Biomedical subjects

Takeo Kondo

Publications and source records attributed to Takeo Kondo.

5 recordsLinked to original sources

PubMed2006

The function of the frontal lobe in neonates for response to a prosodic voice.

We examined how neonates responded at the brain level to an element of acoustic stimulation using near-infrared spectroscopy (NIRS). Twenty full-term, healthy neonates were included in the study. The neonates were tested in their cribs while they slept in a silent room. First, two probe holders were placed on the left and right sides of the forehead over the eyebrows using double-sided adhesive tape. Then the neonates were exposed to the auditory stimuli from an external auditory speaker. The stimuli, readings of the first scene of "Little Red Riding Hood," were made with a digital voice. The stimuli consisted of two conditions: variably pitched speech (variable speech: VS) and monotonous flat-pitched speech (monotonous speech: MS). The analyses focused on changes in O(2)Hb because O(2)Hb is the most sensitive indicator of changes in cerebral blood flow in NIRS measurement. The O(2)Hb level promptly increased at the beginning of the VS condition, and then returned to baseline again, while O(2)Hb did not show any changes during the MS condition. Differences between baseline-stimulation relative values were used to perform a 2 (condition)x2 (recording site)x2 (gender) analysis of variance. The results show that VS (M=0.45, S.D.=1.33) produced a greater increase of oxygenated blood to the frontal area of the brain area than MS (M=-0.19, S.D.=1.28). Neonates' brain activation patterns suggest that they can discriminate differences in the prosodic patterns of utterances.

Acoustic Stimulation↗

PubMed2006

Long-term effect of low-frequency repetitive transcranial magnetic stimulation over the unaffected posterior parietal cortex in patients with unilateral spatial neglect.

OBJECTIVE: To explore long-term effects on unilateral spatial neglect of low-frequency repetitive transcranial magnetic stimulation (rTMS) over the unaffected posterior parietal cortex. DESIGN: Uncontrolled pilot study. SUBJECTS: Two chronic-phase patients with left-sided unilateral spatial neglect from cerebral infarction. METHODS: Six rTMS sessions were undertaken for 2 weeks. Each session included 900 stimuli applied over P5 at an intensity of 95% motor thresholds and a frequency of 0.9 Hz. The Behavioural Inattention Test, either the Mini-Mental State Examination or the Revised Hasegawa Dementia Scale, Brunnstrom Recovery Stage, and Barthel Index were evaluated at 2-week intervals until 6 weeks after rTMS sessions. Single-photon emission computed tomography was performed 2 weeks before and after rTMS. RESULTS: Behavioural Inattention Test scores improved remarkably, especially from 2 to 4 weeks after rTMS sessions. At 6 weeks, Behavioural Inattention Test scores still remained above pre-rTMS levels. Other clinical evaluations as well as single-photon emission computed tomography showed no significant change during the study. CONCLUSION: In this small pilot study, low-frequency rTMS over the unaffected posterior parietal cortex decreased unilateral spatial neglect for at least 6 weeks.

Female↗

PubMed2003

Temporal changes of neurogenesis in the mouse hippocampus after experimental subarachnoid hemorrhage.

Recent studies indicate the existence of progenitor cells and their potential for neurogenesis in the subventricular zone (SVZ) and the hippocampus dentate gyrus (DG) of normal adult mammalian brain. Increased neurogenesis has been shown following cerebral ischemia and traumatic brain injury; however, the involvement of neurogenesis in subarachnoid hemorrhage (SAH) has not been examined. Adult male CD-1 mice were subjected to SAH by endovascular perforation of the left anterior cerebral artery. Mice received intraperitoneal injections of the cell proliferation-specific marker 5'-bromodeoxyuridine (BrdU) after SAH induction. BrdU incorporation was examined from 1 to 30 days after SAH by immunohistochemistry. The BrdU-positive cells were detected in SVZ and DG of normal control brain, and were significantly decreased in both areas three days after SAH. The number of these cells had recovered to its control level seven days after SAH. Double staining with BrdU and NeuN indicated that the majority of the BrdU-positive cells migrating into the granular cell layer of the DG became NeuN-positive 30 days after SAH. In conclusion, temporal changes of the neurogenesis as shown in the present study suggest that neurogenesis in the hippocampus may affect functional outcome after SAH. The induction of the neurogenesis can provide therapeutic value against SAH.

