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Biomedical subjects

Ryuji Kaji

Publications and source records attributed to Ryuji Kaji.

At least 19 recordsLinked to original sources
PubMed2006

Stereotactic surgery for subthalamic nucleus stimulation under general anesthesia: a retrospective evaluation of Japanese patients with Parkinson's disease.

We compared retrospectively the outcome of bilateral subthalamic nucleus (STN) stimulation in 15 patients with Parkinson's disease who underwent the procedure under general anesthesia (GA) with that achieved in 10 patients under local anesthesia (LA). At 3 months postoperatively, all cardinal parkinsonian motor symptoms, evaluated on Unified Parkinson's Disease Rating Scale were significantly improved compared to preoperative baselines in both groups. The administration of GA did not adversely affect postoperative improvements in motor and daily activity scores, except for off-medication bradykinesia. Our results suggest that GA compares favorably with LA in surgical procedure for bilateral STN stimulation.

Aged↗
PubMed2006

Alleviation of camptocormia by bilateral subthalamic nucleus stimulation in a patient with Parkinson's disease.

Camptocormia, known also as "bent spine syndrome", is characterized by involuntary truncal flexion of the thoraco-lumbar spine that appears in the sitting or standing position. Although Parkinson's disease (PD) is the most frequent etiologic factor, this postural disorder responds poorly to levodopa or other medications. We report a PD patient in whom chronic bilateral subthalamic nucleus stimulation produced a striking alleviation of camptocormia.

Aged↗
PubMed2006

Nerve excitability testing and its clinical application to neuromuscular diseases.

Non-invasive nerve excitability testing measures the membrane polarization, ion channel function and paranodal/internodal condition of peripheral nerves. This technique has been recently used for various neuromuscular disorders, such as pure motor conduction block in multifocal motor neuropathy, conduction block in carpal tunnel syndrome and Na(+) channel function disorders in diabetic neuropathy, to shed light on their pathophysiology. Here, we review the basics of ion channel functions and membrane properties that influence nerve excitability, the basic principles of nerve excitability testing and the reported findings in various disorders.

Action Potentials↗
PubMed2006

Effect of repetitive transcranial magnetic stimulation applied over the premotor cortex on somatosensory-evoked potentials and regional cerebral blood flow.

Somatosensory-evoked potentials (SEPs) are attenuated by movement. This phenomenon of 'gating' reflects sensorimotor integration for motor control. The frontal N30 component after median nerve stimulation was shown to be reduced in amplitude prior to hand movement. To investigate the mechanism of this sensory gating, we recorded median SEPs immediately before and after application of monophasic very low-frequency (0.2 Hz) repetitive transcranial magnetic stimulation (rTMS) of 250 stimuli over motor cortex (MC), premotor cortex (PMC), or supplementary motor area (SMA) in 9 healthy volunteers. The stimulus intensity for MC or PMC was set 85% of the resting motor threshold for the hand muscle, and that for SMA was at the active motor threshold for the leg muscle. SEPs showed significant increases in amplitudes of the frontal N30 component after PMC stimulation, but not after SMA or MC stimulation. Low-frequency (1 Hz) biphasic stimulation over PMC showed no significant N30 changes in 6 out of 9 subjects tested, indicating the effect being specific for 0.2 Hz monophasic stimulation. To examine the functional anatomy of the N30 change, single photon emission computed tomography was performed immediately before and after monophasic 0.2 Hz rTMS over PMC in all the 9 subjects. Regional cerebral blood flow showed significant increases mainly in PMC and prefrontal cortex, indicating the involvement of these cortical areas in sensory input gating for motor control.

Adult↗
PubMed2006

Complete suppression of paroxysmal nonkinesigenic dyskinesia by globus pallidus internus pallidal stimulation.

Stereotactic functional surgery is being explored as potential therapies for medically intractable paroxysmal dyskinesias (PxD). We report on a 59-year-old man in whom stimulation of globus pallidus internus produced immediate and sustained relief of paroxysmal non-kinesigenic dyskinesia secondary to a rotator cuff tears on the left shoulder. Our finding strongly suggests that altered function of neuronal circuits of the basal ganglia underlies the manifestation of PxD.

Chorea↗
PubMed2006

Impact of bilateral pallidal stimulation on DYT1-generalized dystonia in Japanese patients.

