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ABSTRACT: To cite this article: Kita T, Banno F, Yanamoto H, Nakajo Y, Iihara K, Miyata T. Large infarct and high mortality by cerebral ischemia in mice carrying the factor V Leiden mutation. J Thromb Haemost 2012; 10: 1453-5.
Journal of Thrombosis and Haemostasis 05/2012; 10(7):1453-5. · 5.73 Impact Factor
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ABSTRACT: We analyzed the incidence of ischemic complications after internal trapping for ruptured VA dissecting aneurysms. Between April 2001 and August 2005, nine cases of ruptured VA dissecting aneurysms, five in women, "proximal" or distal (distal type) to the origin of the PICA, were treated by internal trapping in the acute stage after SAH. There were four cases of proximal type and five of distal type. The demographics of the patients were reviewed in the medical charts and radiological findings were evaluated by neuroradiologists. The dissected site was completely obliterated and PICA was preserved in all cases. Follow-up angiography performed five to 19 days after treatment revealed complete obliteration of the aneurysm and patency of the PICA. The incidence of perioprocedural ischemic complications for the PICA-distal type (75%) was higher than that for the PICA-proximal type (20%). Here we retrospectively analyzed and discussed the incidence and mechanisms of ischemic complications.
Interventional Neuroradiology 03/2007; 13 Suppl 1:157-62. · 0.56 Impact Factor
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ABSTRACT: We report a rare case of a ruptured de novo dissecting aneurysm induced by ethyl 2-cyanoacrylate. A 39-year-old woman underwent microvascular decompression for left hemifacial spasm. The offending vessel was left posterior inferior cerebellar artery (PICA). Left vertebral artery (VA) was mobilized and affixed to the dura mater with cyanoacrylate to remove pressure of PICA to the root exit zone of the facial nerve. The left VA was found to be intact at the time of the operation. One year later, the patient sufferd subarachnoid haemorrhage (SAH) caused by rupture of a newly-developed dissecting aneurysm of the left VA. Endovascular occlusion of the dissecting site was performed using Guglielmi detachable coils. We suppose mechanical injury and chemical reaction of ethyl 2-cyanoacrylate induced dissecting aneurysm.
Interventional Neuroradiology 01/2006; 12(Suppl 1):145-7. · 0.56 Impact Factor
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K Hayashi,
H Seyama,
N Yamada,
K Murao, K Iihara,
J C Takahashi,
N Nakajima,
T Sayama,
M Morimoto,
H Mori,
M Yamamoto,
T Hishikawa,
Y Nonaka,
J Ayabe,
T Kikuchi,
M Hyuga,
M Ookawa,
T Kudo,
S Miyamoto
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ABSTRACT: In the safety stenting, it is important to get to know the characteristics of a plaque. In petrous carotid artery stenosis, it is difficult to know the characteristics of the plaque.We paid our attention to the MPRAGE (Magnetization Prepared Rapid Acquisition with Gradient Echo) method on high resolving power MRI. By the MPRAGE method, low intensity was observed in these lesions of all cases. This result suggested that the plaque in petrous portion was a fibrous plaque. This method is useful to get to know the characteristics of a plaque in petrous portion before endovascular treatment.
Interventional Neuroradiology 01/2006; 12(Suppl 1):193-6. · 0.56 Impact Factor
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ABSTRACT: The purpose of this study was to evaluate the efficacy and safety of staged carotid stenting (CS) and carotid endarterectomy (CEA) for bilateral internal carotid artery stenosis. With this strategy, initial carotid stenting was performed for the high grade carotid stenosis to reduce the risk of subsequent CEA. Eight patients were treated with staged CS and CEA; CS for asymptomatic side followed by CEA for symptomatic side. Sufficient revascularization was obtained in all procedures but one CS procedure. Two minor stroke caused by distal embolism occurred during the perioperative period of CS. Postprocedural persistent hypotension was observed in one CS procedure. The mean interval between CS and CEA was 19.8 days. In conclusion, although our strategy has some advantages such as avoidance of bilateral cranial nerve palsy and shorter admission period over staged CEA, relatively high complication rate was noted at the first CS without any stroke morbidity post CEA. Our preliminary result showed that further reduction of periprocedural complication rate at the initial stenting is mandatory for this approach justified.
