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Biomedical subjects

S Uchigasaki

Publications and source records attributed to S Uchigasaki.

24 records · Page 2Linked to original sources

Two cases of giant serpentine aneurysm.

Giant serpentine aneurysm (GSA) is an entity defined on radiological and pathological grounds as a giant, partially thrombosed aneurysm containing tortuous vascular channels. We have had the opportunity to study two patients with GSAs, which has allowed for a complete comparative anatomical and radiological study. This report emphasizes the etiology of the GSAs. Twenty-two patients with GSAs have been reported in the literature, of which pathological studies were done in 10. In most of these, the aneurysm was found to be filled with an organized thrombus, but in our patients the aneurysm was filled with relatively new clot. The aneurysm enlarged and a change in the tortuous vascular channel was observed over a period of 1 year in the first patient, whereas a globoid aneurysm developed into a GSA in the brief period of just 2 weeks in the second patient. This rapid transformation of a globoid aneurysm into a GSA is of particular interest when the etiology of GSAs is considered. Our patients therefore shed some interesting light on the possible pathophysiology of GSAs. That is, the bloodstream may change dynamically in a giant aneurysm and may become a serpentine channel under conditions that lead to a "Coanda effect."

Adult↗

Normal pressure hydrocephalus. Neuropathological study.

The pathological changes in the brains of seven patients who had been clinically diagnosed as normal pressure hydrocephalus (NPH) are described and the possible etiological mechanisms are discussed. The pathological findings in all cases consisted of demyelination akin to Binswanger's type of encephalopathy, especially in the frontal lobes. Arteriosclerosis accompanied by occasional organized thrombi and scattered microinfarcts in the periventricular white matter were seen. Focal leptomeningeal fibrosis, diminution of arachnoidal granulations, and non-specific aging processes were noted. Among the above of particular interest, was the degeneration of both periventricular and deep white matters with microinfarcts, and moderate to severe arteriosclerosis. On the basis of these observations, we assume that the degeneration in the white matter is not merely a secondary change due to the result of enlargement of ventricle, but plays an important role in the development of NPH. The development of NPH requires not only the disturbance of cerebrospinal fluid, but also the pre- or coexisting vulnerability in the white matter caused by variables such as ischemia, hypoxia, and trauma.

Adolescent↗