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Biomedical subjects

S Wakai

Publications and source records attributed to S Wakai.

At least 163 records · Page 9Linked to original sources
PubMed1984

Congenital brain tumors.

Two cases of congenital brain tumor present at birth are reported. One patient was a baby girl with a huge teratoma measuring 8 X 6 X 5 cm; she died on her fourth day of life. The other patient had a large cystic astrocytoma, which was successfully removed; the patient is alive and in good health at 2 years of age and has no sign of recurrence of the tumor. Each baby had a large head, which caused dystocia at delivery. In addition to these two cases, we reviewed 200 cases of brain tumors reported in the literature presenting or producing symptoms or found incidentally at autopsy within 2 months after birth. We analyzed these cases in terms of initial symptoms and signs, sex distribution, histologic types and sites of tumors, prognosis, associated anomalies, familial occurrence, and hemorrhage from the tumor. The results of these analyses are described in detail, and the etiology of neonatal brain tumors is discussed.

Astrocytoma↗
PubMed1984

Rare combination of spinal lesions and spina bifida occulta: case report.

An infant presented with spina bifida occulta and a rare combination of spinal lesions, consisting of fibrous band with skin tag, lipoma, congenital dermal sinus and arachnoid cyst. The literature concerning the arachnoid cyst in occult spinal dysraphism is reviewed and the embryogenesis of these lesions is discussed.

Arachnoid↗
PubMed1984

Ventricular diverticulum.

A ventricular diverticulum was found on computed tomography in six out of 25 cases of congenital obstructive hydrocephalus. In all six cases, the diverticulum was located on the medial wall of the trigone. In three cases, it was restricted to the tentorial hiatus with a recognisable superior cerebellar cistern (small). In two cases, it occupied the tentorial hiatus without a recognisable cistern (medium). The remaining case had a diverticulum extending into the posterior fossa that caused cerebellar ataxia (large). In all patients, the diverticulum regressed after ventriculo-peritoneal shunt. The characteristics of the computed tomograms, the clinical significance and the pathogenesis of this phenomenon are discussed.

Brain Diseases↗
PubMed1984

Hemangioblastoma presenting with intraparenchymatous hemorrhage.

The authors report six cases of hemangioblastoma presenting with apoplectic symptoms but with no history related to the tumor. In each case, computerized tomography disclosed an intraparenchymatous hemorrhage, which was located supratentorially in four and in the cerebellum in the remaining two. Angiography revealed an abnormal vascular blush in two cases, but no abnormal vessels or tumor blush in the other four. In all cases, a solid tumor with abnormal vessels, such as red veins and feeding arteries, was found within or adjacent to the hemorrhage at surgery. The possibility of hemangioblastoma should be kept in mind as a cause of intraparenchymatous hemorrhage, particularly subcortical. Evacuation of the hematoma should be carefully carried out, and the whole hematoma wall should be thoroughly investigated for abnormal vessels or a solid mass.

Adult↗
PubMed1983

Spontaneous regression of a cerebral arteriovenous malformation. Report of a case and review of the literature.

A cerebral arteriovenous malformation (AVM) spontaneously and completely disappeared on subsequent angiography. Computed tomography revealed a very similar picture to that of angiographically occult AVM, which was histologically thrombotic. Reviewing the literature, we suggest that in many cases the important factor related to regression of AVM is a previous bleeding episode.

Adolescent↗
PubMed1983

Extracerebral neural tissue mass in the middle cranial fossa extending into the oropharynx in a neonate. Case report.

The authors report the case of a newborn baby girl who had a large extracerebral neural tissue mass in the right middle cranial fossa which extended into the oropharynx through an enlarged foramen ovale. The surgical specimen comprised various kinds of neural tissue, including primitive neuroepithelium, mature as well as immature neurons and glia, myelinated fibers, ependyma, choroid plexus, ocular pigmented epithelium, and a number of calcospherites. The mass was partially covered by its own leptomeninges. The question of whether this mass is a true neoplasm or a heterotopia is discussed.

Brain↗
PubMed1983

Diverticulum of the lateral ventricle causing cerebellar ataxia. Case report.

A case of ventricular diverticulum causing cerebellar ataxia is presented. Computerized tomography clearly demonstrated the aperture of the diverticulum in the medial wall of the trigone and its extension into the posterior fossa. The diverticulum regressed and the cerebellar ataxia disappeared after placement of a ventriculoperitoneal shunt.

Brain Diseases↗
PubMed1983

[Peroxidation of arachidonic acid and brain edema].