Interventional Neuroradiology 05/2003; 9(Suppl 1):143-8. · 0.56 Impact Factor
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S Kogure,
N Sakai, K Iihara,
H Sakai,
H Sakaida,
T Higashi,
J C Takahashi,
H Ohta,
T Nagamine,
R Anei,
A Soeda,
A Taniguchi,
I Nagata
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ABSTRACT: The purpose of this study was to evaluate our initial procedural success rate and angiographical outcome of stent placement for vertebral artery (VA) stenosis at the intermediate followup period (11.3 +/- 7.3 months). Stent placement was successfully performed in 20 procedures (19 patients), resulting in a marked reduction of stenosis from 78.7 +/- 12.6 % before to 8.7% +/- 10.6 after stenting. Follow-up angiography, performed after an interval of 11.3 +/- 7.3 months, revealed restenosis greater than 50% in a total of 6 procedures (40%) out of 15. Although PTA with stent placement for stenosis affecting VA origin provided excellent initial success, restenosis occurred at a significant rate even during the intermediate follow-up period.
Interventional Neuroradiology 12/2001; 7(Suppl 1):167-9. · 0.56 Impact Factor
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H Sakaida,
N Sakai,
I Nagata,
H Sakai, K Iihara,
T Higashi,
S Kogure,
J Takahashi,
H Ohta,
T Nagamine,
R Anei,
A Soeda,
A Taniguchi,
A Shindo,
H Kikuchi
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ABSTRACT: The authors report the initial results of stenting in four patients of Takayasu arteritis for 11 occlusive carotid and subclavian arteries between January 1999 and December 2000. The lesions included stenoses of two right subclavian, three right common carotid, two left common carotid, and two left subclavian arteries, and total occlusion of two subclavian arteries. A total of 14 stents were implanted in 10 arterial lesions, resulting in a 91% procedural success rate. One failure was due to inability to cross the total occlusion of the subclavian artery. Procedural complications and problems were pain during balloon angioplasty in three patients, vaso-vagal reflex in two, carotid artery perforation associated with transient horseness in one, and stent migration in one. There was no permanent morbidity. Follow-up over a mean duration of 12 months revealed one symptomatic recurrence of left subclavian stenosis, followed by a successful re-dilatation. The results of the current study indicated that primary stenting is an excellent therapeutic option for the occlusive carotid and subclavian arteries in Takayasu arteritis. A long-term follow-up is required to determine the response or behavior of stented segments of the affected arteries.
No shinkei geka. Neurological surgery 12/2001; 29(11):1033-41. · 0.13 Impact Factor
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ABSTRACT: Brain subjected to acute ischemic attack caused by an arterial blockage needs immediate arterial recanalization. However, restoration of cerebral blood flow can cause tissue injury, which is termed reperfusion injury. It is important to inhibit reperfusion injury to achieve greater brain protection. Because oxidative stress has been shown to activate mitogen-activated protein kinases (MAPKs), and because oxidative stress contributes to reperfusion injury, MAPK may be a potential target to inhibit reperfusion injury after brain ischemia. Here, we demonstrate that reperfusion after forebrain ischemia dramatically increases phosphorylation level of extracellular signal-regulated kinase 2 (ERK2) in the gerbil hippocampus. In addition, i.v. administration of U0126 (100-200 mg/kg), a specific inhibitor of MEK (MAPK/ERK kinase), protects the hippocampus against forebrain ischemia. Moreover, treatment with U0126 at 3 h after ischemia significantly reduces infarct volume after transient (3 h) focal cerebral ischemia in mice. This protection is accompanied by reduced phosphorylation level of ERK2, substrates for MEK, in the damaged brain areas. Furthermore, U0126 protects mouse primary cultured cortical neurons against oxygen deprivation for 9 h as well as nitric oxide toxicity. These results provide further evidence for the role of MEK/ERK activation in brain injury resulting from ischemia/reperfusion, and indicate that MEK inhibition may increase the resistance of tissue to ischemic injury.
