[Surgical treatment of intracranial giant aneurysms].
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Biomedical subjects
Publications and source records attributed to J Suzuki.
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A case of allergic granulomatous angiitis showing various symptoms of the central nervous system is reported. A 29-year-old female was admitted to our hospital because of severe headache and urinary incontinence. Consciousness was drowsy, and right IIIrd cranial nerve palsy was observed. CT scan revealed subarachnoid hemorrhage, hydrocephalus and arachnoid cyst. Since no aneurysm or arteriovenous malformation was detected by angiography, continuous ventricular drainage was performed. Marked hypertension due to renal vascular origin was suggested by means of laboratory data about serum renin etc., so renal as well as cerebral angiography was carried out by Seldinger's method. There revealed aneurysms of the left renal artery and a branch of the left anterior cerebral artery. Then, ventriculo-peritoneal shunt and resection of left frontal aneurysm were done. Microscopic finding of the excised aneurysm was necrotizing angiitis with infiltration of eosinophil. Six days after the operation, CT scan showed asymptomatic subcortical hematoma at the right occipital lobe. The patient was in good condition and had no cerebral or other complication following steroid therapy. The present case was considered as a very rare one because no case with subarachnoid hemorrhage and cerebral aneurysm due to allergic granulomatous angiitis was reported in the previous literature.
Using a bifrontal trans-interhemispheric approach, we have performed direct operations on 206 cases of aneurysm of the anterior communicating artery, 44 of which (21.4%) had vascular anomalies associated with the aneurysm. Those anomalies included 27 cases (13.1%) with median artery of the corpus callosum, 20 cases (9.7%) with duplication of the anterior communicating artery and one case (0.5%) with duplication of the A1 portion. Preoperative diagnosis of the duplications was not possible on the basis of angiograms. Moreover, preoperative diagnosis of the median artery using angiography was unambiguous in only 11 of the 27 cases (41%). The majority (81.5%) of the aneurysms of the anterior communicating artery in cases with a median artery of the corpus callosum were found to develop at the trifurcation of the anterior communicating artery, the A2 portion and the median artery of the corpus callosum.
The authors report twenty-six aneurysms of the proximal anterior cerebral artery (A1 segment). Fourteen cases were male and twelve cases were female. Saccular aneurysms were twenty-four and fusiform aneurysms were two. The incidence of the A1 aneurysms was 0.76%. Clinicopathologically, multiplicity of this aneurysm was distinctive, and eleven cases had multiplicity (42.3%). In the seven cases among them, the A1 aneurysms bled (63.6%). These 26 aneurysms were classified into five types according to the mode of the origin of the aneurysm from the A1 segment: (a) fifteen aneurysms originating from the junction of the A1 segment and the small perforating artery, (b) five from the A1 directly, (c) three from the proximal end of the fenestration of the A1, (d) two were fusiform aneurysms, (e) one from the junction of the A1 and the cortical branch. In CT scan of these aneurysms, bleeding extending to the septum pellucidum is very similar to that of the anterior communicating artery aneurysms.
The effects of combination chemotherapy of ACNU and 5-FU on cells grown exponentially as monolayers, cells in multi-cell spheroids and in s.c. transplanted tumors of rat glioma clone-6 cells were analyzed by the colony-forming assay. The cytotoxic effect of ACNU on cells in spheroids was enhanced by continuous 5-FU pretreatment for several hours, but further enhancement was obtained only if the 5-FU pretreatment lasted for more than 12 hr. The combined effect was decreased by a drug-free interval due to recovery from potentially lethal 5-FU damage, but ACNU treatment immediately after 5-FU treatment suppressed PLD recovery. Analysis with sequential trypsinization of spheroids indicated that ACNU showed more marked cytotoxicity on cells in the deeper layers in spheroids than on those in the outer layers, whereas the effect of 5-FU decreased towards the deeper cell layers. Enhancement of treatment with ACNU combined with 5-FU was evident for cells in the outer layers, but was more remarkable in the deeper layers. The combined effect of ACNU and 5-FU on s.c. tumors was similar to that in spheroids. The effect of combined treatment of ACNU with 5-FU on increase in body weight was within the additive range of both drugs acting independently, but was more than additive for the growth delay of s.c. tumors.
A spin-trapping technique was applied to the detection of free radicals generated in nicotinamide-adenine denucleotide phosphate (NADPH)-dependent lipid peroxidation of rat ischemic brain homogenate. The spin adduct of phenyl-t-butylnitrone (AN = 16.2-16.5 g, AH beta = 3.6-3.8 g) was observed, and it was thought to be derived from NADPH-dependent lipid peroxidation from its oxygen and NADPH dependency. Its intensity was increased in the recirculated condition following ischemic insult, indicating the susceptibility of brain tissue to lipid peroxidation in such a condition.
