A case of priapism with ruptured intracranial aneurysm.

A man of 35 years, who had had three attacks of subarachnoid hemorrhage in the previous 3 years, was admitted to hospital with complaints of headache and priapism. There had been intermittent priapism with abnormal acceleration of sexual desire since the first attack, and erection of the penis had persisted with intolerable pain after the last attack of subarachnoid hemorrhage. A carotid angiogram revealed an aneurysm at the junction of the left internal carotid and posterior communicating arteries. Clipping of the aneurysmal neck was successfully performed. However, priapism continued for 22 days after the operation and resulted in sexual impotence. The neurological problems of priapism are discussed with special reference to a hypothalamic lesion caused by the ruptured intracranial aneurysm in this report.

[The association of intracranial meningioma with arteriovenous malformation and aneurysm (author's transl)].

A rate case was reported in which a brain tumor was also found in a patient who had an intracranial arteriovenous malformation and a cerebral aneurysm separately. A 56-year-old man was admitted with motor weakness and repeated convulsions in the left lower limb. Preoperative right and left carotid angiograms showed an arteriovenous malformation in the left parietal region and a left internal carotid artery aneurysm, but both the carotid angiograms and brain scintigrams could reveal no brain tumor. After the radical operation for these two lesions, pneumoencephalography, right serial carotid angiography and brain scintigraphy were performed, demonstrating a right parasagittal tumor. The tumor was totally removed and histological findings were fibrous meningioma.

[Familial intracranial aneurysms--report of 20 cases in eight families and review of the literature].

Twenty cases with 32 cerebral aneurysms in eight families of familial intracranial aneurysms are presented. The present 20 cases, 191 cases in 81 pedigrees in the prior 48 reports and our 692 cases of nonfamilial intracranial aneurysm are analyzed from the view points of sex incidence, age at onset, location of aneurysm, incidence of multiple aneurysms and familial relationship. In addition, the heredity of familial intracranial aneurysm is discussed. The characteristics of our 20 cases are summarized as follows: (1) Mean age of our cases was 53.8 years but it differed from that (41.7 years) of the prior cases. (2) However, five patients (25.0%) were diagnosed at younger age (under 39 years) as in the previous reports. (3) The incidence of multiple cerebral aneurysms was very high (40.0%). (4) Middle cerebral artery aneurysms showed a higher incidence (50.0%). Furthermore, we observed the familial incidence (0.7 - 3.2%) in the total intracranial aneurysms encountered at the same neurosurgical unit, the incidence (39.5%) of cerebral aneurysm among children in parent-children cases and that (44.4%) among siblings in sibling cases of familial intracranial aneurysm. Therefore, we suggested the possibility of incidental aneurysm in the remaining siblings in the cases of familial occurrence.

[Middle cerebral artery occlusion with Moyamoya phenomenon.--2nd report: report of an autopsy case].

About the middle cerebral artery occlusion with moyamoya phenomenon, we have reported the clinical and angiographical study of 10 cases. Now we present an autopsy case. A 53-year-old female was admitted to our hospital on May, 22, 1978, two hours after an apparent subarachnoid hemorrhage. Neurological examination revealed drowsiness, nuchal rigidity right hemiparesis and motor aphasia. Left carotid angiogram showed an occlusion of the left middle cerebral artery at its origin with moyamoya phenomenon, but did not demonstrate an occlusion and/or stenosis of the intracranial internal carotid artery. Furthermore right carotid and bilateral vertebral angiograms were normal. The hospital course was progressively uphill, and she did not have any focal neurological deficits at discharge. But she committed suicide with a poison (Paraquat) on August, 19, 1978. Histopathologic examination of the left middle cerebral artery revealed a stenosis, with a maximum diameter of 900 microns. In this portion the lumen was not be occluded, and arteriosclerotic and inframatric exchanges were not present. The elastica interna was reduplicated, frayed and at times discontinuous. The tunica media was very thin or disappeared. On the other hand, moyamoya vessels were found between distal and peripheral portion of the stenotic middle cerebral artery as a collateral circulation. These findings suggested that the stenotic arterial wall of the left middle cerebral artery might be a congenital hypoplasia.

