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Biomedical subjects

H Naritomi

Publications and source records attributed to H Naritomi.

At least 19 recordsLinked to original sources
PubMed2005

How to improve repetition ability in patients with Wernicke's aphasia: the effect of a disguised task.

Dissociation "automatico-voluntaire" is a symptom observed in aphasic patients. We elucidated the difference between voluntary and involuntary speech output in a quantitative manner using the same task materials in nine patients with Wernicke's aphasia. All the patients exhibited better ability and less paraphasias in a repetition task elicited in a disguised condition than in an ordinary repetition condition. This result indicates that the output difficulty in Wernicke's aphasia might be a disability of volitional control over the language system.

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PubMed2004

Predictor of cognitive deterioration in elderly subjects by auditory-evoked magnetic signal using magnetoencephalography.

Recent development of auditory-evoked magnetoencephalography (A-MEG) made it possible to measure interhemispheric neural conduction time (INCT) of auditory impulses. We estimated INCT with A-MEG and cognitive function with mini-mental state examination (MMSE) in 85 elderly patients with chronic dizziness (CD) and found that INCT was negatively correlated with MMSE scores (p<0.001). In 11 of 85 patients whose MMSE scores were within the normal range, A-MEG and MMSE were repeated for the subsequent 4 years to find longitudinal changes in INCT and cognitive function. The 11 patients were divided into two groups according to the baseline INCT values, such as Group A with normal INCT (n=7) and Group B with abnormally prolonged INCT (n=4). In Group A, INCT and MMSE scores remained within the normal range throughout the 4-year period. In Group B, INCT showed the tendency towards progressive prolongation during the follow-up period, and MMSE scores decreased to abnormally low levels at the third or fourth follow-up year in all the patients. The present results suggest that rapid neural interaction of both cerebral hemispheres is needed to maintain normal cognitive function. Abnormal INCT prolongation in elderly subjects suggests subclinical cortical network dysfunction and may predict the future development of cognitive deterioration.

Acoustic Stimulation↗
PubMed2004

Losartan, an angiotensin II (AT1) receptor antagonist, preserves cerebral blood flow in hypertensive patients with a history of stroke.

In patients with severe hypertension, chronic heart failure or a history of stroke, the lower limit of autoregulation of cerebral blood flow (CBF) is shifted to higher levels of blood pressure (BP) than those observed in healthy subjects. The aim of pharmacotherapy for hypertensive patients with an impaired autoregulation of CBF should be to reduce BP while preserving an appropriate CBF. In the present study, 16 hypertensive patients who had had an episode of stroke more than 4 weeks previously were administered the angiotensin II (AT1) receptor antagonist losartan at daily doses of 25-100 mg for 4 weeks. Systolic and diastolic blood pressures were recorded for 24 h using an ambulatory BP monitoring system. CBF in both hemispheres of the cerebrum and cerebellum was quantified using single photon emission tomography with N-isopropyl-p-[123I]iodoamphetamine. At baseline, CBF was 29.7 +/- 6.7 ml/min/100 g in the cerebrum and 31.5 +/- 7.5 ml/min/100 g in the cerebellum. At the end of treatment, BP was lower, while CBF increased by 7.7% in the cerebrum, and remained at the baseline level in the cerebellum. Thus, CBF was preserved despite the reduction in BP. We consider the use of losartan is advantageous for hypertensive patients with a history of stroke in whom autoregulation of CBF is potentially impaired.

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PubMed2002

Effect of prothrombin complex concentrate on INR and blood coagulation system in emergency patients treated with warfarin overdose.