Proceedings of the National Academy of Sciences 10/2001; 98(20):11569-74. · 9.68 Impact Factor
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H Sakaida,
N Sakai,
I Nagata,
H Sakai, K Iihara,
T Higashi,
S Kogure,
J Takahashi,
H Ohta,
T Nagamine,
R Anei,
A Soeda,
A Taniguchi,
A Shindo,
H Kikuchi
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ABSTRACT: The authors report the initial results, between January 1998 and February 2001, of stenting utilizing the brachial approach in seven patients for total occlusions at the following locations: two right subclavian, one brachiocephalic, and five left subclavian arteries. All lesions were associated with subclavian steal syndrome. Indications for the treatment included ischemic symptoms in the affected arm (seven patients), and vertebrobasilar insufficiency (five patients). A total of eight stents were implanted in six occluded arteries, resulting in a 75% procedural success rate. Procedural complications encountered were two subintimal dissections by a 0.035-inch guide wire during recanalization, and one stent dislodgement with migration. There was no stroke, presumably because of the previously reported preventive effect of delayed reversal of a stealing vertebral artery. Follow-up over a mean duration of 11 months revealed no sign or symptom of recurrence in cases with initial technical success. The results of the current study, with a literature survey, indicated that percutaneous transluminal angioplasty with primary stent deployment in an occluded prevertebral segment of the subclavian or the brachiocephalic artery should be considered as an available choice for treatment. Further points, such as some remaining technical and clinical problems, will require more experience and consideration.
No shinkei geka. Neurological surgery 09/2001; 29(8):717-25. · 0.13 Impact Factor
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ABSTRACT: Expression of brain-derived neurotrophic factor (BDNF) may play a role in the mechanism of neuronal cell death after cerebral ischemia. We investigated the changes in levels of mRNAs encoding BDNF and its promoters in the rat brain after transient forebrain ischemia. Transient forebrain ischemia was induced by occlusion of bilateral common carotid arteries and systemic hypotension for 8 min. The alterations in BDNF gene expression in the hippocampus and in the cerebral cortex were examined by in situ hybridization using a mouse BDNF cDNA probe and cDNA probes including exon-specific promoters. BDNF transcripts were rapidly enhanced after the ischemic insult, both in the hippocampus and the cerebral cortex. NBQX suppressed the enhanced gene expression of BDNF markedly in the dentate gyrus (DG). In contrast, MK-801 had little effect on BDNF expression. In the piriform cortex, MK-801 or NBQX reduced the expression only moderately. After the ischemic insult, promoter specific BDNF 5'-exon I and exon III were increased remarkably in the DG. The increase in exon I in DG was suppressed partially by MK-801 and NBQX, while the increase in exon III in CA3 was suppressed by MK-801 but that in DG was not suppressed by either antagonist. In the piriform cortex, exon III was increased remarkably and this increase was not influenced by either agonist. These results suggest that the gene expression of BDNF was enhanced by transient ischemia both in the hippocampus and the cerebral cortex and that the cerebral ischemia stimulated at least two different promoter- and neuron type-specific pathways regulating expression of the BDNF gene mediated by glutamate receptors of non-NMDA type and NMDA type.