Recent studies suggest that peroxidation of arachidonic acid (AA) accumulating during ischemic insult, may be related to the occurrence of post-ischemic brain damage. Since the influence of the increased brain content of AA remains unclear, the present study was undertaken to explore whether the intracerebral injection of AA is associated with the injury of the surrounding brain tissues such as brain edema. Rats received the intracerebral injection of 10 microliters of test solution (160 microgram of AA emulsified in 1% bovine serum albumin, BSA) or the same volume of BSA as the control. The measurement of specific gravity (SG) (74 rats) and the local CBF by H2 clearance technique (21 rats), and electron microscopical studies with tracers (Evans blue and horseradish peroxidase, HRP) (24 rats) were carried out. The effect of pretreatment with indomethacin (PI, 10 mg/kg) was evaluated in separate groups. AA transiently produced a significant decrease in SG and in 1CBF adjacent to the injection sites (p less than 0.01). The increased pinocytotic transportation, an accumulation of edema fluid containing HRP in extracellular space and endothelial injuries were observed only after AA injection. The above-mentioned falls in SG and in 1CBF, and the extravasation of HRP were inhibited by PI. The fact that PI prevented the edema formation, 1CBF change and the disturbance of blood-brain barrier induced by AA, indicates that peoxidation of AA through the arachidonate cascade is involved in the mechanism of brain edema formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Selective destruction of the outer leaflet of the capillary endothelial membrane after intracerebral injection of arachidonic acid in the rat.

A peculiar ultrastructural change of the cytoplasmic membrane is described. It concerns selective destruction of the outer leaflet of the luminal side of the capillary endothelium in the white matter of the rat brain, 30 min and 3 h after intracerebral injection of arachidonic acid (AA). The cristae of the mitochondria disappeared in the endothelium of many capillaries. These changes were observed mainly in the central part of brain edema, where the extracellular space was markedly widened. The possible mechanism whereby these changes developed is discussed.

Animals↗
PubMed1982

Spontaneous intracranial hemorrhage caused by brain tumor: its incidence and clinical significance.

Hemorrhage from brain tumor was confirmed clinically, surgically, or on autopsy in 94 of 1861 cases (5.1%) treated during the past 18 years: 49 of 311 pituitary adenomas (15.8%) and 45 of 1550 other brain tumors (2.9%). The higher incidence of hemorrhage from pituitary adenoma was statistically significant (p less than 0.001). In brain tumors other than pituitary adenoma, the incidence of hemorrhage was significantly higher in the patients under 14 years old (17 of the 322 cases, 5.3%) than in the patients over 15 years old (28 of the 1228 cases; 2.3%) (p less than 0.001). Nineteen patients showed no evidence of clinical symptoms related to bleeding. Twenty-six patients had a definite history of an acute episode that suggested sudden bleeding. In 11 of these, the apoplectic syndrome was the initial presenting symptoms. The incidence of hemorrhage was not statistically correlated with sex. The hemorrhage was intratumoral in 30 cases, intracerebral in 7, subarachnoid in 7, and subdural in 1. The tumors were supratentorial in 36 cases, pineal in 1, and infratentorial in 8. Primary and metastatic choriocarcinoma and primary embryonal carcinoma seemed to cause hemorrhage most frequently. The following precipitating factors were found in 7 of the 17 patients aged under 14: ventricular drainage in 2, ventriculoperitoneal shunt in 2, carotid angiography in 1, head injury in 1, and leukemia in 1. Seven of the 17 patients under 14 years old died of massive bleeding from the tumor. Unless there is evidence of vascular disease such as cerebral aneurysm, vascular malformation, or hypertensive cerebrovascular disease, intracranial hemorrhage should be suspected of being due to a brain tumor.

Adenoma↗
PubMed1982

Prevention of cerebral vasospasm after SAH with a thromboxane synthetase inhibitor, OKY-1581.

The efficacy of thromboxane synthetase inhibitor in the prevention of cerebral vasospasm after subarachnoid hemorrhage (SAH) was evaluated in a prolonged experiment using dogs. Changes in the diameter of the basilar artery were followed by angiography, and morphological changes were studied by photomicroscopy and electron microscopy. As a thromboxane synthetase inhibitor, OKY-1581 (sodium-(E)-3-(4(-3-pyridylmethyl)phenyl)-2-methylacrylate) was used. Dogs received intravenous injections of 160 mg of OKY-1581 dissolved in 2 ml of physiological saline immediately after subarachnoid blood injection. Subsequently, the animals received continuous intravenous infusion of the drug at the rate of 4 gm/50 ml/24 hours until sacrifice 4 days after induction of SAH. Control dogs received subarachnoid blood injection without treatment with OKY-1581. Angiographic examination revealed that the late spasm was almost completely abolished by the treatment with OKY-1581. Early spasm was also prevented, but the drug's effect was less prominent than it was on the late spasm. Morphological study revealed degenerative changes in the endothelium and myonecrotic changes in the tunica media following SAH in the basilar arteries of the treated as well as the untreated dogs. However, corrugation of the internal elastic lamina was almost completely absent in the treated dogs. The above results indicate that a disproportionate synthesis of thromboxane A2 plays an important role in the evolution of chronic cerebral vasospasm following SAH, and that drugs such as OKY-1581 that selectively inhibit thromboxane synthetase might be useful in the prevention of vasospasm.

Acrylates↗