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We clearly determined the key to managing patients with brain abscess by retrospectively evaluating the factors affecting poor outcome in these patients. This study included 113 patients with brain abscess diagnosed in the CT era. Basic characteristics and therapeutic parameters were estimated as independent predictors of poor outcome by using univariate and multivariate logistic regression analysis. Patients with poor outcomes more frequently had deeply-located abscesses (p < 0.02), IVROBA (intraventricular rupture of brain abscess (p < 0.001) and were in a severely deteriorated neurological state (p < 0.001) than those with good outcomes. Multiple logistic regression analysis predicted that IVROBA (ORs, 24.5; 95% CI, 3.04 to 197.9) and severely deteriorated cases (ORs, 13.7; 95% CI, 2.34 to 80.8) resulting from IVROBA increased the relative risk of poor outcome. Patients with IVROBA more frequently had also deeply-located abscesses (p < 0.005), positively immunocompromised states (p < 0.05) and were in a severely deteriorated condition (p < 0.003) than those without IVROBA. Patients with metastatic abscess had also IVROBA (p < 0.006). Multiple logistic regression analysis anticipated that deeply-located abscess (ORs, 3.90; 95% CI, 1.38 to 11.04), and metastatic abscess (ORs, 12.26; 95% CI, 1.35 to 111.2) increased the relative risk of IVROBA. Patients in an obtunded state and with marked neurological deficit had IVROBA more often than patients in an alert state and/or mild neurological deficit (ORs, 3.23; 95% CI, 1.17 to 8.86, p < 0.03) before treatment. Our findings suggest that IVROBA strongly influences poor outcome in patients with brain abscess. The key to decreasing poor outcomes may be the prevention and management of IVROBA, by evaluating intracranial pressure pathophysiology. IVROBA should be aggressively treated by aspiration methods for the abscess coupled with appropriate intravenous and intrathecial administration of antibiotics.

We recently encountered a patient with thrombosis of the superior sagittal sinus of an idiopathic cause. The patient was treated initially with combined local thrombolytic therapy through the burr hole over the superior sagittal sinus and systemic anticoagulant therapy. Continuous ventricular drainage and hyperbaric oxygenation therapy were used to control the increased intracranial pressure. The superior sagittal sinus was successfully recanalized. Whereas the patient suffered a complication with subacute subdural haematoma, he was successfully treated with the combination of these therapies. The rationale and approach are discussed.

An encapsulated fluid epidural haematoma in a 9-year-old boy was successfully evacuated by a simple burr hole procedure 5 months after a minor head injury. Clinicopathological findings suggested that chronic expansion of an initially unsuspected epidural haematoma occurred as a result of repeated haemorrhages from the haematoma membrane, resulting in an unusually long delayed appearance of clinical evidence. This case demonstrates that a chronic expanding process similar to that seen in chronic subdural haematoma needs to be considered as a possible complication of epidural haematoma and indicates an important role for the haematoma membrane in the chronic expansion of epidural haematoma.

Many factors have been suggested as possible mechanisms for the development of peritumoural oedema in meningioma. Venous compression by the tumor is thought to be one factor, but reports presenting a direct relationship between venous compression and the formation of oedema are rare. We have recently observed 6 meningioma patients in whom venous stasis contributed to peritumoural oedema. The stasis was due to 1) compression of an adjacent cortical vein by the tumour with stasis at the site of compression and/or its distal portion, 2) compression of adjacent brain by the tumour with prolonged perfusion and delayed venous return (visualized as pial staining in the capillary and venous phases), and 3) presence of an early draining vein linked to a nearby cortical vein with stasis at its periphery. Venous compression and stasis seem to be related not only to the formation of peritumoral oedema but also to the occurrence of haemorrhagic infarction after the resection of meningiomas.

Flow studies using dynamic CT and xenon (Xe) CT were carried out in 25 patients with ischaemic stroke in the territory of the middle cerebral artery to define the clinical characteristics of cerebral ischaemia at a chronic stage. The parameter of peak height/mean transit time (PH/MTT) obtained from dynamic CT can provide an accurate index for blood circulation in the cerebral vascular bed. Xe CT measurements revealed various kinds of ischaemia around the infarction even in the chronic stages. In mild ischaemia of more than 30 ml/100 g/min, reduction of cerebral blood flow (CBF) was well correlated to the PH/MTT. However, in severe ischaemia between 20 and 30 ml/100 g/min, changes of CBF were no longer correlated with the PH/MTT. There were cases showing severe reduction of CBF but which showed sufficient blood circulation (moderate value of PH/MTT). Mild reductions of CBF in parallel with decreased blood supply were often found in the peri-infarct area of infarctions in the centrum semiovale. On the other hand, infarctions in the cortico-subcortical region showed severe ischaemia, in even where blood circulation was relatively well sustained.

