The authors have investigated the relationship between oncogene (N-myc and c-src) expression and major histocompatibility complex (H-2 in the mouse) antigen gene expression at the molecular levels, by using mouse neuroblastoma sublines (NB-1 and NB-V). Fluorescence-activated cell sorter analysis showed that NB-1 cells exhibited positive expression to H-2 K_k, H-2 D_d, and beta-2-microglobulin, while NB-V cells were negative to all three antigens. It was found that dimethyl sulfoxide (DMSO) had a capacity to increase an H-2 class I antigen expression on NB-1 cells, whereas no change was observed on NB-V cells after DMSO treatment. Molecular analysis with deoxyribonucleic and ribonucleic acid (RNA) blot hybridization and immunoprecipitation revealed that the enhancement of H-2 antigen expression on NB-1 cells was modulated at the transcriptional control of the H-2 gene. In contrast, negative H-2 antigen expression on NB-V cells was caused by block at the level of glycosylation of the H-2 heavy chain, although an increase in messenger RNA of the H-2 gene was induced after DMSO treatment. There was neither amplification nor rearrangement of N-myc and c-src oncogenes in either neuroblastoma subline. Nuclear runon transcription assay revealed that the N-myc gene was post-transcriptionally down-modulated by DMSO, whereas the c-src gene was transcriptionally up-regulated. It was thus suspected that N-myc and c-src might be directly associated with cellular proliferation and differentiation in neuronal tumors and that in vivo tumorigenicity could be regulated by the control mechanism of oncogene expression in relation to H-2 gene expression on tumor cells.

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 Medulloblastoma is one of the most common malignant brain tumors in childhood. These cells are immature bipotential cells that could differentiate into both neuronal and glial cells. The authors established two human medulloblastoma cell lines. One was derived from a 2-year-old girl with cerebellar tumor (designated as ONS-76) and another was from a 9-year-old girl with metastatic tumor in the right frontal lobe (ONS-81). Immunohistochemical studies showed that both cell lines possessed 145 and 200 kDa neurofilament proteins and neuron-specific enolase, without glial fibrillary acidic protein and S-100 protein. It was shown that interferon γ could enhance or induce the expression of the major histocompatibility complex (MHC) antigens which play a major role in immune response. Also shown for the first time was the expression of MHC class II antigens on human medulloblastoma (ONS-76 and 81) with neuronal differentiation.

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 A Moloney virus-induced T cell lymphoma, YAC-1, derived from A/Sn (H-2^a) inbred mouse origin, was tested for hybrid resistance (HyR) after subcutaneous (s.c.) or intracerebral (i.c.) tumor cell inoculation into syngeneic and semi-syngeneic mice. The F1 hybrids (H-2^a/b) between A/Sn and C57BL/6 mice more strongly resisted the s.c. inoculation of 10⁶ and 5 × 10⁵ cells than did syngeneic recipients. In contrast, no HyR to the i.c. inoculation of 10⁴ and 10³ cells was seen in the F1 hybrid mice. Natural killer (NK) cell activity was much higher in F1 hybrids than in syngeneic mice. ¹²⁵I-iododeoxyuridine-labeled YAC-1 cells were more efficiently eliminated from the highly resistant F1 hybrids than from the parental strain in both 4 and 18 hour in vivo rejection assays via intravenous (i.v.) and s.c. injection, respectively. The remaining radioactivity of the brain, however, did not differ between these mice. Thus, there was a correlation between the in vivo resistance of F1 hybrid mice to challenge s.c. inoculation of parental tumors and their expression of lymphocyte-mediated natural cytotoxicity in vitro against those tumors. T cell depletion by thymectomy followed by irradiation and fetal liver reconstitution did not abrogate the s.c. HyR against YAC-1, whereas NK cell depletion by i.v. administration of anti-asialo-GM 1 antibodies resulted in the disappearance of the resistance. Furthermore, genotypic study segregating (A/Sn × C57BL/ 6) F1 × A/Sn backcross mice indicated that the s.c. HyR might be attributable primarily to heterozygosity within the H-2 complex. Taken together, it was suggested that HyR to an NK cellsensitive YAC-1 is mediated by an NK cell-dependent cytotoxic effector mechanism with H-2-linked genetic control against s.c. tumor grafts, while such an NK cell-mediated natural resistance does not operate in the brain.

