N Aoyama

Nihon University, Edo, Tōkyō, Japan

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Publications (9)5.35 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Movement disorders associated with cerebral cavernous malformations (CM) are seldom reported, and chorea, in particular, is rarely associated with a CM located in the caudate nucleus. Here we report a 78-year-old female patient with chorea, who presented with choreiform movements due to a CM in the contralateral caudate nucleus. A brain MRI was obtained and compared with that obtained before the onset of chorea. The new images did not reveal further extralesional hemorrhage from the CM when compared with the previous images. The choreiform movements showed spontaneous improvement and then disappeared completely. We reviewed previous reports of patients with chorea associated with a CM, and conclude that CM located in the caudate nucleus can cause chorea.
    No preview · Article · Mar 2011 · Journal of Clinical Neuroscience
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    ABSTRACT: In the present study, we examined the effects of OPC-14117, a superoxide radical scavenger, on the secondary cellular damage and cognitive dysfunction occurring in a rat model of cerebral contusion induced by a controlled cortical impact (CCI). Histological examinations revealed that the contusion necrosis volume reached 13.6+/-5.3 mm(3) in non-treated animals and declined to 1.9+/-0.6 mm(3) in OPC-14117-treated animals (P<0.01). The cell number of the CA3 region was 120.0+/-12.4 cells/mm in the normal controls, 73.6+/-9.9 cells/mm in the non-treated animals, and 111.2+/-10.2 cells/mm in the OPC-14117-treated animals, indicating that CCI-induced selective neuronal cell death in the CA3 region was attenuated by the OPC-14117 administration (P<0.01). The tissue osmolality, as determined with a vapor pressure osmometer, was 314.5+/-15.4 mmol/kg in the normal brain and increased to 426.0+/-20.1 mmol/kg at 12 h following CCI. The increase in tissue osmolality was significantly attenuated by OPC-14117 administration (P<0.01). The OPC-14117 administration also attenuated the CCI-induced cognitive deficits. The OPC-14117-treated animals showed a tendency to improve on the Morris water maze performance test. The impairment of the habituation of exploratory activity elicited by CCI was significantly attenuated by OPC-14117 administration (P<0.05). In conclusion, OPC-14117 may have a potential for decreasing secondary cellular damage due to traumatic brain injury since it is as efficacious as any other compound tested in this model.
    No preview · Article · May 2002 · Brain Research
  • T Kawamata · Y Katayama · T Mori · N Aoyama · T Tsubokawa
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    ABSTRACT: 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. 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. 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. 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.
    No preview · Article · Feb 2002 · Acta neurochirurgica. Supplement
  • T Kawamata · Y Katayama · N Aoyama · T Mori
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    ABSTRACT: Severe cerebral contusion is sometimes associated with early edema formation within 24-48 hours post-trauma, and this frequently results in progressive ICP elevation and clinical deterioration. To investigate the underlying mechanisms of such severe contusion edema, diffusion imaging and ADC mapping were performed in 20 patients with cerebral contusion, employing 1.5 T echo planar MRI. Within 24 hours post-trauma, the diffusion images demonstrated a low intensity core in the central area and a high intensity rim in the peripheral area of contusion. The ADC value increased in the central area (ADC ratio (contusion/normal brain) = 1.13 +/- 0.13) and decreased in the peripheral area (ADC ratio = 0.83 +/- 0.13). This suggested that intra- and extracellular components underwent disintegration and homogenization within the central area, whereas cellular swelling was predominant in the peripheral area. A crescent-shaped zone of very high ADC value (ADC ratio = 1.38-1.61) was observed at the border between these two areas during the period of 24-48 hours post-trauma in some cases, apparently indicating that edema fluid was accumulated within a space formed by homogenization. The ADC values in the peripheral area shifted to an increase after 48-72 hours post-trauma. These findings imply that multiple mechanisms operate in early edema formation in cerebral contusion. It appears that the capacity for edema fluid accumulation increases in the central area and resistance for edema fluid propagation is elevated by cellular swelling in the peripheral area. We suggest that a combination of such events facilitates edema fluid accumulation in the central area and contributes, together with the cellular swelling in the peripheral area, to the mass effect of contusion edema. Diffusion MRI and ADC mapping represent powerful tools for investigating spatially as well as temporally heterogeneous mechanisms of contusion edema.
    No preview · Article · Feb 2000 · Acta neurochirurgica. Supplement
  • Tatsuro Kawamata · Y. Katayama · N. Aoyama · T. Mori
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    ABSTRACT: Severe cerebral contusion is sometimes associated with early edema formation within 24–48 hours post-trauma, and this frequently results in progressive ICP elevation and clinical deterioration. To investigate the underlying mechanisms of such severe contusion edema, diffusion imaging and ADC mapping were performed in 20 patients with cerebral contusion, employing 1.5 T echo planar MRI. Within 24 hours post-trauma, the diffusion images demonstrated a low intensity core in the central area and a high intensity rim in the peripheral area of contusion. The ADC value increased in the central area (ADC ratio (contusion/normal brain) = 1.13 ± 0.13) and decreased in the peripheral area (ADC ratio = 0.83 ± 0.13). This suggested that intra- and extracellular components underwent disintegration and homogenization within the central area, whereas cellular swelling was predominant in the peripheral area. A crescent-shaped zone of very high ADC value (ADC ratio = 1.38 ~ 1.61) was observed at the border between these two areas during the period of 24–48 hours post-trauma in some cases, apparently indicating that edema fluid was accumulated within a space formed by homogenization. The ADC values in the peripheral area shifted to an increase after 48–72 hours post-trauma. These findings imply that multiple mechanisms operate in early edema formation in cerebral contusion. It appears that the capacity for edema fluid accumulation increases in the central area and resistance for edema fluid propagation is elevated by cellular swelling in the peripheral area. We suggest that a combination of such events facilitates edema fluid accumulation in the central area and contributes, together with the cellular swelling in the peripheral area, to the mass effect of contusion edema. Diffusion MRI and ADC mapping represent powerful tools for investigating spatially as well as temporally heterogeneous mechanisms of contusion edema.
    No preview · Chapter · Jan 2000
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    ABSTRACT: Oxygen free radicals contribute to various kinds of tissue injury processes within the central nervous system. It has been suggested that inhibition of free radical formation has the potential to attenuate secondary neural tissue damage involving ischemia or trauma, and antioxidant therapy may offer a promising approach. In the present study, employing a cortical contusion model in the rat, contusion-induced neural damage, was evaluated by investigating edema formation, behavioral activities and histological changes. The effects of the superoxide radical scavenger, OPC-14117, were also tested to determine how free radicals may contribute to such neural damage. The results demonstrated that cerebral contusion induces a progressive decrease in tissue specific gravity representing edema formation, and behavioral deficits in the Morris water maze test and habituation of exploratory activity. Histological examinations revealed necrotic cavity formation in the cortex and selective neuronal death of the hippocampal CA3 region. These changes were significantly attenuated by OPC-14117, which was administered as a single dose immediately following trauma induction. The above results indicate that oxygen free radicals are involved in contusion-induced edema formation, subsequent tissue damage and cognitive deficits. The superoxide radical scavenger, OPC-14117, has a powerful therapeutic potential for preventing secondary cell damage following traumatic brain injury.
    No preview · Article · Feb 1998 · Acta neurochirurgica. Supplement
  • Y. Katayama · N. Aoyama · T. Mori · T. Maeda · T. kawamata

