Neurologia medico-chirurgica
Online ISSN : 1349-8029
Print ISSN : 0470-8105
ISSN-L : 0470-8105
Volume 16pt2, Issue 6
Displaying 1-10 of 10 articles from this issue
    1976 Volume 16pt2 Issue 6 Pages 467-478
    Published: 1976
    Released on J-STAGE: December 28, 2006
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    1976 Volume 16pt2 Issue 6 Pages 479-486
    Published: 1976
    Released on J-STAGE: December 28, 2006
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    1976 Volume 16pt2 Issue 6 Pages 487-495
    Published: 1976
    Released on J-STAGE: December 28, 2006
    This review is based upon 424 cases with the anterior communicating artery aneurysm (Acoma.) directly attended by the author between June 1961 and September 1975.
    350 cases of these had single aneurysm, at this site, 74 cases had multiple aneurysms including one at this site. 1, 000 cases of intracranial saccular aneurysm have been attended directly during this period, the ratio of Acoma. was 42.5% of the total cases.
    As the result, mortality rate during hospitalization was 5.4% in single cases and 6.7% in multiple cases.
    Result of the follow-up study during the period of 6 months to 14 years and 6 months after surgery were as follows : 32 cases died, 15 of which died of other diseases. 10 could not walk. 18 had at least one psychic disturbances, aphasia or disability of walking without assistance. 312 were healthy or in good condition. 38 could not be followed and consequently the follow-up rate was 90%.
    The technical specialities in direct attack of Acoma. were given according to author's experiences:
    1. Acoma. is always approached through bifrontal incision.
    2. Bilateral frontal lobes must be dissected only by blunt technique interhemispherically.
    3. Before exposuring of aneurysm, if possible, bilateral anterior cerebral arteries at proximal and distal portion of the aneurysm must be exposed for the temporary clipping.
    4. Bilateral olfactory nerves must be dissected from the frontal lobes carefully, to prevent falling out of their attachment to the olfactory grooves.
    5. Blood clot in subarachnoid spaces must be aspirated as completely as possible to prevent postoperative vasospasm.
    6. Brain, arteries and veins must not be injured artificially during the surgery.
    7. Of course the growth direction of the aneurysm, the grade of adhesion with four export and import arteries and neighboring tissues, the size of aneurysm and the deformity of anterior communicating artery may have influences upon the difficulty of the procedures.
    8. Anyhow, certification of the four arteries and complete dissetion of aneurysm itself are the fundamental points of the operation.
    9. Aneurysm must be ligated then clipped exactly at its neck, and if necessary, muscle wrapping is added to these procedures.
    10. The time of temporary occlusion of the feeding arteries is approved as long as 40 minutes at one time, if 1, 000 cc of 20% manittol is given intravenously just before the craniotomy.
    The author's policy for preare and postoperative management for ruptured Acoma. as follows :
    1. The most favorable time for surgery is before 40 hours from the onset of the first rupture of aneurysm.
    2. As for the decision of surgical indication, the consciousness level is the most important factor. The patient must be in the state of up-hill course of consciousness. If not, he must be brought to up-hill course by some way.
    3. When the infarctic sign due to vasospasm appears before or after surgery, immediate superior cervical ganglionectomy will be effective to release the vasospasm.
    4. The continuous ventricular drainage is very useful to control the intracranial pressure in acute stage of subarachnoid hemorrhage.
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    1976 Volume 16pt2 Issue 6 Pages 497-504
    Published: 1976
    Released on J-STAGE: December 28, 2006
    In recent years the presence of adrenergic nerve fibers on cerebral arteries as small as 10 to 15 μ both on the pial and within the brain substance has been confirmed morphologically. Although possible roles of the adrenergic fibers in control of cerebral circulation are fairly well clarified, there are few studies as to neural factors in the territory of the basilar artery.
    In the present study, electrical stimulation of the superior cervical ganglion (SCG) was performed to define the contribution of neural mechanism to control of basilar arterial flow. Studies were also made to determine the effects of hexamethonium(C6)and chronic bilateral superior cervical ganglionectomy on autoregulation mechanism and CO2 reactivity in the territory of the basilar artery.
