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T Kawamata

Publications and source records attributed to T Kawamata.

At least 19 recordsLinked to original sources

Extravascular application of an intravascular ultrasound (IVUS) catheter during carotid endarterectomy to verify distal ends of stenotic lesions.

BACKGROUND: Intravascular ultrasound (IVUS) has been developed initially for intravascular imaging of coronary arteries to investigate vascular structures. We applied the IVUS catheter extravascularly to the cervical carotid arteries to obtain intra-operative ultrasound images during carotid endarterectomy (CEA). Intra-operative assessments of the distal ends of the stenotic lesions as well as pathological vascular structures are important, not only for exposing the lesions sufficiently but also for placing the shunt system safely. METHOD: An IVUS catheter (3.2 French/30 MHz) was intra-operatively applied close to the outer surface of the cervical carotid arteries during CEA. Ultrasound transection vascular images were obtained in 33 consecutive patients (30 males and 3 females) with a mean age of 66.5 years. FINDINGS: In 32 of 33 cases, extravascular application of IVUS catheter before making arteriotomies correctly depicted the distal ends of the internal carotid artery (ICA) stenotic lesions as a thin layer of vascular wall [0.64 +/- 0.16 mm (mean +/- SD) compared with 1.66 +/- 0.42 mm for carotid plaque] with intravascular blood flow. Based on the IVUS findings, we were able to adequately expose the normal ICA portion distal to the stenotic lesion before making the arteriotomy even in cases with stenotic lesions at very high positions, and to insert shunts safely. Furthermore, the properties of lesions and blood flow were also verified. However, it was difficult to examine the far vascular wall. CONCLUSIONS: Extravascular application of IVUS catheter is efficient for intra-operative evaluation of the distal end of the stenotic lesion especially in cases with stenotic lesions at very high positions and cases in whom pre-operative angiograms did not clearly demonstrate the distal end. The findings also demonstrate the properties of lesions and completeness of CEA.

Adult↗

Metabolic derangements in interstitial brain edema with preserved blood flow: selective vulnerability of the hippocampal CA3 region in rat hydrocephalus.

Hydrocephalus induces interstitial brain edema, which causes neurological deficits, even if the intracranial pressure is maintained within the normal range, and the cerebral blood flow (CBF) does not decline to an ischemic level. The precise mechanisms underlying such edema-induced neuronal dysfunction remain unclear. In the present study, in an attempt to elucidate the metabolic derangements in brain tissue with interstitial edema, we evaluated the changes in CBF and oxidative/glucose metabolism using a rat model of kaolin-induced hydrocephalus. Hydrocephalus was produced in male Wistar rats by intrathecal injection of 0.1 ml aluminum silicate suspension (200 mg/ml) via the cisterna magna. CBF was determined by 14[C]-iodoantipyrine autoradiography. Oxidative metabolism was evaluated by cytochrome oxidase (CYO) histochemistry, and glucose metabolism by hexokinase (HK) histochemistry. CBF declined with the development of hydrocephalus, but did not reach an ischemic level. The CYO activity was diffusely depressed in both the cortex and hippocampus. The HK activity was preserved at the early stage of hydrocephalus. At the advanced stage, the HK activity was reduced in the hippocampal CA3 region first, and diffusely thereafter. In conclusion, interstitial brain edema impairs oxidative metabolism even at the early stage of hydrocephalus, and shifts the metabolism to anaerobic glycolysis despite a preserved CBF. Impairment of glucose metabolism was first observed in the CA3 region, suggesting that the CA3 is metabolically vulnerable, and CA3 dysfunction may contribute to the memory deficits seen in hydrocephalus.

Animals↗

Edema fluid accumulation within necrotic brain tissue as a cause of the mass effect of cerebral contusion in head trauma patients.