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An autopsy case of cebocephaly-holoprosencephaly at 27 weeks' gestation is reported. Chromosome analysis revealed a 46, XX,-7, +der(7), t(7;13) (q32;q34) pat karyotype. Pathological examination disclosed a hypoplastic aberrant adenohypophysis, in which immunohistochemical localization of four anterior pituitary hormones (ACTH, GH, PRL, TSH-beta) was demonstrated. Malformation of the pituitary gland in holoprosencephaly can include ectopic adenohypophysis as well as pituitary dysgenesis, so a careful search for adenohypophysis should be made in future cases for a better understanding of endocrine dysgenesis associated with holoprosencephaly.
Retrospective examination of lungs from 128 monkey necropsies was attempted for Pneumocystis infection using special strains, including toluidine blue-O and Gomori's methenamine silver nitrate. Four Japanese monkeys (7.7%), Macaca fuscata fuscata, and one crab-eating monkey (7.7%), Macaca fascicularis, were found to have Pneumocystis infection. The organism was found in young and infant animals. At the time of death, one infant and two young monkeys were debilitated and/or emaciated. Pneumocystis infection was considered an important lesion which could have caused reduced respiratory function in two of the Japanese monkeys, but constituted only an incidental finding in the others.
To study the therapeutic effect of phenytoin on cerebral ischaemia and confirm whether or not the effectiveness of phenytoin could be enhanced by combined administration with free radical scavengers, twenty-five dogs were subjected to ischaemia, using the "canine model of the completely ischaemic brain regulated with a perfusion method". Five animals served as untreated controls, fifteen received treatment with several doses of phenytoin and five were treated with 10 mg/kg phenytoin, 2 g/kg mannitol and 30 mg/kg vitamin E. These drugs were administered prior to the production of ischaemia. After one hour ischaemia, cerebral blood flow was restored and the recovery of electrical activity of the brain and the degree of brain swelling were observed for three hours. With regard to the recovery of the EEG, the higher the administered dosage, the better was the degree of recovery of the EEG. And the group which was treated with a combination of phenytoin, mannitol and vitamin E exhibited remarkable recovery of the EEG. With regard to the degree of brain swelling, a similar dose-related suppressive effect was seen in the phenytoin-treated groups. Furthermore, in the combination therapy group, brain swelling was attenuated significantly. Based on these results, it is concluded that phenytoin has a protective effect in cerebral ischaemia and it shows its most remarkable effect when given together with radical scavengers, such as mannitol and vitamin E.
The flow threshold and time threshold for reversibility of cerebral ischemia were studied using a canine model of cerebral ischemia regulated by controlled perfusion of cerebral blood flow (CBF). CBF was continuously monitored with a laser Doppler flow meter, the brain was brought to a constant level of ischemia for a defined period of time, after which recirculation was instituted. The electroencephalogram (EEG) and somatosensory evoked potentials (SEP) were monitored and used as an index of brain function. No recovery of brain function was found following recirculation if the CBF was reduced to a level below 20% of the normal state for more than one hour. When residual blood flow was 30% of the normal level, however, recirculation after one hour of ischemia resulted in nearly complete recovery of brain function. Significant functional recovery was not seen after two or more hours of such ischemia. Nearly complete recovery was also seen following reperfusion within three hours with 40% of normal CBF. It was demonstrated that the reversibility in the ischemic brain was critically correlated to the level of blood flow and its duration. If these results can be applied to the human brain, emergency cerebral revascularization for ischemic stroke should be attempted when critical flow and time thresholds have not been crossed, namely, in less than 1 hour and 3 hours of insult when the residual blood flow is reduced to 30 and 40% of the normal state, respectively. In clinical situations, this "critical time" may be too short for acute revascularization unless cerebral protective measures are applied pre-operatively to prolong the viability period of ischemic cerebral tissue.
Over the past 10 years we have experienced 33 cases of von Recklinghausen's disease, among whom 5 were cases of multiple (3 or more) brain tumours. In the past we have extirpated multiple tumours in a one-stage operation, but the results were poor. Recently, we have done multi-stage operation in two cases thought to require surgical treatment and have obtained satisfactory results. We have discussed the autopsy results of our own case of multiple neurinomas and meningiomas and have reviewed the 44 reported cases of von Recklinghausen's disease in whom the presence of three or more brain tumours had been confirmed at surgery or autopsy.
