Norio Takeda

Magnetic resonance imaging and histopathology of cerebral gliomas.

SummaryThe correlation of magnetic resonance imaging (MRI) with histopathological findings was analysed in 26 patients with untreated cerebral gliomas. In low-grade gliomas, T2-weighted images demonstrated relatively homogeneous high-intensity lesions involving both the grey and the white matter. In high-grade gliomas, especially grade IV, T2-weighted images demonstrated prominent heterogeneity in signal intensity, which consisted of a hyperintense “core”, less hyperintense or normal intensity “rim” and surrounding finger-like areas of high intensity. Marked and irregular contrast enhancement was evident in all but one case of these high-grade gliomas in which gadolinium-DTPA was used. Histological examination revealed tumour cells extending as far as the borders of the high-intensity areas shown on T2-weighted images in both high-and low-grade gliomas, but in 5 of 8 low-grade and 4 of 18 high-grade gliomas, isolated tumour cells extended beyond the hyperintense areas shown on T2-weighted images.

Cerebral glioblastoma with cerebrospinal fluid dissemination: a clinicopathological study of 14 cases examined by complete autopsy

During the last 17 years, complete autopsies were performed on 51 patients who died of cerebral glioblastoma, and 14 were found to have dissemination by cerebrospinal fluid (CSF). In these 14 cases of glioma, the extent of intraparenchymal invasion by the primary tumor and the degree of seeding were studied in connection with histological findings and immunohistochemical staining for glial fibrillary acidic protein (GFAP) as the most reliable marker of astrocytic differentiation. From the findings obtained, the cases were divided into two groups. In one group, consisting of 7 gliomas, autopsy revealed intense seeding, despite only slight invasion by the primary tumor. Among these 7 extensively disseminated gliomas, 4 expressed almost no GFAP, 2 contained only a few GFAP-positive cells, and only 1 displayed an immunohistochemically high degree of astrocytic differentiation. Clinically, 6 of the 7 affected patients developed symptoms attributable to CSF seeding. In the other group consisting of the remaining 7 gliomas, only slight dissemination was seen, despite extensive infiltration of the primary tumor. Each of these 7 gliomas contained many GFAP-positive cells. None of the affected patients developed symptomatic seeding. This study shows the existence of two clinicopathologically distinct groups of disseminated cerebral glioblastomas and suggests that, regardless of morphological features, glioblastomas showing immunohistochemically poor astrocytic differentiation tend to shed tumor cells more vigorously but are less invasive at the primary site than those with many GFAP-positive cells. It is also suggested that, as a consequence, the former glioma type produces symptomatic seeding more frequently than the latter type.

Correlation of computed tomography with the histopathology of primary malignant lymphoma of the brain

SummaryThe authors present seven autopsy cases of non-AIDS primary malignant lymphoma of the central nervous system to correlate the pathology with the findings of the most recent pre-mortem computed tomogram (CT). Of 10 primary contrast-enhancing (CE) lesions treated by chemotherapy alone, radiotherapy alone, radiochemotherapy, or surgery combined with radiochemotherapy, all but one completely disappeared after the initial course of therapy. However, in six of the seven patients, the final pre-mortem CT demonstrated CE lesions. In three cases CE lesions were at the same site as the primary lesion, in one case in a remote location, and in two cases in diffuse and multiple locations. In all but one case these CE lesions corresponded histologically to tumor nodules or to white matter densely infiltrated by tumor cells. The sole exception was diagnosed pathologically as delayed radiation necrosis. The final CT also showed five low-density areas (LDAs) which had evolved from CE lesions after the completion of therapy. These LDAs corresponded to rarefied or necrotic parenchyma in which tumor cells remained, mainly in the perivascular spaces. One case exhibited diffuse tumor infiltration of periventricular structures which appeared to have normal density and no CE on the final pre-mortem CT.

Correlation of MRI and clinical features in meningeal carcinomatosis.

Ten patients with meningeal carcinomatosis associated with nonhaemoatological neoplasms were examined: six with breast, two with gastrointestinal and one with lung cancer, plus one with a tumour of unknown origin. Cytology was positive in all but one. The patients were classified into four groups according to the gadolinium-enhanced MRI (Gd-MRI) appearances: group 1 had pure leptomeningeal carcinomatosis, group 2 dural carcinomatosis, group 3 spinal leptomeningeal carcinomatosis, and group 4 had normal Gd-MRI except for hydrocephalus. In group 1, Gd-MRI showed diffuse enhancement of the subarachnoid space, including the cisterns around the midbrain, the sylvian fissures, or cerebellaar and cerebral sulci. In group 2, Gd-MRI showed diffuse, thick, partially nodular enhancement of the duramater. No leptomeningeal or subependymal enhancement was evident. In group 3, nodular masses were seen only in the spinal canal. In group 4, no definite evidence of meningeal carcinomatosis was demonstrated on contrast-enhanced CT (CE-CT) or Gd-MRI. The median suvival time was 2.0 months in group 1, 1.0 month in group 3, and 4.5 months in group 4, but the two patients in group 2 were alive 10 and 15 months after a definite diagnosis of meningeal carcinomatosis was made. In all patients examined by both CE-CT and Gd-MRI, the latter was superior for identification of meningeal carcinomatosis. Hydrocephalus in an important indirect sign of leptomeningeal carcinomatosis, but was not seen in patients with dural carcinomatosis despite the presence of increased intracranial pressure.

Anomalous origin of the anterior inferior cerebellar arteries from the internal carotid artery

SummaryTwo cases of the anterior inferior cerebellar arteries originating from the cavernous and precavernous segments of the internal carotid artery are reported. In one case the course of the anomalous artery was confirmed by autopsy. This anomalous artery is considered to be a variant of persistent primitive trigeminal artery. The clinical significance is discussed briefly.