    No preview · Article · Jul 1997 · Clinical Neurology and Neurosurgery
  • Takeshi Maeda · Y Katayama · T Kawamata · N Aoyama · T Mori
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    ABSTRACT: Cerebrovascular damages leading to subsequent reductions in regional cerebral blood flow (rCBF) may play an important role in secondary cell damages following traumatic brain injury (TBI). Recent studies have demonstrated that rCBF markedly decrease in experimental model of TBI (e.g. fluid percussion injury, acute subdural hematoma, contusion). However, precise mechanisms underlying post-traumatic CBF reduction remain unclear. In the present study, the rCBF changes and microthrombosis formation were investigated in a cortical contusional model in rats, and the effects of etizolam (platelet activating factor antagonist) on microthrombosis were tested. The rCBF in the peripheral areas increased transiently, and decreased to ischemic level 3 hours post- injury. The histological examinations revealed microthrombosis formation in the contused area, extending from the center to the peripheral areas within 6 hours post-injury. The rCBF decrease and the contusion necrosis volume were significantly attenuated by etizolam administration. These results indicate that platelet activating factor is involved in microthrombosis formation and hemodynamic depression, and resultant ischemic damages within areas surrounding the contusion.
    No preview · Article · Feb 1997 · Acta neurochirurgica. Supplement
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    ABSTRACT: Oxygen free radicals may contribute to tissue injury processes in the central nervous system following ischemia or trauma. Recent studies have suggested that inhibition of free radicals improves the outcome in experimental models involving such conditions, and antioxidant therapy appears promising. In the present study, behavioral changes and edema formation in rat cortical contusion model were investigated, and the effects of a superoxide radical scavenger, OPC-14117, were tested. Wistar rats were anesthetized with halothane inhalation. Cortical contusion was induced in the parietal cortex employing a controlled cortical impact device. Immediately following injury induction, OPC-14117 was administered (300 mg/kg, p.o.). Edema formation was assessed in the center and peripheral areas of the contusion by the specific gravity method. Behavioral changes were evaluated by the Morris water maze test and the habituation of exploratory activity. The results revealed that the vehicle-administered control showed progressive edema formation and behavioral deficits following the injury. These changes were significantly attenuated by the OPC-14117 treatment (p < 0.05). Further, OPC-14117 reduced the size of contusional necrosis (p < 0.05). These findings suggest that superoxide free radicals are involved in contusion-induced edema formation, necrosis formation, and behavioral deficits, and that OPC-14117 has a therapeutic potential to prevent secondary cell damage following traumatic brain injury.
    No preview · Article · Jan 1997 · Acta neurochirurgica. Supplement