M. Sonoo
Teikyo University
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Featured researches published by M. Sonoo.
Neurology | 2005
H. Oba; A. Yagishita; H. Terada; A. J. Barkovich; K. Kutomi; T. Yamauchi; S. Furui; Teruo Shimizu; M. Uchigata; Kiichiro Matsumura; M. Sonoo; M. Sakai; K. Takada; A. Harasawa; K. Takeshita; H. Kohtake; H. Tanaka; S. Suzuki
OBJECTIVEnTo evaluate the area of the midbrain and pons on mid-sagittal MRI in patients with progressive supranuclear palsy (PSP), Parkinson disease (PD), and multiple-system atrophy of the Parkinson type (MSA-P), compare these appearances and values with those of normal control subjects, and establish diagnostic MRI criteria for the diagnosis of PSP.nnnMETHODSnThe authors prospectively studied MRI of 21 patients with PSP, 23 patients with PD, 25 patients with MSA-P, and 31 age-matched normal control subjects. The areas of the midbrain tegmentum and the pons were measured on mid-sagittal MRI using the display tools of a workstation. The ratio of the area of the midbrain to the area of the pons was also evaluated in all subjects.nnnRESULTSnThe average midbrain area of the patients with PSP (56.0 mm2) was significantly smaller than that of the patients with PD (103.0 mm2) and MSA-P (97.2 mm2) and that of the age-matched control group (117.7 mm2). The values of the area of the midbrain showed no overlap between patients with PSP and patients with PD or normal control subjects. However, patients with MSA-P showed some overlap of the values of individual areas with values from patients with PSP. The ratio of the area of the midbrain to the area of pons in the patients with PSP (0.124) was significantly smaller than that in those with PD (0.208) and MSA-P (0.266) and in normal control subjects (0.237). Use of the ratio allowed differentiation between the PSP group and the MSA-P group.nnnCONCLUSIONnThe area of the midbrain on mid-sagittal MRI can differentiate PSP from PD, MSA-P, and normal aging.
Clinical Neurophysiology | 2003
Takaaki Miura; M. Sonoo; Teruo Shimizu
OBJECTIVEnTo establish standard values for tibial nerve somatosensory evoked potentials (SEPs).nnnMETHODSnWe examined SEPs following left tibial nerve stimulation in 65 normal subjects of various ages, and performed multiple regression analysis using height, age, (age-20)(2) and gender as predictor variables. We objectively selected the latency or interval parameters with less intersubject variability as the standard parameters for evaluation.nnnRESULTSnAmong 3 cortical bipolar derivations investigated, the Cz-Cc lead gave a more constant and stable P38 component than the Cz-Fz or Ci-Cc lead. The latencies of the N8o (N8 onset) of the popliteal potential, P15 (P15 peak) in the contralateral iliac crest-ipsilateral greater trochanter lead, N21, N30 and P38o/P38 in the Cz-Cc lead, as well as the intervals between these components were selected as standard parameters. P15 was easily identified in all of the subjects and is expected to be a new parameter to evaluate the proximal segment of the tibial nerve. The amplitudes of P15 and the other components were also evaluated. We present nomograms for the normal limit values of each parameter.nnnCONCLUSIONSnWe present a thorough set of standard values for tibial SEPs where the subject factors were fully considered, and which is easily applicable to clinical practice.
Muscle & Nerve | 2002
M. Sonoo
Quantitative motor unit potential (MUP) analysis, which is a leading method of quantitative evaluation of concentric needle electromyography, has several inherent limitations. First, the most essential features of neurogenic or myogenic changes manifest as recruitment abnormalities, rather than as changes in MUP morphology. Second, two factors related to MUP sampling, focusing and level of contraction, greatly influence the parameters of sampled MUPs. Third, the MUP duration, considered to be the cardinal parameter in MUP analysis, has several drawbacks, including low stability and low discriminant sensitivity. We developed a new MUP parameter, the size index (SI), which is calculated from the MUP amplitude and area/amplitude ratio (thickness). The SI remained almost constant during electrode movements, as demonstrated by manual scanning of MUPs. It is a stable and robust parameter and achieved an extremely high ability to discriminate between normal and large neurogenic MUPs. It identifies features related to the sound produced by the MUP on the audio monitor, which is often used by trained electromyographers for qualitative assessments of MUPs.
Neurology | 2005
Yutaka Ohsawa; K. Kurokawa; M. Sonoo; H. Yamada; S. Hemmi; K. Iwatsuki; Hiroki Hagiwara; Tatsufumi Murakami; T. Shirabe; Teruo Shimizu; Yoshihide Sunada
The authors performed nerve conduction studies in nine PARK2 and eight idiopathic Parkinson disease patients and found a significant reduction of sural sensory nerve action potential (SNAP) amplitude in eight PARK2 patients who mostly remained asymptomatic. These data suggest that sensory axonal neuropathy may be a common clinical feature of PARK2 and a reduced amplitude of sural SNAP could be a diagnostic indicator of PARK2.