A co-operative study for patients with intracranial germ cell tumours was performed to analyze their prognosis and the effectiveness of Cisplatin/Etoposide (CDDP/VP-16) chemotherapy. A total of 46 patients; 30 primary and 16 recurrent cases were registered from 15 participating neurosurgical institutions in Japan. Based on histological criteria and tumour markers, they were classified into three groups; germinoma, germinoma with syncytiotrophoblastic giant cell (STGC), and non-germinomatous malignant tumour. Sixteen patients were treated with CDDP/VP-16 chemotherapy alone and the other 30 patients were treated by a combination of surgery and/or radiation in addition to chemotherapy. Eleven out of 13 patients (85%) with germinoma showed a complete (n = 10) or partial (n = 1) response to CDDP/VP-16 chemotherapy even if their tumours were recurrent and there was evidence of CSF dissemination. For the germinoma with STGC and non-germinomatous malignant tumour, a high response rate; 100% for the former and 78% for the latter, could also be achieved in both the primary and the recurrent cases except in those cases of immature teratoma. Their survival times were still different between them. Two-year survival was 50% in germinoma with STGC and 48% in non-germinoma, while it was 88% in germinoma cases.

The proportion of ganglioside GD3 increases in glioma tissue and GD3 content is correlated with malignancy of gliomas. This ganglioside can be detected in the sera of patients with glioma by thin-layer chromatographic analysis. Ganglioside GD3 was not detected in the sera of healthy donors and astrocytoma grade 2 patients. However, serum GD3 was detected in one of three astrocytoma grade 3 patients and seven of nine glioblastoma patients. These results show that shedding of GD3 increases in proportion to the degree of malignancy of gliomas. Nevertheless, all of the glioblastoma patients in this study were advanced cases. Considering the high reliability of radiological diagnostic techniques in the neurosurgical field, further study will be necessary to clarify the relationships between the GD3 level in serum and the properties of tumours.

The initial dose-escalating clinical trial of a novel calcium antagonist, AT877, in patients with aneurysmal subarachnoid haemorrhage is reported. AT877 is characterized by its strong spasmolytic activity, its inhibition of intracellular calcium ion activity, and the inhibition of several protein kinases. A total of 113 patients (Hunt and Hess grades I to IV) who had undergone surgery within 3 days of aneurysmal rupture entered the study. Patients were divided into 5 groups according to the total daily dose of AT877: I: 20 mg; II: 40 mg; III: 60 mg; IV: 90 mg; and V: 120-180 mg. AT877 was given by intravenous infusion over 30 min two or three times a day for 14 days after surgery. Although AT877 did not completely abolish angiographic vasospasm, severe vasospasm was seen less frequently in patients given higher doses. Vasospasm was the cause of a poor clinical outcome (Glasgow outcome scale rating 3 or greater) in 19%, 7%, 9%, 8%, and 6% of the patients in groups I to V, respectively. The results indicated a favourable clinical effect of AT877 at doses above 40 mg per day. Only mild hypotension was seen, even when 60 mg of AT877 was infused over 30 min. AT877 appears to be effective in patients with subarachnoid haemorrhage. Part of its effect may be attributable to protection of the brain from ischaemic insults due to chronic cerebral vasospasm. However, the drug still needs to be evaluated in a placebo-controlled double-blind trial (which is currently being carried out).

The content of norepinephrine (NE) in the ventricular, basal cisternal and lumbar cerebrospinal fluid (CSF) was determined in 19 patients with ruptured cerebral aneurysms. The cisternal CSF in patients with vasospasm contained a significantly higher level of NE (0.246 +/- 0.0490 ng/ml) compared with those without vasospasm (0.075 +/- 0.001 ng/ml) (p less than 0.001). However, this increase is not considered to be high enough to constrict cerebral arteries, unless there is an increased NE-sensitivity in subarachnoid haemorrhage. Vascular responses to NE in vivo were then studied after reversing blood-induced prolonged vasospasm of the rabbit's basilar artery through a transclival approach as well as a newly developed basal cisternal irrigation model. However, NE in molar concentrations between 1 x 10(-10) and 10(-2) failed to produce further contraction of the artery. In conclusion, the increase in NE with vasospasm might be only a secondary phenomenon, and not a causative factor of vasospasm. Early removal of subarachnoid blood clots seemed to prevent the development of vasospasm.

