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Biomedical subjects

K Osaka

Publications and source records attributed to K Osaka.

At least 55 records · Page 3Linked to original sources
PubMed1978

Myeloschisis in early human embryos.

Four early human embryos with open myeloschisis are reported. These are a thoracolumbar myeloschisis in Carnegie developmental stage 12, a cervical myeloschisis in stage 13, and two lumbosacral myeloschisis in stage 14. All of them are the smallest human embryos with this type of malformation ever reported. In these embryos, the neuroectodermal junction is smooth and there is no microscopic evidence that the neural tube is forced open after its proper closure. The presence of the lesion in such early embryos, especially in one of stage 12, implies that the lesion evolved from the neural plate which never closed. Cellular polarity and the limiting membrane in the lesion are generally well preserved in spite of apparent overgrowth of the neural tissue. These findings do not support the hypothesis of LEMIRE et al. that the defective external limiting membrane predisposes to a loss of cellular polarity and resultant neural overgrowth.

Embryo, Mammalian↗
PubMed1978

Holoprosencephaly in neurosurgical practice.

The clinical, angiographic, and pneumoencephalographic features of seven cases with holoprosencephaly are reported. Three of the alobar type in this series revealed the facial dysmorphia characteristic of the anomaly. In the other four cases (one alobar, one semilobar, and two lobar), such facial anomaly was absent, and the diagnosis was achieved only after contrast studies. An azygous anterior cerebral artery running over the cerebral surface due to a defective interhemispheric fissure is pathognomonic for alobar and semilobar holoprosencephaly. Dysgenesis of the deep venous system was found in alobar, semilobar, and lobar holoprosencephaly, a finding helpful in diagnosis, especially of the lobar type. Air study and computerized tomography scan revealed incomplete separation of the ventricular system. The basic nature of holoprosencephalization and its differentiation from non-holoprosencephalic malformation are discussed. Six of the seven patients reported had hydrocephalus.

Agenesis of Corpus Callosum↗
PubMed1978

Myelomeningocele before birth.

The authors report a study of 92 human embryos and four fetuses with myeloschisis. The characteristics of embryonic myeloschisis compared with spina bifida cystica in infants are: 1) the lesion is often more diffuse, involving the whole spinal cord (12 embryos); 2) the cervical cord is frequently affected (23 of the remaining 80 embryos); 3) holoprosencephaly is frequently associated (18 embryos); 4) meningocele is not found; and 5) hydrocephalus and Arnold-Chiari malformation are not yet developed. Hydrocephalus and Arnold-Chiari malformation are found in myeloschistic fetuses. Almost all embryos with diffuse and cervical myeloschisis or with holoprosencephaly are extruded before birth by spontaneous abortion. Absence of meningocele in the embryonic period implies that its appearance is deferred to the fetal period. The development of hydrocephalus and Arnold-Chiari malformation also seems to be delayed until the fetal period. Our observation implies that myelomeningocele is induced by non-closure of the neural tube, not by rupture once it was closed. "Neural overgrowth" and disturbed "recanalization process" are discussed in relation to the pathogenesis of myelomeningocele.

Abnormalities, Multiple↗
PubMed1977

Dysgenesis of the deep venous system as a diagnostic criterion for holoprosencephaly.

The angiographic features of three cases with holoprosencephaly are reported. In all of them, the galenic venous system seemed to be deficient and the basal ganglia were drained by peculiar veins which coursed laterally and drained directly into the lateral sinus. These peculiar veins are considered to be remnants of the embryonic diencephalic veins, suggesting that these patients retain their early embryonic pattern of venous drainage. The diagnosis of alobar holoprosencephaly is established by the demonstration of the azygos anterior cerebral artery coursing along the frontal bone with excessive undulations. But with lobar holoprosencephaly, this characteristic feature is not present, and dysgenesis of the deep venous system is important for the diagnosis of holoprosencephaly.

Brain↗
PubMed1977

Congenital hypocupraemia syndrome with and without steely hair: report of two Japanese infants.

Two Japanese infants with Menke's kinky hair syndrome are reported. The unusual finding in one infant was the absence of the hair abnormality characteristic of this disease; other findings were consistent with the diagnosis. It is suggested that hair abnormality cannot be relied upon for the diagnosis and that the term "kinky hair" is anappropriate. In its place "congenital hypocupraemia" is proposed as the diagnostic term to embrace patients with and without hair abnormality. Serum copper determination is a simple and reliable test in the diagnosis of this syndrome and should be done routinely in all male patients with unexpected deterioration. The angiographic features present in these patients with unexpected deterioration. The angiographic features present in these patients are characteristic but not pathognomonic of the disease. Subdural hygroma, a common finding, is the result of severe brain atrophy and little can be expected by surgical intervention.

Brain Diseases, Metabolic↗
PubMed1977

Correlation of the response of the flushing device to compression with the clinical picture in the evaluation of the functional status of the shunting system.

