This report provides findings of an investigation of the influence of traumatic subarachnoid hemorrhage on the development of delayed cerebral ischemia caused by vasospasm. The authors prospectively studied 130 patients with closed-head trauma, who exhibited subarachnoid blood on admission computerized tomography (CT) scans. Ten (7.7%) of these patients developed delayed ischemic symptoms between Days 4 and 16 after the head injury. They consisted of three (3.0%) of 101 patients with small amounts of subarachnoid blood and seven (24.1%) of 29 patients with massive quantities of subarachnoid blood on admission CT scans. In each of the 10 patients, severe vasospasm was demonstrated by angiography performed soon after development of ischemic symptoms. There was a close correlation between the main site of the subarachnoid blood and the location of severe vasospasm. In seven of the patients, follow-up CT scans showed development of focal ischemic areas in the cerebral territories corresponding to the vasospastic arteries. These results demonstrate that traumatic subarachnoid hemorrhage, especially if massive, is a predictable indicator of delayed ischemic symptoms.

The present study is a chronological morphological examination on the effects of collagen gel matrix on regeneration of severed sciatic nerves. The nerves (5 mm length) were resected, and both the distal and proximal stumps were inserted into a silicone tube with 5 mm gap in between. In the test side, the gap in the tube was then injected with liquid collagen which gells in the tissue when reconstructed with a certain buffer solution. The gap space in the tube of the control side was left empty. In a chronological examination of the tissue in the tube, considerably more rapid growth of sprouting axons toward the distal stump in the test side was revealed in comparison with the control side. The cells, including both fibroblasts and larger Schwann cells, were less in number. More orderly directions were observed in the collagen matrix than in the control tube. The result indicates that regeneration of the peripheral nerves in the silicone tube can be improved, by using appropriate exogenous fine materials, collagen matrix.

Manganese-containing superoxide dismutase (Mn-SOD) content and its immunohistochemical localization in human thyroid tumours and some other thyroid diseases were examined and compared with adjacent normal thyroid tissue. Enzyme-linked immunosorbent assay (ELISA) was used in this study for the measurement of Mn-SOD. The content of Mn-SOD tended to increase in diffuse hyperplasia, adenomatous goitre, and follicular adenoma. In papillary carcinoma, it was significantly higher than in adjacent normal thyroid tissue. Follicular carcinoma also revealed a markedly high Mn-SOD content. In the immunohistochemical study, adjacent normal thyroid tissue showed granular positive staining of Mn-SOD in the cytoplasm. An increase of Mn-SOD was observed in the papillary proliferative lesion of diffuse hyperplasia and in the follicles adjacent to lymphoid tissue in chronic thyroiditis with hypothyroidism. Strong positive staining of Mn-SOD was observed in papillary and follicular carcinomas, whereas in anaplastic carcinoma staining was markedly less intense. These results indicate that the Mn-SOD content varies according to the degree of differentiation of thyroid carcinomas.

Ultrastructural damage leading to delayed neuronal death was investigated in the mid-CA1 region of the hippocampus from the stratum (str.) moleculare to oriens after transient bilateral forebrain ischemia in Mongolian gerbils. After ischemia for 5 min without recirculation, mild swelling of the peripheral part of the apical and basal dendrites was already apparent in the str. moleculare and str. oriens. Mitochondria in the dendrites were also swollen in the same area. During recirculation for 12 h to 3 days, swelling of the dendritic cytoplasm persisted with formation of microvacuoles, but swelling of mitochondria receded. Microvacuolation and loss of microtubules were also observed in the proximal part of the dendrites during this period, and swelling and disruption of internal cristae were observed in mitochondria after recirculation for 3 days. The dendrites became severely degenerated after recirculation for 4 days. In the pyramidal cell bodies, no abnormality was observed at the end of ischemia for 5 min, but disaggregation of polyribosomes and swelling of the endoplasmic reticulum were observed 12 h after recirculation. Proliferation of the endoplasmic reticulum in parallel arrays occurred after recirculation for 1 day and persisted. Severe degeneration of the pyramidal cell bodies was obvious after recirculation for 4 days. The findings observed in the present investigation suggested that the neuronal structure most vulnerable to ischemia was the peripheral part of the dendrites and postischemic neuronal damage occurred early in this part of the dendrites.

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