We investigated the effect of prothrombin complex concentrate (PCC) on the international normalized ratio (INR) and blood coagulation system in two emergent patients treated with warfarin for secondary prevention of cardioembolic stroke due to nonvalvular atrial fibrillation. An 80-year-old woman developed massive subcutaneous hemorrhage and swelling on her right upper extremity with weak pulsation of the right radial artery and had an INR above 10. An 83-year-old man had pleural effusion with an INR value of 6.69 and pleural puncture was immediately required. We administered 500 IU of PCC to the two patients (17.2 IU/kg and 12.5 IU/kg) with 10 mg of vitamin K. The INR decreased to 1.12 and 1.85, respectively, with an increase of plasma levels of protein C and coagulant factors IIa, VIIa, IXa, and Xa 10 min after administration. The plasma levels of the thrombin-antithrombin III complex increased (from 4.0 to 12.0 micro g/l and from 0.5 to 28.9 micro g/l, respectively, normal value <3.0), but prothrombin fragment 1+2 increased minimally 10 min after administration (from 0.4 to 1.1 nmol/ml and from 0.4 to 0.7 nmol/ml, respectively, normal value 0.4-1.4 nmol/ml). Plasma levels of D-dimer remained unchanged. The massive subcutaneous hemorrhage in the former patient improved in 14 days. Anticoagulation was restarted in the latter patient after 14 days of PCC administration. There were no embolic episodes during the month after PCC administration. In conclusion, a small amount of PCC may be effective in immediately correcting increased INR levels with increased plasma levels of protein C and coagulant factors IIa, VIIa, IXa, and Xa and may partially activate the coagulation system without any effects on plasma levels of D-dimer.

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PubMed2002

Visualisation method of spatial interictal discharges in temporal epilepsy patients using magneto-encephalogram.

The aim of the study was to develop a method for investigating how interictal epileptic discharges in temporal epilepsy patients are activated spatially. The activity was measured using magneto-encephalography (MEG). The MEG data were used to produce a current-arrow map that reflected the topographic distribution of the electrical current for each peak epileptic waveform. A large current distribution was obtained that appeared to be contained in the limbic structure, in each temporal lobe. The large current orientation indicated two opposite directions. Furthermore, the decrease in the maximum strength of the current-arrow, depending on the medication (e.g. the decrease from 11 to 6 pT m-1 in the left temporal lobe (contralateral stimuli)), suggested that the discharge distributions could be used to verify the efficacy of medication. Thus the topographical visualisation method could be a new strategy for diagnosis in temporal epilepsy patients.

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PubMed2001

Homonymous defect of macular vision in ischemic stroke.

It is generally believed that a homonymous defect of macular vision (HMV) is caused by a small lesion restricted to the occipital lobe tip and rarely results from ischemic stroke. The incidence of HMV was studied retrospectively in 54 patients with infarction of the posterior cerebral artery territory who underwent Goldmann's visual field test. HMV was found in 6 patients (11%). In all of them, HMV was first dismissed due to a confrontation test of visual fields at the bedside and later detected by Goldmann's visual field test. All had a relatively large infarction extending from the occipital lobe tip to the posterior part of the calcarine cortex and/or the neighboring subcortical regions. Stroke-induced HMV can be caused by a large lesion involving the occipital pole and may not be so rare as generally considered.

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PubMed2001

[Neuroprotective therapy for the treatment of acute ischemic stroke].

Following cerebral ischemia, various biochemical reactions are provoked in a stepwise manner leading neuronal cells to ischemic death. The prevention of these biochemical reactions may exert neuroprotective actions and consequently reduce the magnitude of ischemic cerebral injury. On the basis of such a view, numerous neuroprotective drugs have been developed during the last decade. Quite a few drugs were found effective in reducing the infarct volume in experimental studies, and more than 15 of them were subjected to clinical phase III trials to see a therapeutic effectiveness. However, the results of phase III trials were disappointing in the majority drugs. Only three drugs, nicaravene, ebselen and edaravone, all radical scavengers, were judged effective by small-sized trials with a wide therapeutic window, 48-72 hours after stroke, in Japan. The fact suggests that a one-point prevention of biochemical reactions by single drug is unable to rescue ischemic neuronal cells. Ischemic insult causes damages of vascular wall including the endothelium which play an important role in the development of hemorrhagic changes or cerebral edema. Vascular protection is considered as important as neuroprotection in treatment of clinical stroke. Mild hypothermia has neuroprotective and vascular protective actions and hence may be more effective than neuroprotective drugs for the treatment of stroke. The prevention of fever, which often occurs in severe stroke, may exert the similar effect as hypothermia in neuroprotection. Neuroprotective therapy in the future should proceed toward the simultaneous protections of neurons and vessels using combination of multiple drugs.

