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Tetsumori Yamashima and Shinjiro Yamamoto

✓ Pathological changes of the cerebral arteries were studied in 30 dogs after subarachnoid injections of saline, fresh autologous blood, epinephrine, blood plus epinephrine, norepinephrine, or blood plus norepinephrine. Macroscopically, the circle of Willis was maximally dilated after the injection of epinephrine and was constricted following administration of blood plus epinephrine. Microscopically, neither saline nor blood produced abnormalities, except for minor changes of the adventitia in the latter. Epinephrine produced frank necrosis of smooth-muscle cells, which was subsequently replaced by fibrosis in the media of larger subarachnoid arteries, and the leakage of necrotic material from the infarcted hypothalamus contributed to these lesions. Blood plus epinephrine produced marked changes in the internal elastic lamina and tortuosities of the nuclei of smooth-muscle cells, while norepinephrine and blood plus norepinephrine produced only minor changes.

Previously reported findings of morphological changes due to vasospasm after subarachnoid hemorrhage were confirmed experimentally, but such changes were found only after application of epinephrine. It is suggested that epinephrine produced the most severe vasospasm among the five substances tested.

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Minoru Hayashi, Hidenori Kobayashi, Hiroyuki Fujii and Shinjiro Yamamoto

✓ The size of the ventricular system and cerebrospinal fluid (CSF) flow were determined in 17 patients with plateau waves, using computerized tomography (CT) and isotope cisternography. Some patients had increased intracranial pressure (ICP) resulting from space-occupying lesions and other causes, and some had normal ICP observed in normal-pressure hydrocephalus. The size and shape of the ventricular system during plateau wave phases as ascertained by CT showed little or no change as compared with its size and shape during the interval phases between two waves. It was also noticed that, in patients with supratentorial masses, the midline shift showed no difference in degree between the two phases. These findings suggest that there is little change in the intracranial CSF volume between the two phases, that is, there is little compensatory outflow of the intracranial CSF for the ICP variations. These results may also support the assumption that the plateau waves are not caused by an intermittent obstruction of the CSF pathways. Isotope cisternography showed a marked delay of clearance of radioactivity from the intracranial CSF in 15 patients. The cisternographic pattern in patients with increased ICP and the absence of ventricular dilatation demonstrated an abnormally large accumulation of radioactivity over the cerebral convexities, and the pattern in patients with normal-pressure hydrocephalus showed complete obstruction of the subarachnoid space over both cerebral convexities. These observations suggest that, in patients with plateau waves, there is a marked delay in CSF absorption. The authors postulate that the reduction of CSF absorption may create a critically tight condition within the cranial cavity and act as a contributory factor in the development of the plateau waves.

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Kiyonobu Ikeda, Toshihiko Kubota, Kengo Kashihara and Shinjiro Yamamoto

✓ Intraoperative monitoring of anorectal pressure was used in a case of sacral lipomeningocele accompanied by congenital dermal sinus to protect the physiological function of the anorectal sphincters. This monitoring system consists of a manometric anorectal balloon and neural electrical stimulation. The system was able to differentiate functioning neural structures from surrounding tissues during the operation.

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Tetsumori Yamashima, Toshihiko Kubota and Shinjiro Yamamoto

✓ A previously unrecognized role of eosinophils in chronic subdural hematomas is described. Outer membranes of hematomas with marked infiltration by eosinophils were studied ultrastructurally with particular attention to the degranulation of these cells. In all of the five cases studied, degranulation was observed. Disintegration of the cells contributed to the release of granules. The free granules, the matrix of which has been demonstrated to contain plasminogen, were often circulating in the vascular lumen and trapped among the aggregated platelets. They were also found within the fragile vascular wall surrounded by fibrinoid material and in the edematous perivascular interstitium. Some of the perivascular eosinophils showed frank solubilization of granule matrix contents in spite of unaltered crystalloids. These findings suggest a role of eosinophils in the development of local hyperfibrinolysis within the outer membranes, which might contribute to the fluidity of chronic subdural hematomas and the resultant leakage of blood from the vessels in the capsules.

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Tetsumori Yamashima, Shinjiro Yamamoto and Reinhard L. Friede

✓ The structure of macrocapillaries (also called “sinusoids”) in the outer membrane of chronic subdural hematomas was investigated by electron microscopy, with particular attention paid to vascular permeability. One characteristic of macrocapillaries is the frequent formation of gap junctions between adjacent endothelial cells. In endothelial gap junctions 0.6 to 8 µm in diameter, numerous blood components, including red blood cells and plasma, can be seen squeezing or spilling into the interstitial space of the outer membrane. Irregularly deformed erythrocytes are located around the macrocapillaries, and amorphous material is seen among scattered thin collagen fibers. It is suggested that endothelial gap junctions of macrocapillaries play an important role in the leakage of blood, causing enlargement of chronic subdural hematomas.