    Fifty-two mongrel adult dogs weighing 8 to 26 kg were anesthetized with pentobarbital and mechanically ventilated. The basilar artery was exposed through the transcervical-transclival approach and the flow was measured with an electromagnetic flowmeter. The unilateral and bilateral SCG were stimulated by square-wave direct current impulses (3-5 v, 2.0 msec duration, 20 Hz). Autoregulation of basilar flow was studied under acute hypertension, which was induced by an intraaortic balloon inflation before and after intravenous administration of C6. The same study was performed in the animals, in which both SCG were removed 2 weeks to 2 months prior to the experiment. Also changes in basilar flow following 7 % CO2 inhalation were studied in the respective experiments.
    The mean percentage reduction of basilar flow was 11.7% on unilateral SCG stimulation and 20.4% on bilateral, associated with a slight rise of systemic blood pressure. The effects of bilateral stimulation were greater than those of unilateral (p<0.01). Inflation of the balloon produced an increase in basilar flow. However, it returned rapidly to the resting level and remained unchanged during 3 minutes period of induced hypertension. After the administration of C6, basilar flow increased along with the rise of blood pressure. CO2 reactivity was well maintained under this condition. Two to four weeks after bilateral SCG-ectomy, fluorescence of the adrenergic fibers disappeared completely from the trunk and main superficial branches of the basilar artery. Studies using chronically bilaterally sympathectomized dogs revealed an impairment of autoregulation in response to rise of blood pressure.
    Adrenergic fibers observed in abundance on the basilar artery may have an important functional role in conveying vasoconstrictive impulses via the SCG. It is assumed that the bilateral SCG contribute to neurogenic control of blood flow in the territory of the basilar artery and the neurogenic control plays an important role in autoregulation of cerebral blood flow in response to rise of blood pressure.
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    1976 Volume 16pt2 Issue 6 Pages 505-513
    Published: 1976
    Released on J-STAGE: December 28, 2006
    The direct observation of the sympathetic vasomotor activity during increase in intracranial pressure (ICP) has seldom been done, although the pressor response following increased ICP is presumed to be due to excitation of the sympathetic nervous system. It is also interesting to know whether the sympathetic nervous system participates in the development of vasoparalysis or plateau wave.
    The activity of the sympathetic vasomotor nerve was assessed by measuring the efferent discharge from the renal nerve of a cat which is known to be a good indicator for evaluating the sympathetic vasoconstrictor tone of the whole body.
    ICP was increased stepwisely by infusing saline into the cistena magna. With each increment of ICP, the renal nerve activity (RNA) was suppressed. Since the suppression of the RNA was not striking in the animals whose baroreceptor nerves had been cut, it is convinced that a reflex mechanism via the baroreceptor depresses the sympathetic vasoconstrictor tone during the initial phase of increased ICP. At cerebral perfusion pressure (CPP) of 30 mmHg, a sudden remarkable increase of the RNA was noted, followed by a significant rise of blood pressure (BP). When increased ICP was lowered, the RNA was decreased to the level below the initial value. After the procedure of raising and lowering ICP was repeated, in one cat out of five, an abrupt disappearance of RNA for five minutes was observed during the state of increased ICP. The renal nerve did not respond to the withdrawal of blood, which usually causes the RNA to increase. The sympathetic vasomotor activity was considered to be paralyzed temporarily during this phase.
    In other animals whose ICP were raised by infusing heparinized arterial blood instead of normal saline, the increase in RNA from the suppressed state occurred at earlier stage, that is, at higher level of CPP. In one cat out of five, the infusion of a small amount of blood caused a remarkable continous increase in RNA followed by a significant rise in BP with tachycardia. These observations indicate the tone of the sympathetic nervous system may be increased in subarachnoid hemorrhage.
    In other five animals, ICP was elevated rapidly beyond the level of mean BP and maintained for seven minutes and then lowered. After this procedure was repeated several times, in three cats out of these five, a gradual decline of RNA was observed following the stage of increase resulted from the elevation of ICP. Thereafter, RNA disappeared completely despite ICP maintained above the level of BP. The absence of RNA persisted several minutes even after the ICP was lowered.The administration of 0.025mg/kg of norepinephrine at this stage resulted in a significant rise in ICP following a rise in BP. Several minutes later, RNA was recovered spontaneously to the level more than that before the procedure. The administration of norepinephrine at this stage of increased RNA resulted in only a slight rise in ICP, while the rise in BP was similar. This phenomenon may strongly suggest the possibility that the tone of the sympathetic vasoconstrictor nerve plays an important role for protecting the brain against the change in BP by preventing the occurrence of sudden rise in ICP.
