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H Nabatame

Publications and source records attributed to H Nabatame.

30 records · Page 2Linked to original sources
PubMed1989

[Left antero-medial thalamic infarction and symptoms of amnesia, aphasia, and dementia].

Three cases of left antero-medial thalamic infarction who showed amnesia, aphasia and dementia were studied comparatively in terms of clinical features and the MRI findings. Case 1 and Case 2, who showed transient amnesia and aphasia respectively, had a single lesion in the left antero-medial thalamus. Case 1 had a lesion in a more ventral part than Case 2, suggesting that Case 1 had a lesion of the bundles into the anterior and dorsomedial thalamic nuclei while Case 2 had a lesion of the ventrolateral thalamic nucleus. On the other hand, Case 3 who showed persistent dementia had multiple lesions in addition to the left antero-medial thalamic infarction. A review of the previous reports and investigations of the present cases suggest that a single ischemic lesion in the left antero-medial thalamus will cause amnesia and/or aphasic symptom while in cases with other multiple lesions it may cause persistent dementia.

Aged↗
PubMed1988

Muscarinic receptor-mediated inhibition of dopaminergic excitatory input to caudate neurons from the substantia nigra.

Microiontophoretic studies using rats anesthetized with chloral hydrate were performed to elucidate the relationship between the striatal cholinergic system and nigrostriatal dopaminergic system. Iontophoretic application of carbachol inhibited the spikes elicited by substantia nigra (SN) stimulation in 21 of 24 caudate neurons in which the spikes induced by SN stimulation were inhibited by microiontophoretically applied domperidone, a dopamine D-2 receptor antagonist. This inhibitory effect was completely blocked by atropine, although the spike generation induced by SN stimulation remained unaffected by the drug. However, carbachol did not affect the glutamate-induced firing of the caudate neurons of which the spikes induced by SN stimulation were inhibited by application of both domperidone and carbachol. Furthermore, carbachol had inhibitory effects on the spikes induced by SN stimulation even after the systemic application of bicuculline. In contrast, in 17 of 24 caudate neurons in which the spikes induced by SN stimulation were not affected by domperidone, carbachol did not inhibit the spikes induced by SN stimulation. These results suggest that the muscarinic receptors located on the SN-derived dopaminergic nerve terminals mainly play a role in inhibiting inputs from the SN to the caudate neurons, probably by reducing the release of dopamine from the nerve terminals.

Animals↗
PubMed1987

Effects of L-threo-DOPS, an L-noradrenaline precursor, on locus coeruleus-originating neurons in spinal trigeminal nucleus.

Electrophysiological studies using reserpinized cats were performed to examine the effects of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS) on the noradrenergic pathway from the locus coeruleus (LC) to the spinal trigeminal nucleus (STN). The spike generation of STN relay neurons induced by trigeminal nerve stimulation was not affected by LC conditioning stimulation nor iontophoretic application of L-threo-DOPS. After intraventricular administration of L-threo-DOPS, the inhibition of the spike generation was seen with LC conditioning stimulation and blocked by iontophoretically applied sotalol, suggesting that L-noradrenaline converted from L-threo-DOPS inhibits transmission of STN relay neurons.

Action Potentials↗
PubMed1987

Pontine ataxic hemiparesis studied by a high-resolution magnetic resonance imaging system.

Using a high-resolution magnetic resonance imaging system, we studied 3 patients who had exhibited pontine ataxic hemiparesis. In each patient, the ischemic lesions responsible for the contralateral ataxia were located in the dorsomedial basis pontis. The isointensity bands in the ischemic area on T2-weighted images showed the spared transverse fibers originating from the contralateral pontine nuclei, and this may explain the cause of the unilateral ataxia.

Ataxia↗
PubMed1987

Acute-onset amnestic syndrome with localized infarct on the dominant side--comparison between anteromedial thalamic lesion and posterior cerebral artery territory lesion.