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 Brain damage in the early stage of experimental head injury was studied under electron microscope, especially with respect to the permeability of the blood brain barrier and damage to nerve fibers. Lightly anesthetized rabbits were treated by intravenous injection of horseradish peroxidase (150-250 mg/kg) and were subjected to occipital impacts with a pendulum impactor. The animals were then perfused with a 2.5% glutaraldehyde mixture. Small blocks of the brain were sampled, incubated, postfixed, and embedded in Epon®. These sections were observed under an electron microscope without staining. The authors' criteria of concussion have been previously published. There were three nonconcussion, 11 nonlethal concussion and seven lethal concussion animals. All cases of lethal concussion showed subarachnoid hemorrhage (SAH) in the brainstem and 57% of them showed microscopic parenchymal perivascular hemorrhages in the brainstem. Fifty-five percent of the nonlethal concussion cases showed SAH in the brainstem with a little parenchymal hemorrhage. The nonconcussion cases showed no hemorrhagic change except contusions and/or SAH of the cerebellum. Hemorrhagic changes were frequently seen in the cerebrum and cerebellum of nonlethal and lethal concussion cases without correlation to the severity of concussion. Under electron microscope, nonconcussion cases showed mild splitting of myelins. In nonlethal concussion cases, swelling of perivascular astrocytic feet was seen to a moderate degree in the cerebrum, pons, and medulla oblongata and damage to axons and myelins were mainly seen in the pons and medulla oblongata. Many cored dense bodies containing peroxidase were diffusely recognized in vascular endothelial cells. In lethal concussion cases, beside findings seen in nonlethal concussion, intravascular peroxidase was seen to leak from the intravascular space through an opened tight junction to the extracellular space, axons and neuropils. Severe splitting of myelins and atrophic axonal changes were seen in the pons and medulla oblongata. In conclusion, irreversible damage to the blood brain barrier and nerve fibers was seen in the brainstem of lethal concussion cases. Reversible changes of increased permeability of the blood brain barrier and mild damage to nerve fibers were seen in nonlethal concussion cases. Even in nonconcussion cases, some minimal damage to myelins was seen.

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 The clinical course of 45 patients treated by carotid endarterectomy over the past 5 years is described with emphasis on the following three points: 1) Diagnostic methods, namely digital subtraction angiography (DSA) and B-mode Doppler imaging technique; 2) surgical procedure using an improved shunt tube and surgical instruments; and 3) monitoring before and during surgery.
 All operations were conducted using a shunt. Morbidity and mortality rates were both 0%. Postoperative transient hemiparesis lasting for 6 hours was recognized in only four cases. The total percentage of correct diagnoses using intravenous DSA compared with conventional angiography was approximately 80%. The accuracy of the non-invasive B-mode Doppler technique in measuring the degree of constriction compared with conventional angiography was 84%. The shunt was made of silicone tubing and was based on a tube 30 cm in length and 3.5 mm in diameter which was a T-shaped loop. Different sized bulbs were fixed to each end of the tube to prevent extravascular deviation. Modified bulldog clamps and Sugita clips were used for fixation in the vessel.
 Regional cerebral blood flow (rCBF) measurement and electroencephalography (EEG) under contralateral Matas procedure were conducted before surgery, and cross circulation during shortterm occlusion of the common carotid artery was evaluated. The emergence or increase of δ waves in EEG during occlusion was observed in six cases. The rCBF of the affected middle cerebral artery territory in these patients was lower than that in patients with no increase of δ waves. Furthermore, the mean stump pressure during surgery in cases with preoperative EEG changes was 40 mmHg and that in cases without changes was 63 mmHg; these values were significantly different. Cases with 50% or more reduction in amplitude of the early component of somatosensory evoked potential during surgery were found to have a stump pressure of less than 40 mmHg. The use of a shunt and intraoperative monitorings are considered necessary in order to minimize postoperative complications.

