The authors studied the changes in neurological signs and cerebral circulation by using dynamic CT scans before and after cranioplasty in six externally decompressed patients. Five of the 6 patients showed some improvements in neurological signs. The results of the dynamic CT scans in 6 cases suggested that increases of bilateral cerebral blood flow may play a role in their neurological improvement.

Phone: þ81 22 215 2281, Fax: þ81 22 215 2302Cleaved ScAlMgO 4 (SCAM) substrates with small lattice mismatch of 1.8% to GaN were used for metalorganic vapor phase epitaxial (MOVPE) growth of GaN. A single crystalline GaN film with a flat surface was obtained on a cleaved substrate without peeling off of the film, which is contrast to the growth on ZnO substrate with comparably small lattice mismatch to GaN. Polarity of the film was proven to be Ga polarity and an interface model was proposed based on the topmost surface structure of the cleaved SCAM. The effect of substrate-cleaning and growth conditions on the surface morphology, crystallographic orientation relationship with the substrate, threading dislocation densities, small residual strains, and small background carrier density of GaN have been studied. To discuss the residual strains, thermal expansion coefficient of SCAM has also been measured.

In our studies of the pathogenesis of cerebral vasospasm, we have been emphasizing that microthrombosis may play an important role in the induction of cerebral ischemic symptoms or cerebral infarction. In this report, multiple microthrombi are demonstrated histologically to be a major cause of cerebral infarction in the autopsied brain of a 63-year-old woman who died from typical cerebral vasospasm that occurred after the rupture of an anterior communicating artery aneurysm. We discuss the significance of thrombus formation and subarachnoid perivascular acidosis in vasospasm.

A comparative investigation of the pathogenetic factor in symptomatic cerebral vasospasm was made by quantitative histological and clinical studies in four patients who died immediately of sympto matic cerebral vasospasm (Cases 1-4) and in two who died without fatal cerebral vasospasm (Cases 5 and 6). Histological examination of the brain from Cases 1 and 2 found many white and fibrin microthrombi together with ischemic and infarctic changes in the territories of spastic arteries, which corresponded to the low-density areas (LDAs) observed on computed tomographic (CT) scans and the typical neurological symptoms. In Case 3, who had suffered severe vasospasms in bilateral ante rior cerebral and middle cerebral arteries, bilateral LDAs were observed on CT scans and multiple fibrin thrombi were seen diffusely throughout the brain. In Case 4, extensive bilateral LDAs (It > rt) were observed on CT scans, and multiple microthrombi were seen diffusely but predominantly in the left cerebral hemisphere. Only in Case 3 the possible complication of disseminated intravascular coagulation could not be ruled out. Only negligible thrombi were observed in Cases 5 and 6, whose immediate cause of death was considered to be acute hydrocephalus and aneurysmal rerupture, re spectively. Distributions of microthrombi were significantly greater in the regions clinically identified to have been ischemic or infarctic.

In the last 9 years, infundibular dilatation (ID) has been sought in 260 aneurysm (An) cases and 398 carotid angiogram's (CAG) to reveal its incidence and morphology. Findings were as follows: The incidence was about double that so far published. Small ID, usually triangular in shape, tended to become round as it grew larger (P less than 0.01). Large ID favored young age (P less than 0.05). In internal carotid-posterior communicating aneurysm (IC-P com An) cases, a high incidence of ID was noted as compared to other An cases (P less than 0.05), and intermediate or large, round ID accounted for high ratios. Cases with a history of hypertension showed a high large ID ratio (P less than 0.05). Cases with well developed P com A had a high ratio of large, round ID (P less than 0.01). In cases with a large divergent angle of ICA and P com A, intermediate or large, round ID was found in high ratio (P less than 0.05). Aggressive follow-up or treatment was thought necessary in cases which possess the factors mentioned.

Evoked action potentials from the internal auditory meatus portion of the cochlear nerve (IAM-EAP's) and brain-stem auditory evoked potentials (BAEP's) from the vertex were simultaneously recorded during cerebellopontine angle (CPA) manipulations (retractions of the cerebellar hemisphere and the cochlear nerve) in dogs. The BAEP changes noted in these dogs were the same as those seen in patients. The IAM-EAP's showed graded deterioration related to BAEP changes. The results are as follows: Prolongation of the I-V interpeak latency of BAEP's, the most common finding during CPA manipulations, is the reflection of prolongation of the I-II interpeak latency, which is caused by conduction impairment or block of the nerve impulses between the extracranial portion of the cochlear nerve and the brain stem. The operative manipulations representing stretch or compression injury to the cochlear nerve in the CPA leads to an acute traumatic cranial nerve root lesion--a retrocochlear lesion. The obliteration of all BAEP components including wave I cannot be caused by conduction block. This is caused by occlusion of the internal auditory artery. Wave I of the BAEP's and the P1-N1 complex of the IAM-EAP's are important indicators of cochlear blood flow during surgical intervention. As possible causes of internal auditory artery obstruction, mechanical distortion of the relationship between the anterior inferior cerebellar artery (AICA) and the internal auditory artery at the junctional portion, mechanical vasospasm of the AICA-internal auditory artery complex, and ensuing no-reflow phenomena are discussed. Evoked action potentials are expected to be a useful intraoperative real-time monitor during CPA surgery that can detect rapid changes derived from cochlear artery insufficency. The real-time aspects can overcome some of the disadvantages of BAEP monitoring.

SummaryThe clinical aspect and mechansims of production of ocular motor disturbances appearing as false localizing signs are discussed in four patients who were observed in a series of 102 consecutive admissions of patients with ruptured intracranial aneurysms. The aneurysms were located on the anterior communicating artery and the precommunicating segment of the right anterior eerebrM artery.In these patients bilateral abdueens nerve palsy, unilateral partial oculomotor nerve palsy and bilateral ophthalmoplegia totalis were observed. Nuclear or internuclear palsy due to vasospasm of the pontine branches of the basilar artery, peripheral oculomotor nerve palsy due to concomitant megadolichobasilar anomaly, and transtentorial axial descent of the midbrain were considered to be responsible.

The possible changes in the subarachnoid space after subarachnoid haemorrhage were studied in animals by using a scanning electron microscope (SEM). About 1 ml/kg of autogenous blood was injected intracisternally in 36 adult mongrel dogs to investigate changes in the subarachnoid space, over periods ranging from immediately after the injection to as long as 6 months. We have come to the conclusion that the injected blood disappears in about one to two weeks; the fibrosis or thickening of the arachnoid membrane appears in one to three weeks, and then returns to normal in a month in instances of rapid recovery, but there are some cases in which fibrosis persists for a long period and becomes chronic. The fact that an increase of fibrous tissue was found in the parietal region, where the injected blood had hardly reached, appears to indicate that the fibrosis is not always limited to the site of the haemorrhage but can occur in remote regions. We also discuss the usefulness of the SEM in the observation of the subarachnoid space, and the finding that vascular specimen preparations can be made by perfusing the brain with 2-10% phosphate-buffered formaldehyde solution.