Neuroendocrine markers in central nervous system neuronal tumors (gangliocytoma and ganglioglioma)

SummaryWe studied five cases of central nervous system neuronal tumor, one gangliocytoma and four gangliogliomas, both ultrastructurally and immuno-histochemically, using antibodies to neuroendocrine markers including tyrosine hydroxylase (TH), serotonin (5HT), somatostatin (SOM), met-enkephalin (MEK), leu-enkephalin (LEK), substance P (SP), gastrin, vasopressin, oxytocin, vasoactive intestinal polypeptide, adrenocorticotropic hormone and calcitonin. In all cases, the presence of dense-core vesicles (60–250 nm) in the neuronal elements was the characteristic ultrastructural finding. Synapses were observed in two cases. Immunohistochemically, variable numbers of neuronal cells showed positive staining for SOM in five cases, TH, MEK and LEK in three cases, and 5HT and SP in one case each. The others were negative. Positive immunoreactivity for multiple markers was shown in all cases. SOM, TH, 5HT and SP were present in the small- to medium-sized cells, while MEK and LEK were almost exclusively confined to the large cells. Our study clearly indicated that these tumors contained neuronal cells which were not homogeneous with regard to neuroendocrine markers.

Symptomatic cerebrospinal fluid dissemination of cerebral glioblastoma

SummaryComputed tomography (CT) findings in eleven patients with symptomatic cerebrospinal fluid (CSF) dissemination from cerebral glioblastoma were analyzed and, in seven cases subsequently autopsied, they were compared with histological observations. Each patient had multiple CT abnormalities including periventricular enhancement (5/11), subarachnoid enhancement (10/11) and progressive hydrocephalus (7/9) by cranial CT, and small filling defects with or without block (5/5) by CT myelography. The areas that showed periventricular or subarachnoid enhancement on CT were confirmed to have macroscopically detectable seeding at autopsy. On the other hand, microscopic deposits were more widely distributed than the enhancement suggested, and were hardly visualized on CT. In association with subarachnoid seeding, we found low-density lesions on CT which had resulted from ischemia or reinvasion of adjacent structures by disseminated glioblastoma and resulting parenchymal edema. By cranial CT, subarachnoid enhancement seems to be a very reliable sign of CSF seeding, whereas periventricular enhancement due to CSF metastases should be carefully distinguished from that due to periventricular tumor infiltration. CT myelography is capable of revealing minute metastatic spinal deposits and may be helpful for ruling out spinal seeding as well as its precise evaluation.

Spinal Metastases of Cerebral Glioblastoma: The Value of Computed Tomographic Metrizamide Myelography in the Diagnosis

Spinal metastases from cerebral glioblastoma via the cerebrospinal pathway are rarely detected when the primary tumors are under apparent control. The authors report two adult patients with cerebral glioblastoma who developed spinal symptoms referable to spinal seeding without neurological and computed tomographic findings of the recurrence of the primary tumors. Computed tomographic metrizamide myelography clearly revealed minute deposits of perispinal metastatic tumors that could not be detected by conventional myelography. Even perispinal mass lesions so minute that they are revealed only by computed tomographic metrizamide myelography can invade the spinal cord and cause clinical symptoms.

Correlation of DNA ploidy and morphological features of human glioma cell cultures with the establishment of cell lines

SummaryEleven gliomas were serially cultivated and examined for DNA distribution by flow cytometry and simultaneously for morphological features by light microscopy at the various passage levels until passage 50 at most. Seven gliomas (four low-grade gliomas, three anaplastic gliomas) showed a similar DNA distribution pattern with a main diploid and small tetraploid peaks at various passages. In this group, only one culture formed a permanent cell line, whereas six cultures showed a limited growth ranging from 6 to 24 passages. In contrast, the other four gliomas (each an anaplastic glioma) showed a marked change of DNA distribution through passages and finally a single DNA aneuploid population prospered. Each of these four gliomas yielded established cell lines. Thus, it is suggested that the change of DNA ploidy and prosperity of DNA aneuploid populations in flow cytometry might be used as early and reliable indices for the later establishment of glioma-derived permanent cell lines. Since the changes of DNA distribution are frequently associated with the morphological changes, as seen in the latter group, careful tracing of morphological features is valuable in determining of the fate of cultures, especially in the absence of a flow cytometer. The correlation between the potential to become established cell lines and histology of the original gliomas is also discussed.

Haemodynamic Evaluation of Cerebral Gliomas Using XeCT

Summary The purpose of this study was to characterize regional blood flow (BF) in untreated cerebral gliomas (CG) using stable Xe-enhanced computed tomography (XeCT). XeCT of 38 patients with untreated CG were analyzed and compared with CT and magnetic resonance images (MRI) and histopathological findings. Individual averaged BF values for tumour in 29 high grade gliomas (HGGs) and 9 low grade gliomas (LGGs) were intermediate between averaged BF values for cortex and white matter in the non-tumour bearing hemisphere. All averaged BF values for cyst and central necrosis were very low. In 27 HGGs, BF in tumour was relatively high in ring-enhancement lesions on CT and MRI, but was low even in viable tumour centers showing no contrast enhancement. In the other 2 HGGs, BF was low in tumour center and relatively high in tumour periphery regardless of homogeneous enhancement. In 5 HGGs, averaged BF value of the cortex outside surrounding oedema was higher than that of cortex in the non-tumour bearing hemisphere. In LGGs, BF distribution in tumour was homogeneously low in 3 small-sized and heterogeneous in 6 large-sized lesions including moderately high and low BF regions. These differences in BF pattern between HGGs and LGGs on XeCT might be helpful in considering to some extent the histopathology of untreated cerebral glioma pre-operatively.