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Biomedical subjects

H Narabayashi

Publications and source records attributed to H Narabayashi.

At least 73 records · Page 4Linked to original sources
PubMed1988

[Metrizamide encephalopathy in a child with hydrocephalus--effects of L-threo-DOPS on persistent disturbance of consciousness and L-dopa on extrapyramidal symptoms].

This report describes a case of metrizamide encephalopathy with persistent disturbance of consciousness and extrapyramidal symptoms. These two conditions have rarely been reported among the various adverse effects of metrizamide. An 11-year-old girl had been in almost good health until she was ten years old, at which time she received a ventriculo-peritoneal shunt operation, suffering from hydrocephalus of unknown etiology. At the age of eleven, she was admitted to our hospital due to hydrocephalus recurrence. She was examined by metrizamide shunt-gram (1200 mg iodide/4 ml). On the next day, she became drowsy. The CT scan disclosed the periventricular penetration of metrizamide into the medial part of the thalamus and the caudate nucleus. Thirteen days later, disturbance of consciousness continued, and extrapyramidal symptoms, that is, rigo-spasticity and postural tremor, were observed. Oral administration of L-threo-DOPS, the direct precursor of noradrenaline, was effective against the persistent disturbance of consciousness and L-DOPA was effective against the extrapyramidal symptoms. She soon recovered almost to normal and no neurological deficit remained. We thus conclude that the CT scan findings and effects of L-threo-DOPS and L-DOPA suggest that metrizamide encephalopathy in this case were respectively due to its periventricular penetration into the medial part of the thalamus and the caudate nucleus, and the resultant deficiency of the ascending noradrenergic reticular activating system and the nigrostriatal dopaminergic system.

Basal Ganglia Diseases↗
PubMed1988

[Lateral coordinate of the thalamic Vim neurons in the cases with dilated third ventricle].

Precise radiographical measurement of the third ventricle in the first and essential procedure in stereotaxic surgery in order to determine the target point. This is done while referring to an available standard brain atlas such as Schaltenbrand & Bailey. However there have been no criteria established for determining the deviation of the coordinates of the thalamic nuclei, especially in their lateral coordinates when the third ventricle is highly dilated. Therefore, in 109 cases encountered recently (81 parkinsonism, 11 essential tremor, 10 cerebral palsy, 3 thalamic pain, 1 Benedikt's syndrome, 1 torticollis, 1 oral dyskinesia, 1 striato-nigral degeneration), we studied the correlation between the width of the third ventricle and the lateral coordinate of the thalamic point where kinesthetic neurons or tremor-synchronously discharging neurons were detected. These neurons were especially related to the arm. According to the width of the third ventricle, we classified the cases into three types: 18 cases with large ventricles (more than 10 mm), 37 cases with medium-sized ventricles (4-10 mm) and 16 cases with small ventricles (less than 4 mm). By plotting the lateral coordinate of the thalamic point where kinesthetic neuron of the upper extremity was recorded in reference to the radiogram of anteroposterior view, we found that the lateral coordinates of large ventricular cases generally tended to show more lateral displacement than cases where the ventricles were narrower. Their mean lateral coordinate was 16.9 mm from midline in contrast ot 14.0 mm in cases with small ventricular width. There was a linear correlation between the width of the third ventricle and the lateral coordinate of the kinesthetic neuron of the Vim nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Mapping↗
PubMed1988

[Visibility of the inferior horns in computed tomography of normal subjects and epileptics].

In recent years brain CT scan has been so popular that many investigators have been trying to clarify the normal CT images. But little attention has been paid to the inferior horns of lateral ventricles in spite of their importance for judging mesial temporal lobe structures. The present study was designed to elucidate how the inferior horns were visualized on brain CT in normal subjects from childhood to aged group, and to evaluate whether the inferior horns were dilated in the epileptics or not. The subjects of the present study were 502 normal controls (2-79 y, mean 36.1 y) and 163 epileptic patients with normal CT image (4-68 y, mean 26.6 y) including 55 cases of temporal lobe epileptics. CT scans were performed with EMI 1010 scanner, and slices were obtained every 10 mm from the projection of 5-10 degrees angle for orbito-meatal line. Inferior horns were examined at the level of basal cisterns. Because inferior horns were not necessarily visible in our cases, we examined the frequency of clearly visualized inferior horns at each decade, and regarded their frequency as the size of inferior horns at each decade. In normal controls, frequency of visible inferior horns was relatively high in early childhood, and decreased as they grew. In the 3 rd to 4 th decades the visibility frequency became the lowest (30-35%), and then gradually increased as the subjects became older.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Magnetic resonance planned thalamotomy followed by X-ray/CT-guided thalamotomy.

