Search

It is possible to diagnose varicose vein from medical history and physical examinations including inspection and palpation. Non-contrast enhanced MRV (magnetic resonance venography) is becoming popular because it can be easily performed without being affected by the radiographer's skill. We thought that the use of MEDIC (multi echo data imaging combination) would enable us to delineate varicose veins within a short acquisition time and without need for synchronization or contrast enhancement. We used the SIEMENS MAGNETOM Avanto 1.5-Tesla unit to acquire images. Our subjects were five healthy volunteers and five patients with varicose vein. The signal strength of deep veins and muscles were measured. The SNR (signal-to-nose ratio) of deep veins and the CNR (contrast-to-noise ratio) between deep veins and muscles were also measured. 1. a) flip angle, b) fat suppression methods, c) MTC (magnetic transfer contrast) pulse, and d) combined echo. Using the optimum image acquisition protocol following our preliminary study with varicose vein patients, the ability of the 3D-MEDIC method to delineate varicose veins was compared with that of the ECG-synchronized 2D-TOF method. We found that the following settings would enable us to acquire images from a wide range=coronal, within short acquisition time and needless ECG-triggering. 1. a) flip angle=20 degrees, b) fat suppression method=water excitation, c) MTC pulse=ON, d) combined echo=2. 3D-MEDIC was better than the 2D-TOF method in delineating the varicose vein itself and the connection between the varicose vein and deep veins. It is expected that 3D-MEDIC may be useful in the clinical diagnosis of varicose veins. (Article in Japanese).

The clinical phenotype of frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) varies. This variability is seen not only between kindreds with different mutations but also in families sharing the same mutation. Inheritance of tau haplotype (H1) and genotype (H1/H1) has been established as a risk factor for some neurodegenerative disorders with parkinsonism. We assessed the effect of tau polymorphism on the clinical features of FTDP-17 in 61 cases from 30 separately ascertained families with four different tau mutations, including P301L, +16, N279K, and P301S. There were no significant differences of age at symptomatic onset and disease duration between H1/H1 and H1/H2 genotypes. The comparison between tau genotype and type of initial clinical sign showed an association between the H1/H1 genotype and parkinsonian phenotype and between the H1/H2 genotype and frontotemporal dementia phenotype (OR=11.7; 95% confidence interval, 1.4-98.7; P=0.008). Our results suggest that tau genotype does not influence the disease course. However, it may predispose to a specific clinical sign in the early stage of FTDP-17.

Unlabelled: This study investigated alterations in regional cerebral blood flow (rCBF) in patients with Parkinson's disease using statistical parametric mapping (SPM)., Methods: Noninvasive rCBF measurements using 99mTc-ethyl cysteinate dimer (ECD) SPECT were performed on 28 patients with Parkinson's disease and 48 age-matched healthy volunteers. The Parkinson's disease patients were divided into two groups, 16 patients with Hoehn and Yahr stage I or II and 12 patients with Hoehn and Yahr stage III or IV. We used the raw data (absolute rCBF parametric maps) and the adjusted rCBF images in relative flow distribution (normalization of global CBF for each subject to 50 mL/100 g/min with proportional scaling) to compare these groups with SPM., Results: In patients with stage I or II Parkinson's disease, we found a diffuse decrease in absolute rCBF in the whole brain with sparing of the central gray matter, hippocampus and right lower temporal lobe compared with healthy volunteers. Adjusted rCBF increased in both putamina and the right hippocampus. In patients with stage III or IV disease, rCBF decreased throughout the whole brain. Adjusted rCBF increased bilaterally in the putamina, globi pallidi, hippocampi and cerebellar hemispheres (dentate nuclei) and in the left ventrolateral thalamus, right insula and right inferior temporal gyrus., Conclusion: SPM analysis showed that significant rCBF changes in Parkinson's disease accompanied disease progression and related to disease pathophysiology in the functional architecture of thalamocortex-basal ganglia circuits and related systems.

