532‐534, 1986)

ISSN:0148-396X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

&NA;The neurovascular relationships in the trigeminal root entry zone were studied in 130 trigeminal root entry zones of 65 cadavers. No history of facial or trigeminal pain had been obtained during life in these subjects. The technique of intravascular injection, which allowed good visualization and evaluation of the neurovascular relationships, is described. A total of 42 examples of contact with the root entry zone and 10 examples of compression were identified. In 30 of the examples of contact, the finding could be related to an artery; in the other examples, it appeared to be due to veins. Of the arterial compressions, the superior cerebellar artery was responsible in 53.8%, the anterior inferior cerebellar artery was responsible in 25.6%, and pontine branches of the basilar artery were responsible for the remaining 20.6%. Only one instance of unequivocal compression by a vein was found. Other anatomical observations of interest are reported. The absence of a history of trigeminal neuralgia in the 7% of examined nerves in which root entry zone showed arterial compression is in marked contrast to the finding of 80% or more in the operative series for trigeminal neuralgia. It seems that vascular compressions may be the predominant but not the sole cause of trigeminal neuralgia. (Neurosurgery19:535‐539, 1986)

ISSN:0148-396X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

&NA;To test the safety and feasibility of using direct instillation of urokinase to induce rapid lysis of intraventricular clots, an animal model of intraventricular blood cast is required. Injections of 11 ml of fresh, unclotted autologous blood into the ventricles of adult mongrel dogs did not produce a solid blood cast in the ventricular system, suggesting that the adult dogs have an unusual ability to clear uncoagulated whole blood from the ventricles and subarachnoid space. Injection of 9 ml of preclotted blood resulted in a subtotal cast of the ventricles, leaving only portions of the occipital horns free of solid clots. This volume of injected clots incurred no mortality and minimal morbidity, whereas injection of 10 to 12 ml resulted in a mortality of 42% and formidable morbidity. The technique of producing this intraventricular blood cast model, as well as that of implanting an indwelling ventricular catheter‐reservoir system useful in chronic urokinase administration, is described. (Neurosurgery19:540‐546, 1986)

ISSN:0148-396X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

&NA;It was determined from in vitro experiments that the minimal dose of urokinase required to lyse 10 ml of clotted canine blood within a closed space must exceed 10,000 IU. We empirically doubled this minimum effective dose and tested the in vivo safety of injecting 20,000 IU of urokinase every 12 hours for 4 days into the ventricles of six adult mongrel dogs through an implanted catheter‐reservoir system. The animals were monitored carefully for local and systemic bleeding by neurological and clinical examination, hematological tests reflecting systemic fibrinolytic status, serial computed tomography, and postmortem histological examinations of the brain, meninges, and peripheral organs. It was found that this intraventricular dose regimen of urokinase did not cause intracranial hemorrhage even though the dogs had recent brain wounds related to transcerebral ventricular catheterization. Mild activation of systemic fibrinolysis, implying passage of the enzyme from ventricle to blood, occurred 4 to 6 hours after each intraventricular injection, but no systemic hemorrhages were seen. This dose regimen also did not cause acute or chronic inflammatory changes in the brain or meninges and did not disturb cerebrospinal fluid circulation. (Neurosurgery19:547‐552, 1986)

ISSN:0148-396X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

&NA;Nine millilitres of preclotted autologous blood was injected into the ventricles of 10 adult mongrel dogs (control dogs) to create subtotal ventricular casts with solid clots. The neurological status and systemic fibrinolytic profiles were closely monitored, and the changes in clot and ventricular volumes were measured by serial computed tomography (CT) for 3 months. The control animals showed severe neurological impairment for 7 to 9 days. No visible lysis of the intraventricular clots occurred for 5 to 7 days, after which slow clot lysis occurred at a constant rate. Complete lysis of the 10 clots took 38 to 65 days, indicating that canine cerebrospinal fluid normally possessed limited capacity for in situ fibrinolysis. Of the 10 control dogs, 8 developed progressive ventricular enlargement after a transient initial shrinkage parallel with initial clot lysis. Their final ventricular volume at 3 months was as much as 14 times the base line ventricular volume. Necropsy studies disclosed increased basal subarachnoid fibrosis and extensive ependymal and subependymal damage in the lateral ventricular walls of the hydrocephalic dogs. Ten other dogs (UK dogs) were given similar ventricular clot injections. Six hours later, each UK dog was begun on a regimen of 20,000 IU of intraventricular urokinase every 12 hours until solid clots were no longer seen in the ventricles on CT. In all 10 UK dogs, intraventricular urokinase induced complete lysis in 3 to 6 days without causing local or systemic hemorrhages. The neurological status of all 10 dogs also improved promptly. In 8 UK dogs, the ventricles that were initially distended by clots showed rapid shrinkage parallel with thrombolysis to a final volume at 3 months of less than four times the initial ventricular volume. Only 2 animals had persistently large or expanding ventricles. At necropsy, the ependymal and subarachnoid spaces of the UK dogs were remarkably free of damage and fibrosis. The possible mechanisms by which intraventricular urokinase may prevent posthemorrhagic hydrocephalus are discussed. (Neurosurgery19:553‐572, 1986)

ISSN:0148-396X    

出版商:OVID    

年代:1986

数据来源: OVID