The early massive edema caused by severe cerebral contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24-72 hours post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration. In order to elucidate the mechanisms underlying the early massive edema, we have carried out a series of detailed clinical studies. Diffusion magnetic resonance (MR) imaging and apparent diffusion co-efficient (ADC) mapping suggest that cells in the central area of contusion undergo shrinkage, disintegration and homogenization, whereas cellular swelling is predominant in the peripheral area during the period of 24-72 hours post-trauma. The ADC values in the central and peripheral areas are maximally dissociated during this period. A large amount of edema fluid accumulates within the necrotic brain tissue of the central area beginning at approximately 24 hours post-trauma. We have found that fluid-blood interface formation within the central area does not represent an uncommon finding in various neuroimaging examinations of cerebral contusions, indicating layering of red blood cells within the necrotic brain tissue accumulating voluminous edema fluid. Intravenous slow infusion of gadolinium-DTPA and delayed MR imaging revealed that the central area of contusion can be enhanced at 24-48 hours post-trauma. implying that water supply from the blood vessels is not completely interrupted. Necrotic brain tissue sampled from the central area of contusion during surgery demonstrates a very high osmolality. It appears that the capacitance for edema fluid accumulation increases in the central area, whereas cellular swelling in the peripheral area elevates the resistance for edema fluid propagation. Combination of these circumstances may facilitate edema fluid accumulation in the central area. We also suggest that the dissociation of ADC values and high osmolality within the necrotic brain tissue may generate an osmotic potential across the central and peripheral areas and contribute to the early massive edema caused by cerebral contusion.

Body Fluids↗

Ultra-early study of edema formation in cerebral contusion using diffusion MRI and ADC mapping.

OBJECTIVE: Our previous studies have reported that heterogeneous mechanisms exist in early edema formation in cerebral contusion, and cytotoxic edema plays an important role within 48 hours post-trauma. It is remains unclear, when edema begins to develop following injury. In order to determine the time course of edema development, diffusion imaging and ADC (apparent diffusion co-efficient) mapping was performed in 10 patients within 24 hours post-trauma with cerebral contusion. METHODS: Diffusion imaging and ADC mapping were performed employing 1.0 T echo planar MRI. ADC values were indicated as a ration relative to the values of intact brain areas. RESULTS: Within 3 hours post-trauma, diffusion MRI showed no remarkable changes, and the ADC values were within normal limit (ADC ratio (=contused/normal brain) = 1.00 +/- 0.21, (mean +/- SD)). At 6 hours post-trauma, diffusion images demonstrated a low intensity core in the contusion proper and a high intensity rim in the peripheral area of contusion. The ADC value increased in the contusion proper (ADC ratio = 1.26 +/- 0.13) and decreased in the peripheral area (ADC ratio = 0.58 +/- 0.19). CONCLUSIONS: These findings indicated that early cellular swelling in the peripheral area of contusion begins within 6 hours following injury. This delayed occurrence of contusion-induced cellular swelling suggests that the CBF does not decrease to ischemic level immediately following injury.

Brain Edema↗

Pneumocephalus following an epidural blood patch.

Pneumocephalus is a rare complication of epidural block. We report a case of pneumocephalus complicating an epidural blood patch performed 3 days after unintentional dural puncture. Pneumocephalus may occur during an epidural blood patch procedure, even if the epidural needle tip is within the epidural space.

Aged↗

Infantile gliosarcoma: a case and a review of the literature.

INTRODUCTION: Gliosarcoma in infant is a very rare entity. CASE REPORT: The authors present a case of gliosarcoma in a 23-month-old boy. The patient was admitted to our hospital with persistent headache and frequent vomiting. MR imaging demonstrated a large frontal well-circumscribed lesion with a heterogeneous gadolinium enhancement. Although macroscopically the tumor was totally extirpated, the boy died of rapid tumor regrowth 2 months after surgery. The surgical specimens obtained from the tumor showed an admixture of two distinctive neoplastic tissues. One was a malignant mesenchymal feature. Its fibrosarcomatous nature was characterized by spindle-shaped cells with fine fibers that were deeply stained in silver preparations for reticulin. The other was gliomatous tissue forming islands surrounded by the sarcomatous tissues. Its glioblastomatous nature was obvious, as it was characterized by endothelial proliferation and perinecrotic pseudopalisading. Both tissues were histologically malignant, as evidenced by mitotic figure, high cellularity, atypical features, and variability. DISCUSSION: The literature concerning gliosarcomatous tumors is reviewed, and pathological and clinical features of the tumor are briefly discussed.