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    1976 Volume 16pt2 Issue 6 Pages 515-523
    Published: 1976
    Released on J-STAGE: December 28, 2006
    Disturbance of cerebral circulation during intracranial hypertension is not only caused by vasoparalytic effect of the cerbral vessel, but also caused by alteration of the perfusion pressure. The perfusion pressure, which is the difference between mean arterial pressure and cerebrospinal fluid pressure (Miller), does not always indicate real perfusion pressure during intracranial hypertension. Appearance of intercompartment pressure gradient during intracranial hypertension might be important to control perfusion pressure as reported by Symon et al. In the mechanism of alteration of cerebral circulation during intracranial hypertension, the change of the real perfusion perssure, vasopressor response and vasoparalysis have to be observed.
    In 40 mongrel dogs under pentobarbital anesthesia with artificial respiration (PaCO2 35-38 mmHg), pressures at the epidural space, the cisterna magna, the sagittal sinus, the femoral artery, the cerebral pial artery, the vein and cerebral tissue fluid were continuously recorded during intracranial hypertension induced by incremental inflation of the extradural balloon placed at the right frontal region or at the posterior fossa.
    The perfusion pressure was analysed by means of two factors: One is upstream perfusion pressure (mean arterial pressure —pial arterial pressure) and the other is downstream perfusion pressure (pial arterial pressure — pial venous pressure). Each perfusion pressure was divided by mean arterial pressure as indicated by the formula in Fig. 2.
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    1976 Volume 16pt2 Issue 6 Pages 525-534
    Published: 1976
    Released on J-STAGE: December 28, 2006
    Experimental subarachnoid hemorrhage was produced by the injection of fresh arterial blood (2-4 ml) into the cisterna magna of adult cats. Spasm of intracranial major vessels with more than 50 per cent decrease in the size of the vessels was observed angiographically, and lasted for 60 to 90 minutes in all the cases studied. Repeat angiograms revealed biphasic vasospasm in 10 out of 21 cases. The late spasm occurred in 3 days, reaching a maximum in 3 to 5 days after the hemorrhage.
    The basilar artery was microscopically exposed by a transclival approach in the normal cats as well as those at 3 days after the cisternal injection of blood. Vasospasm of the basilar artery in normal cats lasted for 20 to 30 minutes with a 2 minute period of topical application of those vasoactive substances such as noradrenaline (100 ng/ml), serotonin (100 ng/ml), prostaglandin E1 and F2α (10 μg/ml), fresh blood and a 3 days long incubated CSF-blood mixture. In cats 3 days after the subarachnoid hemorrhage, spasm was produced with much lower concentration of noradrenaline (5-10 ng/ml) and lasted for longer time up to 40 minutes. Blood and incubated CSF-blood mixture also produced marked arterial spasm for more than 60 minutes.
    Serotonin, noradrenaline, prostaglandin E1 and F2α were determined in the blood mixed with CSF in cats. Concentrations of those vasoactive substances were less than 10 ng/ml of the mixed fluid, except that of serotonin. An incubation of the mixed fluid at 37 °C for 3 days lowered concentrations of these vasoactive substances down to less than 5 ng/ml of the fluid.
    Enzyme dopamine-β-hydroxylase (DBH) activity and noradrenaline concentration of major vessels at the base of the brain and locus ceruleus area were determined in normal (control) cats and in those with experimental subarachnoid hemorrhage. Subarachnoid hemorrhage produced a biphasic response in the DBH activity of the vessels and locus ceruleus, consisting of a reduction to 60% of control during the first 24 hours followed by a marked increase to approximately 250% of control reaching a maximum at 3 days, and a gradural recovery to the control level by 7 days after the hemorrhage. Noradrenaline concentration of the vessels and locus ceruleus showed biphasic response similar to that of DBH activity.
    Several agents were used to relieve the vasospasm produced by the topical application of noradrenaline (5-10 ng/ml) to the exposed basilar artery 3 days after the cisternal injection of blood. Phenoxybenzamine (α-adrenergic blocker) and fusaric acid (DBH enzyme inhibitor) were more effective in reversing the vasospasm than dopamine and salbutamol (β2-adrenergic stimulant), when applied topically.
    These results demonstrated that late cerebral vasospasm is likely due to a hyperreaction of cerebral vessels to spasmogenic substances which would remain in the subarachnoid space, in the ciscumstances of excessive accumulation of DBH enzyme and noradrenaline in cerebral vessel wall.