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 The clinical status of patients with glioma is influenced by 1) the histological malignancy of the tumor, 2) the tumor volume, 3) secondary status such as brain edema or intracranial hypertension due to the tumor, and 4) the host immunity. Due to some improvement in at least 2) and 3) by the initial treatment, most low grade glioma cases pass through a clinically silent postsurgical period. However, at a certain point, transition to a high grade tumor malignant transformation may occur with exacerbation of the symptoms. Twenty-two cases of histologically established low grade glioma experienced over the past 7 years, in which immunological status was evaluated, were analyzed. Nine cases (41%) showed malignant transformation. Characteristic pictures of the clinical symptoms, computed tomography (CT) scan findings, immunological status, and morphological findings (mainly immunohistochemical examination) in nine cases were delineated. The findings at the time of exacerbation of the symptoms were as follows. In all cases CT scan demonstrated the change in the main lesion from low density to mixed density and were compatible with a high grade glioma. Reduction in host immunity was verified. Morphological increase in the tumor volume, increase in histological malignancy and deterioration in the secondary status due to the tumor were confirmed. Necrosis of the tumor cells as well as increase in giant cells and gemistocytes were observed. Immunohistochemical analysis revealed a decrease and irregularity in glial fibrillary acidic protein positive cells and positive processes as well as increase in vimentin intensity. These findings demonstrate change in the biological characteristics of the tumor. It was not possible, however, to clarify the factors causing malignant transformation in low grade glioma.

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 The authors report two cases of rapid resolution of acute subdural hematoma. Case 1, a 78-year-old male, sustained head trauma and became unconscious for a few minutes, but on arrival he was alert and neurological examination was normal. A computed tomography (CT) scan taken 5 hours after the injury showed a high-dense subdural hematoma partly containing low-density area over the right cerebral hemisphere. He was conservatively treated. A CT scan taken 33 hours after the injury disclosed diminution of the hematoma and appearance of a thin high-density layer in the subdural space adjacent to the tentorium. The high-density layer disappeared on a CT scan taken 7 days after the injury. Case 2, an 84-year-old female, struck her head in the occipital region. On arrival she was drowsy but otherwise had no neurological abnormality. A CT scan taken 1 hour after the injury demonstrated a high-dense subdural hematoma partly containing low-density area over the right cerebral hemisphere. She was conservatively managed and became asymptomatic. A CT scan taken 14 hours after the injury disclosed complete resolution of the hematoma and appearance of a thin high-density layer in the subdural space adjacent to the falx and the tentorium. This highdensity layer also completely disappeared on a CT scan taken 14 days after the injury. It was suggested that a mechanism of rapid resolution of the acute subdural hematoma was attributable to washing-out by cerebrospinal fluid.

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 A 17-month-old boy was admitted to our hospital in a semicomatose state after a minor head injury. Computed tomography (CT) scans revealed a posterior interhemisphericand athin convexity subdural hematoma. Two and a half hours later, repeated CT scans disclosed a development of the right hemispheric diffuse low density and an enlargement of the interhemispheric subdural hematoma. Decompressive craniectomy and removal of the hematoma was performed immediately. On the second postoperative day, the diffuse low density areas developed in the contralateral frontal and temporal lobes. On the 14th postoperative day, the gyri which had been low in density were markedly enhanced with contrast enhancement. On the 16th postoperative day, CT scans showed a diffuse hemispheric gyral high density with bleeding in the right parieto-occipital lobe. A right occipital lobectomy and removal of the hematoma was performed. Histological examination suggested cerebral infarction probably due to venous congestion. It is also suggested that the diffuse hemispheric gyral high density observed on the 16th postoperative day was the hemorrhagic cerebral infarction.

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 A 40-year-old female, who had taken low-dose oral contraceptives for 2 months before onset, developed transient dysarthria, left hemiparesis, and left hemihypesthesia. One month later, a computed tomography (CT) scan revealed a uniformly enhanced, convex-shaped, hypertrophic membrane with a lobulated lumen in the subdural space of the right parietal region. A right parietal craniotomy was performed. The membrane, consisting of elastic-hard, hypertrophic granulation tissue and yellowish, sticky fluid in the lumen, was readily freed and totally extirpated. Subsequently, the patient recovered without persistent symptoms. Light microscopic examination detected the sinusoidal channel layer and the fibrous layer in an alternating configuration, along with intramembranous hemorrhagic foci. Such hypertrophy must have been caused by repeated intramembranous hemorrhages and reactive granulation. Such findings of hematoma membrane have never previously been reported. Thus, this is an interesting case, clearly distinguished from typical chronic subdural hematoma.

