Hitoshi Mochizuki

Fukushima Medical University, Hukusima, Fukushima, Japan

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Publications (73)168.56 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Using NIRS (near-infrared spectroscopy) and multi-channel probes, we studied hemoglobin (Hb) concentration changes when single-pulse transcranial magnetic stimulation (TMS) was applied over the left hemisphere primary motor cortex (M1). Seventeen measurement probes were centered over left M1. Subjects were studied both in the active and relaxed conditions, with the TMS intensity set at 100%, 120%, and 140% of the active motor threshold. The magnetic coils were placed so as to induce anteromedially directed currents in the brain. Hb concentration changes were more prominent at channels over M1 and posterior to it. Importantly, Hb concentration changes at M1 after TMS differed depending on whether the target muscle was in an active or relaxed condition. In the relaxed condition, Hb concentration increased up to 3-6 s after TMS, peaking at around 6 s, and returned to the baseline. In the active condition, a smaller increase in Hb concentrations continued up to 3-6 s after TMS (early activation), followed by a decrease in Hb concentration from 9-12 s after TMS (delayed deactivation). Hb concentration changes in the active condition at higher stimulus intensities were more pronounced at locations posterior to M1 than at M1. We conclude that early activation occurs when M1 is activated trans-synaptically. The relatively late deactivation may result from the prolonged inhibition of the cerebral cortex after activation. The posterior dominant activation at higher intensities under the active condition may result from an additional activation of the sensory cortex due to afferent inputs from muscle contraction evoked by the TMS.
    Journal of Neurophysiology 12/2012; · 3.30 Impact Factor
  • Clinical Neurophysiology. 09/2012; 123(9):e91.
  • Clinical Neurophysiology. 09/2012; 123(9):e97–e98.
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    ABSTRACT: BACKGROUND: Imaging studies investigating repetitive transcranial magnetic stimulation (rTMS) mediated hemodynamic consequences revealed inconsistent results, mainly due to differences in rTMS parameters and technical difficulties with simultaneous recordings during rTMS. OBJECTIVE: /Hypothesis: Quadri-pulse rTMS (QPS) induces bidirectional long-term plasticity of the human primary motor cortex (M1). To evaluate its on-line effects, near infrared spectroscopy (NIRS) recordings were performed during QPS. We hypothesized that on-line effects during QPS are different from long-term aftereffects. METHODS: Using a novel TMS - on-line multi-channel NIRS setup we recorded hemoglobin concentration [Hb] changes at the stimulated M1 and adjacent sensory-motor areas during QPS protocols inducing oppositely directed aftereffects (QPS-5: interstimulus interval (ISI) 5 ms, potentiation; QPS-50: ISI 50 ms, depression). In two experiments we studied NIRS changes during either single or repeated QPS bursts. RESULTS: The repetitive QPS-5 bursts significantly decreased oxyhemoglobin concentration ([oxy-Hb]) in the ipsilateral M1. A single QPS-5 burst decreased [oxy-Hb] in the M1 and premotor cortex. QPS-50 induced no significant NIRS changes at any sites. CONCLUSIONS: QPS can significantly alter cortical hemodynamics depending on the stimulation frequency. While bidirectional long-term aftereffects of QPS reflect synaptic efficacy changes, unidirectional on-line effects during QPS may represent pure electrophysiological property changes within the cell membrane or synapse. Since neuronal postexcitatory inhibitory postsynaptic potentials typically peak within the first 10-20 ms, only pulses delivered at higher frequencies may lead to summation of the inhibitory effects, resulting in [oxy-Hb] decrease only after QPS-5. Our new TMS-NIRS setup may be valuable to investigate TMS induced neurovascular coupling mechanisms in humans.
    Brain Stimulation 02/2012; · 4.54 Impact Factor
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    ABSTRACT: Quadripulse transcranial magnetic stimulation (QPS) is a newly designed patterned repetitive transcranial magnetic stimulation (TMS). Previous studies of QPS showed bidirectional effects on the primary motor cortex (M1), which depended on its inter-stimulus interval (ISI): motor evoked potentials (MEPs) were potentiated at short ISIs and depressed at long ISIs (homotopic effects). These physiological characters were compatible with synaptic plasticity. In this research, we studied effects of QPS on the primary sensory cortex (S1). One burst consisted of four monophasic TMS pulses at an intensity of 90% active motor threshold. The ISI of four pulses was set at 5 ms (QPS-5) or at 50 ms (QPS-50). Same bursts were given every 5s for 30 min. QPS-5 and QPS-50 were performed over three areas (M1, S1 and dorsal premotor cortex (dPMC)). One sham stimulation session was also performed. Excitability changes of S1 were evaluated by timeline of somatosensory evoked potentials (SEPs). QPS-5 over M1 or dPMC enhanced the P25-N33 component of SEP, and QPS-50 over M1 depressed it. By contrast, QPSs over S1 had no effects on SEPs. QPSs over motor cortices modulated the S1 cortical excitability (heterotopic effects). Mutual connections between dPMC or M1 and S1 might be responsible for these modulations. QPSs induced heterotopic LTP or LTD-like cortical excitability changes.
    Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology 01/2012; 123(7):1415-21. · 3.12 Impact Factor
  • Brain Stimulation 10/2011; 4(4):303-5. · 4.54 Impact Factor
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    ABSTRACT: To evaluate on-line effects of quadripulse stimulation (QPS) over the primary motor cortex (M1) on cortical areas in the contralateral hemisphere. QPS consisted of 24 bursts of transcranial magnetic stimulation (TMS) pulses with an inter-burst interval of 5 s for 2 min (for on-line effect study) or 360 bursts for 30 min (for after-effect study). Each burst consisted of four TMS pulses (i.e. QPS) separated by an interstimulus interval of 5 or 50 ms (QPS-5 or QPS-50). QPSs were delivered over the left M1. Experiment 1 [on-line effect on somatosensory evoked potential (SEP)]: Left median nerve SEPs were recorded before, during and after QPS. Experiment 2 (after effect on SEP): After-effects of QPS were evaluated by following up SEPs after the QPS sessions. Experiment 3 (on-line effect on NIRS): Near infrared spectroscopy (NIRS) was also recorded at the right hemisphere during all QPS paradigms. Both QPS-5 and QPS-50 enlarged a cortical component of the contralateral SEP during stimulation. On the other hand, concerning the after effects, QPS-5 over M1 potentiated the contralateral SEP and QPS-50 tended to depress it. In NIRS study, both QPS-5 and QPS-50 induced a significant oxy-Hb decrease (deactivation pattern) at the right hemisphere during stimulation whereas sham stimulations unaffected them. We have shown the unidirectional on-line effects evoked by QPS-5 and QPS-50 on both SEP and NIRS, and bidirectional after effects on SEP at the contralateral hemisphere. The discrepancy between on-line effect and after effect may be explained by the differences in the underlying mechanisms between them. The former may be mainly explained by pure electrophysiological property changes in the membrane or synapses. The latter may be explained by synaptic efficacy changes which need some protein syntheses at least partly. Another discrepancy shown here is the direction of on-line effects. Electrophysiological (SEP) function was potentiated by both QPSs whereas hemodynamic (NIRS) function was depressed. This may be explained by which sensory areas contribute to NIRS or SEP generation.
    Experimental Brain Research 09/2011; 214(4):577-86. · 2.22 Impact Factor
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    ABSTRACT: We have reported two patients with posterior spinal artery syndrome. Both of them had sudden onset back pain, paraparesis, loss of deep sensation and bladder-bowel disturbances. MRI disclosed spinal cord lesions positioned at its posterior part including the posterior column or posterior horn at thoracic levels. Spinal artery syndrome is a rare disorder, especially the posterior spinal artery syndrome (PSAS). In our department, only ten patients had spinal artery syndrome out of 2,064 patients admitted to our hospital these 20 years. All the other 8 patients had anterior spinal artery syndrome. It supports the notion that PSAS is rare. The detection rate of PSAS may increase after the routine use of spinal MRI in clinical practice. Our two patients had bilateral, symmetric symptoms. These symmetric signs and symptoms are usually seen in PSAS. The bilateral posterior spinal arteries connect with each other through many complex anastomoses. Moderate blood flow insufficiency may produce no clinical symptoms because of compensation by these anastomoses. When symptoms appear, these anastomoses do not compensate blood flow deficit and may produce bilateral symptoms.
    Rinsho shinkeigaku = Clinical neurology 09/2011; 51(9):699-702.