We developed a questionnaire for the study of background factors and quality of life (QOL) in elderly patients with cerebral vascular disease (CVD) and Parkinson's disease (PD). The questionnaire covered the background factors and four sections such as physical, functional, psychological and social health sections. Each section had 15 questions and disease-specific questions for CVD or PD were included in the physical health section. We analyzed 107 patients with CVD (76 elderly patients, aged 65 or more, 31 non-elderly patients under 65) and 136 patients with PD (91 elderly, 45 non-elderly). In the background section, of a total of 243 patients with CVD and PD, the elderly patients needed the assistance of their spouse and their sons wives more frequently than non-elderly patients. With regard to rehabilitation, non-elderly CVD patients had rehabilitation more frequently than the elderly CVD patients, while a higher percentage of elderly patients with PD had rehabilitation training more frequently than the non-elderly PD patients. In the QOL section, there was no difference between elderly and non-elderly CVD patients, while elderly PD patients were statistically more significantly disabled physically and weak-minded psychologically. The physical disabilities of the elderly PD patients in this statistical investigation included slow motion, stooped posture, frozen gait, difficulty in turning and standing up, constipation and dysuria. The psychological problems of elder PD patients included forgetfulness and a feeling of aging. These patients had significantly fewer consultations by family and relatives than the non-elderly PD patients. The overall tendency of QOL in patients with CVD and PD was similar to that of PD patients.

We performed a detailed study of swollen neurite aggregation surrounding extracellular neurofibrillary tangles (ghost tangles, GTs) in brains of patients with progressive supranuclear palsy (PSP) by immunohistochemistry and electron microscopy (EM). The complex structures, designated as tangle-associated neuritic clusters (TANCs), were found in the hippocampus and parahippocampal cortex in all five PSP brains examined. TANCs measured from 20 to 40 microm across; twice as large as nearby neurons. Each neurite was globular or fusiform in shape, measured up to 10 microm in diameter, and was found between loosened fascicles of GTs or along their outer rims. There were several subsets of neurites that were argyrophilic or immunoreactive against antibodies to either phosphorylated tau protein, phosphorylated neurofilaments, ubiquitin, or synaptophysin. On EM, TANCs consisted of numerous axon terminals of varying size, which were filled with flocculate dense bodies, vesicular profiles, and synaptic vesicles, as well as normal-looking and degenerating cell organelles. Some axons had 13- to 15-nm-thick straight tubules that showed tau immunoreactivity; however, there was little neurofilament accumulation. Most of the swollen axon terminals conformed to the ultrastructural features of either reactive or degenerating terminals. The neurites identified by immunohistochemistry only represented a minority of the swollen axons visualized by EM. Tubules of GTs were dispersed in the extracellular space, but no amyloid fibrils were found. TANCs may constitute a distinctive form of neuronal degeneration in PSP cortices. We hypothesize that axon terminal accumulation may occur in response to GT-formation.

We examined neuronal cytoplasmic inclusions (NCIs) and oligodendrocytic glial cytoplasmic inclusions (GCIs) in the pontine nuclei in multiple system atrophy (MSA) using antibodies against the non-amyloid beta component of Alzheimer's disease amyloid precursor protein (NACP/alpha-synuclein). Our immunohistochemical study revealed that anti-NACP antibodies labeled both NCIs and GCIs. Immunoelectron microscopy showed that positive reaction products were localized on the 15- to 30-nm-thick filamentous components of NCIs and GCIs. The present study demonstrates that NACP is associated with cytoplasmic inclusions of MSA, and suggests a role of NACP in abnormal filament aggregation in neuronal degeneration.

To assess the action of neurotrophin in human dopaminergic neurons, we studied the immunolocalization of neurotrophins or trks in human substantia nigra pars compacta (SNc). The neuromelanin-containing neurons in the SNc showed immunoreactivities for neurotrophins or trks, suggesting an autocrine/paracrine regulation. Quantitative analysis revealed that the percentage of those expressing NGF-like immunoreactivity (NGF-LI), BDNF-LI, NT3-LI, trkA-LI, trkB-LI, or trkC-LI was 66%, 74%, 85%, 66%, 71% or 86%, respectively. The percentage of cells expressing neurotrophins or trks was higher in the medial part than in the lateral part of the SNc. The preferential expression of neurotrophin-trk systems in the medial neurons may, at least partially, explain the differential susceptibility in Parkinson's disease.