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 A 56-year-old female experienced sudden excruciating pain extending from the upper neck to the lower back. She had mild disturbance of consciousness, and a lumbar puncture revealed bloody cerebrospinal fluid. The positive neurological findings were meningitis, spastic paraparesis, hyperesthesia of the left L3 dermatome, bilateral Babinski, disappearance of anal reflex, and urinary retention. Computed tomography scans, myelography, and magnetic resonance images revealed diffuse subarachnoid hematoma and hematomyelia from Th12 to L3. Spinal angiography was tried twice before surgery but no origin of this diffuse hematoma could be found. Laminectomy was performed from Th12 to L1 and organized hematoma was found in the subarachnoid space. After the hematoma removal, non-pulsating tortuous vessels were observed on the surface of the spinal cord at the L1 level which ran into the intramedullary region. However, there was no further abnormality to define spinal arteriovenous malformation or fistula within the limits of exposure. The postoperative course was uneventful and about 2 months later she was able to walk by herself.

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 A 65-year-old female was admitted because of progressive vertigo, truncal ataxia, and unsteadiness of gait for the past 6 years. Computed tomography (CT) and magnetic resonance imaging revealed a non-enhanced, large midline cyst in the posterior fossa and slightly dilated lateral and third ventricles. Metrizamide CT cisternography showed no communication between the cyst and the subarachnoid space. Suboccipital craniectomy, laminectomy of the atlas, and membranectomy of the cyst were performed. On light microscopic examination, the cyst wall was composed of arachnoid cells and connective tissues. Thus, this lesion was not an epithelial cyst but an arachnoid cyst occupying the fourth ventricle. An arachnoid cyst of the fourth ventricle is extremely rare, and only two cases were previously reported.

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 The patients was a 27-year-old female, gravida 0, para 0, with complaint of headache and visual disturbance for about 1 month. Ophthalmological examination showed impaired visual acuity and enlargement of Mariotte's spot on the left. A computed tomography scan disclosed an enhanced mass in the sellar and suprasellar region. Endocrinological examination revealed slight elevation of thyroxin, growth hormone, and prolactin. A trans-sphenoidal hypophysectomy was carried out with a preoperative diagnosis of nonfunctioning pituitary adenoma. Histological examination showed a marked infiltration of lymphocytes and interstitial fibrosis, diagnosed as lymphocytic adenohypophysitis. She received hormone-replacement therapy owing to postoperative hypopituitarism. Twenty-eight cases of lymphocytic adenohypophysitis including the authors' are classified clinically into two types; fluminant type and chronic type. The former type occurs frequently with disturbance of consciousness because of the end organ insufficiency and proceeds to death in a fluminant course. The latter type occurs frequently with headache and visual disturbances, closely related to pregnancy and the postpartum period and survival occurs with hormone replacement therapy. This disease should be kept in mind in the diagnosis of sellar and suprasellar mass lesions.

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 A 55-year-old female was admitted to the Juntendo Izunagaoka Hospital, because of sudden onset of motor aphasia and right hemiparesis. Neurological examination on admission revealed drowsy state, bilateral papilledema, motor aphasia, and right hemiparesis. Computed tomography showed a subcortical hematoma in the left frontoparietal region associated with perifocal edema. Left carotid angiography revealed a fusiform aneurysm at a peripheral branch of the central artery. There was no tumor stain on cerebral angiograms. A combination procedure was carried out during emergency surgery, including evacuation of the intracerebral hematoma and removal of the thrombus-like material from the aneurysmal cavity followed by wrapping the aneurysm with fascia. Histological examination of the thrombus-like material demonstrated that it was a neoplastic embolus of choriocarcinoma. Serum (2600 mIU/ml) and urinary (7200 mIU/ml) human chorionic gonadotropin levels were elevated. The features of neoplastic aneurysm due to choriocarcinoma are reviewed and discussed.