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    ABSTRACT: The aim of this study was to investigate physiological mechanisms underlying ataxia in patients with ataxic hemiparesis. Subjects were three patients with ataxic hemiparesis, whose responsible lesion was located at the posterior limb of internal capsule (case 1), thalamus (case 2), or pre- and post-central gyri (case 3). Paired-pulse transcranial magnetic stimulation (TMS) technique was used to evaluate connectivity between the cerebellum and contralateral motor cortex. The conditioning cerebellar stimulus was given over the cerebellum and the test stimulus over the primary motor cortex. We studied how the conditioning stimulus modulated motor evoked potentials (MEPs) to the cortical test stimulus. In non-ataxic limbs, the cerebellar stimulus normally suppressed cortical MEPs. In ataxic limbs, the cerebellar inhibition was not elicited in patients with a lesion at the posterior limb of internal capsule (case 1) or thalamus (case 2). In contrast, normal cerebellar inhibition was elicited in the ataxic limb in a patient with a lesion at sensori-motor cortex (case 3). Lesions at the internal capsule and thalamus involved the cerebello-thalamo-cortical pathways and reduced the cerebellar suppression effect. On the other hand, a lesion at the pre- and post-central gyri should affect cortico-pontine pathway but not involve the cerebello-thalamo-cortical pathways. This lack of cerebello-talamo-cortical pathway involvement may explain normal suppression in this patient. The cerebellar TMS method can differentiate cerebellar efferent ataxic hemiparesis from cerebellar afferent ataxic hemiparesis.
    The Cerebellum 07/2011; 11(1):259-63. · 2.60 Impact Factor
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    ABSTRACT: Skeletal muscle metabolism is a major determinant of resting energy expenditure (REE). Although the severe muscle loss that characterizes Duchenne muscular dystrophy (DMD) may alter REE, this has not been extensively investigated. We studied REE in 77 patients with DMD ranging in age from 10 to 37 years using a portable indirect calorimeter, together with several clinical parameters (age, height, body weight (BW), body mass index (BMI), vital capacity (VC), creatine kinase, creatinine, albumin, cholinesterase, prealbumin), and assessed their influence on REE. In addition, in 12 patients maintaining a stable body weight, the ratio of energy intake to REE was calculated and defined as an alternative index for the physical activity level (aPAL). REE (kcal/day, mean±SD) in DMD patients was 1123 (10-11 years), 1186±188 (12-14 years), 1146±214 (15-17 years), 1006±136 (18-29 years) and 1023±97 (≥30 years), each of these values being significantly lower than the corresponding control (p<0.0001). VC (p<0.001) was the parameter most strongly associated with REE, followed by BMI (p<0.01) and BW (p<0.05). The calculated aPAL values were 1.61 (10-11 years), 1.19 (12-14 years), 1.16 (15-17 years), and 1.57 (18-29 years). The REE in DMD patients was significantly lower than the normal value in every age group, and strongly associated with VC. Both the low REE and PAL values during the early teens, resulting in a low energy requirement, might be related to the obesity that frequently occurs in this age group. In contrast, the high PAL value in the late stage of the disease, possibly due to the presence of respiratory failure, may lead to a high energy requirement, and thus become one of the risk factors for development of malnutrition.
    Brain & development 05/2011; 34(3):206-12. · 1.74 Impact Factor
  • Hitoshi Mochizuki, Yoshikazu Ugawa
    Movement Disorders 04/2011; 26(8):1577. · 5.63 Impact Factor
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    ABSTRACT: A 22-year-old man with a previous uveitis episode was admitted to our hospital because of persistent hiccup. On admission, he presented right-upper quadrantanopia, mydriasis and lack of the light reflex in the left eye, left-sided hemiplegia, and bilateral pathologic hyperreflexia. The MR fluid attenuated inversion recovery images showed left side dominant, high intensity lesions on the brainstem and the diencephalon. The HLA-B51 was positive. The CSF IL-6 was extremely elevated (998 pg/ml: reference value < = 6.0 pg/ml). Based on these, we concluded he had the neuro-Behçet's disease and treated him by high dose intravenous corticosteroids. This treatment improved his symptoms and MRI lesions, and decreased the CSF IL-6 levels initially. On 13th day after the first his discharge, however, dysarthria appeared and the CSF IL-6 levels elevated again. In addition to the high dose intravenous corticosteroids therapy for acute attack, 15 mg/week of methotrexate was started to prevent the recurrence. Even with this prevention, meningitis related to neuro-Behçet's disease occurred within six weeks. We administered 5 mg/kg of infliximab intravenously at 0, 2, 6, and 14 weeks. After the infliximab treatment, his symptoms improved and the IL-6 levels decreased, and no recurrence has occurred. This case supports that infliximab, anti-TNF-alpha agent, is a good candidate for neuro-Behçet's disease treatment when it is resistant to conventional immunosuppressive agents such as corticosteroids or methotrexate.
    Rinsho shinkeigaku = Clinical neurology 04/2011; 51(4):261-6.
  • Clinical Neurophysiology - CLIN NEUROPHYSIOL. 01/2011; 122.
  • Clinical Neurophysiology - CLIN NEUROPHYSIOL. 01/2011; 122.