Animals↗

PubMed2003

[Unawareness for homonymous visual field defect].

BACKGROUND: There was no report which dealt with the relationship between emotional state, degree of defective visual search, severity of hemianopic dyslexia, the episode when the patient became aware of the defect, and unawareness of visual loss in homonymous hemifield. OBJECTIVE: To investigate the relationship between degree of awareness and those factors that might be responsible for the unawareness, including the aspects listed above. METHODS: Four patients with visual field defects caused by a brain lesion after a stroke was investigated. Self rating of emotional state, search performance for an object among many placed on a table, and for text reading, as well as visual field, visual positive phenomena, and hemispatial neglect were evaluated. Degree of unawareness for field loss was evaluated by modified version of the method of Bisiach et al. (1985). In addition, the episodes when the patient became aware of the defect were asked. RESULT: In accordance with the previous studies, we found no relationship between the degree of awareness of field defect and anatomic lesions, co-existence of hemispatial neglect, or the degree of awareness of hemiplegia. However, the patient with neglect was unaware of their troubles in vision at all, whereas the patients without neglect were aware of the troubles but misinterpreted them as problems of the eyes including acuity. In accordance with previous studies, co-existence of visual hallucinations or illusions seemed to be associated with awareness of visual field defect. No relationship was found between the degree of awareness of field defect and emotional state, degree of field loss, degree of defective visual search, or severity of hemianopic dyslexia. Their responses to the inquiry about the degree of awareness of field defect were not consistent. Thus, the awareness of the field defect seemed to be difficult to be kept firmly in their mind. On the other hand, the patients could remember the episode when they became aware of the defect for the first time, being able to specify time, place, and situation. CONCLUSION: Levine (1990) suggested that the sensory loss in this sort of patients was never phenomenally immediate but instead must be discovered by observation and inference. Non-specificity of the lesion, qualitative difference in awareness between the patient with and without hemispatial neglect, association of positive visual phenomena and awareness, fluctuation of awareness, and dependence of awareness on personal experiences found in our patients, can be explained with this 'discovery' hypothesis.

Aged↗

PubMed2002

Manganese superoxide dismutase deficiency exacerbates cerebral infarction after focal cerebral ischemia/reperfusion in mice: implications for the production and role of superoxide radicals.

BACKGROUND AND PURPOSE: Superoxide anion radicals (O2*-) are implicated in ischemia/reperfusion injury, although a direct relationship has not been elucidated. Recently, a specific method of hydroethidine (HEt) oxidation by O2*- was developed to detect O2*- production in a variety of experimental brain injury models. To clarify the role of O2*- in the mechanism of ischemia/reperfusion, we investigated O2*- production after ischemia/reperfusion and ischemia/reperfusion injury in mutant mice deficient in mitochondrial manganese superoxide dismutase (MnSOD) and in wild-type littermates. METHODS: Ischemia/reperfusion was performed for 60 minutes using intraluminal suture blockade of the middle cerebral artery in the mutant or wild-type mice. We evaluated fluorescent kinetics of HEt or ethidium, the oxidized form of HEt, in brains after an intravenous injection of HEt, followed by measurement of cellular O2*- production using specific HEt oxidation by O2*- before and after ischemia/reperfusion. Furthermore, we compared O2*- production and subsequent infarct volume in the mice using triphenyltetrazolium chloride after ischemia/reperfusion. RESULTS: HEt oxidation to ethidium is primarily a result of mitochondrially produced O2*- under physiological conditions. Cerebral ischemia/reperfusion produced O2*- prominently in neurons shortly after reperfusion, followed by a delayed increase in endothelial cells. A deficiency in MnSOD in mutant mice increased mitochondrial O2*- production and exacerbated cerebral infarction, worsening neurological deficits after ischemia/reperfusion. CONCLUSION: These results suggest that mitochondrial O2*- production may be a critical step underlying the mechanism of ischemia/reperfusion injury and that MnSOD may protect against ongoing oxidative cell death after ischemia/reperfusion.

Animals↗