Chronic subdural hematoma is a common disease. Occasionally, however, it is so puzzling to make a diagnosis clearly and immediately, that the delay of the manage ment may occur. So the purpose of this paper is to clarify the general picture of chronic subdural hematoma from a statistical analysis in 309 adult cases. Through this survey the role of trauma as the triggering factor is to be checked and the signs and symptoms will be summarized and divided into groups according to clinical features, which will make the diagnosis easy and useful to dissolve the pitfall. Pathophysiology and dy namics of the capsule of the hematoma are investigated in some cases, and the dys function of the liver is also inquired. Follow-up study was performed, which will con tribute to the selection of the operative method. Materials and Methods Statistical Analysis History of Trauma History of trauma preceeding the onset of the disease was noted in 276 cases (89%), in which were the traffic accidents 47%, ordinary life 35%, sport accidents 10 %, industry accidents 3 %, and so on (Table 1). In sport accidents 9 cases were

The case of a 52-year-old woman with acromegaly, diabetes insipidus, and visual impairment caused by a metastatic growth hormone-releasing hormone (GRH)-produced pancreatic tumor is reported. Serum growth hormone (GH) and somatomedin C levels were elevated to 14 ng/ml (normal < 5 ng/ml), and 3.20 U/ml (normal < 1.88 U/ml), respectively. Paradoxical increases were observed in GH levels after glucose tolerance and thyrotropin-releasing hormone-stimulation tests. Biopsy of a pituitary tumor observed on computerized tomography scans and magnetic resonance studies revealed a metastatic cancer. When circulating GRH levels were measured, a marked increase in plasma GRH (1145 pg/ml; normal < 4-1 pg/ml) was observed. The patient died of cachexia due to metastases. Postmortem examination revealed that a primary tumor, a malignant endocrine lesion, was present in the pancreas, with metastatic tumors in the pituitary, lung, liver, and adrenal glands. Synthesis and production of GRH by the tumor was demonstrated by Northern blotting and immunohistochemical analysis. The pituitary gland showed hyperplastic, but not adenomatous changes. The authors stress the importance of both exploration for an ectopic source of GRH and the search for a GH-producing pituitary adenoma when unusual signs and symptoms are seen in patients with acromegaly.

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To clarify the pathogenesis of delayed cerebral vasospasm after subarachnoid hemorrhage (SAH), the authors studied changes in lipid peroxides (measured as thiobarbituric acid reactive substances, TRS) and their scavenging enzyme, glutathione peroxidase (GPx), in the cerebrospinal fluid (CSF) and the serum of SAH patients and normal subjects. The CSF of the normal subjects was almost devoid of both TRS and GPx. A sudden increase in GPx activity in the CSF of SAH patients appeared to be due to the efflux of serum GPx to the subarachnoid space. GPx in the CSF decreased within 2-4 days after SAH, and in some cases the TRS content then became elevated and delayed vasospasm ensued. Following SAH, serum TRS increased, reaching a plateau 4-5 days after onset. GPx also increased 1 or 2 days later. The increase in serum TRS appeared to be a consequence of blood clotting within the subarachnoid space and may have stimulated GPx activity. The findings suggest that lipid peroxi des present in the CSF and the serum of SAH patients may be responsible for development of delayed vasospasm and that serum GPx might play an important role in controlling it.

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