[Epidermoid of the third ventricle--report of a case].

A rare case of epidermoid of the third ventricle was experienced. The patient was a fifteen years old boy, who had been hospitalized four years earlier due to acute hydrocephalus. The ventriculography at that time revealed a large cystic tumor containing heterogeneous mass filling the entire third ventricle, which seemed to be a dermoid or epidermoid. Ventricular drainage and ventriculo-peritoneal shunt were performed and he was discharged one month later without any complaint. On February 10th 1983, he was re-admitted with severe headache, nausea and showing markedly increased intracranial pressure and right hemianopsia. Computerized tomography scans demonstrated a large round low density mass in the entire third ventricle extending into the prepontine cistern. Radical operation was performed by the anterior transcallosal approach. After dissecting the interhemispheric fissure, a longitudinal incision about 15 mm long was made in the anterior part of the corpus callosum and the tumor was removed. Mild diabetes insipidus and subdural effusion appeared postoperatively. The patient was discharged on April 7th with right hemianopsia and returned to school. The anterior transcallosal approach seemed to be a good operative procedure in such large third ventricle tumor cases since it allowed excellent exposure of the third ventricle and minimized postoperative neurological deficits.

[A case with a diagnosis of apparent functional sylvian aqueductal stenosis].

A case with a presumptive diagnosis of a functional sylvian aqueductal stenosis is presented. The patient was a 64-year-old female, who suffered from progressive gait disturbance and dementia. On admission, CT-scan showed lateral and third ventricular dilatations. The pattern of the ventricular dilatation suggested an aqueductal stenosis. But CT-scan showed no tumorous lesion. RI-cisternography, RI-ventriculography, aqueductgraphy, and continuous monitoring of the intraventricular pressure of the third ventricle were performed in order to make a diagnosis. The results of these examinations led to the following conclusion. "Although there was no apparent mechanical obstruction or stenosis, the presence of circulatory failure of CSF, demonstrated apparent functional stenosis of the aqueduct sylvii." A VP-shunt operation was performed a month after her admission. Her symptoms improved remarkably.

[Regression of a recurrent malignant glioma by combined chemoradiotherapy utilizing carboquone, FT-207 and telecobalt--report of a case (author's transl)].

Current chemotherapy of malignant brain tumor bases on cell kinetics. Chemotherapeutic agents are devided into two, cell cycle specific (CCS) and cell cycle non specific (CCNS) agents. A case of malignant glioma successfully treated by chemo-radiotherapy using a new combination of the two agents , Carboquone (CQ) as CCNS, which has not appeared in literature, and FT-207 as CCS is reported. A malignant glioma in the right frontal lobe in a case of 51-year-old male was removed subtotaly on Dec. 10th, 1971 in our clinic. Three years and five months after the surgery, the patient was diagnosed as having a recurred malignant glioma in the left frontal lobe from the clinical symptoms. This was supported by a positive brain scan and carotid angiography. A total dose of 57mg of CQ was continuously into the left internal carotid artery during two months. Simultaneously, 16g of FT-207 as a total dose was given orally and 4,550 rads of Telecobalt-60 were irradiated. One month after the beginning of these treatments, clinical symptoms improved obviously. Four months later, the size of the tumor shadow on the brain scan decreased remarkably and the shifted anterior cerebral artery returned to normal position on the carotid angiogram. Anemia, leucopenia, thrombocytopenia, nausea, and anorexia were the side-effects of these treatments. But these complications disappeared six weeks after the termination of the treatments.

[Spontaneous thrombosis of an azygos anterior cerebral artery aneurysm--report of a case (author's transl)].