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 A 56-year-old male was admitted with the complaints of nasal bleeding, gait disturbance, and disturbance of consciousness. Neurological examination revealed drowsiness, right hemiparesis, and choked discs. Computed tomography scan showed an enhanced mass at the frontal base, which extended to the left nasal and paranasal cavities. Angiography showed a tumor stain with a mass sign. The intracranial part of the tumor was removed completely and he was discharged ambulatorily. Two months after surgery, however, he was admitted again for the regrowth of the tumor. Ventriculoperitoneal shunting was emplaced and radiation therapy was given to the brain and nasal cavity. After 3000 rad irradiation the clinical condition suddenly became worse because of pneumocephalus. The cranial tumor disappeared after irradiation but he died of metastases and general prostration. Clinically this case was diagnosed as an olfactory groove meningioma at first, but immunohistochemical diagnosis was olfactory neuroblastoma.

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 Involvement of the choroid plexus by malignant lymphoma is rare. This case showed mass lesions at the choroid plexus in the first stage of systemic non-Hodgkin's malignant lymphoma. A 53-year-old female was admitted with headache, diplopia, and gait disturbance. The patient was alert but had left supraclavicular and axially lymph node swelling. Computed tomography scan revealed enhanced masses at the lateral and fourth ventricles. The lymph node biopsy disclosed non-Hodgkin's malignant lymphoma, diffuse large cell type. The immunological marker was the B-cell type. At surgery, there was highly vascular white tumor at the choroid plexus of the right lateral ventricle. The tumor also involved adjacent brain tissue. Pathological examination revealed infiltration of lymphoma cells to the choroid plexus. The subependymal and perivascular spaces of the choroid plexus were filled with lymphoma cells. Virchow-Robin space and white matter of adjacent brain tissue were also involved by lymphoma. After surgery, whole brain irradiation of 35 Gy and chemotherapy were performed. However, 14 months after initial diagnosis, the patient expired because of systemic involvement by the lymphoma.

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 A 61-year-old female was referred because of headache and gait disturbance. A computed tomography (CT) scan revealed a midline isodense mass lesion. The limit of the tumor was equivocal even after administration of contrast medium. Magnetic resonance imaging (MRI) study, however, clearly showed the relationship between the tumor and the surrounding structures, such as the corpus callosum, the ventricular cavities. The tumor had originated from the region of the septum pellucidum and positioned just beneath the corpus callosum from the genu to the splenium with the roof of the third ventricle pushed downward. The tumor was totally extirpated via the interhemispheric paratranscallosal route. The tumor was typical subependymoma. The postoperative course was uneventful. Transient psychiatric disturbance and inability to retain recent memory were observed and the former subsided in several weeks. CT and MRI characteristics of subependymoma are summarized and the usefulness of MRI to locate tumors and to plan proper surgical approaches are emphasized.

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 A 68-year-old female was admitted with mild headache in the right frontal region. Physical and neurological findings were normal. Plain X-rays revealed a poorly circumscribed, osteoblastic lesion in the right frontal bone. Computed tomography scan showed that the diploic space was destroyed but that the inner and outer tables were intact. On ^99mTc bone scan, a hot lesion was visible in the same region. The lesion was expressed as a low-signal intensity area on T₁-weighted magnetic resonance (MR) image and as a high-signal intensity area on T₂-weighted MR image. The tumor was broadly resected together with peripheral normal bone, and cranioplasty using a resin plate was performed. The tumor was mainly composed of mature, regularly aligned bone (lamellar bone) and intermingled fibrous tissue. Ossifying fibroma is a rare, benign fibro-osseous tumor that mainly involves the craniofacial bone. A few cases involving the cranial vault alone have been reported. The relevant literature is reviewed, and discussion focuses on the differential diagnosis between ossifying fibroma and monostotic fibrous dysplasia.