Among 39 cases with acute-onset amnestic syndrome having unilateral localized infarct, 8 cases with anteromedial thalamic infarct ("thalamic" amnesia), and 18 cases with medial temporal lobe infarct including hippocampus in the posterior cerebral artery territory ("PCA" amnesia) were studied in terms of X-CT and MRI findings and neuropsychological examinations. Results were as follows: 7 out of 8 cases with thalamic amnesia (88%), and 15 of 19 cases with PCA amnesia (78%) showed left side lesions on CT scan. All groups showed a prolonged recent memory loss with little loss of immediate recall and remote memory, and disorientation and dyscalculia. In both types of amnesia, patients having a left sided lesion showed recent memory loss with new learning disabilities of verbal materials. Patients having a right sided lesion showed recent memory loss with new learning disabilities of both verbal and visuospatial materials. Judging from the X-CT and MRI findings, the lesions most probably causing amnesia in these cases seemed to be the anterior and dorsomedial nuclei of the thalamus in thalamic amnesia and hippocampus in PCA amnesia. Differential diagnosis in amnestic syndrome with localized infarct is also discussed.

Adult↗
PubMed1986

Activation of lateral vestibular nucleus neurons by iontophoretically applied phencyclidine.

Microiontophoretic studies were performed to elucidate the effects of phencyclidine (PCP) on neuronal activity in the lateral vestibular nucleus (LVN) of cats anesthetized with alpha-chloralose. Spikes elicited in the monosynaptic LVN neurons by vestibular nerve stimulation were not affected by iontophoretic application of PCP up to 100 nA, but they were blocked by atropine (30-50 nA). A dose-dependent increase in spontaneous firing during application of PCP was obtained in 11 of 15 monosynaptic neurons, in all of which firing was increased by iontophoretically applied acetylcholine (ACh). Simultaneous application of atropine completely inhibited the PCP- and ACh-induced increase in the firing without affecting the glutamate-induced firing. These results indicate that PCP acts on the LVN monosynaptic neurons receiving input from the vestibular nerve in a similar manner to ACh.

Acetylcholine↗
PubMedDate not supplied

High intensity areas on noncontrast T1-weighted MR images in cerebral infarction.

Among 46 noncontrast magnetic resonance studies on patients with cerebral infarction, 11 showed areas of high signal intensity of the involved brain on T1-weighted images. These areas were more frequent in cerebral or cerebellar cortical lesions. Lacunar infarcts in lenticular nuclei, internal capsules, corona radiata, or brain stem did not show any high signal intensity areas on T1-weighted images, whereas the thalamic infarcts did. Sequential studies revealed that these lesions displayed low signal intensity on T2-weighted images at first, and then a high signal intensity area appeared on T1-weighted images. We suggest that these high signal intensity areas on the T1-weighted images in cerebral infarction are caused by hemorrhagic changes at the periphery of the infarction, where blood flow is restored by recanalization or collateral supply.

Adult↗
PubMedDate not supplied

Spinocerebellar degeneration: qualitative and quantitative MR analysis of atrophy.

Magnetic resonance imaging at 1.5 T was performed in 27 patients with either the cerebellar or spinocerebellar form of spinocerebellar degeneration and in 10 control subjects. Neither T1- nor T2-weighted images (T1WIs and T2WIs) of the patients showed any abnormal intensity areas within the cerebellum or in any other structures of the brain. The T2WIs delineated normal configurations of symmetrical dentate and red nuclei. On T1WIs two patterns of atrophy were detected: (a) moderate to severe shrinkage of the basis pontis and the middle cerebellar peduncles associated with atrophy of the cerebellum, and (b) moderate atrophy of the cerebellum with a preserved basis pontis. The former morphological changes are consistent with the pathology of pontocerebellar atrophy (PCA) and the latter with those of cerebellar cortical degeneration (CCD). In 11 patients, only after a quantitative analysis of the images were we able to classify them in one of the two morphological categories (PCA or CCD). There was a significant correlation between atrophy of the cerebellum and atrophy of the basis pontis. Furthermore, in the PCA group the anterior portion of the body of the corpus callosum was significantly smaller in comparison with the control subjects.

Adult↗