Peritumoral brain edema and cortical damage by meningioma.

Forty supratentorial meningiomas were analyzed to identify factors causing peritumoral brain edema. Parasagittal, sphenoid ridge, and olfactory groove meningiomas induced edema more frequently than those in other locations. Meningothelial meningiomas were more invasive than other types and were associated with more peritumoral edema. Brain edema correlated significantly with tumor size and histological evidence of leptomeningeal and cortical damage from the tumor. Larger tumors destroy the leptomeninges and cerebral cortex, allowing direct transmission of edema fluid into the white matter, resulting in vasogenic edema.

In vivo and in vitro activation of macrophages with a cyanine photosensitizing dye, platonin.

A cyanine photosensitizing dye, platonin, is a potent macrophage-activating agent. Four days after the administration to mice of small amounts of platonin (20-40 ng/mouse), peritoneal macrophages exhibited greatly enhanced Fc-receptor-mediated phagocytic and superoxide-generating capacities. Much higher doses (more than 3000 ng/mouse) did not have this effect. Photodynamic experiments for macrophage activation were performed by exposing mouse peritoneal cells (mixture of macrophages and B and T lymphocytes) to white fluorenscent light (3 J m-2s-1) in media containing various low concentrations of platonin. A short exposure to white fluorescent light (5 s, 15 J m-2) of peritoneal cells in a medium containing 3 ng platonin/ml produced a maximal level of phagocytic capacity of macrophages. Although platonin absorbs light poorly at wavelengths longer than 630 nm, the region of the spectrum in which the tissues are transparent allows reasonable penetration of light. Thus, we designed experiments in which peritoneal cells were exposed to a red fluorescent light (0.5 J m-2s-1). In a medium containing 10 ng platonin/ml with 15 J m-2 red light, a markedly enhanced ingestion activity of macrophages was observed. Photodynamic treatment of peritoneal macrophages alone did not activate macrophages. Thus, participation of nonadherent cells is required for photodynamic activation of macrophages, implying that a macrophage-activating factor is generated within the nonadherent cells and transmitted to macrophages.

Activation of mouse macrophages by in vivo and in vitro treatment with a cyanine dye, lumin.

The cyanine photosensitizer, lumin, is a potent macrophage activating agent: 4 days after administration of small amounts of lumin to mice (20-40 ng mouse-1), peritoneal macrophages exhibited a greatly enhanced Fc-mediated ingestion activity; higher doses (more than 3000 ng mouse-1) did not have this effect. The in vitro photodynamic activation of macrophages in mouse peritoneal cells exposed to white fluorescent light (3 J m-2 s-1) was also studied in media containing various concentrations of lumin. A short light exposure (45 J m-2) with 10 ng lumin ml-1 produced a maximum ingestion activity of macrophages. Lumin has absorption peaks at 670 and 760 nm. Therefore we designed experiments in which peritoneal cells were exposed to a red fluorescent light (emission, 660 nm; 0.5 J m-2 s-1). In a medium containing 3 ng lumin ml-1 with 7.5 J m-2 of red light, a markedly enhanced ingestion activity of macrophages was observed. The photodynamic treatment of peritoneal macrophages alone did not stimulate phagocytic activity, but the photodynamic treatment of a mixture of non-adherent (B and T) cells and macrophages resulted in a greatly enhanced ingestion activity of macrophages. Thus non-adherent cells are required for the photodynamic activation of macrophages, implying that an activating factor is generated within the non-adherent cells and transmitted to the macrophages. This hypothesis was confirmed by the observation that co-cultivation of photodynamically treated non-adherent cells with untreated macrophages resulted in a greatly enhanced ingestion capacity.

Peritumoral brain edema associated with meningioma--histological study of the tumor margin and surrounding brain.

Thirty-nine cases of intracranial meningiomas were analyzed to identify factors causing brain edema. Edema was significantly correlated with tumor size and the destruction of the leptomeninges and cortex. Meningotheliomatous meningioma tended to have more peritumoral edema. There was no correlation between the presence of edema and location of the tumor or histological features including lymphocytic infiltration and the presence of glial fibrillary acidic protein-positive cells in the tumor tissue. Larger tumors destroy the leptomeninges and cerebral cortex, allowing direct transmission of humoral edema-promoting factor or edema fluid into the white matter, resulting in vasogenic edema.