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    1976 Volume 16pt2 Issue 6 Pages 535-544
    Published: 1976
    Released on J-STAGE: December 28, 2006
    Clinical manifestations including the angiographic findings suggest that the spontaneous carotid-cavernous fistulae (CCF) are more likely considered etiologically to be one type of the dural arteriovenous fistulae in the cavernous region. This concept have been elaborated by Newton and Hoyt (1970) and also by us (1971) . However, this is not beyond working hypothesis. Recently we have encountered an autopsied case of spontaneous CCF. This 54-year-old female was expired from incidental apopletic complication two weeks after the selective external carotid ligation combined with embolization by polyurethane foam. At autopsy the sphenoid bone was removed including the sella turcica. After fixation, micropaque solution mixed with Evans blue was injected through the internal carotid artery. Blocks were cut in coronal section and stained with HE and Elastica van Gieson. Cavernous sinuses were divided into several sizes of small venous lakes, whose septa of connective tissues contained small arteries and veins. Injected dye not only was found in the arterioles in the septa, but also leaked out into the veins, connective tissues of the septa and also into the venous sinus. Walls of the arterioles running in the septa were partly thick and partly thin due to proliferation and interruption of the internal elastic lamina, and their lumina were irregularly narrowed and obstructed with concomitant organized thrombi. In addition, there were vessels which were hardly called either arteries or veins, and which had the appearance of venous or capillary angioma. Another interesting findings were observed in the thickened septa of the sinus wall, which are characterized by proliferation of elastica especially around the thrombosed small arteries. These histological features are reasonably considered to be that of arteriovenous malformation. Discussions were made from the histopathological standpoint on atherosclerosis, moya-moya disease, fibromuscular hyperplasia and Ehlers-Danlos syndrome.
    From the clinical point of view, spontaneous CCF can be differentiated from the traumatic one. The former were commonly seen amongst the middle aged female and frequently accompanied by headache. Multiple feeders mostly of external carotid artery contribute to the fistula. Furthermore, except for a few cases, they were rarely cured with surgery but rather cured or improved either spontaneously or in the process of the angiographic examinations.
    According to these clinical, angiographic and histological observations, it should be reasonably said that the spontaneous CCF is one type of dural arteriovenous fistula in nature and is the result of the rupture of the arteriovenous malformation of the dural vessels in the septa of the cavernous sinus directly into the cavernous sinus or via bleeding into the connective tissue of the septa.
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    1976 Volume 16pt2 Issue 6 Pages 545-553
    Published: 1976
    Released on J-STAGE: December 28, 2006
    Thirty-five patients with primary malignant brain tumor were treated with scheduled combination chemotherapy using Adriamycin and BCNU, CCNU or methyl CCNU after surgical treatment and BAR therapy. Adriamycin (0.8 mg/kg) on the first and second day and 100 mg/m2 of BCNU, CCNU or methyl CCNU on the second or the third day were given. This combination chemotherapy was repeated every two months. The survival rates at 1 and 1.5 year after operation of highly malignant glioma (13 patients : 11 with glioblastoma, 1 with oligodendroblastoma and 1 with medulloblastoma) were 83%, 45% respectively, and for moderately malignant glioma (15: 11 with low grade astrocytoma, 2 with oligodendroglioma and 2 with ependymoma), they were 86%, 78% at 1 and 2 years respectively. The 1 year survival rate of this chemotherapy with BAR therapy is better than that of BAR only in highly malignant glioma. The average survival time of pontine glioma was 13.8 months. The complications were alopecia (49%), nausea and vomiting (46%) and leucocytopenia below 4, 000 (60%). When 0.8 mg/kg of Adriamycin and 100 mg/m2 of BCNU were administered, the sudden leucocyte decrease was frequently observed after days from the administration, whereas 0.4 mg/kg of Adriamycin and 60 mg/m2 of BCNU or methyl CCNU was given, decrease of WBC was moderate.
    The minimum duration for the repopulation of treated human glioblastoma may be computed with the knowledge of a cell cycle time of 3 days and growth fraction of 0.3. For one tumor cell to become 100 cells without cell loss, it will take a minimum of 53 days. In this case, chemotherapeutic agents resulting in a 2 log cell kill will be effective. Therefore, in order to obtain a stepwise reduction in tumor mass using agents of 2 log cell kill, a second course of therapy should be administered within 53 days. It is reasonable that the administration of Adriamycin and BCNU or CCNU is repeated every 8 weeks, assuming this combination chemotherapy results in 2 log kill.
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    1976 Volume 16pt2 Issue 6 Pages 555-562
    Published: 1976
    Released on J-STAGE: December 28, 2006
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