Animals↗
PubMed2000

Definition of the anterior choroidal artery territory in rats using intraluminal occluding technique.

This manuscript delineates the territory of the anterior choroidal artery (AChA) in rats, as defined by the induction of an AChA infarction. By advancing a 0.24-mm surgical suture up the internal carotid artery (ICA) to a point 0.5-2 mm proximal to the middle cerebral artery (MCA) origin, the AChA could be occluded and a reliable AChA distribution infarction was produced in 62% (23/37) of animals. The infarct volume, as defined by TTC staining, was 55+/-7 mm(3). Maps of the infarction, generated by measuring the entire area of overlapping coronal slices, demonstrated that the internal capsule was always damaged. Other areas that might be affected included the hippocampus, thalamus, amygdaloid complex, piriform cortex, dorsal caudatoputamen, and lateral ventricular wall. Positioning the coated suture proximal to the AChA produced a much smaller infarct involving the medial and lateral hypothalamus, preoptic region, optic chiasm, and marginal region of the internal capsule near to the lateral hypothalamus exempt from AChA territory damage. A causative relationship between AChA occlusion and a deep cerebral infarct centered on the internal capsule was further established by: (1) identifying the AChA on the non-ischemic side with colored silicone perfusion, and subsequent similar delineation on the ischemic side, and (2) delineating infarction in the silicone perfused AChA region using hematoxylin and eosin staining and the TUNEL method. The AChA usually originated from the ICA (91% of cases), 1.75+/-0.12 mm proximal to the MCA bifurcation. Approximately 27% of the AChAs had periamygdaloid branch(es) on its initial segment.

Animals↗
PubMed2000

Prevention of rat cerebral aneurysm formation by inhibition of nitric oxide synthase.

BACKGROUND: Cerebral saccular aneurysm is a major cause of subarachnoid hemorrhage, one of the cerebrovascular diseases with the highest mortality. The mechanisms underlying the development of aneurysms, however, still remain unclear. We have made a series of reports on an animal model of experimentally induced cerebral aneurysms that resemble human cerebral aneurysms in their location and morphology, suggesting that the arterial wall degeneration associated with aneurysm formation develops near the apex of arterial bifurcation as a result of an increase in wall shear stress. Using the animal model and human specimens, we examined the role of nitric oxide (NO) in the degenerative changes and cerebral aneurysm formation. METHODS AND RESULTS: Inducible NO synthase (iNOS) was immunohistochemically located at the orifice of human and rat aneurysms. Nitrotyrosine distribution was also seen in the human aneurysm. Although no iNOS immunostaining was found in normal arteries, iNOS immunoreactivity was observed in parallel with the development of early aneurysmal changes in rats. In contrast, during the early development of aneurysm, endothelial NOS immunostaining in the endothelium was weakened compared with that in the control arteries. An NOS inhibitor, aminoguanidine, attenuated both early aneurysmal changes and the incidence of induced aneurysms. A defibrinogenic agent, batroxobin, which may diminish shear stress by reduction of blood viscosity, prevented iNOS induction as well as early aneurysmal changes. CONCLUSIONS: The evidence suggests that NO, particularly that derived from iNOS, is a key requirement for the development of cerebral aneurysm. The iNOS induction may be caused by an increase in shear stress near the apex.

Animals↗
PubMed2000

[An autopsy case of dementia with Lewy bodies who showed the typical parkinsonism in the initial five years].