Early-onset generalized dystonia attributable to a DYT1 gene mutation is a hyperkinetic movement disorder that responds poorly to pharmacotherapy. In this video brief, we show that continuous bilateral stimulation of the globus pallidus internus produced sustained and marked improvements in the motor symptoms and functional disabilities of Japanese patients with DYT1-generalized dystonia.

Adolescent↗
PubMed2006

Attenuation of MPTP-induced neurotoxicity and locomotor dysfunction in Nucling-deficient mice via suppression of the apoptosome pathway.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity is one of the experimental models most commonly used to study the pathogenesis of Parkinson's disease (PD). Although the biochemical mechanisms underlying the cell death induced by MPTP remain to be clarified, it has been found that the mitochondrial apoptotic signaling pathway plays an important role in the neurotoxicity of MPTP. Nucling is a novel type of apoptosis-associated molecule, essential for cytochrome c, apoptosis protease activating factor 1 (Apaf-1), pro-caspase-9 apoptosome induction and caspase-9 activation following pro-apoptotic stress. Here we found that Nucling-deficient mice treated with MPTP did not exhibit locomotor dysfunction in an open-field test. The substantia nigra dopaminergic neurons of Nucling-deficient mice were resistant to the damaging effects of the neurotoxin MPTP. Up-regulated expression of apoptosome was attenuated in Nucling-deficient mice treated with MPTP. These results indicate an important role for Nucling in MPTP-induced neuronal degeneration and suggest that the suppression of Nucling would be of therapeutic benefit for the treatment of neurodegeneration in PD.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2006

[A case of hyperglycemic neuropathy with possible dysfunction of axonal excitability].

A 66-year-old woman with SLE who recently started oral steroid was admitted to our hospital because of subacute numbness of the bilateral legs and gait disturbance, despite of the stable symptoms of SLE and its serology. Blood tests revealed hyperglycemia. Nerve conduction study showed decreased nerve conduction velocities consistent with demyelinative neuropathy. On initiation of insulin to control hyperglycemia, conduction velocities were rapidly increased in one week, suggesting hyperglycemic neuropathy. The rapid improvement of the conduction velocities was argued against mechanical "demyelination", rather suggesting axonal dysfunction, possibly associated with impaired function of Na(+)-K(+)-ATPase in hyperglycemic state.

Aged↗
PubMed2006

[Neuroradiological study of a possible progressive multifocal leukoencephalopathy using diffusion tensor imaging and proton magnetic resonance spectroscopy].

We report a possible case of progressive multifocal leukoencephalopathy (PML) that was attempted to evaluate the pathogenesis by a novel brain MRI techniques. A 72-year-old woman had developed subacute visual disturbance, right hemiparesis and sensory disturbance. Laboratory examinations revealed liver dysfunction and pancytopenia due to liver cirrhosis (type C) and preclinical status of multiple myeloma. Thus, this patient had these two underlying diseases, while anti-HIV antibody was negative. She was suspected with PML by detection of JCV-DNA in cerebrospinal fluid using with PCR. MRI showed multifocal T2-high signals in the bilateral parieto-occipital deep white matter, basal ganglia and right cerebellar hemisphere. No gadolinium enhancement was found. On FLAIR and diffusion weighted images (DWI), the lesion showed hyperintensity. The hyperintense areas on DWI showed various pattern on apparent diffusion coefficient (ADC) and fractional anisotropy (FA). In particular white matter changes, the course of FA reflected the clinical course more than ADC. Proton magnetic resonance spectroscopy (1H-MRS) in deep brain white matter showed ratios of reduced N-acetyl aspartate (NAA) and increased choline (Cho) to creatine. 1H-MRS by chemical shift imaging were undergone three times between 4 and 6 months after the onset. The change of these chemical markers correlated with her clinical course. We conclude that the approach of diffusion tensor imaging (DTI) and 1H-MRS are useful for evaluating neuropathologic observations and clinical course.

Aged↗
PubMed2005

Modulation of torsinA expression in the globus pallidus internus is associated with levodopa-induced dyskinesia in hemiparkinsonian rats.

