Localization of nucleoside diphosphatase (NDPase) and 5'-nucleotidase (5'-Nase) activity in rat choroid plexus epithelial cells was studied electron microscopically. NDPase activity was observed only in the cytoplasm on the Golgi cisternae of the epithelial cells, and was positive on the pericyte and endothelial cells. 5'-Nase activity was found on the lysosomes and along the basal plasmalemma or basal infoldings of the epithelial cells. The reaction products were also found on the pericytes.
The role of these enzymes in the choroid plexus was briefly discussed.

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A nonsuture anastomotic method for small vascular replacement using a microballoon catheter and plastic adhesive was devised. Various-sized balloon catheters (0.4-2.0 mm in external diameters) were made of latex balloons and polyethylene tube. Both ends of a balloon were fixed to the polyethylene tube so that the size and shape could be controlled more easily than in free-end balloon catheters. Alpha-ethylcyanoacrylate monomer, a plastic adhesive, was used instead of suture. Eleven common carotid and femoral arteries of dogs were used for end-to-end arterial anastomosis by this method. Nine femoral or saphenous veins were used as autogenous vein grafts and eleven expanded polytetrafluoroethylene (EPTFE) grafts as artificial grafts. In follow up studies from 2 days to 6 months, the patency rate of endto-end arterial anastomosis, end-to-end vein grafting, and end-to-end artificial grafting were 90.9%, 88.9%, and 66.7%, respectively. It took about 5 minutes for end-to-end arterial anastomosis and about 10 to 15 minutes for vascular replacement. One or two stay sutures were used effectively in autogenous vein grafting. The advantages of this method were good and free control of the vascular caliber and shape during vascular anastomosis and a diminishment of endothelial damage. Clinical application of this method of vascular replacement is expected in the near future.

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The relationship between residual cerebral blood flow and cerebral edema as well as hemorrhagic infarction seen following acute restoration of cerebral blood flow in an ischemic brain was experimentally studied. Dogs were divided into two groups with different mean arterial blood pressures (MABP) which were sustained at low levels by arterial exsanguination pretreatment: Group A with MABP of 40 mmHg and group B with MABP of 60 mmHg. The right middle cerebral artery (MCA) was occluded by an aneurysmal clip for one hour under these two hypotension levels. The occlusion was then released and MABP recovered towards normal levels.
In group A, MCA occlusion brought the local cerebral blood flow (1CBF) down to less than 8 ml/100 g/min. from 69 ml/100 g/min. Ten minutes after the release of MCA occlusion, the 1CBF increased to 109 ml/100 g/min. and was recognized as reactive hyperemia. Ninety minutes after the release, marked subarachnoid hemorrhage was seen in 5 out of 14 animals, and Evans Blue was extravasated into the cerebral tissue in one of three. Evidences of accumulation of water (85%) and sodium (555 mEq/kg), and decreases of potassium (395 mEq/kg) in the cerebral cortex were observed 6 hours after the release of MCA occlusion. The 1CBF in group B decreased to 20 ml/100 g/min. from 54 ml/100 g/min. after MCA occlusion. It regained its previous levels however, with or without mild reactive hyperemia after the release of the MCA occlusion. No subarachnoid hemorrhage or extravasation of Evans Blue or changes in the cerebral water and electrolyte contents were recognized.
When the residual cerebral blood flow is extremely limited, as in group A, the acute restoration of the blood flow by bypass surgery may be dangerous because of possible complications such as hemorrhagic infarction or severe edema, even if done within a short period after occlusion. The same procedure could, however, be performed without any complication if it is done within a short period after the onset of occlusion and if the residual cerebral blood flow of the ischemic area is maintained at a level of 20 ml/100 g/min. or approximately 37% of its previous level.