Neurochemistry International 09/1998; 33(2):201-7. · 2.86 Impact Factor
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ABSTRACT: Nerve growth factor, brain-derived neurotrophic factor, and other neurotrophic factors have been reported to have neuroprotective effects against global ischemia. To investigate whether the homodimer of platelet-derived growth factor B-chain (PDGF-BB) can protect neurons against focal temporary ischemia, PDGF-BB was administered to the rat brain for a prolonged period prior to, during, and after ischemia, since PDGF-BB protected rat neurons from global ischemia in our previous study. A total of 82 male Sprague-Dawley rats were used. Recombinant PDGF-BB, or saline was administered into the left neocortex via an implanted osmotic pump for 3 days (1.2 microg in total), 7 days (2 microgram or 4 microgram in total), or 14 days (4 microgram in total) pre-ischemia and 2 days post-ischemia. In an additional group, PDGF-BB (4 microgram in total) was administered for 14 days by osmotic pump and focal ischemia was induced after an additional 7-day interval following removal of the pump. Focal temporary ischemia was induced in the left MCA territory by bilateral CCA and MCA occlusion for 2 h. All rats were sacrificed 2 days after ischemia and the volume of cerebral infarct was analyzed using TTC staining. In a separate set of animals, regional cerebral blood flow (rCBF) was monitored by the hydrogen clearance method and laser Doppler flowmetry (LDF) of the neocortex after 14 days of intracerebral administration of PDGF-BB or saline. In the group receiving PDGF-BB (4 microgram in total) for 7 or 14 days pre-ischemia, there was a significant reduction of neocortical infarction compared to that in the control or saline-infused group. The size of cerebral infarct was smallest in the group that received PDGF-BB for 14 days, when ischemia was induced 7 days after removal of the pump. Regarding rCBF measurement, there were no significant differences in groups receiving PDGF-BB or saline infusion for 14 days. The potent neuroprotective effect of PDGF-BB on global ischemia was also demonstrated in the focal ischemia model. However, prolonged intracerebral infusion for 7 to 14 days was necessary to achieve a significant reduction of infarct volume. Neuroprotection was not due to increased collateral flow during ischemia.
Brain Research 03/1998; 784(1-2):250-5. · 2.73 Impact Factor
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ABSTRACT: Our previous studies demonstrated coordinate expression of platelet-derived growth factor (PDGF) -B chain and beta-receptor in neurons at risk in the rat brain with focal ischemia. To clarify a role of the -B chain in the brain further, we examined whether PDGF-A or -B chain protects CA1 pyramidal neurons from delayed neuronal death after forebrain ischemia in rats. Pretreatment with PDGF-BB, but not -AA, at 120 ng/d for 2 days until forebrain ischemia was performed markedly ameliorated delayed neuronal death in CA1 pyramidal neurons on day 7 after ischemia. This neuroprotective effect of PDGF-BB was dose-dependent, and pretreatment with PDGF-BB at 240 ng/d showed almost complete inhibition of delayed neuronal death. In contrast, posttreatment with PDGF-BB at 120 ng/d starting 20 minutes after ischemia demonstrated no significant neuroprotective effect. The current study established marked neuroprotective actions of PDGF-BB in ischemic neuronal damage.
Journal of Cerebral Blood Flow & Metabolism 11/1997; 17(10):1097-106. · 5.01 Impact Factor
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ABSTRACT: Our previous study on the ischemia-induced expression of platelet-derived growth factor (PDGF)-B chain in the rat brain prompted us to examine expression of PDGF beta-receptor in the ischemic brain. Focal ischemia was induced by permanent tandem occlusion of middle cerebral and common carotid arteries in spontaneously hypertensive rats. Northern analysis revealed that ischemia significantly increased expression of the receptor in the ischemic neocortex at 4 and 7 days (328 +/- 109%; 323 +/- 119%, respectively, over control: n = 4, p < 0.05 versus sham). Neurons in infarct transiently showed increased immunostaining for the receptor at 1 day, whereas neurons in periinfarct area showed sustained and increased immunoreactivity from 1 to 14 days post-ischemia. Reactive glial cells in the external capsule and in molecular layer of the neocortex adjacent to infarct possessed enhanced immunoreactivity from 1 to 21 days. Furthermore, marked immunoreactivity was observed on brain macrophages in infarct and on the abluminal side of capillaries surrounding infarct from 4 to 7 days. These results demonstrated that ischemic insult increases expression of the PDGF beta-receptor at both the mRNA and protein level in the brain, suggesting its important role in cellular cascade of the ischemic brain.