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 A 50-year-old female was admitted because of nausea, vomiting, and cerebellar ataxia. Computed tomography scan revealed an enhanced mass accompanied with a cyst in the right cerebellar hemisphere. The mass situated in the subcortical region was removed. Histologically, highly vasculated tumor cells lined the cavities. Postoperative radio and chemotherapy were administered and the clinical symptoms improved gradually. Two months later, the patient complained of dyspnea. Chest X-ray on second admission demonstrated cardiomegaly. Hemorrhagic pericardial effusion amounting to 1000 ml was aspirated by pericardial puncture. Papillary clusters of tumor cells were demonstrated in the pericardial effusion. The patient died of cardiac failure. At necropsy solid tumors were located in the heart, lung, left inguinal region, and cerebellum. Histological diagnosis was mesothelioma arising from the heart. Primary pericardial mesotheliomas are rare; approximately 106 cases have been reported. Pericardial mesothelioma frequently spreads to the adjacent pleura and mediastinum, but distant metastases are extremely rare because patients with pericardial mesothelioma tend to die early due to cardiac failure or cardiac tamponade.

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 A 49-year-old male was admitted with a history of radiotherapy for a pituitary adenoma 9 years earlier. Three weeks prior to admission, he noticed visual loss in the left eye. Computed tomography (CT) scan revealed a sellar tumor. The patient underwent craniotomy and the tumor was partially resected. The histological diagnosis was benign pituitary adenoma. Two months after surgery, he began to complain of headache and left hemiparesis. CT scan at that time showed a large parasellar tumor extending into the right temporal lobe. A second craniotomy was performed and a firm tumor was partially removed. Under light microscopy, the tumor was composed of anaplastic spindle cells showing a fascicular pattern. Ultrastructurally, the tumor cells were spindleshaped with elongated nuclei. The cytoplasm contained numerous distended rough endoplasmic reticula and free ribosomes, Golgi apparatus as well as glycogen granules. Some desmosome-like intercellular adherents were observed. Collagen fibers were scattered in the extracellular space. There was no apparent formation of a basement membrane. These findings suggested a close morphological similarity between tumor cells and fibroblasts, conforming to ultrastructural diagnostic criteria for fibrosarcoma. In spite of intensive treatment, such as a second radiotherapy and subsequent craniotomy, the patient died 9 months after admission. The clinical course and pathological findings of the post-irradiation pituitary fibrosarcoma are discussed.

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 The authors report two cases of vertebral dissecting aneurysm. The first case, a 49-year-old female, developed severe headache and computed tomography scan showed subarachnoid hemorrhage (SAH), but 4-vessel cerebral angiography failed to show an aneurysm. The second angiograms obtained 2 weeks later showed possible aneurysmal dilatation on the right vertebral artery. The third angiograms, 2.5 months after SAH, disclosed a right vertebral fusiform aneurysm on the arterial phase and it was diagnosed as a dissecting aneurysm since the contrast medium remained until the very late venous phase. The previous angiograms were reviewed using the subtraction technique, which revealed retention of the contrast medium. The second case, a 42-year-old female, suffered from SAH. Left vertebral angiography revealed a fusiform aneurysm and tapered narrowing just distal to the aneurysm, which was a typical “pearl and string sign.” The subtraction film of the venous phase also showed retention of the contrast medium in the aneurysmal portion. These findings accurately diagnosed dissecting aneurysm of the vertebral artery. Since the classical true diagnostic “double lumen sign” was rarely observed in the angiograms, it was not easy to diagnose dissecting aneurysm of the vertebral artery. The authors emphasize the angiographic findings of retention of the contrast medium in the venous phase as a “true diagnostic sign” for correct diagnosis of dissecting aneurysm.

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 A 64-year-old, hypertensive female suddenly experienced severe headache. On admission, the patient had almost clear consciousness but was slightly restless and complained of severe headache and nausea. Neurological examination revealed only neck stiffness. A computed tomographic scan revealed subarachnoid hemorrhage. Angiographically, bilateral internal carotid and vertebral arteries had the “string of beads sign” at their cervical portion, and the left internal carotid artery also had the same sign at its cavernous portion. The left vertebral artery had low-origin posterior inferior cerebellar artery and a berry-shaped aneurysm at its distal trunk. A diagnosis of cervical and intracranial fibromuscular dysplasia (FMD) with a ruptured berry-shaped aneurysm of the distal vertebral trunk was made. The berry-shaped aneurysm was successfully treated with proximal clipping. Angiographically, right renal and axillary arteries also had the “string of beads sign, ” and the patient's hypertension seemed to be renovascular in etiology. The co-existence of intracranial FMD and cerebral aneurysm of unusual location suggests a possible relationship between the FMD and the development of cerebral aneurysm.