Lexical agraphia in the Japanese language. Pure agraphia for Kanji due to left posteroinferior temporal lesions.

A new syndrome of 'pure agraphia for Kanji' is described in 3 Japanese subjects with lesions in the left posteroinferior temporal region. Kanji (ideogram or morphogram) can be compared with orthographically irregular or ambiguous words in some European languages, since it is impossible to write Kanji characters unless each one of them is learned and memorized. In contrast, Kana (phonogram or syllabogram) words are comparable with orthographically regular words or nonsense words, because the Kana writing system depends on strict phonological rules (almost one-to-one correspondence between syllable and syllabogram). We conclude that 'lexical agraphia' reported in European languages can also be observed in the Japanese language where it is expressed as 'pure agraphia for Kanji'. 'Lexical agraphia' is a useful concept with general application regardless of language system.

[Case of intracranial and spinal dissemination of primary spinal glioma].

A case of glioblastoma multiforme of spinal cord followed by intracranial dissemination was reported. A 20-year-old man was admitted on Sep. 22, 1981, with motor disturbance of both legs and loss of urinary control. Neurological examination showed spastic paraplegia with bilateral Babinski signs. Abdominal and cremaster reflexes were absent. There was no abnormalities in cranial nerves and upper limbs. Cerebral CT was normal at that time. Myelography showed complete block at the level of 8th thoracic vertebra. Spinal angiography revealed abnormal vascularity at the level of Th7 fed via anterior spinal artery. Intramedullary tumor was partially removed through 5th-8th thoracic laminectomy. Total 5600 rads of irradiation was administered after the operation. The postoperative course was deteriorating. Two months after the operation paresis of both upper extremities had been developed. State of consciousness had been disturbed due to increased intracranial pressure which was subsided for a time while by ventriculoperitoneal shunt. Repeated CT showed high density spots scattered in basal cisterns spreading to all ventricular systems. He expired Feb. 21, 1982. Autopsy revealed that the whole spinal cord was covered by tumor tissue. Basal cisterns were filled with tumor tissue. The tumor was infiltrated subependymally into ventricular systems with intramedullary invasions in some places. Histological diagnosis was glioblastoma multiforme.

[Rathke's cleft cyst. Report of two cases].

Two cases of Rathke's cleft cysts were reported. Case 1. A 57-year-old man was admitted to our hospital on Sep. 29th. 1982, complaining of visual field defect. Visual acuity was 0.7 in the left eye and 0.1 in the right eye. Visual field examination revealed upper temporal quadrantanopsia on the left side and incomplete temporal hemianopia on the right side. He was neurologically free otherwise. Endocrinological study disclosed general hypopituitarism except for elevated serum prolactin level. CT scan showed a high density mass in the enlarged sellar cavity extending to suprasellar area. Right frontal craniotomy was performed on Oct. 26th, 1982, and about 3 ml of reddish-brown colloid substance was aspirated and the capsule of the cyst was excised. Postoperative course was uneventful. The visual acuity and field defects were improved. Microscopic section of the cyst demonstrated a loose fibrous wall, lined by single layer of ciliated columnar epithelial cells containing secreting vesicles. Histological diagnosis was Rathke's cleft cyst. Case 2. A 43-year-old female was attacked by subarachnoid hemorrhage on Jan. 1st, 1983. Angiography revealed an anterior communicating aneurysm. Operation was performed on Jan. 18th, 1983 and the aneurysm was successfully clipped. During surgery a suprasellar cystic mass was incidentally discovered and the cyst wall was resected. Microscopic section of the cyst demonstrated one layer of cuboidal cells supported by thick connective tissue. Precise check of her early history disclosed that her menstruation had been delayed and visual acuity had been impaired. CT scan was negative as far as the suprasellar region was concerned.

[Gangliogliomas in cerebral hemisphere].