Magnetic resonance imaging (MRI) is currently the optimal neuroradiologic technique for visualizing the anterior and posterior commissure for defining the AC-PC line. CT is the optimal technique for electrode and probe guidance during stereotactic thalamotomy. Various possibilities of transferring or overlying MRI and CT are outlined which in some future might result in more refined methods of CT-MRI guidance for stereotactic surgery.

Humans↗
PubMed1987

Long-term follow-up study of nucleus ventralis intermedius and ventrolateralis thalamotomy using a microelectrode technique in parkinsonism.

Long-term observation over 3-8 postoperative years of cases of Parkinson disease operated by stereotactic thalamotomy using a microelectrode recording technique is reported. The procedure is specifically useful in the following four groups: (1) tremor-dominant cases, (2) hemiparkinsonism, (3) cases with marked asymmetry in motor symptoms and (4) juvenile parkinsonism presenting levodopa-induced dyskinesia.

Follow-Up Studies↗
PubMed1987

Similarity and dissimilarity of MPTP models to Parkinson's disease: importance of juvenile parkinsonism.

Clinical, pharmacological and neuropathological features of MPTP-induced parkinsonism in humans and animals were compared with those of the Parkinson's disease (PD) and juvenile parkinsonism (JP). Some dissimilarities between both the conditions noticed in earlier investigations have been dissolved by starting a well-prescribed chronic administration of subliminal dose of MPTP in old matured monkeys. The MPTP model is now more resembling parkinsonism. However, it is to be emphasized that the MPTP model is more similar to JP than to PD in clinical and pharmacological terms. JP has been considered idiopathic in nature and seems to be important in understanding of etiopathogenesis of PD. Findings in one sectioned brain of JP were described with stronger pharmacological changes in the striatum than in the nigra and preservation of nigral neurons. It is thus questioned whether PD is the disease starting by striatal chemical changes or by nigral pathology.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

[A mouse model of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine induced parkinsonism: effect of norepinephrine terminal destruction].

N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been reported to cause chronic Parkinsonism in humans, primates, and long lasting striatal dopamine depletion in mice. Acute animal models thus produced closely resemble Parkinson's disease. There are, however, two major differences. The one is a lack of Lewy bodies and the other is that norepinephrine system is relatively well preserved in the model. So the acute animal model is better considered a nigrostriatal dopamine deficiency model. We have produced another model by adding N-2-chloroethyl-N-ethyl-2-bromobenzyl-amine (DSP4) to MPTP. This material is known to produce selective destruction of norepinephrine terminal in the central nervous system as well as in the periphery. Both norepinephrine system and dopamine system are severely depressed in this model, and the functional role of norepinephrine system was investigated by comparing two models. 90 male C57 black mice weighing 20-25 grams were used. MPTP (Aldrich) was dissolved in sterile distilled water with 5% ethanol solution. Experimental animals were divided into three groups. i) control group; in this group animals received vehicles alone. ii) MPTP group; in this group, mice received daily i.p. doses of MPTP 30 mg/kg for consecutive 10 days, thus total doses of MPTP was 300 mg/kg. iii) MPTP & DSP4 group; in this group animals received daily i.p. doses of MPTP 30 mg/kg for consecutive 10 days and at the last day of MPTP injection they received DSP4 50 mg/kg i.p.. 7 to 14 days after the last injection of MPTP both treated and control mice received an intraperitoneal injection of L-DOPA (200 mg/kg & aromatic L-amino acid decarboxylase mg/kg) and the effect of this drug on three groups were investigated by using behavioral, biochemical and histofluorescence method. Histofluorescence studies by GA-FAS method revealed severe reduction of nigrostriatal dopamine in MPTP treated mice. Mesolimbic and mesocortical dopamine systems seemed relatively preserved. There was no apparent changes in locus coeruleus norepinephrine system. In MPTP & DSP4 treated mice marked reduction of norepinephrine terminal fluorescence as well as nigrostriatal dopamine system was observed. Chemical analysis of norepinephrine and dopamine by HPLC confirmed histofluorescence studies. Behavioral studies were analyzed by Automex locomotor activity meter. Marked increase of locomotor activity was observed in MPTP treated mice after L-DOPA administration.(ABSTRACT TRUNCATED AT 400 WORDS)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

Regulation of phosphofructokinase in perfused rat heart. Requirement for fructose 2,6-bisphosphate and a covalent modification.