The functional status of cerebrospinal fluid shunting systems provided with flushing devices has commonly been assessed by the response of the flushing device to digital compression and a review of the clinical status of the patient. In order to study the reliability of the response of the flushing device as an indicator to shunt function, 47 hydrocephalic children with implanted shunts were studied. In 40% of these children, the flushing device was pumping well at the time of shunt obstruction, and in 50% it was not, although the patient's clinical status was perfectly normal. Accordingly, we conclude that the flushing device is a very poor indicator of shunt functioning.

Cerebrospinal Fluid Shunts↗
PubMed1977

Congenital brain defect masked by subdural fluid collection.

Two rare cases of subdural fluid collection are reported. In these cases, the subdural space was in direct communication with the lateral ventricle through the congenital brain defects. The subdural fluid was formed by the cerebrospinal fluid which passed from the lateral ventricle through the brain defects. The difficulty to diagnose these cases from the usual subdural hygroma is emphasized.

Brain↗
PubMed1977

Prolonged vasospasm produced by the breakdown products of erythrocytes.

The cause of cerebral vasospasm has been generally attributed to the vasoconstrictive substances released from platelets. The role of extravasated erythrocytes in vasospasm has never been well analyzed. To elucidate this point, the basilar arteries of cats were exposed and subjected to topical application of various blood fractions in their fresh state and after prolonged incubation for 1 to 7 days. Incubation was done to test stability of the vasoconstrictors. Severe vasospasm was induced by application of fresh and incubated fractions of lysed erythrocytes. Fresh, intact erythrocytes had no vasoactivity, but by incubation they lysed and gained vasoconstrictors. Vasospasm induced by lysed erythrocytes both in their fresh state and after prolonged incubation never relaxed, and tended to increase in severity during observation up to 24 hours. Fresh serum and platelet-rich plasma had vasoconstrictors, but they were lost after incubation. Apparently platelet-induced vasoconstriction is of short duration and contributes only to the early phase of vasospasm. Later, 12 to 24 hours after hemorrhage, iron pigments released by lysis of extravasated erythrocytes (oxyhemoglobin or methemoglobin) irritate the arterial wall and induce prolonged vasospasm. It is emphasized that the study of cerebral vasospasm should be focused on the role of the breakdown products of extravasated erythrocytes.

Animals↗
PubMed1977

[The stress ulcer in the neurosurgical disease and the warning data (author's transl)].

Twelve cases of G.I. tract bleeding, treated in the Department of Neurosurgery, Kobe University School of Medicine, were analyzed with the special reference to clinical data before the episode of G.I. tract bleeding. These 12 cases consist of 10 cases of aneurysm, 1 of metastatic brain tumor, and 1 of chronic subdural hematoma. The anterior communicating artery has the majority in the case of aneurysm by 50 per cent. In each case, C.B.C., bleeding time, coagulation time, serum electrolytes, serum glucose, glucosuria, steroid administration, blood pressure, hyperthermia, and water balance were reviewed retrospectively. Only serum glucose showed the specific abnormality with the average of 135 mg/dl (Hoffman method) before the episode of G.I. tract bleeding among them. In 1931, Cushing reported the clinical case of G.I. tract bleeding with intracranial disease and also experimental G.I. tract bleeding, in which discussion he concluded only parasympathetic nerve system has the involvement in the mechanism. In 1952, French, however, certified also the involvement of sympathetic nerve system in G.I. tract bleeding with the experimental results. In addition to this report, many experimental works under the standpoint of hypothalamus involvement in stress ulcer were undertaken. On the other hand, hyperglycemia and glycosuria in the stress have been reported as the results of clinical and experimental works. In 1971, Frohman concluded that only ventromedial nuclei has relation to the control of glycogen metabolism in hypothalamus from his experimental results. We concluded that this hyperglycemia before the evidence of G.I. tract bleeding due to the involvements of hypothalamus or other parts of C.N.S. in the neurosurgical disease is one clinical sign of the stimualtion to sympathetic nerve system that also can be a cause of G.I. tract bleeding, and this hyperglycemia before the evidence of G.I. tract bleeding should be paid attention as a warning datum.

Adult↗
PubMed1977

[Subdural hematoma after cerebrospinal fluid shunt for hydrocephalus following subarachnoid hemorrhage-report of two cases (author's transl)].

