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Biomedical subjects

S Sakaki

Publications and source records attributed to S Sakaki.

At least 91 records · Page 5Linked to original sources
PubMed1995

[Operative results in fourteen cases of paranasal sinus and anterior cranial fossa lesions surgically treated by an extended transbasal approach].

We describe the outcomes and complications of 14 patients with paranasal sinus and anterior cranial fossa lesions surgically treated by an extended transbasal approach, originally described by Kawakami, in our department. They were 10 patients with malignant tumors, 2 with benign tumors, and 2 with inflammatory diseases. A bifrontal craniotomy was performed using a high coronal skin incision, and the orbital rim and roof were removed after the dissection of the dura mater from the anterior skull base. Transcranial resection of the tumor was performed, and assisted by transnasal and transmaxillar resection using a nasal endoscope. Reconstruction of the anterior skull base was performed with the fasica lata and galeopericranial flap in all cases, temporal musculo-pericranial flap in 3 and free bone flap from the cranial convex in 3. Among 10 patients with malignant tumors (malignant melanoma; 4, squamous cell carcinoma; 2 adenocarcinoma; 1, malignant plemorphic adenoma; 1, chondrosarcoma; 1, and neuroblastoma; 1), total removal was performed in 5 patients and subtotal removal in 5 patients. Though local recurrence of the tumor was recognized in 6 patients, only one underwent additional surgery. Eight patients survived, and 2 patients died of systemic metastasis of the tumor and complications due to liquorrhea. Seven patients obtained a good quality of life, and the mean survival period in 8 patients still living was 27 months after the first surgery. In 2 patients with benign tumors (chordoma and osteoma), partial and total removal was performed. The patient with chordoma was operated on several times by this approach and the transoral approach, respectively. Each had a good postoperative course.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Spontaneous regression of cerebral arterio-venous malformation following major artery thrombosis proximal to dominant feeders: a case report].

A rare case of spontaneous regression of cerebral arterio-venous malformation (AVM) is reported. A 76-year-old male was admitted to Juzen General Hospital due to generalized convulsion on August 24, 1987. On admission, results of physical and neurological examinations were normal. Plain CT scans showed an iso-density lesion with a slightly high density spot in the left frontal lobe, and enhanced CT scans showed multiple, irregularly tubular enhancements in the lesion. Left carotid angiogram (CAG) demonstrated an arteriovenous malformation (AVM) in the left frontal lobe, which was fed by the left ACA and MCA and drained by the ascending cerebral vein and superficial Sylvian vein. There was also an anterior communicating artery aneurysm. At the patient's request, he was treated conservatively and was discharged without neurological deficit. Though he continued to take anticonvulsants thereafter, he felt weakness or numbness of the right extremities once a year. Five years after the first admission, he developed sudden onset of right hemiparesis, aphasia and consciousness disturbance. On admission, his platelet aggregation function was elevated. At this time, enhanced CT scans did not show any enhanced area in the left frontal lobe where AVM had been found previously. T2-weighted magnetic resonance image showed a mixed intensity area without any flow void phenomenon suggesting thrombosis of the nidus. Left CAG demonstrated occlusion of the A1-A2 junction of the anterior cerebral artery and disappearance of the AVM. He was treated conservatively again, and was discharged without neurological deficit.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Basic fibroblast growth factor-like immunoreactivity in the rat basilar artery with reference to co-localization with NADPH-diaphorase in the trigeminal ganglion.

The location of basic fibroblast growth factor (bFGF)-like immunoreactivity and nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase (neuronal nitric oxide synthase) activity in the rat basilar artery and in the trigeminal, sphenopalatine and superior cervical ganglia was investigated. bFGF immunoreactivity was seen mainly in adventitial nerve fibers of the rat basilar artery, but not in the endothelium. Electron microscopy of the tunica media showed a number of immunoreactive nerve endings in the vicinity of local smooth muscle cells. Among the cranial ganglia that innervate the basilar artery, only the trigeminal ganglion had bFGF-immunoreactivity neurons. Nerve cells and fibers with NADPH-diaphorase activity were detected in the basilar artery and in the sphenopalatine and trigeminal ganglia, and the co-localization of bFGF and NADPH-diaphorase was noted only in the trigeminal ganglion. Furthermore, Fluro-gold tracing in combination with bFGF immunohistochemistry demonstrated that bFGF-containing nerve fibers in the wall of the basilar artery arise from the trigeminal ganglion. These findings provide a morphological basis for the nitric oxide-mediated dilatation of cerebral arteries by bFGF.