TorsinA is the causative protein of DYT1 dystonia, a major representative of hyperkinetic movement disorders. In this study, the distribution of torsinA was investigated in the basal ganglia of hemiparkinsonian rats with or without levodopa-induced dyskinesia (LID). Two months after 6-hydroxydopamine (OHDA) treatment, Wistar-albino rats were subjected to intermittent intraperitoneal injection of levodopa/benserazid (LID-group, n=5) or vehicle (control, n=5) for 21 days. Immunohistochemical analysis disclosed that in the caudal portion of the entopeduncular nucleus (EP), homologous to the globus pallidus internus (GPi) in primates, on the parkinsonian side, there was a significant decrease of torsinA-immunopositive neurons in rats with LID, but not in those without LID. However, Nissl-staining showed no loss of GPi neurons in rats with LID. In both groups, there was no significant difference between ipsi- and contralateral sides with respect to the density of torsinA-positive neuronal cells in the striatum, globus pallidus externus, and subthalamic nucleus. Ours are the first data to demonstrate the specific modulation of torsinA expression in the basal ganglia of the hyperkinesia model, suggesting that GPi neurons containing torsinA possess pathologic plasticity for LID.

Animals↗
PubMed2005

Influence of a tumor necrosis factor gene polymorphism in Japanese patients with multiple system atrophy.

We studied promoter region polymorphisms in the tumor necrosis factor (TNF), interleukin (IL)-6, IL-10, and transforming growth factor (TGF)-beta1 genes in Japanese patients with multiple system atrophy (MSA) (n=122) and normal controls (n=277). The frequency of the TNF-1031C, a high producer allele of TNF, was increased significantly in MSA patients compared with controls (chi2=12.36, P=0.0021, Pc=0.0084). In contrast, there was no difference in the genotype or allele frequency in the other cytokine gene polymorphisms. We also failed to detect any difference in the disease onset between each genotype of the polymorphisms examined. Our findings suggest that TNF might have a toxic effect in MSA.

Adult↗
PubMed2005

Functional anatomy of the basal ganglia in X-linked recessive dystonia-parkinsonism.

Dystonia is a neurological syndrome characterized by sustained muscle contractions that produce repetitive twisting movements or abnormal postures. X-linked recessive dystonia parkinsonism (XDP; DYT3; Lubag) is an adult-onset disorder that manifests severe and progressive dystonia with a high frequency of generalization. In search for the anatomical basis for dystonia, we performed postmortem analyses of the functional anatomy of the basal ganglia based on the striatal compartments (ie, the striosomes and the matrix compartment) in XDP. Here, we provide anatomopathological evidence that, in the XDP neostriatum, the matrix compartment is relatively spared in a unique fashion, whereas the striosomes are severely depleted. We also document that there is a differential loss of striatal neuron subclasses in XDP. In view of the three-pathway basal ganglia model, we postulate that the disproportionate involvement of neostriatal compartments and their efferent projections may underlie the manifestation of dystonia in patients with XDP. This study is the first to our knowledge to show specific basal ganglia pathology that could explain the genesis of dystonia in human heredodegenerative movement disorders, suggesting that dystonia may result from an imbalance in the activity between the striosomal and matrix-based pathways.

Adult↗
PubMed2005

Glutathione-S-transferase-1 and interleukin-1beta gene polymorphisms in Japanese patients with Parkinson's disease.

We studied genetic polymorphisms in the glutathione-S-transferase-1 (GST-1) gene region and the interleukin-1beta (IL-1beta) promoter region in patients with Parkinson's disease (PD, n = 361), as well as controls (n = 257). Although we have confirmed the previous results, in a larger sample, that the IL-1beta genotype has affected the age at onset of PD patients, no contribution of the GST-1 gene polymorphism was observed in the allele frequency or the onset age of the disease in Japanese persons.

Adult↗
PubMed2005

Brain-derived neurotrophic factor gene polymorphisms in Japanese patients with sporadic Alzheimer's disease, Parkinson's disease, and multiple system atrophy.

We studied two genetic polymorphisms (240C/T and 480G/A) of the brain-derived neurotrophic factor (BDNF) gene in Japanese patients with Alzheimer's disease (AD, n = 172), Parkinson's disease (PD, n = 327), and multiple system atrophy (MSA, n = 122), as well as controls (n = 275). The distribution of the 240 C/T polymorphism was significantly different between AD patients and controls, whereas there was no difference in the genotype of the two polymorphisms between MSA and controls or between PD and controls. Our data suggest that BDNF might play a role in AD.

Aged↗