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Changes in N₁ amplitude of somatosensory evoked potential (SEP) with median nerve stimulation, cortical blood flow (CoBF) by a hydrogen clearance method, and histology were studied during brain retraction with graded local compression pressure (LCP) in 56 dogs. Local brain compression was applied with a brain spatula on the primary somatosensory cortex after right frontotemporal craniectomy and opening of the dura. In the first experiment, cerebral perfusion pressure (CPP) was reduced by three different methods, namely, exsanguination, infusion of saline solution into the cisterne magna, and continuous local brain compression. CPP was reduced by a 10 mmHg step every 30 minutes. Continuous local brain compression decreased both N₁ amplitude and CoBF more markedly than did the other two methods. N₁ amplitude decreased as soon as the local compression was started, and was reduced to 50% at 50 mmHg of LCP (CPP, 90-100 mmHg), and became null when LCP was elevated over 90 mmHg (CPP, below 60 mmHg). CoBF was significantly reduced at 110 mmHg of CPP. This suggests that immediate and severe neural dysfunction in local brain compression was due not only to destruction of the neural architecture by brain distortion but also to disturbance of cerebral circulation. As the second experimental step, intermittent local compressions with initial pressures of 20, 40, 60, and 80 mmHg was performed. Local compressions were applied four times for 30 minutes duration with five minute intermissions. At the initial levels of 40 mmHg of LCP, and higher the more the compressions were repeated or the higher the LCP was raised, the more both N₁ amplitude and CoBF decreased. At 60 and 80 mmHg of LCP, N₁ amplitude decreased significantly to 35% and 11% during compression and remained reduced to 70% and 35% at two hours after decompression, respectively. When the N₁ amplitude was reduced more than 50% during compression, it remained suppressed to 55% 2 hours after decompression. In these dogs, histological study of the compressed area showed cortical microhemorrhage and edema.
This study suggests that LCP over 40 mmHg and/or reduction of N₁ amplitude by greater than 50% during brain retraction produce postoperative neuronal dysfunction and histological changes.

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Among the variety of meningiomas, the so-called “angioblastic meningiomas” originally described by Harvey Cushing and his associates have been controversial in terms of their exact cytogenesis. The most recent WHO classification has dropped the term “angioblastic meningioma” but compromized it by including three additional subtypes of meningiomas, i.e., angiomatous, hemangiopericytic, and hemangioblastic, so as to perpetuate the traditional notion that they are of meningeal origin. In the authors' experience with over 200 cases of meningiomas, four types of histologically and cytogenetically distinct neoplasms which would potentially be called or have actually been called “angioblastic meningioma” by unwary pathologists have been recognized. They are: 1) meningiomas with abundant vascular stroma in which the meningeal tumor parenchyma was obscured; 2) intracranial hemangiopericytomas which were histologically identical to those arising outside of the central nervous system; 3) extra-cerebellar hemangioblastomas, especially those located in the supratentorial regions, which were histologically identical to those of the cerebellar primary but found in patients with no stigmata of von Hippel-Lindau disease; and 4) benign hemangioendotheliomas which were often attached to the dural tissue. Except for the first type, all of these neoplasms are apparently originated from the cellular elements of blood vessel and should not be classified as any type of meningiomas. The distinct histological characteristics of these four types of tumors were described in detail, and their clinical features were discussed. It is emphasized that the term “angioblastic meningioma” should be abandoned and that hemangiopericytoma, hemangioblastoma, and hemangioendothelioma should be recognized as separate entities among the neoplasms of blood vessel origin within the central nervous system, and not as subtypes of meningiomas with prefixed adjectives.