Animals↗
PubMed1994

Evaluation of risk of hemorrhagic transformation in local intra-arterial thrombolysis in acute ischemic stroke by initial SPECT.

BACKGROUND AND PURPOSE: Thrombolytic therapy was carried out on patients with acute ischemic stroke, and the risk of hemorrhagic transformation was evaluated from the residual cerebral blood flow (CBF) by pretherapeutic single-photon emission-computed tomography (SPECT). METHODS: Local intra-arterial thrombolytic therapy was carried out using urokinase or recombinant tissue plasminogen activator (rt-PA) within 6 hours from the onset in 34 patients in whom no hypodensity areas were observed on the initial computed tomography examination. In the 20 patients with carotid territory occlusion who underwent 99mTc-labeled hexamethylpropyleneamine oxime (99mTc-HMPAO) SPECT, the residual CBF of the ischemic region was evaluated semiquantitatively by calculating two parameters: the ischemic regional activity to cerebellar activity ratio (R/CE ratio) and asymmetry index (AI). RESULTS: The occluded vessels could be recanalized in 22 (92%) of the 24 patients in the urokinase group and in all 10 of the patients in the rt-PA group. Hemorrhagic transformation appeared in 4 patients in the urokinase group and 3 patients in the rt-PA group. Among the 20 patients who underwent SPECT before the treatment, the residual CBF was lower in the 5 patients who developed hemorrhagic transformation than in the 15 who did not (P < .05). Hemorrhagic transformation occurred in all patients with R/CE ratio of less than 0.35 and AI of more than 1.5. CONCLUSIONS: The risk of hemorrhagic transformation after recanalization of occluded vessels by local intra-arterial thrombolytic therapy was considered to be high when the pretherapeutic residual CBF was markedly reduced.

Acute Disease↗
PubMed1994

Primary Ewing's sarcoma of the occipital bone--case report.

A 12-year-old boy presented with primary Ewing's sarcoma of the occipital bone manifesting as intermittent high fever and local pain in the occipital region. Plain skull x-ray films disclosed an unclear lytic lesion in the occipital bone. Computed tomography and magnetic resonance imaging demonstrated the irregularly enhanced mass. The tumor was removed totally. He received intensive chemotherapy and radiation therapy postoperatively. No recurrence or metastasis has been noted, and he was in good condition 18 months after the operation.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Large cystic cavernous angioma of the cerebellum--case report.

A 40-year-old female presented with gait disturbance and dysarthria. Computed tomography revealed a large cystic tumor in the cerebellar vermis with a mural nodule located in the deepest portion of the cyst. The magnetic resonance (MR) imaging appearance suggested cavernous angioma. The solid nodule was completely removed through the suboccipital approach. The cyst was filled with transparent yellowish fluid which showed positive Froin's sign. The histological diagnosis of the mural nodule was cavernous angioma. The cyst wall consisted of gliosis and contained no angiomatous tissues. Postoperative MR imaging demonstrated that the nodule was totally removed and the cyst size was reduced. The neurological deficits improved postoperatively. The mechanism of formation of the large cyst was assumed to be repeated peritumoral hemorrhage.

Adult↗
PubMed1994

Chronic subdural hematoma associated with middle fossa arachnoid cysts--three case reports.

Three patients with chronic subdural hematoma associated with middle fossa arachnoid cyst were treated by irrigating the hematoma through burr holes, because the symptoms were considered mainly due to increased intracranial pressure caused by the subdural hematoma. The symptoms disappeared immediately afterwards, so no surgery for the middle fossa arachnoid cyst was done. The patients were followed by magnetic resonance imaging. No subdural hematoma recurred during a postoperative period of 11 months to 2.5 years, and the arachnoid cyst reduced in size in two patients. We recommend irrigation of the subdural hematoma as the initial procedure of choice for such cases.