Gangliogliomas are rare central nervous system neoplasms. The clinical features, radiological findings and surgical results in 6 histologically proven cases of gangliogliomas in the cerebral hemisphere are reviewed. The ages varied between 8 and 58 years old at the time of diagnosis. Five patients had seizure disorders without focal neurological deficit or clinical signs of increased intracranial pressure. These 5 patients had been treated as epilepsy for 6 months to 12 years. The other one patient had right sided motor weakness and left homonymous hemianopsia without seizure disorder. Plain roentgenograms of the skull revealed abnormal calcification in 3 out of 6 patients. Angiography showed an avascular mass in all 6 patients. CT scan were examined in 5 patients. In 3 patients the tumor were isodense, 2 of which demonstrated contrast enhancement. The other 2 showed low density lesion. One showed a single large cyst and another ill-defined low density containing high density calcification. In all 5 patients mass effect was slight. Three tumors were located in the temporal lobe and another 3 in the parietal lobe. At surgery total removal was accomplished in 3 patients. One patient had subtotal removal and 3 patients partial removal. Histological study revealed figures characteristic to the ganglioglioma. The predominant glial cell was astrocytic in 4 cases and oligodendroglial component was found in the other 2 cases. All patients either completely or nearly asymptomatic at the follow up for 1 to 12 years. The clinical study in 6 cases, along with a review of the literature suggest that these epileptogenic neoplasms should be aimed at surgical removal or total extirpation if possible.

A randomized clinical trial of adjuvant chemotherapy after resection in patients with stomach cancer.

A study group including 55 institutions in Japan evaluated the effect of adjuvant cyclophosphamide therapy on 461 patients who had undergone curative resection for stomach cancer. Patients, who were followed up for over three years, were randomly divided into three groups: curative resection and long-term drug therapy; curative resection and short-term drug therapy; and curative resection and no drug therapy. Long-term therapy consisted of (a) twice-weekly intravenous doses of 500 mg of cyclophosphamide for four weeks and, after five weeks with no medication, (b) 100 mg/day, given orally, for 40 days and, after ten weeks with no medication, (c) 100 mg/day, given orally, for 40 days. Short-term therapy consisted of only the first course of therapy (ie, twice-weekly intravenous doses of 500 mg for four weeks). The effect of cyclophosphamide differed, depending on the patients' levels of serosal and lymph node invasion: Short-term therapy was more effective in patients with lymph node involvement, and long-term therapy was more effective in patients with serosal involvement.

[Histographic analysis of computed tomography of cerebral hemispheric tumors].

The aim of this report is to assess the possibility of digital processing of computed tomography for histological diagnosis of brain tumors. For this purpose, percent histograms of x-ray attenuation value of lesions were analysed in 113 cases of histologically verified hemispheric tumors. Sixteen histograms obtained from normal brain parenchyma served as controls. Histograms were made from the same slices before and after contrast enhancement. The result were as follows; Histograms of benign tumors such as meningiomas and low grade astrocytomas characteristically showed similar pattern with normal subjects, whereas histographic patterns of the more malignant tumors such as malignant astrocytomas, metastases and glioblastomas were more heterogeneous with lower peak and wider curve. Displacement of the histogram to the higher density following contrast material administration was important clue in histographic analysis. The most prominent displacement was observed in meningiomas, followed by metastases with nodular type enhancement and malignant astrocytomas. Displacement in low grade astrocytomas and oligodendrogliomas was very slight and less than that of normal brain. Tumors showing ring enhancement such as glioblastomas and brain abscesses had wide histogram curve with twin peaks. Conclusively, it is possible to detect histological nature of cerebral tumors through CT scanning, using histographic analysis of the digital data.

[A case of arachnoid cyst associated with chronic subdural hematoma].

An 11-year-old boy was admitted to our clinic with complaint of headache. On admission he was in drowsy state and neurological examination revealed minimal motor weakness of the right hand. Plain skull roentgenogram demonstrated a thinning of the left temporal bone and elevation of the left sphenoidal wing. CT showed marked displacement of the midline structures from left to right. The left lateral ventricle was collapsed. A well circumscribed, homogenous, high density area was delineated in the left middle fossa. Contrast enhancement was negative. A-P view of left CAG showed a crescent shaped subdural avascular area in the parietal region. The anterior cerebral artery was roundly shifted from left to right. Chronic subdural hematoma due to bleeding of arachnoid cyst was most likely. Subdural collection was evacuated by trephination. The postoperative course was uneventful. Postoperative CT 3 week after operation delineated the arachnoid cyst more clearly as round low density area. Follow-up CT 6 months later showed the arachnoid cyst markedly reduced in size.