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Nine-hundred-thirty intracranial aneurysms in 774 cases were analyzed to investigate the relation of cranial nerve involvement to the location of intracranial aneurysms.
The commonest aneurysm site was the region of the anterior communicating artery (Aco) (28.3%), followed by the region of the main branchings (M₁-M₂) of the middle cerebral artery (22.0%) and the region of the internal carotid-posterior communicating junction (IC-PC) (20.6%). There were 411 males (53%) and 363 females (47%). Females cases were predominant in IC-PC (142 females, 50 males), while males were predominant in Aco (173 males, 90 females), and the sex incidence was approximately equal in M₁-M₂ aneurysms (106 males, 99 females). Oculomotor nerve involvement had its highest incidence in IC-PC aneurysms (34.4%), followed by oculomotor palsies due to IC aneurysms (30.2%) and basilar top aneurysms (18.2%). Second, fourth, fifth, and sixth cranial nerve involvement caused by IC aneurysms, IC-ophthalmic aneurysms, or Aco aneurysms were observed less frequently. Other cranial nerve involvement was very rare.
Isolated abducens nerve palsy due to an intracranial aneurysm is uncommon. Only two cases were observed in which the abducens nerve had been initially affected. In the 14 most recent patients complaining of isolated abducens palsy, no aneurysm was verified by angiography. In this series, however, a vascular tumor, a dural AVM, and a carotid-cavernous fistula were encountered in 3 cases (20%). Angiography seems to be useful in investigating the pathogenesis of isolated abducens nerve palsy.

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Forty consecutive patients suspected of cervical lesions were examined with a Gitroscope VS-10 egtxipt with an image intensifier TV system. Lateral C1-C2 puncture was easily performed during TV fluoroscopy in the lateral view with the patient in a prone position and the neck hyperextended. A needle was inserted into the dorsal third of the spinal canal between the laminae, and when cerebrospinal fluid was obtained, the contrast medium was injected under fluoroscopic control. The table tilt could be adjusted to avoid intracranial flow of the medium. A U-shaped chin and head fixation device was used to fix the head and to provide maximum cervical lordosis. Metrizamide 200-230 mgI/ml in concentration and 5-8 ml in volume was used in most cases. After this procedure all patients were hydrated and kept in bed for 12 hours with the head elevated 10-15 degrees.
Good quality films were obtained except for the initial case. Of many side effects, mild to severe headaches occurred only in 17 %, which was much fewer than in many previous reports.

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A case of cerebral fat embolism is reported. A 18-year-old patient with multiple bone fractures was in semicoma immediately after an injury. Brain CT showed no brain swelling or intracranial hematoma. Hypoxemia and alcoholemia were noted on admission, which returned to normal without improvement of consciousness level. In addition, respiratory symptoms with positive radiographic changes, tachycardia, pyrexia, sudden drop in hemoglobin level, and sudden thrombocytopenia developed. These symptoms were compatible with Gurd's criteria of systemic fat embolism. Eight days after injury, multiple low density areas appeared on CT and disappeared within the subsequent two weeks, and subdural effusion with cerebral atrophy developed. These CT findings were not considered due to cerebral trauma. Diagnosis of cerebral fat embolism was made. The subdural effusion was drained. Neurologic and pulmonary recoveries took place slowly and one month following the injury the patient became alert and exhibited fully coordinated limb movement. The CT scans of the present case well corresponded with hitherto reported pathological findings. Petechiae in the white matter must have developed on the day of injury, which could not be detected by CT examination. It is suggested that some petechial regions fused to purpuras and then gradually resolved when they were detected as multiple low density areas on CT. CT in the purpuras phase would have shown these lesions as high density areas. These lesions must have healed with formation of tiny scars and blood pigment which were demonstrated as the disappearance of multiple low density areas by CT examination. Cerebral atrophy and subsequent subdural effusion developed as a result of demyelination. The patient took the typical clinical course of cerebral fat embolism and serial CT scans served for its assessment.