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 A 69-year-old male presented with a 4-month episode of tonic seizures of the right arm and leg. Neurological examination revealed no abnormal findings. In the electroencephalogram, sharp wave trains were seen dominantly in the left frontal region. Computed tomography scans showed a spotty hyperdense lesion in the left insular area with minimal enhancement. Left carotid angiogram demonstrated no abnormalities in the arterial and capillary phases. In the venous phase, however, a varicose dilatation of the posterior insular vein was found, which was also noticed in the delayed phase. Magnetic resonance T₁-weighted images failed to detect the lesion, but T₂-weighted images showed a slight signal focus in the same area. After administration of 300 mg of phenytoin daily, the frequency of attacks markedly decreased and the patient was kept under close outpatient observation.

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 A 59-year-old female was hospitalized because of disturbance of consciousness and convulsive seizures. She had taken a hormonal drug for 15 months after breast cancer surgery. A computed tomography scan revealed multiple high-density areas in the left temporal and frontal and the right parietal lobes. Angiography showed a dural arteriovenous malformation (AVM) in the posterior fossa fed by the occipital and the middle meningeal arteries and draining into the transverse sinus. It also demonstrated occlusion of the left sigmoid sinus in the venous phase. She complained of headache in the occipital region and dizziness. On day 13, the left occipital artery was ligated and cut, and then abnormal arterial anastomoses around the lesion were coagulated. After surgery, clinical symptoms disappeared. The etiology of dural AVM is controversial, but in this case it is suspected that sinus thrombosis due to the drug caused the dural AVM. The authors discuss the etiology and treatment of dural AVM in the posterior fossa.

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 A 32-year-old female (gravida 2, para 2) was admitted at 15 weeks of gestation with a chief complaint of left homonymous hemianopsia accompanied by frontal headache. Computed tomography scan and cerebral angiography were performed with the lead shield and probe for X-ray exposure placed on the patient's body. Angiography revealed an arteriovenous malformation (AVM) located in the posterior part of the right temporal lobe. Total dose of the diagnostic X-ray radiated to the fetus was measured 2.5 mrem at the most. The AVM and the hematoma were totally removed successfully at 19 weeks of gestation. A male infant weighing 3180 g was delivered at full term by cesarean section without congenital anomalies and he has been growing up without mental deficits. These results suggest that diagnostic X-ray examination during pregnancy has little risk and that surgical treatment should be given to the mother immediately after the rupture of an AVM if she is in good condition and the gestational date is past 12 weeks.

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 A 45-year-old male was admitted for evaluation of left facial pain of 11-years' duration. Fifteen years prior to admission, he had had an episode of subarachnoid hemorrhage. Neurological examination revealed no definite abnormalities except for trigeminal neuralgia involving the left second division of the nerve. Computed tomography scan showed an irregulary enhanced lesion involving the lateral aspect of the left cerebellar hemisphere. Vertebral angiograms revealed an arteriovenous malformation (AVM) fed by both the dilated left anterior inferior cerebellar (AICA) and superior cerebellar arteries (SCA) and draining into the superior petrosal and transverse sinuses via three enlarged draining veins. A saccular aneurysm was incidentally visualized at the proximal portion of the dilated AICA. The AVM was successfully extirpated through the left retromastoid craniectomy. The trigeminal nerve was directly compressed both rostrally and caudally at its entry zone by two dilated feeding arteries of the SCA and the AICA. The aneurysm was simultaneously obliterated. The postoperative course was uneventful, and the excruciating facial pain completely subsided. Postoperative angiograms confirmed disappearance of both the AVM and the aneurysm. Posterior fossa AVMs causing trigeminal neuralgia in the literature are reviewed, and the association of the AVM and the aneurysm in the posterior fossa is also discussed.

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