Adolescent↗
PubMed1994

Changes in Ca(++)-ATPase activity in smooth-muscle cell membranes of the canine basilar artery with experimental subarachnoid hemorrhage.

Changes in Ca(++)-adenosine triphosphatase (ATPase) activity in the plasma membrane of smooth-muscle cells in the basilar arteries of dogs with experimental subarachnoid hemorrhage (SAH) were examined. The study methods included electron microscopic histochemistry and bioassay of the enzyme that exports cytoplasmic Ca++ to extracellular spaces. The Ca(++)-ATPase activity in the basilar artery increased significantly in response to the application of vasoconstrictive agents (prostaglandin F2 alpha and a phorbol ester), but decreased significantly 24 hours after experimental SAH, inversely with basilar artery contraction. Dogs that had undergone two arterial blood injections (double SAH) exhibited a further decrease in Ca(++)-ATPase activity as well as persistent contraction of the basilar artery for a longer period (at least 7 days) than was seen in animals with a single arterial blood injection. Bioassay of the enzyme also demonstrated a decrease in vascular Ca(++)-ATPase activity in dogs subjected to double SAH. These findings suggest that the early occurrence of and long-lasting decrease in Ca(++)-ATPase activity in dogs with experimental SAH induces a persistent disturbance of Ca++ homeostasis and indicates that damage to the plasma membrane in the cerebral arterial smooth-muscle cells proceeds to myonecrosis after SAH.

Animals↗
PubMed1994

Evaluation of regional myocardial perfusion in areas of old myocardial infarction after revascularization by means of intraoperative myocardial contrast echocardiography.

Because myocardial revascularization to areas of old myocardial infarction brings about functional recovery to some extent to myocytes in those areas, the assessment of regional myocardial perfusion on those areas after myocardial revascularization may allow myocardial viability to be estimated. Using intraoperative myocardial contrast echocardiography by direct injection of 2 ml sonicated 5% human albumin into saphenous vein grafts, we assessed regional myocardial perfusion in 16 revascularized areas of old myocardial infarction. We estimated the myocardial viability of areas with respect to myocardial perfusion, and we compared these results to both the improvement of regional wall motion after myocardial revascularization (increase in segmental wall thickening during systole) and relative thallium 201 activity obtained by quantitative analysis of preoperative exercise myocardial thallium 201 distribution on delayed images. The background-subtracted peak peak intensity of myocardial enhancement and the ratio of endocardial to epicardial intensity were determined in each revascularized area. An inverse correlation existed between peak intensity (18 +/- 7) and the endocardial/epicardial ratio (0.88 +/- 0.17) (r = -0.63, p < 0.01). A good correlation was found between peak intensity and both the percent increase in segmental wall thickening (r = 0.73, p < 0.005) and the relative thallium 201 activity (r = 0.81, p < 0.005). These results suggested that regional myocardial perfusion after myocardial revascularization in areas of old myocardial infarction distributed better to the epicardial halves than to the endocardial halves, and that the peak intensity could be related to myocardial viability.

Aged↗
PubMed1994

[A case of subacute stroke with high uptake of 99mTc-HMPAO in the reperfused infarct corresponding to low perfusion area].

We reported a case of subacute stroke which showed high uptake of 99mTc-d,l-hexamethylpropyleneamine oxime (HMPAO) in the reperfused infarct corresponding to slightly decreased perfusion by 133Xe inhalation CBF measurement. In the chronic stage, both SPECT images of 99mTc-HMPAO and 133Xe showed low perfusion in the affected lesion. It was, therefore, considered that the high uptake of 99mTc-HMPAO had represented luxury perfusion. In the subacute stage of stroke, high uptake of 99mTc-HMPAO may imply luxury perfusion but not always hyperperfusion. It is suggested that the fractional fixation of 99mTc-HMPAO temporarily change in the affected lesion and it is essential to take into consideration the clinical stage for the interpretation of SPECT images.

Acute Disease↗
PubMed1993

The role of early Ca2+ influx in the pathogenesis of delayed neuronal death after brief forebrain ischemia in gerbils.

