Hakone National Hospital

Odawara, Japan

Hakone National Hospital

Odawara, Japan
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Kimura K.,University of Tokyo | Takenaka K.,University of Tokyo | Ebihara A.,University of Tokyo | Uno K.,University of Tokyo | And 15 more authors.
International Journal of Cardiology | Year: 2013

Background The reported prevalence of left ventricular noncompaction (LVNC) varies widely and its prognostic impact remains controversial. We sought to clarify the prevalence and prognostic impact of LVNC in patients with Duchenne/Becker muscular dystrophy (DMD/BMD). Methods We evaluated the presence of LNVC in patients with DMD/BMD aged 4-64 years old at the study entry (from July 2007 to December 2008) and prospectively followed-up their subsequent courses (n = 186). The study endpoint was all-cause death and the presence of LVNC was blinded until the end of the study (median follow-up: 46 months; interquartile range: 41-48 months). Results There were no significant differences in baseline characteristics between patients with LVNC (n = 35) and control patients without LVNC (n = 151), with the exception of LV function. Patients with LVNC showed, in comparison with patients without LVNC, a significant negative correlation between age and LVEF (R = - 0.7 vs. R = - 0.4) at baseline; and showed a significantly greater decrease in absolute LVEF (- 8.6 ± 4.6 vs. - 4.3 ± 4.5, p < 0.001) during the follow-up. A worse prognosis was observed in patients with LVNC (13/35 died) than in patients without LVNC (22/151 died, Log-rank p < 0.001). Multivariate Cox analysis revealed that LVNC is an independent prognostic factor (relative hazard 2.67 [95% CI: 1.19-5.96]). Conclusion LVNC was prevalent in patients with DMD/BMD. The presence of LVNC is significantly associated with a rapid deterioration in LV function and higher mortality. Neurologists and cardiologists should pay more careful attention to the presence of LVNC. © 2012 Elsevier Ireland Ltd.


Kokubun N.,Dokkyo Medical University | Sonoo M.,Teikyo University | Imai T.,Sapporo Medical University | Arimura Y.,Kagoshima University | And 9 more authors.
Clinical Neurophysiology | Year: 2012

Objective: The aim of this study is to establish reference values for single-fibre electromyography (SFEMG) using concentric needles in a prospective, multicentre study. Methods: Voluntary or stimulated SFEMG at the extensor digitorum communis (EDC) or frontalis (FRO) muscles was conducted in 56-63 of a total of 69 normal subjects below the age of 60. years at six Japanese institutes. The cut-off values for mean consecutive difference (MCD) of individual potentials were calculated using +2.5 SD or 95% prediction limit (one-tail) of the upper 10th percentile MCD value for individual subjects. Results: The cut-off values for individual MCD (+2.5 SD) were 56.8μs for EDC-V (voluntary SFEMG for EDC), 58.8μs for EDC-S (stimulated SFEMG for EDC), 56.8μs for FRO-V (voluntary SFEMG for FRO) and 51.0μs for FRO-S (stimulated SFEMG for FRO). The false positive rates using these cut-off values were around 2%. Conclusions: The +2.5 SD and 95% prediction limit might be two optimal cut-off values, depending on the clinical question. The obtained reference values were larger than those reported previously using concentric needles, but might better coincide with conventional values. Significance: This is the first multicentre study reporting reference values for SFEMG using concentric needles. The way to determine cut-off values and the statistically correct definition of the percentile were discussed. © 2011 International Federation of Clinical Neurophysiology.