  • Journal of neurology, neurosurgery, and psychiatry 12/2010; 81(12):1406-7. · 4.87 Impact Factor
  • Hitoshi Mochizuki, Yoshikazu Ugawa
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    ABSTRACT: In this review, we have mainly discussed the cerebellar ataxic gait. The cerebellum can be divided into 3 phylogenically different lobes: the archicerebellum, paleocerebellum, and neocerebellum. The main components of the cerebellar circuit are 2 types of neurons, i.e., the Purkinje cells and granule cells and 3 types of fibers, i.e., mossy fibers, climbing fibers (cerebellar afferent fibers), and parallel fibers (axons of granule cells) Theoretically, cerebellar ataxia is considered to be caused by any lesions that develop within this circuit. Before diagnosing any symptoms as ataxia, we should first exclude weakness, sensory disturbances or vestibular dysfunction to explain those symptoms. Cerebellar ataxia usually causes several neurological deficits such as antagonist hypotonia, asynergy, dysmetria, dyschronometria, and dysdiadochokinesia. Ataxic gait is one of the cardinal features of the cerebellar symptoms. The clinical features of cerebellar ataxic gait usually include a widened base, unsteadiness and irregularity of steps, and lateral veering. Locomotion in individuals with cerebellar ataxia is characterized by a significantly reduced step frequency with a prolonged stance and double limb support duration. All gait measurements are highly variable in cerebellar ataxia. The characteristic clinical features of several cerebellar diseases have been summarized in this review. Even though the rehabilitation for cerebellar ataxia is not fully supported by much enough clinical evidence, repeated motor training, bandages or light weights has sometimes beneficial effects on ataxic limbs.
    Brain and nerve = Shinkei kenkyū no shinpo 11/2010; 62(11):1203-10.
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    ABSTRACT: A 75-year-old man with diabetic nephropathy treated with hemodialysis visited to a medical office because of slight fever, and received intravenous glucose infusion without any vitamins. Thereafter, he noticed gait disturbance and began to tell inconsistent stories. He was admitted to our hospital due to aggravation of these symptoms. On admission, he was disoriented and not able to sit by himself because of severe truncal ataxia without weakness. He had also gaze direction nystagmus. Based on clinical features, we considered him as having Wernicke's encephalopathy (WE) and treated him with 100 mg thiamine per day. The thiamine supply diminished these symptoms soon. Plasma thiamine level prior to the administration was 7 ng/ml, which confirmed the diagnosis. MRI did not disclose any abnormalities frequently seen in WE. WE is a life-threatening disease, and 'early detection, early cure' is important for recovering without sequelae. The thiamine deficiency is often seen in dialysis patients because of dietary restrictions as well as its loss during dialysis. This case gives us the caution; when hemodialysis patients present acute/subacute gait disturbance and/ or abnormal mental state, we should consider WE. Furthermore, high-risk patients, such as elderly patients under hemodialysis may need some supplement including thiamine even at preclinical stage.
    Rinsho shinkeigaku = Clinical neurology 06/2010; 50(6):409-11.
  • Clinical Neurophysiology - CLIN NEUROPHYSIOL. 01/2010; 121.
  • H. Mochizuki, Y. Ugawa
    Clinical Neurophysiology - CLIN NEUROPHYSIOL. 01/2010; 121.
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    ABSTRACT: A 41-year-old man with multiple sclerosis (MS) complained of nocturnal enuresis at the third exacerbation. Neurological examination revealed echopraxia, forced grasp reflexes and palmo-mental reflexes. The urodynamic studies showed neither spinal cord nor peripheral nerve involvements. His brain magnetic resonance images (MRIs) revealed new lesions at the bilateral medial frontal lobes. The intravenous methylprednisolone therapy improved nocturnal enuresis and made brain MRI lesions smaller and gone. In addition to frequently observed spinal cord lesions, we should consider some medial frontal lesions to be responsible for micturitional disturbance in patients with MS.
    Neurological Sciences 11/2009; 31(2):205-7. · 1.41 Impact Factor

Publication Stats

879 Citations
168.56 Total Impact Points


  • 2008–2012
    • Fukushima Medical University
      • Department of Neurology
      Hukusima, Fukushima, Japan
    • University Hospital Medical Information Network
      Edo, Tōkyō, Japan
  • 1998–2008
    • The University of Tokyo
      • Department of Neuroscience
      Tokyo, Tokyo-to, Japan
  • 2003–2006
    • National Hospital Organization Kurihama Medical and Addiction Center
      Йокосука, Kanagawa, Japan
  • 1997–2006
    • National Defense Medical College
      • Department of Internal Medicine
      Tokorozawa, Saitama, Japan