The authors reported previously on a method of producing brain stem infarction in the dog by segmental embolization of the basilar artery using a silicone rubber cylinder. In the present study the course of infarction in the brain stem was followed and the pathogenesis of hemorrhagic infarction was also explored.
A total of 28 adult mongrel dogs were used in this study. Five of them belonged to the control group and the others belonged to the embolized group. The dogs were anesthetized by intravenous injection of sodium pentbarbital and ventilated mechanically through an endotracheal tube. A silicone rubber cylinder was injected into the unilateral cervical vertebral artery to embolize the basilar artery segmentally. In the control group animals, only saline solution was injected into the right cervical vertebral artery and they were sacrificed after observation for 6 hours. The embolized group animals were sacrificed 1 hour, 6 hours, 3 days, or 1 week after embolization. Before sacrificing the animals, final vertebral angiograms were obtained to determine the distal migration of the embolus, and 1% trypan blue was administered, except in the animals sacrificed 1 week after embolization, to examine the blood-brain barrier status. Thereafter, the brain was perfused with 50% microbarium containing 5% gelatin in order to evaluate the microcirculation in the brain stem. The brain was fixed in 10% formalin for one to three weeks and then embedded in paraffin. The histological specimens were stained with hematoxylin eosin and in some cases with luxol fast blue.
One hour after embolization, the lesions could not be observed macroscopically, but there was a slight extravasation of dye. Microangiograms revealed interruption and disappearance of perforating arteries and avascular areas. Histologically, some small vessels were not perfused with microbarium. Six hours after embolization these lesions could be easily observed macroscopically and some of them were hemorrhagic. Diapedesis and edema could be observed histologically at this stage. On the third day extravasation of dye was slight. Microangiogram revealed extravasation of microbarium in addition to the earlier findings. The major histological findings were microangionecrosis and hemorrhage due to rupture of the necrotic vessels. The additional findings were fine vasculature around the avascular area and tortuosity of the perforating arteries on the microangiogram 1 week after embolization. Newly developed blood vessels and many gitter cells were observed histologically. Distal migration of the embolus could not be observed on the vertebral angiogram at any time.
When the basilar artery was embolized segmentally and the brain stem was infarcted, diapedesis developed in the brain stem 6 hours after embolization, which was attributable to increased permeability of small vessels, and hemorrhage occured in the infarction area due to rupture of the necrotic vessels on the third day.

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Experimental cerebral infarction was induced in 33 dogs by injecting a silicone rubber cylinder through the cervical internal carotid artery. The embolus was found to have obstructed the osseous portion of the internal carotid artery in 15 dogs, trifurcation of the internal carotid artery into the posterior communicating, anterior cerebral, and middle cerebral arteries in ten dogs, and the proximal portion of the middle cerebral artery in eight dogs.
The non-perfused areas in seven standard coronal sections of each brain were shown by carbon perfusion 24 hours after embolization. The following four different patterns of cerebral infarction were established: (1) Large sized infarction of the cerebral hemisphere showing a large carbon perfusion defect in the cerebral cortex, the subcortical and deep white matter, and in the basal ganglia. Area of the perfusion defect was larger than fifty percent of the total area of the hemisphere in each of three serial slices. One of six infarcts was hemorrhagic. (2) Small sized infarction of the cerebral hemisphere showing an area of perfusion defect smaller than fifty percent of the total area of the hemisphere. All of seven infarcts were ischemic. (3) Watershed infarction demonstrating multiple carbon perfusion defects in the arterial borderline and terminal zone of the cortex and white matter or in the basal ganglia. Eight of 17 infarcts were hemorrhagic. (4) Thalamic infarction showing a carbon perfusion defect in a wide area of the thalamus. Two of three infarcts were hemorrhagic.
This classification of infarction in the dog may play an important role in evaluating the computed tomographic findings of cerebral infarction in clinical cases.

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Twenty one patients with giant aneurysms of the intracranial internal carotid artery were experienced from 1961 to the end of 1980. Three out of 21 were given no treatment and the remaining 18 were treated by indirect surgery; carotid ligation was performed in 13 cases and carotid ligation with STA-MCA anastomosis in five. At follow-up, 15 cases were living useful lives; nine of these cases were treated by carotid ligation, five by carotid ligation with STA-MCA anastomosis and one had no surgical treatment. Fourteen out of 15 living cases were examined by CT scan to investigate the fate of the giant aneurysm following carotid ligation. Sequential CT findings of the giant aneurysm were as follows. The cavity of the giant aneurysm was filled with clots within one week after ligation. Most of the cavity was thrombosed and a small residual cavity was visualized within 2 to 3 weeks after surgery. A thick mural thrombus was organized gradually between 4 and 6 weeks but a narrowed residual aneurysmal cavity still existed. Further organization and calcification of the thrombus and aneurysmal wall progressed for several years. More than 5 years following carotid ligation, a small residual cavity was thrombosed and the aneurysm could not be detected by CT scan. CT findings which prove the effectiveness of indirect surgical treatment were observed in 11 out of 13 patients (84.6%). However, complications after carotid ligation cannot be neglected; four out of 18 patients were lost. Therefore, combined therapy consisting of neck internal carotid ligation and STA-MCA anastomosis is recommended to prevent complications due to carotid ligation. Sequential CT scans are very useful for observation of the fate of the giant aneurysm after carotid ligation and the effectiveness of therapy, and for evoluation of the prognosis of patients.