Journal of Cerebral Blood Flow & Metabolism 09/1996; 16(5):941-9. · 5.01 Impact Factor
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ABSTRACT: 1. The present study was conducted to analyse the release and production of mitogen in cultured aortic endothelial cells of stroke-prone spontaneously hypertensive rats (SHRSP), for the further understanding of the role of arterial endothelial cells in the genesis of vascular lesions in hypertension. 2. The cultured aortic endothelial cells derived from SHRSP increased released mitogens were compared with those from control Wistar-Kyoto rats (WKY) with respect to cultured vascular medial smooth muscle cells and fibroblasts. 3. Biochemical analyses determined that the major part of mitogen released from aortic endothelial cells of both SHRSP and controls was the platelet-derived growth factor B-chain. 4. Further northern analyses revealed that the transcripts of PDGF B-chain were constitutively accumulated three- to four-fold in quiescent aortic endothelial cells from SHRSP, compared with those from WKY through passages 2 to 5. 5. However, the half-lives of the transcripts after actinomycin D treatment were 1.12 h (s.d. = 0.14, n = 4) and 1.28 h (s.d. = 0.08, n = 3), in SHRSP and in WKY, respectively, showing no significant difference. 6. These suggest that the increased accumulated transcripts of PDGF B-chain in SHRSP are due to an enhanced transcriptional rate. These enhanced release and production of PDGF-B chain in arterial endothelial cells, which may be induced under chronic hypertensive conditions, is suggested to contribute to the genesis of vascular lesion in hypertension, through the stimulation of vascular smooth muscle cell proliferation and hypertrophy.
Clinical and experimental pharmacology & physiology. Supplement 01/1996; 22(1):S123-5.
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ABSTRACT: To elucidate the role of the platelet-derived growth factor (PDGF)-B chain in the brain, we examined its expression in rat brains with focal ischemia. Focal ischemia was induced by permanent tandem occlusion of the middle cerebral and common carotid arteries in spontaneously hypertensive rats (SHRs). Northern analysis demonstrated that ischemia transiently increased mRNA expression of the PDGF-B chain, but not the PDGF-A chain, in the injured neocortex. The larger transcript (3.5 kb) of the B chain gradually increased to threefold by 16 h, whereas the smaller transcript (2.6 kb) of the B chain markedly increased sixfold by 4 h. Immunohistochemistry revealed enhanced immunoreactivity in the neurons in the infarct and in the periinfarct area from 16 h to days 4-7, with a peak at 24 h. Furthermore, the brain macrophages that accumulated in the infarct showed intense immunostaining in their perinuclear region from days 2 to 14, with a peak at days 5-6. The present study demonstrates that ischemia induces the expression of the PDGF-B chain, first in neurons and later in brain macrophages, and suggests an important role of the PDGF-B chain in the healing process of the injured brain.
Journal of Cerebral Blood Flow & Metabolism 10/1994; 14(5):818-24. · 5.01 Impact Factor
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ABSTRACT: Platelet-derived growth factor (PDGF) is a potent mitogen for mesenchymal cells and glial cells. For a better understanding of the role of PDGF B-chain in the brain, the expression of PDGF B-chain was examined immunohistochemically in penetrating injury to the rat brain. Shrunken neurons were distributed with enhanced PDGF B-chain-related immunoreactivity (PBRI) in the vicinity of the lesion during a period from day 1 to day 4 post injury. Platelet-derived growth factor B-chain-related immunoreactivity was transiently observed also in the cytoplasm of the numerous brain macrophages in the lesion on day 3 and day 4. These distributions of PBRI in the lesion were closely related to the neovascularization and astrogliosis there. The close time and spatial correlation between the expression of PBRI and cellular responses to injury seen in this study suggests PDGF B-chain has an important role in the healing process of cerebral wound.
Brain Research 09/1994; 653(1-2):131-40. · 2.73 Impact Factor
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ABSTRACT: In this contribution the clinical features of eleven patients suffering from a neurinoma in the cauda equina and around the conus medullaris are analysed. Because of the relative mobility of the roots and the wide space in the spinal canal, tumours arising in the cauda equina or around the conus medullaris can become larger than any other spinal tumours. Lumbago was the predominant symptom as the initial complaint. Nocturnal pain relieved by walking was noticed in one patient. Two cases showed spontaneous remission and relapse. Multiple tumours were found in 6 cases (55%). Macroscopic cyst formation was found in 5 cases (45%). Among the eleven patients, total removal of the tumour, including the involved root, was performed in ten. The numbers of the resected nerve roots were one root in 6 cases, two roots in 2, and three roots in 2. Only one patient showed postoperative slight weakness of the leg.