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Toshihiko Kubota, Kazufumi Sato, Shinjiro Yamamoto and Asao Hirano

✓ The fine structure of psammoma bodies was examined in four cases of fibroblastic meningioma. In general, large numbers of various-sized calcified bodies (psammoma bodies) were scattered among the interstitial fibers. In these bodies, the smallest calcific site was found in the extracellular membrane-bound matrix vesicles, which measured approximately 0.1 to 0.2 µ in diameter. In addition, extracellular “matrix giant bodies,” with or without hydroxyapatite aggregates and measuring up to 3 µ in diameter, were frequently encountered. These bodies were apparently invested with single, double, or multiple concentric walls averaging nearly 0.1 µ thick. They presumably originated from the neoplastic cells as a consequence of cytoplasmic residuals associated with cellular degeneration or necrotic cell processes. Hydroxyapatite crystals precipitated repeatedly within the bodies. The precipitate may gradually aggregate within the bodies, and gather in clusters, resulting in a large psammoma body. Finally, collagen fibers around the calcified giant bodies accrued deposits of apatite crystals to make a huge psammoma body. These findings suggest that both matrix giant bodies and matrix vesicles may serve as initial nidus of calcification of psammoma bodies in fibroblastic meningioma. Consequently, this mineralization process may represent a certain dystrophic calcification of meningocytic cells.

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Haruhide Ito, Toshio Komai and Shinjiro Yamamoto

✓ Active plasmin, available plasmin, and total plasminogen were measured by Enzodiffusion fibrin plate techniques in 11 cases and level of tissue activator and tissue fibrinolytic activities in another 11 cases with chronic subdural hematoma. The values were too small to be measured in some instances. Anti-plasmin in the hematoma was less than in the blood plasma. The outer membrane contained about three times more tissue activator than the dura mater, although the inner membrane contained none. Increased tissue activator, which exudes from the extremely vascular outer membrane, transforms plasminogen into plasmin in subdural hematoma, so that plasmin breaks down fibrin and fibrinogen and induces continuous hemorrhage.

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Shinya Kida, Tetsumori Yamashima, Toshihiko Kubota, Haruhide Ito and Shinjiro Yamamoto

✓ The structure of human arachnoid villi was investigated by light and electron microscopy with the aid of immunohistochemical techniques. The human arachnoid villi examined were basically composed of four portions: a fibrous capsule, an arachnoid cell layer, a cap cell cluster, and a central core. The arachnoid cell layer encompassing the central core was mostly covered by the thin fibrous capsule with an endothelial investment. However, the fibrous capsule was often absent at the apical portion of the villus and a factor VIII-related antigen stain failed to confirm the investment of endothelial cells. Instead, the arachnoid cell layer abutted directly upon the lumen of a lateral lacuna or the sinus. The arachnoid cell layer was thickened in places, forming cap cell clusters; it usually consisted of outer and inner zones. On vimentin staining, the former was slightly positive while the latter was strongly positive. The central core contained a network of arachnoid cells intermingled with connective tissue fibers and was in continuity with the cranial subarachnoid space. Electron microscopy showed that the arachnoid cells contained a larger number of intermediate filaments in the inner zone than the outer zone. Ultrastructural immunohistochemical localization showed that vimentin was localized at the intermediate filaments and desmosomal plaques of the arachnoid cells. The arachnoid cells showed a marked variety in both the cell forms and the number of intermediate filaments or desmosomes, depending on their location.

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Takeshi Hasegawa, Haruhide Ito, Shinjiro Yamamoto, Katsuhiko Haba and Hideaki Murata

✓ The authors describe a case of atypical unilateral prominent hyperostosis frontalis interna in a 50-year-old Japanese woman with psychiatric symptoms. Radiological, computerized tomographic, operative, and histological findings of this rare case are presented.

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Minoru Hayashi, Hidenori Kobayashi, Hirokazu Kawano, Shinjiro Yamamoto and Toshio Maeda

✓ Cerebral blood flow (CBF) was measured, the intracranial pressure (ICP) was continuously recorded, and the ventricular system size was evaluated on serial computerized tomography scans in 43 patients. These patients all had communicating hydrocephalus after subarachnoid hemorrhage (SAH) from rupture of an intracranial aneurysm. The studies were carried out both in the acute stage (within 7 days after SAH) and in the communicating hydrocephalus stage. In patients in the acute stage who had no ventricular dilatation, but who later developed communicating hydrocephalus, the mean CBF was reduced; lower CBF was associated with poorer clinical grades and a higher resting pressure range. Communicating hydrocephalus produced a significant decrease in CBF. The ICP tracing showed continuing plateau waves in conjunction with B-waves in patients in whom recordings were begun within 63 days after SAH. In general, patients with more dilated ventricular systems, with less frequent ICP irregularities, and with lower resting pressure ranges had a more marked decrease in CBF. A significant decrease in CBF was also found in patients with diffuse vasospasm in comparison to those without vasospasm. Patients with communicating hydrocephalus in whom ICP recordings were started more than 6 months after SAH showed no ICP irregularities. In these patients, a mean CBF of less than 25 ml/100 gm/min and a markedly low resting pressure range were observed. Shunting procedures were never effective in any of these patients. The results suggest that, in patients with communicating hydrocephalus, a mean CBF below this level may cause irreversible damage to the brain tissue in the terminal stage, and may inhibit the cerebral vasomotor reaction that participates in the development of ICP irregularities.