Cerebral embolism and hormone replacement therapy.

Few studies have focused on the relationship between hormone replacement therapy (HRT) for postmenopausal women or those with breast cancer and the occurrence of cerebral embolism. Results are conflicting as to whether there is a link between the two. We describe three patients who experienced cerebral embolism during HRT. A 73-year-old woman had a transient ischemic attack (TIA) 6 years prior to the present admission. She then took HRT oestrogen plus medroxyprogesterone acetate for about 6 years. The HRT had been prescribed by a gynaecologist for amelioration of postmenopausal symptoms. Six years after beginning HRT, she experienced sudden onset left hemiparesis due to cerebral embolism. Two other patients had been taking HRT for breast cancers. One, a 47-year-old woman, had taken medroxyprogesterone acetate for more than one year, for recurrence of breast cancer. She had developed sudden complete left hemiparesis due to an embolism at the carotid bifurcation. The other patient, a 72-year-old woman who was taking tamoxifen citrate for prevention of breast cancer relapse, experienced cerebral embolism just 2 months after beginning tamoxifen. The risk of cerebral embolism in those on HRT should be emphasized, along with the beneficial effects in terms of postmenopausal symptoms and prevention of breast cancer recurrence.

[Radiological anatomy of the vein of Labbé].

The development and radiology of the vein of Labbé (VL) were investigated using the brains of 19 aborted human fetuses and 6 normal adults injected at autopsy with radiopaque material through the venous system. Carotid angiograms taken in stereoscopic pairs (110 cases, 167 hemispheres) were also analyzed in detail. Developmental alterations of the cerebral structures, particularly those of the opercula and cerebral sulci, are reflected in our classification of the pial veins of the lateral cerebral convexity into the superior, middle and inferior groups. The anastomotic veins of Trolard and Labbé were already recognizable at the fetal age of 6 to 7 months, as development of the opercula and resultant depression of the insula became advanced. In our series, superficial draining veins opening into the VL were 14 to 20 mm (average 16.8 mm) in length. Anastomoses among the superior, middle and inferior groups were analyzed angiographically: single anastomosis was found in 23 percent of cases, while double and triple anastomoses were found in 32 and 45 percent, respectively. A majority of the veins at the sites of anastomosis were found to have calibers of less than 1 mm. The VL, therefore, should be considered in most cases as an independent major superficial draining venous channel of the cerebral convexity with insignificant connections with the superior and middle groups.

Venous architecture of cerebral hemispheric white matter and comments on pathogenesis of medullary venous and other cerebral vascular malformations.

The parenchymal veins, especially the deep medullary veins, of the cerebral hemispheres were studied in detail by analyzing the stereoroentgenograms of multiple brain slices of postmortem injected brain specimens (injected into the internal carotid arteries in 17 cases and into the jugular veins in 12 cases). The presence of four zones--the first (or outer), the second (or candelabra), the third (or palmate) and the fourth (or subependymal) zone--of venous convergence was confirmed within the centrum semiovale, particularly in the frontoparietal area. Other venous convergences such as those related to the optic radiation in the para-atrial area were also found. Arterial branching zones were also observed in the areas similar to those of the medullary veins. It appears that these converging zones are created by rapidly growing crossing nerve fiber tracts, i.e., projection, commissural, and association fibers which grow rapidly during intrauterine and postnatal life. Pathogenesis of medullary venous malformation is also discussed from anatomical viewpoint, venoarchitecture of the pial, parenchymal, and subependymal veins and of the dural venous sinuses. The possibility of a similar mechanism (partial, mild, repetitive venoocclusive disease developing over a long period with fluctuating venous pressure) leading to formation of most (if not all) cases of medullary venous malformation and in some, if not many, cases of cerebral vascular malformations [aside from gene abnormality (chromosome 7) in familial cavernous angiomatosis, particularly in Hispanic American or other familial hereditary conditions] has been postulated.

Treatment of scalp arteriovenous malformation.

We report seven patients with scalp arteriovenous malformations, including two patients with lesions > 10 cm in diameter, who were successfully treated. The principal complaint of each patient was a deforming mass. Each of four patients had a history of blunt traumatic injury. The lesions, each consisting of the nidus, feeders, and draining veins, evolved in all patients. The nidus consisted of fistulae, which exhibited various angioarchitectures as revealed by angiography. A hemangiomatous component was histologically recognized in one patient. In five patients, in whom the lesions were relatively small and whose nidi included only large fistulae, the malformations were remedied by surgical intervention alone or were cured with embolization alone using liquid adhesives. In the two patients with lesions > 10 cm, the nidi consisted of numerous large fistulae and plexiform fistulae in one patient and plexiform fistulae and a hemangiomatous component in the other patient. These patients were treated with a combination of transarterial embolization and surgical intervention. Preoperative embolization greatly reduced blood loss during resection. Total excision and scalp reconstruction using a soft tissue expander were performed in both patients. The cosmetic results were excellent in all of the patients, and no recurrence has been recognized during the follow-up period, which ranges from 31 to 99 months. The treatment of scalp arteriovenous malformations should strive to improve deforming features and to attain a permanent cure. Because each nidus includes a variety of anomalous angioarchitectural features, there should be different means and a combination of treatments for each patient. Embolization alone could be adequate treatment in relatively small lesions, the nidi of which consist only of several large fistulae. For malformations with more extensive, large fistulae or with anomalous components other than large fistulae, a combined endovascular and surgical approach and scalp reconstruction seems to be the best treatment.