A 76-year-old man with parkinsonism and dementia was reported. He developed resting tremor at age 69 followed by hypokinesia, rigidity and small step gait. L-dopa ameliorated his symptoms with no hallucinations for the initial 5 years. His mental level did not decrease during that period. He was admitted to our hospital because of dehydration and fever at age 74. Subsequently, his cognitive function deteriorated, with visual hallucination. Serial brain CT studies displayed a progressive cerebral cortical atrophy without focal lesions. He died of respiratory distress syndrome and disseminated coagulopathy resulting from pneumonia, dehydration and syndrome malin. Postmortem examination revealed a marked bilateral loss of melanin-containing neurons with Lewy bodies in the substantia nigra and locus ceruleus. Lewy bodies were also in the basal nucleus of Meynert, with moderate neuronal cell loss. The distribution of Lewy bodies was widespread in the cerebral cortical areas, corresponding to the neocortical subtype according to the consensus guideline for the pathologic diagnosis of dementia with Lewy bodies. According to the criteria of the Consortium to Establish a Registry for Alzheimer's Disease, the age-related plaque score in the present case suggested Alzheimer's disease, although cortical neurofibrillary changes corresponded to stage II by the criteria of Braak and Braak. These pathological findings established the diagnosis of dementia with Lewy bodies from the quantitative and distributional viewpoints. Based on recent neuropathological evidence, a spectral theory, which presents idiopathic Alzheimer's disease and Parkinson's disease as the two extremes of a spectrum of neurodegeneration, has been proposed. Dementia with Lewy bodies is located in the middle of this spectrum. Pathological evaluation based on quantitative consensus guidelines is important to establish the diagnosis in patients with parkinsonism and dementia, since neuropathological changes of Alzheimer's disease, Parkinson's disease and dementia with Lewy bodies are often observed in a mixed manner in these patients.

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PubMed2000

[A case of agnosia for streets and houses unaccompanied by prosopagnosia of familiar faces due to the right occipital lobe infarction].

We reported a patient who showed agnosia for streets and homes unaccompanied by prosopagnosia of familiar faces following infarction in the right occipital lobe. A 70-years-old right-handed man admitted to our department because of sudden development of visual impairment. He had left hemianopsia, left unilateral spatial neglect and slight visual memory disturbance but no other neurological abnormalities. His verbal memory was maintained intact. He was, however, unable to distinguish the sceneries of buildings and streets regardless of their familiarities and often got lost in the hospital. His topographical abilities in map-sketching and route-description were partially impaired depending upon the familiarity of targets; the disability was observed toward unfamiliar targets. His ability in facial recognition was also partially impaired depending upon the familiarity of persons. The patient was unable to distinguish faces of unfamiliar persons, such as nurses and doctors whom he met following stroke, whereas he was able to distinguish faces of familiar persons, such as his family and friends. The brain MRI demonstrated infarction in the right medial occipital lobe including parahippocampal gyrus, lingual gyrus and fusiform gyrus. In general, the manifestation of agnosia for streets and houses is associated with prosopagnosia. The present case, however, exhibited only the former in association with the partial manifestation of the latter. The fact suggests that those two are independent syndromes. The present case also showed a dissociation in the abilities of topographical and facial recognition according to the familiarity of targets. The process for the retrieval and reference of acquired information and that for the acquirement of new visual information may work in an independent manner.

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PubMed1999

Rhabdomyolysis lesions showing magnetic resonance contrast enhancement.

Although T2-weighted magnetic resonance imaging (MRI) was reported to be useful for depicting rhabdomyolysis lesions, little is known as to the usefulness of gadolinium-enhanced T1-weighted imaging. The authors performed noncontrast and postcontrast T1-weighted MRI along with T2-weighted MRI in a patient with rhabdomyolysis in the chronic phase. Non-contrast T1-weighted imaging revealed no abnormality, whereas postcontrast T1-weighted imaging demonstrated lesions more definitively than T2-weighted imaging. Gadolinium-enhancement study may contribute to the MRI diagnosis of rhabdomyolysis.

Contrast Media↗
PubMed1999

Experimental model of small deep infarcts involving the hypothalamus in rats: changes in body temperature and postural reflex.