Dependence on S. typhimurium enzymes of mutagenicities of nitrobenzene (NB) and o-, p-chloronitrobenzenes (o-, p-CNBs), which are only mutagenic in the presence of S9 and norharman (NOH), was investigated using a nitroreductase-deficient strain TA98NR and an esterifying enzyme-deficient strain TA98/1,8-DNP6. NB exhibited mutagenicity towards TA98 but did not towards TA98NR strain in spite of the presence of S9 in the assay system. The mutagenicity of o-CNB towards TA98NR was significantly lower than that of o-CNB towards TA98. In contrast to NB and o-CNB, synthesized phenylhydroxylamine (PHA) and o-chlorophenylhydroxylamine (o-CPHA) exhibited approximately the same mutagenicity towards both tester strains. These results indicate that the nitroreduction required for the appearance of mutagenicity of the nitrobenzene derivatives in the presence of S9 and NOH is dependent on the nitroreductase of the tester strain. In addition, the mutagenicities of PHA and p-CPHA were significantly higher towards TA98/1,8-DNP6 than towards TA98, suggesting that the esterification of their hydroxylamines produced inactivation rather than activation. From these results, it was concluded that S9 and NOH play a role in metabolic activation other than the reduction of the nitro group to hydroxylamine and subsequent esterification for the mutagenesis of NB and its derivatives.
Temporal sequences of estrogen-induced embolization were studied in both in vivo and in vitro models. Infusion of the estrogen compound into rat mesenteric artery caused local spherocytosis and severe rapid degeneration of endothelial cells, followed by injury to the underlying muscle cells and fibroblasts. These changes were regarded as mainly the results of the embolization effect of conjugated estrogen. A study of cultured vascular endothelial cells suggested narrow margins of effective drug concentrations for cell damage. Also, nuclear disintegration with relative sparing of cytoplasmic constituents seemed to be characteristic of estrogen-induced cell damage in both in vivo and in vitro models.
The effect of colchicine on the fine structure of the retinal pigment epithelium (RPE) was investigated morphometrically in ICR mice bred in a condition of 12-hr light: 12-hr dark cycle since birth. In untreated mice, the number of phagosomes in RPE, containing packets of rod outer segment (ROS) discs, increased maximally at 1.5 hr after light onset, and progressively declined to the bottom value at around the time of lights off. Intraperitoneal injection of mice with colchicine (1 mg per 100 g body weight) prior to a peak of phagocytosis (4 hr before light onset) resulted in a marked increase in the number of phagosomes and a clustering of lysosomes in the apical cytoplasm of RPE and a decrease in the number of microtubules. The colchicine treatment also induced the dispersion of mitochondria from a basal cytoplasmic portion to the whole cytoplasmic area. These changes became dominant at 8 hr after the treatment and continued thereafter for a period of 12 hr. On the other hand, when colchicine was given during the period in which phagocytosis is inactive (8 hr after light onset), it induced only a slight increase in the number of phagosomes which recovered to the normal level earlier than the above. Clustering of lysosomes and dispersion of mitochondria continued to the same extent as in mice treated with colchicine at 4 hr before light onset. It was suggested that the effect of colchicine on the phagocytosis of ROS by RPE might depend on the functional state of RPE during the lighting cycle.
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Seven VLBW infants with pulmonary hypoplasia (P.H.) were studied retrospectively and their necropsied lungs were analyzed morphologically and histometrically in an attempt to establish the clinical and pathological criteria of P.H. Clinically they had various features as follows; 1) causes with oligohydramnios due to amniotic fluid leakage, 2) bell-shaped chest and/or small lung radiographically, 3) severe respiratory distress immediately after birth, 4) frequent complications with air leaks, lethal within several hours after birth. Pathologically they showed a series of changes; 1) remarkably decreased LW: BW ratios, less than 0.015, 2) decreased number of alveoli per alveolar duct, less than 3 or 4 alveoli/duct compared with 6.5 of normal controls at 28 weeks' gestation, 3) immature duct system and increased interstitium which suggested delay in growth and structural maturation of the lungs. It is suggested that the tendency to develop pulmonary air leaks is not only due to high pressure ventilation but also to histological immaturity of the lungs.
The effects of body position during the neonatal period on subsequent functional and postural behaviours were examined in relatively low-risk preterm infants. 44 infants were nursed in the supine position and 37 in a prone position throughout their admission period. Persistent head-turning to the right was observed more often and continued longer in the infants lying in supine. Asymmetrical postures, e.g. of skull and trunk, were more often seen in infants lying in supine than in prone. The prone position was thought to help prevent infantile scoliosis. At nine months, preference for the right hand was more marked in infants lying in supine, whereas infants lying in prone used their hands bilaterally, a tendency that persisted at 18 months. Asymmetrical gait pattern with mild gait disturbance was found more often in infants lying in supine than in prone. The prone position was thought to prevent asymmetrical posture and excessive functional asymmetries.