Clinical pathology of primitive gliomas in the cerebrum

Summary To clarify the biological features of primitive gliomas in the cerebrum and clearly distinguish them from malignant or anaplastic gliomas and glioblastomas, we studied eight cases clinically and pathologically. Our evaluations included immunohistochemical and electron microscopic observations. We divided the patients into two groups, children and young adults. Most tumours appeared as ring-like, enhanced masses on computed tomography and avascular or ring-like, vascular masses on angiography. Macroscopically, the tumours were well demarcated and contained cysts. Ocassionally we found tumour dissemination. Microscopically, the tumours were composed of small, round cells without remarkable structural features. Ependymal, astroglial, and oligodendroglial differentiation was evident, in varying proportions; tumours in which the differentiated areas constituted more than half of the mass were classified as poorly differentiated gliomas. By these criteria, this series comprised four undifferentiated and four poorly differentiated gliomas. Cell anaplasia and polymorphism were rare in both undifferentiated and differentiated areas of the tumours. Immunohistochemical and electron microscopic examinations also revealed glial differentiation. These primitive gliomas appear to be biologically similar, but not identical, to cerebellar medulloblastomas. In this series, five patients died because of recurrence or dissemination. Whole brain and spinal irradiation should be considered after total or subtotal surgical removal.     

The study of a case of single coronary artery using stress 201thalium single photon emission computed tomogram

A 48-year-old female, who had been having episodes of chest discomfort and oppression lasting for several minutes for 15 years was diagnosed as having a single left coronary artery by coronary angiography. The electrocardiogram taken during a chest pain attack demonstrated the depression of the ST-segment in leads II, III, aVF, and V4-6. The chest pain was relieved, and the ischemic change in ECG was improved by sublingual nitroglycerine. 201Thalium single photon emission computed tomography under stress indicated poor uptake in both the anterior and infero-posterior myocardium, which was compatible with the change in ECG either during the attack or during exercise. The anterior myocardial ischemia was reduced by propranolol and the chest pain was successfully relieved by propranolol. The chest pain in this case might have partly been due to the myocardial ischemia in the anterior and infero-posterior myocardium, under stress, which could have been the steal phenomenon to lateral myocardium due to the anatomical anomaly, besides other possible mechanisms for chest pain proposed in the case of single coronary artery. Our findings suggested that 201Thalium stress single photon emission computed tomography is a useful method for detecting the myocardial ischemia in patients with single coronary artery and those suffering from chest pain without any coronary stenosis.     

Whole-body hyperthermia-induced renal atrophy of mice as evinced by obstruction and degeneration of renal tubules caused by acute ischemia

Effects of microwave-induced whole-body hyperthermia (WBH) on the mouse kidney were examined histologically for acute and late effects up to 150 days after WBH treatment at 43.5 degrees C (rectal temperature) for 20 min or 42 degrees C for 40 min. As a whole the damage could be divided into two types. One was the damage to distorted epithelial cells in the subcapsular region. This lesion was common in most animals, possibly caused by direct hyperthermic effect of microwave. The other was general renal atrophy accompanied with aqueous or protein-rich cysts due to a chain of physiological reactions of the whole body to WBH. The first reaction was characterized by general stasis of the blood stream in all parts of the kidney, which resulted in acute ischemia of some tissues. This was seen immediately by dilatation of the renal and interlobular veins as well as the bundles of capillaries in the medulla region. The subsequent event was rather specific cell necrosis of distal and collecting tubular epithelium as compared to proximal tubules. The cell destruction induced cell proliferation of the proximal tubular epithelia after two days. Later on, in accord with the recovery of the blood circulation, the proliferated cells were carried away into the lumen, these processes then resulting in obstruction of tubules through formation of protein casts in the lumen. The block incidentally led to the destruction of nephrons. The degenerated area sometimes consisted of aqueous or protein-rich cysts of various sizes after 7 to 30 days. Thereafter these cysts degenerated, decreasing in both number and size. Thus irreversible atrophy of the kidney developed after WBH.     

Modulation of glial cell signaling by adenosine and pharmacological reinforcement

In view of the increasing evidence that a pathological glial activation plays a significant role in the development of neurodegenerative diseases, we investigated the underlying molecular signaling as a possible target for a pharmacological therapy. Here, we are particularly focusing on the endogenous modulation of the Ca²⁺ and cyclic nucleotide-dependent signaling by the nucleoside adenosine and its reinforcement by the xanthine derivative propentofylline (PPF). As an experimental model, we used cultured rat microglial cells and astrocytes that are immature, show a high proliferation rate, and resemble in several aspects pathologically activated glial cells. A prolonged increase of the cellular cAMP level favored the differentiation of cultured astrocytes and associated properties required for the physiological nerve cell function. On the other hand, a strengthening of the cyclic nucleotide-dependent signaling inhibited potentially neurotoxic properties of cultured microglial cells. Similar effects were obtained by treatment with propentofylline, which mimicked modulatory adenosine effects and increased the intracellular level of cAMP and cGMP. Such a pharmacological glial cell conditioning, obtained by modifying the strength and the timing of these second messengers, may provide a therapy of neurodegenerative diseases in which a pathological activation of microglial cells and astrocytes is discussed to play a pathogenic role.     