BACKGROUND AND PURPOSE: Intraluminal middle cerebral artery (MCA) occlusion in rats has been reported to cause hyperthermia assumed to be caused by hypothalamic damage. To clarify the effects of hypothalamic ischemia on body temperature and to obtain a model simulating lacunar infarction, we attempted to produce small infarcts in deep structures (including the hypothalamus). METHODS: A surgical suture was advanced to occlude the origin of the hypothalamic (HTA) and/or anterior choroidal arteries (AChA) without compromise of the anterior or middle cerebral artery origins. After treatment, rectal temperature and postural reflex were examined repeatedly for 3 days under nonanesthetic conditions. The AChA and HTA and their link with small deep infarction were then confirmed by TTC, hematoxylin and eosin, and TUNEL stains and by microsurgical dissection after colored silicone perfusion into the cerebral arteries. RESULTS: Advancement of the suture near to but not occluding the MCA origin (0.5 to 1.9 mm proximal) produced small, deep, nonneocortical strokes in 25 of 36 animals without producing MCA ischemic changes. These infarctions mainly affected the hypothalamus in 13 animals (HTA area: infarct volume 6+/-1 mm(3)) and involved both the internal capsule and hypothalamus in 12 animals (HTA+AChA area infarct volume 48+/-10 mm(3)). Rats with HTA infarction alone exhibited persistent hyperthermia for 72 hours; some also had transient mild postural abnormality. The AChA+HTA infarct group showed a transient elevation of body temperature for 24 hours and definitive postural abnormality. In the remaining 11 animals, the suture was inadvertently advanced across the MCA origin, producing a large infarct that affected both the neocortex (MCA territory) and nonneocortical structures (volume 381+/-30 mm(3), n=11). The MCA infarct group displayed a transient hyperthermia and severe postural abnormality. CONCLUSIONS: When properly positioned, the intraluminal suture method permits selective AChA and/or HTA obstruction without inducing MCA territory ischemia. This model confirms that selective hypothalamic infarction produces significant and sustained temperature regulation abnormalities. The model also may be useful in investigating the pathophysiology of small, deep, end-vessel infarction.

Animals↗
PubMed1998

Neurological function after deep hypothermic circulatory arrest in the rat.

BACKGROUND: Integrated neurological function, behavior, and somatic recovery were studied in 35 rats undergoing 5 to 80 minutes of hypothermic circulatory arrest (HCA). METHODS AND RESULTS: A closed extracorporeal circulation system (ECC) consisting of a miniature oxygenator and heat exchanger, primed with 6 mL of asanguinous solution, was connected to a closed-chest rat with cannulae in the right atrium for venous drainage (ID = 1.7 mm) and in the ascending aorta for arterial return (ID = 1.0 mm). The rat was surface- and core-cooled until rectal temperature reached 18 degrees C, when ECC was stopped and cardioplegic solution delivered. After 5, 10, 20, 40 (each n = 5), and 80 minutes (n = 15) of HCA, the rat was reperfused, weaned from ECC, and followed with behavioral scoring, passive avoidance tasks, and cardiopulmonary exercise testing until euthanized for morphological study. Every rat resumed weight gain in the first week after HCA and regained preoperative exercise capacity by the fourth week. Only rats undergoing 80 minutes of HCA showed behavioral abnormalities such as stereotypy and incomplete righting reflex, which eventually disappeared in the fourth week. Learning ability was preserved in all except for rats after 80 min of HCA, who failed to acquire new memory to avoid electric stimuli (n = 10) up to 3 months after HCA, when pyramidal cells were partly replaced by astroglia in the cerebral cortex and CA1 sector of hippocampus. Nonetheless, old memory established before HCA was preserved even after 80 minutes of HCA and allowed rats (n = 5) to avoid electric stimuli. CONCLUSIONS: Homogeneity of animals, miniature ECC system, and an established testing system allowed evaluation of rats after HCA, which disclosed learning disability (functional disorder) and pyramidal cell loss (organic defect) after 80 minutes of HCA despite recovery of somatic function, behavior, and growth.

Animals↗