Cellular synchronization using Colcemid as pretreatment for combined chemoradiotherapy was investigated. C6 rat brain tumour was cultured in RPMI medium containing 10(-5)-10(-7) Mol. of Colcemid for 24 hours. The basic cell kinetics were analysed with a Pulse Cytophotometer, which facilitated the analysis of tumour cell cycle phase distribution according to the DNA content. The effect of Colcemid depended on the concentration, and the minimal concentration showing continuous blocking during 48 hours after removal of the drug was 10(-6) Mol. G1 fraction of 2 C DNA content was reduced from 74% to 36%. G2-M phase of 4 C DNA content increased from 9% to 28%. S phase cells increased from 17% to 31%. Polyploid cells in the Tetraploid cell cycle could be recognized. The remaining 36% of cells within the GO + G1 peak of 2 C DNA content were considered to be diploid GO cells.

The relationship of supratentorial intracranial pressure (ICP) and cerebral perfusion pressure (CCP) with serial changes in auditory evoked brain stem responses was investigated. Eighty-one patients without primary brain stem damage admitted to our emergency unit were studied. When ICP over 50 mm Hg persisted for 4 hours, the I-V interpeak latency was significantly prolonged. The threshold of this prolongation was 8 hours for the ICP over 45 mm Hg and 24 hours for that of over 40 mm Hg. The ICP of 35-40 mm Hg for 24 hours was the border zone. CCP did not show a significant relation with I-V interpeak latency changes. The loss of wave V was observed in a wide range of the ICP (30-147 mm Hg) and CPP (0-60 mm Hg). Wave III disappeared when the ICP exceeded 50 mm Hg. Wave I became undetectable with an ICP above 50 mm Hg or a CPP below 40 mm Hg. These results indicate that an increase of ICP over 40 mm Hg definitely initiates secondary brainstem dysfunction if it lasts for more than 24 hours and that the ICP should be reduced below this level, preferably below 35 mm Hg, to maintain brain function. The fact that both low CPP and high ICP were involved in the loss of wave I clearly shows that both ischaemia and displacement of the brain stem are the important pathophysiological factors for the disappearance of wave I.

In 1974, the Japanese EEG Society's Ad Hoc Committee on Brain Death published criteria for determining brain death only in cases of acute gross primary brain lesions. In 1983, a new brain death study group was organized to re-evaluate these criteria. During a 6-month period from March 1, 1984, 217 neurosurgical and neurological clinics and emergency services throughout Japan reported 718 brain deaths caused not only by primary lesions but also by secondary brain lesions and diagnosed as such on the basis of the 1974 criteria excluding the condition of "abrupt fall of blood pressure followed by persistent hypotension". The data derived from the 718 cases in this collaborative study were pooled and analyzed, and it became known that the 1974 criteria still are generally reliable. Some changes have been made, however, and new criteria for determination of brain death adopted.

A case of anterior sacral meningocele which was clearly visualized on whole body computerized tomography is presented. Posterior surgical approach with ligation of the narrow communication between the sacral dural sac and the meningocele alleviated the subjective complaints of a feeling of abdominal distention and of dysuria. For the purpose of postoperative follow-up study, examination by whole body computerized tomography proved to be the best method of evaluating the size of the meningocele and also the state of neighbouring structures.

The existence of insulin receptors and biological responses to insulin on macromolecular synthesis have been studied in C6 glioma cells. Binding of 125I-insulin to C6 glioma cells was specific, time- and PH-dependent. Porcine insulin competed for 125I-insulin binding in a dose-dependent manner. Unlabeled polypeptides, including glucagon, bovine growth hormone, bovine prolactin did not compete for 125I-insulin binding. Scatchard analysis of the binding data gave a curvilinear plot which may indicate negative co-operativity or the existence of both high and low affinity (Ka = 7.55 x 10(10) - 4.25 x 10(9] sites. Incubation of cultures with insulin caused a time and dose-dependent stimulation of DNA, RNA and protein synthesis in C6 glioma cells (measured by 3H-thymidine, 3H-uridine or 3H-leucine incorporation into DNA, RNA, or protein respectively). The increase of macromolecular synthesis was admitted at more than 2 nM concentration of insulin. Maximal stimulation of DNA synthesis (142% of control) occurred 6 hours after incubation with 167 nM insulin. The same concentration of insulin caused a 45% increase in 1 hour on RNA synthesis, a 37% increase in 2 hour on protein synthesis. These results indicate that C6 glioma cells have specific insulin receptors capable of mediating effects of insulin on macromolecular synthesis. Insulin in the brain and even blood may be an important growth factor in the glioma cells of the patients with disrupted blood-brain-barrier.