Post-shunt subdural hematoma was found in two patients with hydrocephalus due to subarachnoid hemorrhage. The first case was a 46-year-old man with two episodes of subarachnoid hemorrhage from anterior communicating aneurysm. Two weeks after neck-clipping for the aneurysm, a ventriculo-peritoneal shunt with Pudenz's system was performed since hydrocephalus with moderately increased pressure had been found. He did well for one month, then soon after mild head injury, disorientation and right hemiparesis developed. Cerebral angiogram revealed avascular space in the left parietotemporal region. After the ligation of the shunt tube, subdural hematoma was removed. The symptoms improved in two weeks. The second case was a 62-year-old man with an aneurysm at the trifurcation of the right middle cerebral artery. One month after successful clipping of the aneurysm, he received a ventriculoperitoneal shunt with Pudenz's system for normal pressur hydrocephalus. One and a half years after the operations he hit his head against the ground during his convulsive seizure. Since then, disorientation, urinary incontinence and gait disturbance appeared. After cerebral angiogram, the subdural hematoma was removed and the shunt tube was ligated. He became free of these symptoms in two weeks. The cerebrospinal fluid shunt is recommended for hydrocephalus induced by subarachnoid hemorrhage, but careful follow-up is necessary since these patients might develop post-shunt subdural hematoma, especially after head trauma as shown in our cases.

Cerebrospinal Fluid Shunts↗
PubMed1977

[Post-shunt subdural hematoma in infants and children--analysis of eleven cases (author's transl)].

Out of 122 hydrocephalic infants and children treated by cerebrospinal fluid shunt, post-shunt subdural hematoma was found in 11 patients in total, 8 cases with non-tumorous hydrocephalus and 3 cases with brain tumors obstructing the cerebrospinal fluid pathway. In most cases the diagnosis of subdural hematoma was delayed since signs of increased intracranial pressure were absent initially. The signs of increased intracranial pressure appeared later, when the shunted venricle collapsed and could not give any more space to the growing subdural hematoma. At this stage those cases were easily misdiagnosed as shunt dysfunction. Post-shunt subdural hematoma was apparently induced by the tear of the bridging vein or leakage of the cerebrospinal fluid into the subdural space through the torn arachnoid membrane due to over-drainage of the cerebrospinal fluid, especially when the patients took the erect position. Since such a complication is not rare and difficult to be diagnosed, intensive follow-up is necessary in the post-shunt period. The precautionary measures as well as the treatment for these subdural hematoma were also discussed.

Cerebrospinal Fluid Shunts↗
PubMed1977

["Compensated hydrocephalus" (author's transl)].

Out of 60 consective cases with hydrocephalus of pediatric age group, 8 cases were found to be so-called "compensated" hydrocephalus and their clinical features were reported. "Compensation" of hydrocephalus in our cases was probably induced by increased ventricular absorption of cerebrospinal fluid since moderate to severe ventricular dilatation was present in all cases. Such "compensation" of hydrocephalus is apparently made at the expense of normal development of the brain function. Therefore, such "compensation" of hydrocephalus is not the condition to be aimed for, but to be avoided for preservation of normal brain function. In order to prevent such "compensation" of hydrocephalus, shunt function should be followed carefully especially in those whose initial shunts were placed at older age, and in whom symptoms of increased intracranial pressure were not so apparent before the initial shunt-placement. Further treatment for hydrocephalus was considered to be necessary in our cases since unrolling of the anterior cerebral artery was invariably present. Unrolling of the anterior cerebral artery was found even in such cases whose cerebrospinal fluid pressure was normal, head circumference did not show any increase, and IQ test was normal. In one case, "compensated" hydrocephalus became later "decompensated" with apparent signs of increased intracranial pressure. Other supplementary tests for cerebrospinal fluid dynamic such as saline infusion test or RISA cisternography were also discussed.

Child↗
PubMed1977

[The development of cerebro-spinal fluid pathway in human embryos (author's transl)].

The early development of the subarachnoid space, the choroid plexus, and the arachnoid villi was studied in 60 normal human embryos ranging from Carnegie stage 12 to 23. The embryos were fixed in Bouin's fluid, paraffin-embedded, serially sectioned and stained with hematoxylin-eosin and Azan. One abnormal human embryo with exencephaly and myeloschisis in the high cervical cord was added for the study. A primitive subarachnoid space (future subarachnoid space) is first distinguishable as cavity formation within the meninx primitiva in the areas ventral to the middle brain vesicle at stage 14. The development of the primitive subarachnoid space precedes the appearance of the choroid plexus. The primitive subarachnoid space appears earlier in the region ventral to the rhombencephalon than in the region posterior to the fourth ventricle. By stage 20, a primitive subarachnoid space almost completely surrounds the neural tube. A fairly-well developed primitive subarachnoid space was observed in the abnormal human embryo, in which the fourth ventricle was open to the amniotic cavity and the ventricular system was completely separated from the primitive subarachoid space. These findings imply that the extraventricular spread of fluid of choroid plexus origin is not an essential factors, and that probably it is not even an important factor, for the development of the subarachnoid space. The arachnoid villi dose not appear even at the end of the embryonal stage. Absorption of the cerebrospinal fluid in an embryo should be done by the way other than the arachnoid villi.

Brain↗