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Biomedical subjects

M Kagawa

Publications and source records attributed to M Kagawa.

At least 145 records · Page 8Linked to original sources
PubMed1980

[Case report of paraventricular cerebral cyst of infant (author's transl)].

A case of paraventricular cerebral cyst was reported. A 48-day-old infant was admitted to the Department of Neurosurgery with an enlargement of head circumference. Cerebral angiography, pneumoventriculography, and computed tomography showed a cyst in the trigon of the right lateral ventricle and unilateral hydrocephalus. Right-parieto-occipital craniotomy was done. The trigone of the right lateral ventricle was opened and the wall of the cyst was subtotally removed. A partial defect of the corpus callosum and other additional cysts at the quadrigeminal region were identified. On light microscopy, the inner layer of the cyst, protruding into the lateral ventricle, consisted of columnar cells and outer part of the wall was formed of loose connective tissue and glial tissue. On electron microscopy, the cells of the cyst wall was formed of loose connective tissue and glial tissue. On electron microscopy, the cells of the cyst wall had microvilli and abnormal cilia, and desmosome was recognized. And the cells of the cyst were bordered by a continuous basement membrane. According to pathological finding, the cyst was considered to be classified as a transitional type between chroidal epithelial cyst and ependymal cyst.

Agenesis of Corpus Callosum↗
PubMed1980

[A case of aortitis syndrome associated with basilar aneurysm (author's transl)].

A case of aortitis syndrome (pulseless disease) associated with basilar aneurysm is reported. This patient was 52-year-old woman suffering from pulseless disease for past fifteen years. She was admitted to our hospital with severe headache, nausea and vomiting. Four vessel angiograms revealed an aneurysm of the basilar artery and occlusion of the right vertebral artery. The internal carotid artery in the left side and the subclavian artery in the right side were not demonstrated even by the serial aortography. As regard to the pathogenesis of cerebral aneurysms associated with aortitis syndrome, questions are in discuss whether the aneurysm is of congenital nature or the result of acquired arteriosclerosis due to aortitis syndrome. In addition, the rupture mechanism of basilar aneurysm associated with aortitis syndrome is discussed.

Aortic Arch Syndromes↗
PubMed1979

[A case of congenital dermal sinus in the parietal region (author's transl)].

A congenital dermal sinus at the midline of the parietal region, which extends into the falx, is relatively rare. The following case is illustrative. A 3-year-old girl was noticed by her parents to have tumor at the midline of the parietal region without other disturbances and complaints. This girl had the normal mental and motor development, and was admitted to our clinic for cosmetic surgery. A round, elastic soft tumor, roughly 1x1x1 cm in diameter, was located at the midline of the parietal region. This tumor had a port wine cutaneous discoloration and an absence of normal hair growth in this area. Abnormal hair did not protrude from the sinus. This tumor had no dimple nor sinus opening. Skull XP showed a round lucent bone defect at the midline of the parietal region. This bone defect with sclerotic margin, was about 1 cm in diameter. Skull XP and tomography, with contrast medium injection into the tumor, showed that this tumor extended into the falx through bone defect. Angiography showed that there were no relations between the tumor and the superior sagittal sinus. PEG showed that there were no mass lesion nor dilatation of ventricles. Both spinal tap and EEG were normal. Operation for the congenital dermal sinus was performed on Nov. 4, 1977. This congenital dermal sinus extended into the falx and congenital cell rest tumor was not elicited.

Child, Preschool↗
PubMed1979

[Brain abscess (Part 5)--Brain abscess following internal carotid occlusion (author's transl)].

Three cases of brain abscess following an occlusion of the internal carotid artery were reported. Case 1: A 6-year-old girl with congenital heart disease was admitted with headache, disturbance of consciousness and left hemiparesis. Right carotid angiography revealed an occlusion of the right internal carotid artery. After 6 months, she was readmitted with high fever. CT scan revealed a low density area and a ring-like shadow at the same site of cerebral infarction. Case 2: A 69-year-old man was admitted in semicoma and with right hemiplegia. Left angiography revealed an occlusion of the left internal carotid artery. After 2 months, a brain abscess was noted in the infarcted area. Case 3: A 20-year-old man with congenital heart disease, was admitted due to headache, vomiting and high fever. CT scan revealed a brain abscess in the right frontal lobe. Carotid angiography showed bilateral internal carotid artery occlusion. We concluded that diminution of cerebral oxygen and encephalomalacia are predisposing factors to the evolution of brain abscess.

Adult↗
PubMed1977

[Fibrinolytic activity of cerebrospinal fluid in subarachnoid hemorrhage (author's transl)].

This study was aimed to investigate the correlation between recurrent hemorrhage of ruptured intracranial aneurysm and local fibrinolytic activity of aneurysmal fibrin plug. The fibrinolytic activity of cerebrospinal fluid (CSF) was investigated in 63 patients with various neurological diseases by means of modified fibrin plate method. No plasmin was elicited in normal CSF, however, it was confirmed that CSF contained an incomplete activator which became a complete activator inthe presence of streptokinase, and plasminogen was identified in the presence of urokinase. In 26 cases of subarachnoid hemorrhage, the fibrinolytic activity of CSF occurred in the patients within two weeks following hemorrhagic ictus. In almost cases, the fibrinolytic activity of CSF was not increased in the first three weeks after the onset of hemorrhage. This result agreed with the fact that rebleeding of intracranial aneurysm tended to occur within two weeks after the hemorrhage. Therefore, intensive antifibrinolytic therapy for two weeks after onset of hemorrhage is necessary in order to prevent recurrent hemorrhage of intracranial aneurysm, and its doses should be sufficient to inhibit local fibinolysis. It has been suggested that the local fibrinolysis after subarachnoid hemorrhage would be caused by activators released from damaged surrounding brain tissues. Furthermore, it is strongly suggested from the result of our in vitro experiments that coexistence of CSF and blood play an important role to increase local fibrinolysis.

Fibrinolysis↗