Brain Neoplasms↗

Deep brain stimulation therapy for a persistent vegetative state.

Twenty cases of a persistent vegetative state (PVS) caused by various kinds of brain damage were neurologically and electrophysiologically evaluated at 3 months after persistence of the PVS, and were treated by deep brain stimulation (DBS) therapy. The stimulation sites were the mesencephalic reticular formation (2 cases) and CM-pf complex (18 cases). Seven of the patients emerged from the PVS, and became able to obey verbal commands. However, they remained in a bedridden state. These 7 cases revealed a desynchronization or slight desynchronization pattern on continuous EEG frequency analysis. The Vth wave of ABR and N20 of SEP could be recorded even with a prolonged latency, and the pain-related P250 was recorded with an amplitude of over 7 microV. We conclude that chronic DBS therapy may be useful for allowing the patient to emerge from a PVS, if the candidates are selected according to the neurophysiological criteria. In view of the severely disabled state of the patients who emerged from the PVS, a special rehabilitation program which includes neurostimulation therapy may be necessary for treatment of the PVS.

Adult↗

Control of post-stroke movement disorders using chronic motor cortex stimulation.

The effects of motor cortex (MC) stimulation on post-stroke movement disorders were analyzed in 50 patients. These individuals either underwent MC stimulation primarily for the purpose of controlling their post-stroke involuntary movements (n = 8) or underwent MC stimulation for the purpose of controlling their post-stroke central pain (n = 42). In the latter patients, the effects of MC stimulation on co-existent involuntary or voluntary movement disorders were analyzed retrospectively. Good control of involuntary movements was observed in 2 of 3 patients with hemichoreo-athetosis, 2 of 2 patients with distal resting or action tremor, and 1 of 3 patients with proximal postural tremor. Subjective improvements in motor performance were reported by 8 patients who had mild motor weakness, and the effects appeared to be attributable to attenuation of rigidity. We consider that these findings justify further clinical studies on MC stimulation for the control of post-stroke movement disorders.

Electric Stimulation Therapy↗

Mechanisms of the mass effect of cerebral contusion: ICP monitoring and diffusion MRI study.

OBJECTIVE: Cerebral contusion is sometimes associated with a non-hemorrhagic mass effect which progresses rapidly within 12-48 hours post-trauma. In order to determine the mechanisms underlying such a mass effect, we analyzed data obtained from ICP monitoring and diffusion MRI in a total of 38 patients with cerebral contusion. METHODS: Diffusion imaging and ADC mapping were performed employing 1.5 T echo planar MRI. ADC values were expressed as a ratio relative to the values of intact brain areas. RESULTS: In 6 patients, ICP became uncontrollable medically and surgical resection of the contused brain tissue was eventually performed. Within 24 hours post-trauma, diffusion images revealed a low intensity core and a high intensity rim in the contusion. The ADC ratio increased in the central area (1.13 +/- 0.21) and decreased in the peripheral area (0.67 +/- 0.14). A crescent-shaped zone of very high ADC ratio (1.45 +/- 0.14) was observed at the border between these two areas during the period of 24-48 hours. CONCLUSIONS: It appears that the capacitance of edema fluid accumulation is elevated by cellular disintegration in the central area, whereas the resistance to edema fluid propagation is elevated by cellular swelling in the peripheral area. We suggest that such events facilitate extracellular edema fluid accumulation within contused brain tissue and contribute, together with cellular swelling itself, to the non-hemorrhagic mass effect of cerebral contusion.