[Intracranial hematoma secondary to chronic DIC (author's transl)].

Five cases of intracranial hematoma secondary to chronic disseminated intravascular coagulation syndrome (DIC) were reported. Intracranial hematomas included a case of acute subdural hematoma combined with intracerebral hematoma and 4 cases of acute or subacute hematoma. Primary diseases which caused DIC were cancer; a case of carcinoma of choledochus and 4 cases of gastric carcinoma. All cases were in the advanced stage of carcinoma or at least, had metastasis to other organs. They showed coagulation disorders, such as, the reduction of platelets and the hemorrhagic diastasis, which were referred as chronic DIC, before the onset of intracranial hematoma. After the onset of intracranial hematoma, their coagulation disorders got worse and were diagnosed as acute DIC. They showed the rising of FDP, reduction of the serum fibrinogen and platelets and others. The blood transfusion and the trivial head injury were considered a triggers of exacervation from chronic DIC to acute DIC, that is, from compensated DIC to decompensated DIC. The long-term administration of anticancer drugs might play a part of the role as triggers. Initial symptoms of intracranial hematoma were headache in 4 case and dullness in a case. Three cases immediately lapsed into coma after 1 to 2 hours from the onset. Two cases turned out coma state after 4 to 5 days from the onset. Evacuations of hematoma were performed in 3 cases but they gave rise to rebleeding of intracranial hematomas later. All of 5 cases including surgically and non-surgically treated cases died at last. It is certain that DIC is rather common in the advanced stage of cancer. Matsuda reported that DIC existed in 20% of died patients with cancer. Though the incidence of intracranial hematoma secondary to DIC were less than that of cerebral infarct, it is no reasonable to assume that the actual number of the intracranial hematoma secondary to chronic DIC is rare.

[Head injury in children--with special reference to CT findings (author's transl)].

Findings of computerized tomography (CT) in 183 cases of head injury in children were investigated with special reference to CT findings of mild head injury. As was expected, CT findings of mild head injury fell within the normal range, in almost all cases. However, abnormal findings were noticed in 4 out of 34 cases (12%) in acute stage and 7 out of 76 cases (9%) in chronic stage. They were 3 cases of localized low density area in acute stage and 6 cases of mild cerebral atrophy in chronic stage, etc. There were some cases of mild head injury in which CT findings were normal while EEG examination revealed abnormality. Also in some cases, x-ray study demonstrated linear skull fracture which CT failed to show. These conventional techniques could be still remained as useful adjunct aid in diagnosis of head injury. CT findings of cases of cerebral contusion in their acute stage were divided as follows; normal, low density, small ventricle and ventricular and/or cisternal hemorrhage, frequency of incidence being 38, 17, 22, 11% respectively. These findings were invariably converted to cerebral atrophy from 10 days to 2 months after the impacts. In the cases with intracranial hematoma revealed by CT, only 32% of them showed clinical signs of Araki's type IV in their acute stage and 63% of them showed no neurological defects, that is Araki's type I & II. A case of extreme diffuse cerebral atrophy which followed acute subdural hematoma caused by tear of bridging veins without cortical contusion was presented.

[Computed tomography in the diagnosis of hemorrhage secondary to intracranial aneurysm. (author's transl)].