Development of posterior fossa dural sinuses, emissary veins, and jugular bulb: morphological and radiologic study.

PURPOSE: To report the anatomic and radiologic development of the transverse, sigmoid, and occipital sinuses, the emissary veins, and the jugular bulb formation from the jugular sinus in humans before and after birth. METHODS: Roentgenograms of 33 injected brains showing the cranial venous system in human fetuses from 3 to 7 months of gestational age and cerebral angiograms of newborns and infants up to 6 years of age (23 clinical cases) were made and analyzed in detail. Special attention was focused on the inner diameters of the transverse and sigmoid sinuses and of the internal jugular veins, particularly at the sigmoid sinus-internal jugular vein junction. RESULTS: Marked increase in venous flow from the rapidly growing cerebral hemispheres leads to ballooning of the transverse sinuses in the absence of an increase in the inner diameters of the sigmoid and jugular sinuses. The ballooning also results in formation of the occipital sinus, marginal sinus around the foramen magnum, and emissary veins. The formation of the jugular bulbs from the jugular sinuses begins after birth when a shift from a fetal to a postnatal type of circulation (or from a lying-down position to an erect posture) takes place. CONCLUSION: The morphological changes of the posterior fossa dural sinuses, emissary veins, and jugular bulb are closely related to the development of the brain, shift to postnatal type of circulation, and postural hemodynamic changes.

Intracranial cavernous angioma manifesting as subarachnoid hemorrhage--case report.

A 56-year-old male presented with a posterior fossa cavernous angioma manifesting as persistent headache with mild neck stiffness. Lumbar puncture revealed subarachnoid hemorrhage (SAH). Repeated four-vessel angiography failed to identify the source of the SAH. Magnetic resonance (MR) imaging demonstrated multiple small lesions in the posterior fossa and cerebral hemispheres, and the SAH. A mass arising from the biventral lobule of the right cerebellar hemisphere extended exophytically into the cisterna magna with intratumoral hemorrhage. These findings were compatible with the presumptive diagnosis of SAH from the mass at the right biventral lobule. The lesion was totally removed through a suboccipital craniectomy without sequelae. The histological diagnosis was cavernous angioma. Intracranial cavernous angioma presenting only as SAH has never been reported before. The use of MR imaging in establishing the diagnosis of vascular malformations is emphasized, particularly when neither computed tomography nor angiography can adequately visualize the origin of SAH.

Aqueductal stenosis due to mesencephalic venous malformation: case report.

The authors report the case of a 43-year-old woman with a venous malformation of the mesencephalon occluding the sylvian aqueduct. Neuroradiological investigations suggested aqueductal stenosis, while the presence of a venous malformation was diagnosed by both magnetic resonance imaging and an angiogram, and was visualized using a neuroendoscope. This is the first reported instance of a venous malformation being observed in situ and the subependymal course taken.

[Clinicopathological evaluation of EVAL embolization in arteriovenous malformations].

The clinical and pathological aspects of two large arteriovenous malformations which were removed totally after preoperative embolization using ethylene vinyl alcohol copolymer (EVAL) were studied. The material, which is not adhesive, is handled easily during the procedure of embolization. However, it involves some risks because it might migrate to and occlude the normal branches of the brain and pass through the nidus to the venous system. Histopathological study of AVM nidus which was removed showed embolic materials within the vessels and inflammatory reaction of the vessel wall and its surrounding tissue. There were patchy hemorrhages within the AVM nidus and its surrounding brain tissue. Recanalization was also found within the occluded vessels. These findings suggest that preoperative embolization has some risk of causing intracerebral hemorrhage after the embolization. AVM should be removed surgically as a radical treatment if the patient is able to tolerate the operation.

Aneurysm of the lenticulostriate artery--report of four cases.

Four rare cases of aneurysm of the lenticulostriate artery (LSA) are presented. LSA aneurysms were located at the origin in three patients and distally in one. Two cases were of multiple aneurysms, one was associated with hypertensive intracerebral hematoma (putaminal hemorrhage), and the other with moyamoya disease. Two patients were successfully treated by microsurgical procedures. The occurrence of LSA aneurysm suggests that aneurysm formation and growth are accentuated by hemodynamic alteration and stress.