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Ten cases of chronic subdural hematoma that were followed by a sequential study with computerized tomography (CT) from an early posttraumatic period to evolution of chronic subdural hematoma were reported.
The initial head injuries were mild except for two cases. Case 2 had been suffering from thrombocytepenic purpura, but the others has no specific past history. These cases were divided into two groups on the basis of the density of subdural collections on the initial CT.
In four of these 10 cases, the initial CT showed thin subdural collections of high density suggesting acute subdural hematoma. Two weeks later, the density of subdural collections reduced, but their volumes increased. Clinical symptoms such as headache and disorientation occurred three or four weeks later. Preoperative CT showed similar huge subdural collections of low density and marked mass effect. These cases underwent surgery from 24 to 44 days after injury (average: 30 days), and development of neomembranes was confirmed.
In the remaining six cases, the initial CT showed thin subdural collections of low density suggesting subdural hygroma. In five of the six cases, the density of the subdural collections was slightly higher than that of cerebrospinal fluid, and in one case, an area of spotted high density was shown. It was suggested that these were mixtures with blood. Follow-up CT scans revealed that the subdural collections increased in size but remained at a uniformly low density for the first month after the head injury, and then the increase in density occurred. Operations were performed 55 to 76 days after injury (average: 63 days), and operative findings were not different from those of common chronic subdural hematoma.
From these investigations, it was suggested that there were two types of evolution of chronic subdural hematoma. One is the development from acute subdural hematomas, and the other from subdural hygromas. It is supposed that blood and cerebrospinal fluid are very important factors in the evolution of subdural collections into chronic subdural hematomas.

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Findings obtained by CT scan in 45 cases of metastatic brain tumor, 1 case of leptomeningeal metastasis, 1 case of dural metastasis, and 3 cases of metastatic skull tumor were analized. Primary lesions were lung carcinomas in 24 cases, breast carcinomas in 6 cases, renal carcinomas in 4 cases, stomach carcinomas in 4 cases, other malignant tumors in 6 cases, and unknown of origins in 6 cases. In 15 cases of metastatic brain tumor, the lesion was solitary, while in 30 cases the lesions were multiple.
Enhancement effect was found in 93% of 118 metastatic tumors. Patterns of enhancement were divided into two types: solid and ring enhancements. Solid enhancement was found in 48.3% of 118 metastatic brain tumors and ring enhancement in 44.7% of them. The Hounsfield numbers of the enhanced areas of the tumors of the solid enhancement type were similar with those of the ring enhancement type both in plain and enhancement CT. Ring enhancement was predominant in tumors larger than 2 cm in diameter, but was not related to the difference of the primary lesions nor to the pathological patterns.

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A case of angiographically demonstrated fenestration of the internal carotid artery in association with an aneurysm arising from the anterior communicating artery is reported.
The patient was a 58-year-old man and was admitted because of consciousness disturbance. The patient was semicomatose, and the neurological examination revealed nuchal stiffness and bilateral retinal hemorrhage. Right carotid angiography showed an aneurysm of the anterior communicating artery and fenestration of the internal carotid artery.
Fenestration of the vertebral artery at its origin was well known. However, no previous reports of angiographically demonstrated fenestration of the internal carotid artery were seen among 43 cases of fenestration in Japanese subjects found in the literature. Only a case of duplication of the internal carotid artery was reported in U.S.A.
In the authors' case, fenestration of the internal carotid artery started at 15 mm distal to its bifurcation or at the level of the second vertebra. This fenestration presumably developed by anomalous connection of the third aortic arch with the dorsal aorta, or by persistence of the cranial part of the ductus caroticus.