Yokoyama T.,Hakone National Hospital | Yokoyama T.,National Sagamihara Hospital | Hasegawa K.,National Sagamihara Hospital | Obama R.,Hakone National Hospital | And 2 more authors.
Neuropathology | Year: 2010

Up to now diffuse white matter demyelination of the cerebrum has been reported in only a few cases of mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS). Here we document an autopsy case with this rare neuropathology. Most MELAS cases are diagnosed antemortem by A3243G transition of mitochondrial DNA. While cerebral damage including necrotic foci in the cerebral cortex are common findings in MELAS, prominent white matter involvement best characterizes this MELAS case. There were numerous necrotic foci, varying in size and chronological stage, in the cerebral white matter. In the areas of the white matter without necrotic foci, there was diffuse fibrillary gliosis with the loss of axons and oligodendrocytes. The gliosis was dominant in the deep white matter, sparing the U-fiber. The cerebral cortex showed diffuse cortical atrophy with few scattered necrotic foci. Distribution of the cerebral lesions does not coincide with the territory of blood supply. The vascular wall presented only slight to mild hyalinosis. We assumed a common pathogenesis to the cortical lesions and the white matter change. The pathogenesis of the present diffuse cerebral lesions may not be just secondary to circulatory disturbance but partly due to metabolic abnormality. © 2009 Japanese Society of Neuropathology.


Hamada K.,Hakone National Hospital | Yamanaka K.,Yamanaka Orthopaedic Clinic | Uchiyama Y.,Tokai University | Mikasa T.,Red Cross | Mikasa M.,Matsudo Orthopaedic Hospital
Clinical Orthopaedics and Related Research | Year: 2011

Background: In 1990, Hamada et al. radiographically classified massive rotator cuff tears into five grades. Walch et al. subsequently subdivided Grade 4 to reflect the presence/absence of subacromial arthritis and emphasize glenohumeral arthritis as a characteristic of Grade 4. Questions/purposes: We therefore determined (1) whether patient characteristics and MRI findings differed between the grades at initial examination and final followup; (2) which factors affected progression to a higher grade; (3) whether the retear rate of repaired tendons differed among the grades; and (4) whether the radiographic grades at final followup differed from those at initial examination among patients treated operatively. Patients and Methods: We retrospectively reviewed 75 patients with massive rotator cuff tears. Thirty-four patients were treated nonoperatively and 41 operatively. Results: Patients with Grade 3, 4, or 5 tears had a higher incidence of fatty muscle degeneration of the subscapularis muscle than patients with Grade 1 or 2 tears. In 26 patients with Grade 1 or 2 tears at initial examination, duration of followup was longer in patients who remained at Grade 1 or 2 than in those who progressed to Grade 3, 4, or 5 at final followup. The retear rate of repaired supraspinatus tendon was more frequent in Grade 2 than Grade 1 tears. In operated cases, radiographic grades at final followup did not develop to Grades 3 to 5. Conclusions: We believe cuff repair should be performed before acromiohumeral interval narrowing. Our observations are consistent with the temporal concepts of massive cuff tear pathomechanics proposed by Burkhart and Hansen et al. Level of Evidence: Level III, Therapeutic study. See Guidelines for Authors for a complete description of levels of evidence. © 2011 The Association of Bone and Joint Surgeons®.


PubMed | Hakone National Hospital
Type: Case Reports | Journal: Neuropathology : official journal of the Japanese Society of Neuropathology | Year: 2010

Up to now diffuse white matter demyelination of the cerebrum has been reported in only a few cases of mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS). Here we document an autopsy case with this rare neuropathology. Most MELAS cases are diagnosed antemortem by A3243G transition of mitochondrial DNA. While cerebral damage including necrotic foci in the cerebral cortex are common findings in MELAS, prominent white matter involvement best characterizes this MELAS case. There were numerous necrotic foci, varying in size and chronological stage, in the cerebral white matter. In the areas of the white matter without necrotic foci, there was diffuse fibrillary gliosis with the loss of axons and oligodendrocytes. The gliosis was dominant in the deep white matter, sparing the U-fiber. The cerebral cortex showed diffuse cortical atrophy with few scattered necrotic foci. Distribution of the cerebral lesions does not coincide with the territory of blood supply. The vascular wall presented only slight to mild hyalinosis. We assumed a common pathogenesis to the cortical lesions and the white matter change. The pathogenesis of the present diffuse cerebral lesions may not be just secondary to circulatory disturbance but partly due to metabolic abnormality.

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