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Twenty cases of primary pontine hemorrhage (PPH) were diagnosed by CT scan over a period from June 1979 to March 1982, and were treated conservatively. They were classified into four types according to their outcome. Five cases in Type I showed a full recovery or could resume most activities (ADLI or II). The initial clinical picture of this type was characterized by alertness, no disturbance of autonomic function, and mild hemiparesis. CT scan demonstrated a small hematoma which was localized in the unilateral region or midportion of the pontine tegmentum. In four cases, the largest diameter of the hematoma on a transverse section through the pons was less than 20 mm, and its extension was limited to 2 slices, (each 10 mm in width). EEG performed on two patients were normal. Three cases of. Type II recovered to daily life partially assisted (ADL III). Clinical manifestations consisted of mild disturbance of consciousness, severe hemiplegia, cerebellar signs, and minor autonomic dysfunction. Hematoma was located in the bilateral pontine tegmentum and partially involved the pontine basis. The size of hematoma was less than 30 mm and its extension was 2 to 3 slices. EEG performed on one patient consisted of alpha activity with some theta waves. Seven cases of Type III were severely disabled in prolonged coma or the “locked-in” syndrome (ADL IV). Their clinical findings were coma in four patients, tetraplegia in seven, decerebrate regidity in two, respiratory disturbance in two, and hypertension in three. Hematoma was located in the entire pontine tegmentum and unilateral pontine basis extending to the midbrain. The size of hematoma was less than 30 mm in five patients and more than 31 mm in two. EEG was carried out on five patients in the comatose state. Alpha-pattern coma was present in two cases and beta-coma was observed in two. All five cases of Type IV died within a few days after the onset. The clinical picture was coma, tetraplegia, respiratory failure, hyperthermia, and hypertension in all cases. Hematoma involved the entire tegmentum and basis pontis and extended to the cerebellum and midbrain. The size of hematoma was less than 30 mm in two patients and more than 31 mm in three. The sagittal extension was 3 to 6 slices. The importance of systematic investigations of the clinical, computed tomographic, and electroencephalographic findings were recognized.

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Drip infusion of a very small amount of aqueous pitressin (AP) and a patient weighing system were jointly used in fourteen patients with acute postoperative diabetes insipidus (D. I.).
In the acute stage of postoperative D. I., urine volume was measured every hour. AP drip infusion was started when the urine volume was over 300 ml per hour. Urine volume over 1, 000 ml per hour was effectively treated with AP doses from 1 to 3 pitressin units administered over one-hour period. Urine volume of about 500 ml per hour could be controlled by 0.5 pitressin unit. Effectiveness of AP lasted only two to three hours. AP drip infusion was resumed when the urine volume again reached 300 ml per hour. As a result, the daily urine volume of most cases treated with AP could be kept under 6 liters. The intake and output of water were controlled by an hourly check of the body weight using a patient weighing system. Body weight was controlled so as to stay between plus one kilogram and minus one kilogram during AP use. AP side effects were pallor in 6 patients and headache in one. No change in blood pressure or pulse rate was recognized.

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Experimental and clinical investigations were made to determine the suitability of the Nd-YAG laser in neurosurgical operations.
The vaporization effect of the Nd-YAG laser coagulator (Molectron 8000, Medilas YAG) was experimentally examined using various materials. When boiled fish paste and a human skull were irradiated at a distance of 2 mm, vaporization occurred at the energy level of 70 watts, 1 sec. and 80 watts, 1 sec., respectively. At an energy level of 50 watts, 5 sec., rabbit livers was vaporized to the depth of 1 mm and kidney to a depth of 2.3 mm. From these experiments, the vaporization effect of the Nd-YAG laser proved adequate for clinical use.
Using a Nd-YAG laser coagulator, 38 brain tumors were removed; they consisted of 19 pituitary adenomas, 10 meningiomas, 3 gliomas, 1 multiple myeloma, 1 fibrous dysplasia, 1 arteriovenous malformation, and 2 other brain tumors. The Nd-YAG laser had a greater hemostatic effect than the CO₂ laser and it appeared suitable for highly vascular tumors. Since the laser beam of the Nd-YAG laser was transmitted by a flexible quartz fiber, it could be freely moved under the operative microscope. Thus, coagulation and hemostasis of a specific target site could be performed with ease making the laser highly suitable for the removal of deep seated tumors. In the transsphenoidal approach, the Nd-YAG laser permitted easy opening of the sella and sphenoid, even in the conchal type and presellar type sphenoid.
Thus, with its strong hemostatic effect and flexible quartz fiber, the Nd-YAG laser has wide application in microneurosurgery especially with regard to easy removal of brain tumors.

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