To examine the role of calcium influx in the early phase after brief forebrain ischemia and subsequent delayed neuronal cell death in the hippocampus, 45Ca autoradiography and electron microscopic cytochemistry, by a combined oxalate-pyroantimonate method, were carried out in gerbil brains after 5 min bilateral common carotid arterial occlusion. Further, neuronal damage during the ischemic and postischemic periods was determined by conventional or immunohistochemical staining for microtubule-associated protein 2 (MAP2) with and without calcium-entry blockers. 45Ca autoradiography showed a high peak of calcium in the hippocampus at 5 min of recirculation. Electron cytochemical microscopy also demonstrated accumulation of intracellular calcium pyroantimonate deposits in the neuronal cells in all regions. At 30 min of reperfusion, amounts of calcium in the hippocampus returned to the control levels, and intracellular dense calcium pyroantimonate deposits were reduced in these areas. Loss of the reaction for MAP2 was noted in the medial CA1 of the hippocampus immediately after 5 min ischemia and at 5 and 30 min after reperfusion. MK-801 (10 mg kg-1), an N-methyl-D-aspartate (NMDA) receptor antagonist, injected intraperitoneally 1 h before ischemia, suppressed the early increase of calcium in the forebrain and neuronal cell necrosis in the CA1. However, neither injection of MK-801 30 min after reperfusion nor preischemic treatment with 0.5 mg kg-1 Nimodipine or 1 mg kg-1 Nicardipine, voltage-sensitive calcium channel antagonists, prevented neuronal death. In immunohistochemical staining for MAP2, the ischemic lesion in the medial CA1 maintained after 5 min ischemia and the subsequent early reperfusion period in the untreated brains was protected by the preischemic injection of 10 mg kg-1 MK-801, but was not restored by the injection of 0.5 mg kg-1 Nimodipine or 1 mg kg-1 Nicardipine. In conclusion, it is suggested that an early excess of calcium influx could be caused mainly by excitatory amino acid overload through NMDA receptor-mediated calcium channels during the ischemic and early postischemic periods.

Animals↗
PubMed1993

Transient increase in endogenous basic fibroblast growth factor in neurons of ischemic rat brains.

An antiserum against basic fibroblast growth factor (bFGF) was shown to recognize an 18-kDa protein (possibly bFGF) in crude neocortical extracts by immunoblot and used to investigate the changes of bFGF immunoreactivity in neurons and astrocytes of the cerebral cortex of rats 1-21 days after unilateral occlusion of the middle cerebral artery (MCA). The mildly ischemic neocortex exhibited no signs of cell loss or degeneration in Nissl-stained sections 1-14 days after MCA occlusion, but it contained pyramidal cell bodies and processes with more intense bFGF immunoreactivity than did the control neocortex. bFGF immunoreactivity in the ischemic hemisphere gradually declined in intensity and by 21 days after MCA occlusion, it had reached the control level. On the other hand, there were many bFGF immunoreactive astrocytes in the primary olfactory cortex on the side of infarction. These findings suggest that MCA occlusion causes an increase in bFGF content not only in astrocytes but also in neurons, depending on the severity of the ischemic insult in individual cortical regions. The transient augmentation of bFGF expression or accumulation in mildly ischemic pyramidal neurons but not in astrocytes is in line with previous studies suggesting the neurotrophism of exogenously applied bFGF.

Animals↗
PubMed1993

Recovery of protein synthesis in tolerance-induced hippocampal CA1 neurons after transient forebrain ischemia.

Protein synthesis at various recirculation times after 5-min transient forebrain ischemia was evaluated in gerbil hippocampal CA1 pyramidal neurons that had acquired tolerance to delayed-type ischemic injury. Evaluation was performed by observing polyribosomes under electron microscopy, and by [14C]leucine autoradiography. Hippocampal CA1 pyramidal neurons in the gerbils acquired stable and reproducible tolerance to delayed-type ischemic injury subsequent to a 5-min ischemia by pretreatment that consisted of loading two 2-min ischemic periods at a 1-day interval, followed by 48 h of recirculation. During the early phase following the 5-min ischemia, polyribosomal disaggregation, loss of dendritic microtubules, and significant suppression of radiolabeled leucine incorporation were observed in the tolerance-induced CA1 neurons as well as in the non-tolerance-induced neurons. While these findings persisted in the non-tolerance-induced neurons throughout the duration of the experiment, most of the tolerance-induced neurons demonstrated reaggregation of cytosomal ribosomes, increase in the number of dendritic microtubules, and restoration of impaired amino acid incorporation 24 h after the ischemia. These findings suggest that recovery of protein synthesis during the early post ischemic phase is essential for CA1 neuron survival after ischemic injury.