Brain Concussion↗

Ectopic clival craniopharyngioma.

Ectopic craniopharyngioma is a rare entity. The authors present a very rare case of an ectopic clival craniopharyngioma completely separate from the sella turcica.A 44-year old woman presented with abducens palsy. A MR imaging study and a CT scan revealed a cystic clival lesion separate from the sella turcica. Surgical resection was performed successfully with flexible endoscope-assisted procedure using an endonasal transsphenoidal approach. No evidence of involvement of the sellar region was found according to radiological, intra-operative, and clinical findings.A review of the literature revealed no other such cases. The discussion includes the formation of craniopharyngioma from the ectopic Rathke's pouch remnants and the surgical approach for clival lesions. We believe that our approach provides good results with minimal invasiveness for some clival lesions.

Adult↗

Expression of cyclin kinase inhibitor p21/WAF1 protein in pituitary adenomas: correlations with endocrine activity, but not cell proliferation.

p21/WAF1 blocks cell cycle progression through inhibition of cyclin/cyclin-dependent kinases (cdks) complexes and, simultaneously, has been associated with cell cycle exit and the process of differentiation. In this series, the expression of p21/WAF1 was assessed immunohistochemically in 47 cases of pituitary adenomas in relation to endocrine activity and cell proliferation. To evaluate cell proliferation, a monoclonal antibody, MIB-1, against Ki-67 antigen was used in all of the available cases. The study revealed positive p21/WAF1 staining in 24 cases of 26 functioning parenchymas, whereas 14 cases of 21 non-functioning parenchymas stained negative. The MIB-1 index ranged from less than 1% to 5.1% (mean: less than 1.7%) in functioning adenomas, and from less than 1% to 3.6% (mean: less than 1.6%) in non-functioning adenomas. Regardless of endocrine activity, p21/WAF1 positivity did not correlate with the MIB-1 index. Double staining techniques revealed the co-expression of p21/WAF1/GH or p21/WAF1/PRL in functioning adenomas. In 22 cases of p21/WAF1-positive functioning adenomas, p21/WAF1 immunoreactivity was seen in the cytoplasma as well as nuclei. These results indicate that in pituitary adenomas, p21/WAF1 expression is associated with endocrine activity, but not with cell proliferation. Taken together with recent findings demonstrating that cytoplasmic p21/WAF1 acts as an inhibitor of apoptosis, it is possible that pituitary adenomas expressing cytoplasmic p21/WAF1 have resistance against DNA-damaging agents such as ionizing radiation.

Adenoma↗

Flexible endoscope-assisted endonasal transsphenoidal surgery for pituitary tumors.

We have performed rigid endoscope-assisted endonasal transsphenoidal microsurgeries for pituitary tumors in 230 patients. Recently, we further introduced the use of a flexible endoscope to inspect the tumor bed and suprasellar structures more extensively. We report our experience with the flexible endoscope in endonasal transsphenoidal surgery for pituitary tumors. The endoscopes were used to complement the microscope in visualization. The flexible endoscopes were used in 34 recent cases with suprasellar and/or lateral tumor extension. During or after removal of the main tumor bulk, the flexible endoscope together with a rigid endoscope was used to inspect the tumor cavity, especially at the blind spot of the microscope. Despite limited resolving power, in all the 34 cases the flexible endoscope was a highly efficient tool permitting extensive visualization of almost the whole surgical area, even in narrow surgical fields and spaces not visible with an operating microscope or a rigid endoscope, and allowing continuous change of viewing angle. The residual tumor situated laterally or in the suprasellar areas that could not be reached and was impossible to remove by a rigid endoscope could be dissected and extirpated under a flexible endoscope using grasping forceps in 5 patients with pituitary adenoma and all the craniopharyngioma cases. The flexible endoscope may be more efficient in the lateral and suprasellar areas than the rigid endoscope in compensating for the narrow surgical field in endonasal pituitary surgery, despite its limited resolving power. Surgeons should make the best use of the advantages of each instrument.