In 168 patients with ruptured intracranial aneurysms, the pathology of intracranial hemorrhage visualized on CT was analyzed. Blood in the subarachnoid space could be visualized in 95% of cases within three days after SAH and 75% of 106 cases within two weeks after SAH. In one case blood clot in the subarachnoid space visible up to 13 days after SAH. Concerning the cases within two weeks after the bleeding, intracerebral hematomas were observed in 36% of anterior cerebral aneurysms and middle cerebral aneurysms, 16% of internal carotid aneurysms and none of vetebro-basilar aneurysms. The incidence of the intraventricular hemorrhage was as follows; vertebro-basilar, 44%; anterior cerebral, 38%; internal carotid, 28%; middle cerebral, 12%. On the basis of the pattern of distribution of extravasated blood the location of the ruptured aneurysm was properly predicted in 58% of anterior cerebral, 81% of middle cerebral, 58% of internal carotid and 30% of vertebro-basilar. Especially CT could contribute to predict which aneurysm has ruptured in patients with multiple aneurysms. It was possible to localize the site of bleeding in 11 out of 12 CT positive cases. The development of intracranial hemorrhage demonstrated by CT well correlated with the clinical grading of the patients and the clinical outcome. Patients merely showing subarachnoid hemorrhage were more likely to have good neurological grades, but ones showing complicated intracerebral hematomas and intraventricular hemorrhage had poor neurological grades at the time of the scan. The findings of extensive subarachnoid clot, which were followed by severe vasospasm, and marked intraventricular hemorrhage, usually correlated with poor prognosis. These pathology recognizable on CT was very helpful in determination of the timing of surgery and management of such patients. In conclusion CT is of great value in the examination of SAH when performed in the acute stage and should be the initial examination followed by angiography.

[An attempt to numerical diagnosis by computed tomography (author's transl)].

In the previous report, the authors described a method obtaining numerical values of 'standard deviation (SD)' and deviation coefficient (DC) from printed out data of a brain CT slice picking up the basal ganglia. In the report, using these values, a possibility of numerical discrimination between normal and abnormal was also discussed. In the present investigation, it was attempted to apply admissible linear discriminant analysis to numerical diagnosis using SD value and DC value. From fifty normal scans and fifty abnormal ones of proved pathology, the admissible linear discriminant function, as below, was extracted, its misdiscriminant rate being 7.6% theroretically. S=-0.4248(SD)-6.4709 (DC) S larger than or equal to -11.447; normal, S < -11.447; abnormal. By this analysis, 98% of abnormal scans and 92% of normal scans were correctly judged without referring to analogue display and actual misdiscriminant rate was 5.0%. Furtermore, for the purpose of confirming reappearance of this result, another twenty normal scans and twenty abnormal scans were investigated by this method. Only one normal scan was judged uncorrectly and all abnormal scans were judged correctly. Accordingly misdiscriminant rate of this sample was 2.5%. It would be emphasized that this method was useful for screeing examination by CT, not only because the total discriminant rate was high, but also false negative rate was relatively low.

Quantitative investigation of the x-ray absorption coefficient in computed tomography. An approach to numerical diagnosis.

From printout data of 50 normal and 50 abnormal scans of a brain slice picking up the basal ganglia the numerical values of SD and DC were obtained and those values lying inside M + 2sigma were arbitrarily regarded as normal. By these criteria two cases (4%) were diagnosed as false negative and three cases (6%) as false positive, with a misdiagnosis rate of 5%.

[Two cases of nonketotic hyperosmolar coma in neurosurgery (author's transl)].

Hyperosmolar nonketotic coma is characterized by hyperglycemia, hyperosmolarity and dehydration in the absence of ketoacidosis. Two cases of hyperosmolar nonketotic coma, in which both the patients recovered, were presented. One of the cases was a 59-year-old female who had suffered from a metastatic brain tumor. After removal of the tumor, the patient's condition improved for a period. This was followed by a period of frequent vomiting, subsequently followed by coma. The laboratory data showed the absence of ketoacidosis in the blood sugar measured at 672 mg/dl and serum osmolarity at 343.1 mOsm./kg. The other case was a 74-year-old female who was admitted to the clinic because of cerebral thrombosis. Her caloric in-take was restricted and insulin was administered because of a mild diabetes mellitus which occured after admission. Then she entered a hyperosmolar non-ketotic coma. The laboratory data revealed blood sugar to be 1068 mg/dl and serum osmolarity to be 418 mOsm./kg. Immediately after large amounts of intravenous drip infusion and insulin were administerd, she recovered from the syndrome. The clinical observations and the pathogenesis of this syndrome were discussed.