Amino Acids↗
PubMed1993

Successful total removal of intramedullary hemangioblastoma from the medulla oblongata.

The case of a large solid hemangioblastoma embedded wholly in the medulla oblongata is reported. Preoperative magnetic resonance imaging provided precise indications of the anatomical location and radiologic features of the tumor, which facilitated its total removal by microsurgery. Short-latency somatosensory evoked potentials were monitored throughout the operation.

Adult↗
PubMed1993

Differential vulnerability in the hindbrain neurons and local cerebral blood flow during bilateral vertebral occlusion in gerbils.

Differential vulnerability in the hindbrain neurons was examined immunohistochemically during hindbrain ischemia in the gerbil. Hindbrain ischemia was produced by extracranial occlusion of the bilateral vertebral arteries just before their entry into the transverse foramen of the cervical vertebra. Local cerebral blood flow was measured by quantitative autoradiographic technique after 5 min of ischemia and was reduced to less than 5 ml/100 g per min in the cerebellum, the pons, and the medulla, indicating that severe and reproducible hindbrain ischemia was induced immediately after occlusion. For immunohistochemical investigation, four gerbils each were used for each ischemic period of 5, 10, 15, and 30 min. Immunohistochemical lesions, detected by the reaction for microtubule-associated protein 2, were visible in the lateral vestibular nucleus and the cerebellar interpositus nucleus even after 5 min of ischemia. These results suggested that these areas were more vulnerable than others, although blood flow was markedly reduced in various regions of the hindbrain. In contrast, areas related to respiratory or cardiovascular control were rather resistant to ischemia. The present study suggests that selective vulnerability during hindbrain ischemia depends mainly on different metabolic characteristics inherent to various neurons in the hindbrain.

Animals↗
PubMed1993

Role of protein kinase C in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage.

This study investigated the role of protein kinase C (PKC) in the pathogenesis of vasospasm after experimental subarachnoid hemorrhage (SAH). PKC activation by intracisternal injection of a phorbol ester [12-O-tetradecanoylphorbol-13-acetate (TP)] induced dose-dependent, slowly developing, severe contraction of the basilar artery. A single intracisternal injection of TP (5 x 10(-9) M in the CSF) induced sustained contraction lasting over 3 days, which almost paralleled the changes of membrane-bound PKC activity in the basilar arterial wall. In a two-hemorrhage SAH model, membrane-bound PKC activity in the basilar artery increased up to day 4 and returned to the control level by day 14, whereas angiographic contraction reached a maximum on day 7 and still persisted at a moderate level on day 14. Thus, there was a discrepancy between arterial PKC activity and arterial contraction. Multiple intracisternal injections of TP produced 30-40% sustained contraction of the basilar artery lasting for more than 10 days along with sustained activation of PKC to levels compatible with that observed in the SAH model. However, TP injection caused considerably milder histological changes in the basilar artery than those noted in the SAH model. We concluded that cerebral vasospasm after SAH cannot be explained solely on the basis of activation of the PKC pathway.

Animals↗
PubMed1993

A case of distal anterior choroidal artery aneurysm: case report and review of the literature.

We describe a very rare case of distal anterior choroidal artery aneurysm. A 34-year-old woman was admitted to our hospital because of headache and vomiting. Computed tomographic scans revealed a diffuse intraventricular hematoma and a thin subarachnoid hemorrhage. Cerebral angiography disclosed a saccular aneurysm in the peripheral portion of the right anterior choroidal artery, which was located in the temporal horn of the right lateral ventricle. We approached the temporal horn through a small inferior temporal incision, and the aneurysm was resected without any neurological damage. A histological examination of the surgical specimen revealed it to be a true aneurysm.

Adult↗