Phosphofructokinase from rat heart perfused with epinephrine was purified to homogeneity and various allosteric properties were determined under conditions which approximate physiological concentrations of the substrates, effectors, and pH. The molecular weights of the protomer of the enzyme isolated from the hormone-stimulated and the control hearts are both approximately 83,000. The epinephrine-stimulated and the control enzymes contain 1.1 and 0.66 mol of phosphate/mol of protomer, respectively. Both enzymes can be fully phosphorylated by cAMP-dependent protein kinase indicating that the phosphorylation site is new and distinct from the known phosphorylation site of skeletal muscle phosphofructokinase. Pure phosphofructokinase isolated from the epinephrine-stimulated heart is significantly less sensitive to inhibition by ATP and citrate, and the K0.5 values for Fru-6-P (0.18 mM) and Fru-2,6-P2 (3 microM) are one-half those for the enzyme from control hearts. In the presence of in vivo concentrations of ATP, citrate, and Fru-6-P at pH 7.1, both enzymes are inactive in the absence of Fru-2,6-P2. Moreover, the K0.5 values for Fru-2,6-P2 of the hormone-stimulated and untreated enzymes are 3 and 6 microM, respectively. These differences in the allosteric properties of phosphofructokinases from the hormone-treated and the control hearts disappear when the enzymes are dephosphorylated by alkaline phosphatase. Determination of the glycolytic intermediates showed a 2-fold increase in Fru-6-P, Fru-2,6-P2, and AMP and 13-fold increase in Fru-1,6-P2. Partially purified Fru-6-P,2-kinase from epinephrine-stimulated and control hearts show KFru-6-P0.5 = 4 and 15 microM, respectively. These results indicate that rat heart phosphofructokinase in vivo requires Fru-2,6-P2 for its activity. Epinephrine stimulates phosphorylation of phosphofructokinase which results in a more active form. The hormone also increases Fru-2,6-P2 which appears to be the result of an activation of Fru-6-P,2-kinase by a covalent modification.

Animals↗
PubMed1985

Tryptophan hydroxylase activity in the brains of controls and parkinsonian patients.

The activity of tryptophan hydroxylase was measured in nine regions of human brains from controls and patients with Parkinson's disease, striatonigral degeneration, Shy-Drager syndrome and progressive supranuclear palsy by high performance liquid chromatography with fluorescence detection. The regional distribution of the enzyme activity in control brains was similar to that of serotonergic neurons; relatively high activity was found in the raphe nucleus, locus coeruleus and substantia nigra. The activity in the thalamus in Parkinson's disease and that in the locus coeruleus, raphe nucleus and substantia nigra in striato-nigral degeneration were significantly lower than that of controls (p less than 0.05). In most other brain regions in parkinsonian patients the activity was relatively lower than that of controls except the caudate nucleus and nucleus accumbens where the activity was relatively higher than that of controls. Marked decrease in the enzyme activity in various brain regions was observed in striato-nigral degeneration, Shy-Drager syndrome, and progressive supranuclear palsy. These results suggest that the activity of tryptophan hydroxylase in serotonergic neurons is reduced in the brains of parkinsonian patients and of patients with degenerative nervous diseases.

Adolescent↗
PubMed1985

Effects of bromocriptine on parkinsonism. A nation-wide collaborative double-blind study.

The effects of bromocriptine in patients with Parkinson's disease manifesting various problems in levodopa therapy were tested in a double-blind manner with the collaboration of 59 institutions. The slow and low principle was in part adopted. Either bromocriptine or placebo was added to levodopa. Twenty-nine % of the bromocriptine-treated patients (n = 108), in contrast to 14.8% of the placebo-treated (n = 108), showed either marked or moderate improvement (P less than 0.05). Twenty to 37% improvement was noted in most of the symptoms studied in those treated with bromocriptine. The significant superiority of bromocriptine was also noted in the effects on wearing-off phenomena and frozen gait. No irreversible side effects were noted. It is concluded that bromocriptine is useful in patients who are manifesting various difficulties in levodopa therapy. Our results are comparable to those using higher maintenance doses. Dopamine antagonistic actions were not observed. This is unlike the case with experimental animals.

Bromocriptine↗