Conditions of Alzheimer-type dementia in the old-old and oldest-old patients with special reference to extreme conditions of brain aging

A neuropathological study on 1540 consecutive autopsy brains ranging from 60 to 107 years of age revealed the following points. (1) Of the of the demented cases of the plaque-predominant type, 93% were complicated with multiple tiny cortical infarcts. They showed a tendency for dementia to develop before or after the appearance or worsening of a systemic disorder such as cardiovascular disease, respiratory infection and cancer. However, there was no case showing Alzheimer-type dementia (ATD). (2) The plaque-predominant type might be an extreme condition of brain aging in terms of senile plaques (SP). It is likely that although the pathological appearance of SP alone is not responsible for dementia, its coexistence with multiple cortical infarcts could be the cause of dementia. Therefore, this type should be distinguished from ATD. (3) Primary hippocampal degeneration could also be an extreme condition of brain aging in terms of neurofibrillary tangles. This condition was different pathologically from the hippocampal lesion in ATD. (4) Several characteristics of old-old and oldest-old patients were clarified.     

Effects of calcium in continuous cardioplegia on myocardial protection

The effects of calcium (Ca) on a hyperkalemic cardioplegic solution for continuous cardioplegia were examined in an isolated perfused working rat heart model. The coronary arteries were perfused with a modified Krebs-Henseleit bicarbonate buffer (K-H) solution, containing various concentrations of Ca(0.1, 0.6, 1.2, and 2.5 mmol/l) and a high concentration of potassium (20 mmol/l), for 180 min, after which cardiac arrest was induced at 37°C for 180 min. Cardiac function and creatine kinase (CK) were measured. In the control group, K-H solution was infused in place of the cardioplegic solution, and cardiac arrest was not induced. No significant differences were observed between the groups infused with the K-H solution containing Ca concentrations of 0.6, 1.2, and 2.5 mmol/l in the percent recovery of aortic flow (82.1±2.9%, 80.6±2.0%, and 71.5±3.7% (mean±SEM) respectively) or in the recovery of other indices of cardiac function, or in CK leakage. There were also no significant differences in the recovery of cardiac function and CK leakage between these groups and the control group. In the Ca 0.1 mmol/l group, however, the characteristic Ca paradox was observed. These findings suggest that if the Ca concentration in a cardioplegic solution is higher than 0.6 mmol/l during continuous cardioplegia, excellent cardioprotective effects will be achieved.     

Biliary cystadenoma with mesenchymal stroma of the liver: Correlation between unusual MR appearance and pathologic findings

We reported a case of the biliary cystadenoma of the liver. The cystic mass had labulation and septation and showed marked hyperintensity on T1-weighted images and hypointensity on T2-weighted images; MR findings were very unusual for cystadenoma. The content of the cystic mass was jelly-like, thick mucinous fluid without intracystic hemorrhage. We concluded that these unusual signal intensities of the cyst were due to hyperproteinous mucinous fluid.     

A case of Raeder's syndrome caused by metastatic malignant lymphoma

A case of Raeder's syndrome caused by metastatic malignant lymphoma was reported. The patient was 67-year-old male. He had complained of diplopia, ptosis and frontal headache at the left side. Neurological examinations revealed left incomplete Horner's syndrome (miosis and ptosis, but normal facial sweating) and left abducens palsy, which was considered to be Raeder's syndrome Group 1 (Boniuk and Schlazinger's classification). CT scan, MRI and angiography demonstrated a mass lesion in the left cavernous sinus extending to the sphenoparietal sinus, and a mass lesion in the anterior part of the superior sagittal sinus. During his hospitalization, enlargement of the left cervical lymph nodes was noticed. "Malignant lymphoma (non-Hodgkin)" was diagnosed on the basis of biopsy. Group 1 of Raeder's syndrome is rare, but it is important to define the site of lesion, which is located around the paratrigeminal region at the middle cranial fossa. Because these lesions are very small and metastatic in many cases, various neuroradiological investigations, especially MRI, are necessary for early diagnosis and early treatment.