[Clinicopathological study of meningiomas of the tentorium and its surrounding structures].

We report the clinical features, radiological studies, operative procedures and results, and follow-up data in 29 patients with meningiomas of the tentorium and its surrounding structures. The cases represented 22.5% of all the intracranial meningiomas operated on in a 15 year period and were divided into three groups, depending on their main attachments, tentorial, cerebellopontine angle (dorsal aspect of the petrous ridge) and others. Tumor size was generally large and 13 cases were larger than 5 cm. The most common tumor site was along or near the superior petrosal sinus and transverse-sigmoid junction in cases involving the tentorium, and medial to the porus acousticus in cases involving the cerebellopontine angle. Different operative approaches to these tumors were carried out, depending on their location. The tumors in the lateral or medial petrous ridge were approached mainly with a suboccipital craniectomy using a retromastoid incision. Total removal was carried out in 80% of the tentorial cases, in 46.2% of cerebellopontine angle cases, and in the 83.3% in the others. Total operative mortality rate was zero. Follow-up periods ranged up to 5 years 5 months in the tentorial cases, 4 years 6 months in cerebellopontine angle cases, and 7 years 1 month in the others. Long-term results were good in 21 cases (72.4%), fair in 3 cases (10.3%) and poor in 2 (6.9%). Three patients died due to tumor recurrence. One of them suffered lung metastasis, and two of them suffered extensive local recurrences. We recommend the retromastoid approach combined with the petrosal approach, if the CPA tumor is large enough and extends to the retroclival region.

[An unusual association of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and central diabetes insipidus associated with spontaneous pituitary apoplexy].

Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.

Medullary venous malformation with an arterial component associated with a ruptured aneurysm--case report.

We report the rare of occurrence of a medullary venous malformation (MVM) with an arterial component associated with a saccular aneurysm on the opposite side. This 49-year-old male patient was admitted with headache and vomiting. He was diagnosed as having a subarachnoid hemorrhage on the basis of bloody cerebrospinal fluid. Angiography revealed a saccular aneurysm at the junction of the internal carotid and posterior communicating arteries on the left side. A MVM with an arterial component was also seen in the right basal frontal lobe. On the seventh hospital day, the aneurysm was clipped via a left frontotemporal craniotomy. The postoperative course was uneventful. There are many hypotheses concerning cerebral aneurysms; some are thought to derive from persistent primitive arteries in the early fetal period. On the other hand, MVM is thought to be intimately related to arteriovenous malformation, which is believed to develop from the premordial vascular plexus, also in early fetal life.

[Current status of radiation therapy in the treatment of malignant glioma:].

The patients of malignant glioma mostly consisting of anaplastic astrocytoma (AA) and glioblastoma (GM) were surveyed at the Committee for Compiling the Manual of Radiotherapy in the Treatment of Brain Tumors, organized by Japanese Association for Radiotherapy Research. Total 286 patients were treated at ten institutes during the period from January 1985 through December 1987. Numbers of cases with AA and GM were 130 and 156, respectively. Concerning the treatment volume, the medium field (50-100 cm2) was applied to 127 patients (37.4%) and the whole brain to 25 one (7.4%). The total dose was given by the range from 56 Gy to 65 Gy in 158 patients (47.6%). One-year survival ratio of AA and GM were 60-75% and 40-65%, respectively. For obtaining the improvement of local control rate, it is considered that the beam focusing onto the target lesion and the sufficient removal of the tumor are necessary and essential.

[Complication of irradiation in brain tumors].

Examination by questionnaire throughout the country revealed 97 cases of radiation brain necrosis (RN). Of the above 97 cases, histologically confirmed 39, having received one course of radiation therapy received an average dose of 62 +/- 10.6 Gy. Minimal total dose provocative of RN is estimated statistically to be 40.6 Gy. Safety fractionation for total dose is regarded as standard in case of 1.8 Gy per once by 22 fractionations for a total dose of 40 Gy and of 1.4 Gy per once by 36 fractionations for a total dose of 50 Gy. After left frontotemporal craniotomy for pituitary adenoma, postoperative opposing 2 fields irradiation brought about right RN on the right side. Examination by means of PET is useful for the differentiation RN from recurrence of malignant glioma. The appearance of foam cells in tunica intima arteriole in substance alba and subsequent luminal narrowing are interesting histological findings in RN.

Multiple intracerebral arteriovenous malformations: report of two cases.