Adenoma↗

Involvement of capsaicin-sensitive fibers in spinal NMDA-induced glutamate release.

The activation of spinal NMDA receptors can evoke glutamate release through the production of nitric oxide (NO) within the spinal cord, resulting in pain-relating behavior. In this study, we investigated the involvement of capsaicin-sensitive primary afferents in this phenomenon using in vivo intrathecal microdialysis. Intrathecal NMDA perfusion evoked increases in the concentrations of NO metabolises and glutamate and in pain-related behavior in both neonatal capsaicin and vehicle-treated rats. Although the degrees of increase in NO metabolises in capsaicin- and vehicle-treated rats were not significantly different, capsaicin-treated rats showed significantly smaller increases in glutamate concentration and pain-related behavior than did vehicle-treated rats. Our results showed that glutamate release from capsaicin-sensitive primary afferent terminals is involved in spinal NMDA-induced pain.

Animals↗

Peripheral nitric oxide in carrageenan-induced inflammation.

Recent studies have suggested that nitric oxide (NO) peripherally produced by different nitric oxide synthase (NOS) isoforms contributes to edema formation and development of hyperalgesia. The present study was designed to examine the effects of NOS isoforms on NO release in carrageenan-induced inflammation at various time points. A microdialysis probe was implanted subcutaneously into the glabrous skin of hindpaws of Sprague-Dawley rats under pentobarbital anesthesia. After sample collection to obtain the basal level of the total amount of nitrite and nitrate (NO2-/NO3-), modified Ringer solution, a non-selective NOS inhibitor, NG monomethyl-L-arginine acetate (L-NMMA), or an iNOS inhibitor, aminoguanidine hemisulfate (AG) was perfused through the microdialysis probe. 2 mg of carrageenan was injected into the plantar surface of the probe-implanted hindpaw. Carrageenan was also injected in rats that had undergone sciatic nerve sectioning. Carrageenan significantly increased the dialysate concentrations of NO2-/NO3- for more than 8 h. L-NMMA suppressed the carrageenan-induced increase in NO2-/NO3- concentration. Although AG did not suppress the increase in NO2-/NO3- for the first 2 h after carrageenan injection, significant suppression of the increase in NO2-/NO3- was observed from 2.5 h after carrageenan injection. In the rats in which the sciatic nerves had been denervated, the increases in concentrations of NO2-/NO3- were completely suppressed up to 3 h and partially suppressed 4.5-8 h after carrageenan injection. The results of the current study show that carrageenan induces peripheral release of NO, the production of which is mediated by nNOS in the early phase and by both nNOS and iNOS in the late phase of carrageenan-induced inflammation.

Animals↗

Microglial signaling by amyloid beta protein through mitogen-activated protein kinase mediating phosphorylation of MARCKS.

Myristoylated alanine-rich C kinase substrate (MARCKS), an acidic protein associated with cell motility and phagocytosis, is activated upon phosphorylation by protein kinase C (PKC) and proline-directed protein kinases. In Alzheimer disease (AD), activated microglia expressing MARCKS migrates around senile plaques. We reported that amyloid beta protein (A beta), a major component of senile plaques, activated MARCKS through a tyrosine kinase and PKC-delta. We have now identified another A beta signaling pathway through a mitogen-activated protein kinase (MAPK) involved in the phosphorylation of MARCKS and analysed cross-talk between PKC and MAPK pathways in primary cultured rat microglia. A selective inhibitor for MAPK kinase, PD098059, significantly inhibited the phosphorylation of MARCKS induced by A beta. Extracellulary regulated kinases, the activities of which were induced by A beta, directly phosphorylated a recombinant MARCKS in vitro. The MAPK pathway was sensitive to wortmannin, but not to a PKC inhibitor or to tyrosine kinase inhibitors. The activation of PKC by A beta was not sensitive to wortmannin. Our findings suggest involvement of the MAPK pathway through phosphoinositol 3-kinase in the phosphorylation of MARCKS in rat cultured microglia, an event may be associated with mechanisms activating microglia in AD.