A case of spontaneous thrombosis of azygos anterior cerebral artery aneurysm was reported. A 39-year-old man was admitted to our hospital on April 23, 1979, 5 days following an apparent attack of subarachnoid hemorrhage. On admission, he complained a headache and left hemiparesthesia. Neurologic examination revealed a very slight nuchal rigidity, left hemihypesthesia and hypalgesia. Routine laboratory studies were noncontributory. Left and right carotid angiograms showed an azygos anterior cerebral artery aneurysm. Twelve days after the attack, a left carotid angiogram demonstrated a segmental narrowing and widening of an azygos anterior cerebral artery, and then the aneurysm was filled incompletely. Nineteen days after the attack, the aneurysm was not visualized on right carotid angiogram. Neck clipping and resection of the aneurysm was performed on May 8, 1979. Cross section of the aneurysm exposed a thrombus. He showed postoperatively a slight hypesthesia in the left lower limb. Complete thrombosis of intracranial aneurysm occurring spontaneously is rare. We collected 42 such cases including the present case from the literature and discussed some factors facilitating intraluminal thrombosis. Although the shortest previous period of thrombosis is noted to be over a course of 5 days, the thrombosis in our case in 19 days after subarachnoid hemorrhage was certainly a relative rapid event.

[Chronic subdural hematoma associated with malignancy: report of three cases].

Three cases of chronic subdural hematoma (CSH) associated with malignancy are reported. Case 1; A one-year-old girl was referred for vomiting and convulsions. Left CSH was removed, and her symptoms disappeared. Cytological examination of chronic subdural hematoma revealed abnormal white blood cells. A clinical diagnosis of acute monocytic leukemia was made after the laboratory examination. Remission was achieved by chemotherapy, but she died one year after the operation. Case 2; A 72-year-old woman was referred for right hemiparesis and urinary incontinence. Left CSH was irrigated, and her clinical symptoms immediately disappeared. Cytological examination of chronic subdural hematoma revealed abnormal white blood cells. A clinical diagnosis of chronic lymphocytic leukemia was made after the laboratory examination. No treatment was given since there were no clinical symptoms of chronic lymphocytic leukemia. Case 3; A 70-year-old woman who had been affected with early gastric cancer and mammary cancer for the previous two years was admitted to our clinic because of headache, right hemiparesis and consciousness disturbance. Left CSH was irrigated, and her clinical symptoms improved. However, there was a tendency to bleed because disseminated intravascular coagulation had occurred, and CT showed bilateral subdural hematoma. A second irrigation was performed, but her symptoms did not improve. Left acute subdural hematoma, which was removed by craniotomy, occurred three days after the second operation. Pathological examination of the outer membrane of the subdural hematoma revealed invasion of adenocarcinoma. She died three days after the third operation. It is recommended that both the cytological and the histological examinations be performed when possible, since they are simple to perform and very useful in some cases.

[A case of thymic carcinoma with brain metastasis].

A 43-year-old female with a thymic carcinoma spreading to the extrathorac region is reported. She had received radiation and chemotherapy, after that thymic carcinoma was extirpated. Five months later, the patient was noticed to have a right side hemiparesis, following consciousness disturbance. CT and MRI revealed a left thalamic mass with a heterogenous enhancement effect. The tumor was diminished dramatically due to radiation. Metastasis of thymic carcinoma to the central nervous system is discussed.

A mitochondrial tRNA(Leu)(UUR) mutation at 3,256 associated with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS).

Enzymatic and molecular analyses were conducted on the muscular tissue of a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Significant decreases in activity of complexes I and IV were found and three nucleotide substitutions in the mitochondrial tRNA genes were detected. Two of the substitutions were detected in unaffected members of the family and in some healthy controls. A C-to-T transition mutation at the nucleotide position 3,256 in the mitochondrial tRNA(Leu)(UUR) gene was detected only in the patient and not in unaffected members of the family or 100 healthy controls. The data strongly suggest that this mutation at nucleotide position 3,256 in the mitochondrial tRNA(Leu)(UUR) gene is associated with MELAS.