We report the cases of two patients, each of whom had two separate angiographically demonstrable intracerebral arteriovenous malformations (AVMs). One patient had an intraventricular hemorrhage with AVMs in the basal ganglia and the insula on the left side, and the other had a pontine hemorrhage with AVMs in the pons and the occipital lobe on the right side. The AVMs in the former patient were removed totally without residual neurological deficit. We discuss the diagnostic problems of multiple intracerebral AVMs and stress the need for thorough neuroradiological evaluation so as not to miss an occult AVM. We also stress the necessity of total excision of all the lesions and point out several problems faced in surgery for AVMs.

[Two adult cases of moyamoya disease with intraventricular hemorrhage--angiographic evaluation of periventricular vascular anatomy].

In order to show the vascular anatomy in periventricular region, two adult cases of moyamoya disease with intracerebral hemorrhage extending into lateral ventricle were presented. And we discussed the relation between the vascular anatomy and the form of hemorrhage in moyamoya disease. The first case was a 46-year-old woman admitted for nausea and vomiting following headache for four days. CT scan revealed a high density area in the upper portion of body of right lateral ventricle showing intracerebral hemorrhage which extended into the lateral ventricle. On angiogram, typical moyamoya disease was noted. The ventriculofugal arteries from the posterior lateral choroidal artery was detected which indicated developed ventriculofugal perfusion. The second case was a 52-year-old man who was hospitalized sudden onset of headache, vomiting and consciousness disturbance. CT scan revealed a high density area suggesting of hemorrhage in the head of right caudate nucleus. It perforated into the right anterior horn of lateral ventricle with spreading over the other ventricles. We observed similar findings on the angiograms to the first case. In this case, however, the lateral striate arteries were involved instead of the posterior lateral choroidal artery. It should be pointed out that, in both cases, the area of hemorrhage in CT scan coincided with the area of developed ventriculofugal perfusion in angiograms.

[Two cases of intracerebral hemorrhage in full-term neonatal infants].

Intracranial hemorrhage in neonatal infants is mostly noted in the subependymal or subdural space. The former is characteristically noted in premature infants and is attributed to hemorrhage from the subependymal germinal matrix layer. The latter is prevalently noted in full-term neonatal infants and is thought to be associated with injury in the vicinity of the falx cerebri or tentorium cerebelli. We report two cases of intracerebral hemorrhage, which is relatively rare in full-term neonatal infants. In both of them hematoma was located in the left frontal area adjacent to the coronal suture. Angiogram did not reveal any causative abnormality. From CT scan and intraoperative findings it is speculated that the hemorrhage was caused by moulding at the coronal suture. In other words, moulding made the frontal bone slipped in beneath the parietal bone at the coronal suture causing pressure over the brain. The hemorrhage is thought to be caused by contusion of fragile vasculature of neonatal infants.

[Ganglioglioma in a child--report of a case].

A seven-year-old boy who was admitted for surgical treatment for intractable epilepsy was found to have a ganglioglioma in his left parietal lobe. Since four years old, he had been suffering from the seizure and treated with various anticonvulsants without satisfactory effects. As its frequency increased, the dose had to be increased. Thus, it was sought for the possible surgical approach. On the CT scans, an egg size low density zone without contrast enhancement was observed in the subcortical region of his parietal lobe. There was marked thinning on inner table of the skull immediately above the zone. He was operated under fronto-temporo-parietal craniotomy. When the dura matter was opened, pale cerebral cortex protruded. Complete removal of the tumor was not possible, since there was not clear boundary between the mass and normal tissue. Based on histological study, it was diagnosed as ganglioglioma, because its main body contained increased number of glia which had deeply stained ununiform size nuclei. After the operation, he showed neither motor paralysis nor sensory disturbance and was able to sustain his activity with less amount of anticonvulsant.

[Cerebellar astrocytoma presenting with cerebellar hemorrhage: a case report].

UNLABELLED: A rare case of cerebellar astrocytoma presenting with cerebellar hemorrhage is reported. On reviewing the literature, we could collect only four other cases of spontaneous hemorrhage in cerebellar astrocytomas. CASE: On April 5, 1984, a 15-year-old boy noted a sudden onset of headache, vomiting and vertigo and became lethargic and confused. He was admitted on the next day. General examinations, including bloodpressure, temperature and laboratory tests, were found to be normal upon admission. The patient was in somnolence with nystagmus and left dysdiadochokinesis. The result of the left nose to finger test was poor. Computerized tomography revealed a mass leison with calcification and hemorrhage in the paramedian part of the cerebellum. Fourty days after admission, suboccipital osteoplastic craniotomy was performed. A hematoma was found in the paramedian part of the cerebellum. A tumor mass with rich vascularity was completely removed together with the hematoma. Histologically this tissue was a low grade fibrillary astrocytoma accompanying calcification and hemosiderin suggesting tumoral hemorrhage. He regained his neurological functions satisfactorily and was discharged 2 months later.