Amyloid beta-Peptides↗

Amyloid beta protein activates PKC-delta and induces translocation of myristoylated alanine-rich C kinase substrate (MARCKS) in microglia.

The increased accumulation of activated microglia containing amyloid beta protein (Abeta) around senile plaques is a common pathological feature in subjects with Alzheimer's disease (AD). Much less is known, however, of intracellular signal transduction pathways for microglial activation in response to Abeta. We investigated intracellular signaling in response to Abeta stimulation in primary cultured rat microglia. We found that the kinase activity of PKC-delta but not that of PKC-alpha or -epsilon is increased by stimulation of microglia with Abeta, with a striking tyrosine phosphorylation of PKC-delta. In microglia stimulated with Abeta, tyrosine phosphorylation of PKC-delta was evident at the membrane fraction without an overt translocation of PKC-delta. PKC-delta co-immunoprecipitated with MARCKS from microglia stimulated with Abeta. Abeta induced translocation of MARCKS from the membrane fraction to the cytosolic fraction. Immunocytochemical analysis revealed that phosphorylated MARCKS accumulated in the cytoplasm, particularly at the perinuclear region in microglia treated with Abeta. Taken together with our previous observations that Abeta-induced phosphorylation of MARCKS and chemotaxis of microglia are inhibited by either tyrosine kinase or PKC inhibitors, our results provide evidence that Abeta induces phosphorylation and translocation of MARCKS through the tyrosine kinase-PKC-delta signaling pathway in microglia.

Amyloid beta-Peptides↗

Injuries to the posterolateral aspect of the knee accompanied by compression fracture of the anterior part of the medial tibial plateau.

We present 12 cases of patients with injury to the posterolateral aspect of the knee accompanied by a compression fracture of the anterior part of the medial tibial plateau. There were 11 male patients and 1 female patient with an average age of 26 years (range, 17 to 44 years). There were 4 cases of posterolateral rotatory instability and 8 cases of straight lateral instability of the knee. The size of the compression fracture was classified into 2 types, small (8 cases) and large (4 cases). Although the mechanism of injury was considered to be hyperextension and varus force, the pattern of cruciate ligament injuries varied from case to case. The following 3 questions should be considered to determine which cruciate ligament is damaged: (1) Was the ipsilateral foot fixed to the ground? (2) Was forward inertia involved? (3) Was there a direct blow to the anteromedial aspect of the tibia or to the femur? Accompanied fractures of the medial tibial plateau were considered to have been compressed by the medial femoral condyle. The size of the accompanying compression fracture varied; 7 of 8 cases with a small-type fracture had posterior cruciate ligament injuries and 3 of 4 cases with a large-type fracture had anterior cruciate ligament injuries. The size of the fracture is determined by which point of the medial tibial plateau touched the medial femoral condyle. We propose that a compression fracture of the anterior part of the medial tibial plateau indicates a coexistent posterolateral aspect injury, and that especially a small compression fracture strongly suggests an accompanying posterior cruciate ligament injury, as well.

Adolescent↗

Surgical treatment of falcotentorial meningioma.

Meningiomas arising from the falcotentorial junction are rare. Among our surgical experience of 375 meningiomas, only 4 cases of so-called falcotentorial meningiomas were encountered. We present these four surgical cases. An occipital transtentorial approach was used in three cases, and a combined midline occipital and suboccipital approach in one case. Total tumour excision was impossible in two cases because of engulfing deep venous structures including the great vein of Galen. Postoperative Gamma knife radiosurgery was performed in these two cases. On the other hand, a posteriorly located tumour was relatively easy to remove, and macroscopic total removal was accomplished. In conclusion, precise microvascular anatomical knowledge is indispensable to satisfactorily excise meningiomas in the falcotentorial area without significant morbidity.

Craniotomy↗