Clinical Neurophysiology | 2006
M. Sonoo; Y. Tsaiweichao-Shozawa; M. Oshimi-Sekiguchi; Y. Hatanaka; Teruo Shimizu
OBJECTIVEnTo investigate the occurrence of the spread of the radial sensory nerve action potential (SNAP) among patients with carpal tunnel syndrome (CTS) during standard median orthodromic sensory conduction study (SCS) using index finger stimulation.nnnMETHODSnWe prospectively examined 74 hands in 56 CTS patients. We stimulated the index finger using ring electrodes. SNAPs were recorded at wrist over median and radial nerves.nnnRESULTSnA spread of radial SNAP was clearly identified over the median nerve despite its small amplitude, in 72/74 hands during stimulation of the base of the index finger. In hands with delayed median SNAP, two peaks were observed; however in hands with absence of genuine median SNAP, only one peak of the spread was noticed. The proximal interphalangeal joint (PIP) stimulation still elicited an identifiable spread in 47/74 hands.nnnCONCLUSIONnThis spread phenomenon is a previously undescribed pitfall during the standard median orthodromic SCS, frequently occurring in CTS patients.nnnSIGNIFICANCEnIn severe CTS cases, one may make wrong conclusion of normal median sensory latency if unaware of this pitfall.
Neurology | 2005
M. Sonoo; A. Katayama; T. Miura; Teruo Shimizu; Kiyoharu Inoue
There is controversy regarding the initial pathology of tabes dorsalis. In a patient with early tabes dorsalis, tibial nerve somatosensory evoked potentials elicited normal P15, a delayed traveling peak in the lumbar bipolar leads, and absent subsequent components. Based on the comparison with normative data and stimulation at different intensities, the authors conclude that only the slower conducting antidromic motor volleys are preserved, whereas the dorsal root is damaged at its distal end.
Clinical Neurophysiology | 2004
M. Sonoo; Y. Hatanaka; H. Tsukamoto; Y. Tsai-Shozawa; Teruo Shimizu
OBJECTIVEnTo test the hypothesis that the N10 far-field potential in median nerve somatosensory evoked potentials is generated by the motor axons by examining patients with amyotrophic lateral sclerosis (ALS).nnnMETHODSnSubjects were 5 ALS patients showing pronounced or complete denervation of median-innervated small hand muscles. We evaluated N10 over scalp, and proximal plexus volleys (PPVs) at lateral or anterior cervical electrode.nnnRESULTSnN10 and PPVs were definitely preserved for every ALS subject. N10 amplitudes of ALS subjects were even significantly larger than control subjects. In one ALS patient completely lacking motor axons, N10 was larger than the largest one among control subjects.nnnCONCLUSIONSnPresent results clearly indicate that N10 is not predominantly generated by motor axons but by the whole median nerve dominated by sensory axons. We propose a theory that N10 is a junctional potential generated by the entrance of the median nerve into bone at the intervertebral foramen, producing a positive pole at the non-cephalic reference electrode. Significantly larger N10 in ALS subjects may be due to the lack of cancellation by slower motor axons.nnnSIGNIFICANCEnThe hypothesis that N10 is generated by motor axons is refuted, and a new theory of its generation is presented.
Journal of Neurology, Neurosurgery, and Psychiatry | 2004
Michiko Kobayashi; M. Sonoo; Teruo Shimizu
A selective weakness of a particular group of fingers due to cortical infarction has been reported by several authors.1–3 This finding is related to the controversy over the somatotopic organization of the primary motor cortex (M1). Traditionally, a discrete somatotopic arrangement for individual fingers, with the radial fingers represented laterally and the ulnar fingers medially, has been assumed. However, recent theories have suggested functional overlapping of the cortical representation of the fingers. We describe here a case presenting with major weakness of the index finger due to a cortical infarction confirmed by MRI.nnA 71 year old right handed man noted difficulty in using his toothbrush one morning. He complained of weakness in his right index finger and was admitted to our hospital on the day of onset. He had no previous illnesses nor risk for stroke. Neurological examination revealed the following muscle weaknesses: extension, abduction, and adduction of the right index finger (2-/5 as scored by the Medical Research Council (MRC) grading …
International Congress Series | 2005
Hiroyuki Fukuda; M. Sonoo; Teruo Shimizu
Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine | 2006
M. Sonoo; Y. Hatanaka