Neurochirurgia 10/1992; 35(5):145-9.
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ABSTRACT: The authors reported their clinical experience with devices, which have been recently introduced for spinal surgery. The main roles of such devices are to correct malalignment of the spine and stabilize the spinal instability. Although Harrington's device has been widely used since 1962, its use is gradually decreasing due to its having several weak points, such as its low resistance to distorting forces and its imperfect ability to correct malalignment of the spine. In the present manuscript, the authors describe clinical experience with three kinds of spinal devices. They are Steffee's transpedicular screw for 5 cases of lumbar spondylolisthesis, Roosen-Trauschel compression clamp for 2 cases of atlanto-axial dislocation and Kaneda's device for one case of metastatic T-11 tumor. Good fixation was obtained in 4 cases using Steffee's devices. The injury of the nerve root is one of the most serious disadvantages in this device. Although Roosen-Trauschel compression clamp needs improvement in some aspect, it was able to bring about good stabilization without using sublaminar wiring, which may be a dangerous procedure in the cervical region. Kaneda's device seemed to be useful for the thoracolumbar lesion. Although it needs a relatively radical approach, such as thoracotomy, Kaneda's device brought about good stabilization and corrected the kyphosis. The devices, which are described in the present manuscript, will probably play important roles in spinal surgery in the future.
No shinkei geka. Neurological surgery 04/1992; 20(3):243-8. · 0.13 Impact Factor
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ABSTRACT: A 46-year-old female was admitted complaining of progressive, severe girdle pain consistent with the left Th3 dermatome. Neurological examination on admission revealed dysesthesia and radiating pain in the left Th3 territory. Plain X-rays and tomograms of the thoracic spine revealed a beak-like bony excrescence arising from the lamina and projecting moderately to the Th3/4 intervertebral foramen, suggesting ossification of the thoracic ligamentum flavum (OYL). Myelography showed the dural sac compressed from laterally just below the left Th3 pedicle, which suggested that the Th3 nerve root was compressed by the OYL. After Th3 nerve root decompression through hemilaminectomy and foraminotomy, the girdle pain disappeared. OYL is known to cause thoracic radiculomyelopathy, but presentation with intercostal neuralgia only is very rare. The authors review the literature and stress the importance of myelography for diagnosis.
Neurologia medico-chirurgica 01/1992; 31(13):999-1002. · 0.61 Impact Factor
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ABSTRACT: A case of atrial myxoma with cerebral oncotic aneurysms was presented. A 37 year-old woman was admitted complaining of right hemiparesis, and episodes of syncope. Neurological examination on admission revealed a right arm monoparesis, a right hemisensory disturbance, and a motor aphasia. Computed tomography (CT) demonstrated low density areas in the left fronto-parietal region, and multiple discrete enhancing high density spots scattered bilaterally in the parietal lobes. Cerebral angiography showed multiple fusiform peripheral aneurysms especially in the distribution of the bilateral middle cerebral arteries. Cerebral emboli from the cardiac source were suspected, and an echocardiography was performed, which disclosed a huge villous mass in the left atrium. The cardiac mass was resected uneventfully under cardiopulmonary bypass. It proved to be a left atrial myxoma. Postoperatively, her neurological deficit persisted. After the resection of the cardiac tumor, follow-up angiographies were undertaken twice. The second angiography performed 6 months later revealed spontaneous resolution or stabilization of most of the aneurysms detected before. On the other hand, newly-developed aneurysms were seen at the sites which had seemed normal previously on the first angiography. No remarkable changes were seen on the third one except the slight enlargement of one of the aneurysms in the middle cerebral territory. At 3 years she was neurologically stable. Because of the paucity of knowledge concerning the natural history of cerebral oncotic aneurysms and lack of definite treatment for them, long-term follow-up including serial angiography is mandatory after the resection of left atrial myxoma.
No shinkei geka. Neurological surgery 10/1991; 19(9):857-60. · 0.13 Impact Factor