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It has been generally accepted that the direct approach to the cavernous sinus under normal temperatures is very difficult and that the radical removal of tumors which have invaded the cavernous sinus cavity is usually impossible. The partial removal of tumors which have grown into the sinus in the form of a small nodule may cause major venous bleeding which is thought to be very difficult to control.
The purpose of this paper is to describe surgical techniques for radical operation on the cavernous sinus under normal body temperatures. Thirteen cases of tumors which had invaded the cavernous sinus and 6 cases of vascular cavernous sinus lesions were operated on in the semi-sitting position which decreased venous pressure in the sinus. Biobond-soaked Oxycel was inserted into the opened cavernous sinus to control bleeding.
There are four possible approaches to the cavernous sinus; the position and extent of the tumor determine which is optimal. When the tumor involves the external wall of the cavernous sinus, the tumor is removed with the external wall of the sinus. The second is the lateral approach to the cavernous sinus through the opening of Parkinson's triangle. The third is the subfronto-pterional approach with removal of the planum sphenoidale, the tuberculum sellae, and the anterior wall of the sella turcica to expose the entire optic nerve in the optic canal. Through this approach, the anterior inferior cavity and the medial cavity of the cavernous sinus could be opened in order to expose the C-3 and C-4 segments of the internal carotid artery. The last approach is the posterior approach to the cavernous sinus through the transpetrosal approach combined with the subtemporal approach, which is suitable for exposure of C-5 and the posterior part of C-4 of the internal carotid artery.
Out of these 19 cases, one patient with an ophthalmic aneurysm complicated by a malignant glioma died 6 months after surgery, and another one with a pituitary adenoma which invaded the cavernous sinus died of meningitis 20 days after the operation. A case of meningioma of the petroclival portion extending into the cavernous sinus developed right hemiparesis and aphasia due to postoperative intracerebral hemorrhage. One case with subtotal removal of a medial sphenoid wing meningioma which had invaded the sinus did not regain his visual acuity postoperatively. The remaining 15 cases returned to normal social activity, although one of petroclival meningiomas developed third through sixth nerve palsy and a teratoma case showed third and fifth nerve palsy.

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An autopsy case of intracranial and intraspinal subdural hematomas secondary to invasion of the dural and epidural vessels by a metastatic adenocarcinoma was presented. The extremely rare occurrence of such lesions was reviewed in the literature and the mechanism of hematoma formation was discussed.A 45-year-old woman, who had a partial gastrectomy for adenocarcinoma of the stomach 12 years previously, showed increased serum alkaline phosphatase level and multiple high uptake areas on a radioisotope bone scan. Physical and neurological examination on admission showed no definite abnormalities. Ten weeks later, she complained of double vision and became semicomatose within a few days. Brain CT showed the presence of subdural hematoma in the right parietal region. Laboratory examinations, suggested the presence of disseminated intravascular coagulation (DIC). A burrhole was placed and bloody fluid was evacuated from the subdural space. The level of consciousness gradually improved, but again deteriorated progressively into a comatose state. Brain CT showed bilateral subdural hematomes. She died on the 7th postoperative day.
Autopsy revealed metastatic adenocarcinoma foci in various tissues such as the lungs, left retroperitoneal space, lymphnodes, and bones, although no evidence of local recurrence was found in the stomach. In the lungs and the bone marrow of the skull and vertebrae, many tumor cell nests were found only within the dilated vessels. Subdural blood clots were found bilaterally over the frontoparietal lobes and around the lower thoracic and lumbar segments of the spinal cord. Histologicaly, an extensive permeation of tumor cells into the lumina of the vessels was observed in the cranial dura over the subdural hematoma. The spinal dura covering the subdural hematoma contained a large number of engorged vessels without tumor cells. Veins in the spinal epidural tissue were distended and filled with tumor cells. Therefore, both intracranial and intraspinal subdural hematomas were assumed to be the result of obstruction of the dural or epidural veins by the tumor cells and of the subsequent bleeding from the capillaries of the inner vascular or areolar layer of the dura. In addition, the coagulation defect, or DIC, may have played a significant role in the development of the subdural hematomas.

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A case of intracranial sarcoidosis was presented with a review of twelve operated cases reported in the literature.
A 29-year-old female was admitted with a fifteen month history of headache, anosmia, and convulsion. Neurological examination revealed only bilateral anosmia. CT scan showed two enhanced areas. One was on the left half of the tentorium cerebelli and the other was at the anterior part of the falx. The tumor of the tentorium cerebelli was totally removed. Histologically, the tumor was confirmed to be sarcoidosis. Kveim test was positive. The patient returned to her previous work.

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Reports on brain abscess in addicts are surprisingly limited in the literature.
Presented is a 37-year-old male, who had been an amphetamine addict for four years and was hospitalized under suspicion of a brain tumor.
Neurological examination revealed somnolence, left homonymous hemianopsia, bilateral choked disks, mydriasis with sluggish response to light on the right, and left hemiparesis. CT scan showed a low density area with a markedly enhanced ring-blush in the right occipital lobe. Angiography showed an avascular area with a halo formation in the venous phase. A brain abscess was diagnosed and an emergent operation was performed. Fifty ml of yellowish pus was aspirated through a right occipital craniotomy and the abscess was totally extirpated. Staphylococcus aureus grew from the pus.
The possibility of brain abscess should be kept in mind when an addict shows focal neurological signs, or the signs of increased intracranial pressure. CT with contrast enhancement is the most useful diagnostic tool in such cases.

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