Fumio Yamamoto

Kumamoto University, Kumamoto, Kumamoto Prefecture, Japan

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Publications (6)6.24 Total impact

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    ABSTRACT: When cerebral infarction develops during pregnancy, treatment without adverse effects must be considered not only for the mother but also for the fetus. Because pregnant women were excluded from many clinical trials, clear treatment guidance for them is not shown in the package inserts or guidelines of many drugs. We report the case of a 35-year-old woman (gravida 3, para 2) who developed sudden onset of left visual field defect, left hemiparesis, and dysesthesia over the left forearm during her fourth month of pregnancy. Brain diffusion-weighted MRI showed high intensity areas in the right occipital lobe, and magnetic resonance angiography revealed an occlusion of the right posterior cerebral artery. She was treated with an intravenous injection of recombinant tissue plasminogen activator 2 h 55 min after symptom onset, and the visual field and sensorimotor deficits improved. MRA obtained 3 days after the onset showed recanalization of the right posterior cerebral artery. We also conducted electrocardiography, neck vascular ultrasound, cardiovascular ultrasound, transcranial Doppler recordings from the temple area, and laboratory examinations for complete blood count, biochemistry, coagulation factors, endocrine secretion, and autoantibodies. Reduced protein S activity (35%) along with high intensity transient signals on transcranial Doppler indicated microemboli to be the embolic source. All other tests were negative. Anticoagulation therapy was initiated to prevent recurrence. She was initially given intravenous heparin, and then switched to warfarin therapy at 15 weeks of gestation. The patient delivered a healthy infant via caesarean section. Although reports and experiences of thrombolytic therapy with injection of recombinant tissue plasminogen activator during pregnancy remain scant, this therapy might be carefully used, especially after due consideration and understanding of the risks and benefits for both mother and fetus.
    03/2013; 53(3):212-6. DOI:10.5692/clinicalneurol.53.212
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    ABSTRACT: In clinical practice, secondary prevention in patients with ischemic stroke (IS) needs to be continued permanently; however, antithrombotic agents are sometimes stopped by clinicians or the patients themselves. The rate of non-taking oral antithrombotic agents was evaluated in IS patients. 266 consecutive patients (154 men and 112 women; age, 73.6 +/- 11.5 years) with first-ever acute IS were studied. Patients with transient ischemic attack (TIA) were also included. Emboligenic heart diseases, frequency of past stroke, oral antithrombotic agent use just before IS, and secondary prevention were evaluated. The number of past strokes was 0 in 182 cases (68.4%), 1 in 66 cases (24.8%), 2 in 14 cases (5.3%), 3 in 3 cases (1.1%), and 9 in 1 case (0.4%; 3 times with stroke, and 6 times with TIA). There were 42 cases (15.8%) with TIA, 47 (17.7%) with lacunar infarction, 69 (25.9%) with atherothrombotic infarction, 62 (23.3%) with cardioembolic infarction, 23 (8.7%) with other types of infarction, and 23 (8.7%) with stroke of unknown etiology. Although 15-26% of patients with their first IS had taken antithrombotic agents just before IS, about 40% of the patients with a previous IS history were not taking antithrombotic agents just before their recurrent IS. About 40% of the patients with recurrent IS were not taking antithrombotic agents at the time of their recurrent IS; had they been taking antithrombotic agents at the time, the recurrent IS might have been prevented. Clinicians must recognize the importance of antithrombotic agents in patients with IS, and patients must continue to take antithrombotic agents permanently.
    Rinsho shinkeigaku = Clinical neurology 01/2011; 51(1):35-7. DOI:10.5692/clinicalneurol.51.35
  • E. Kimura · F. Yamamoto · A. Migita · S. Mita · H. Teramoto · M. Uchino ·

    Neuromuscular Disorders 09/2009; 19(8):567-567. DOI:10.1016/j.nmd.2009.06.077 · 2.64 Impact Factor
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    ABSTRACT: We describe three cases of HTLV-I-associated myelopathy (HAM) with abnormal spinal magnetic resonance imaging (MRI) findings. The serum and cerebrospinal fluid (CSF) of all 3 patients tested positive for anti-HTLV-I antibody. Swelling of the spinal cord with high-intensity lesions on T2-weighted images was observed. Corticosteroid treatment in the case of two patients gradually improved the symptoms, decreased the protein and IgG levels as well as the cell count, and reduced the abnormal MRI findings. To confirm the assumption that abnormal spinal MRI findings are reflective of active inflammation, we compared the clinical parameters, namely, the protein content, IgG level, and cell count, in the CSF of patients exhibiting abnormal spinal MRI findings with those in the case of patients without spinal MRI lesions. The protein contents, IgG levels, and number of cells in the CSF of patients with MRI lesions were significantly higher than those in the CSF of patients without lesions. These findings support the fact that abnormal MRI findings in the spinal cord may be reflective of active inflammation in the early stages of rapidly progressive HAM.
    Clinical neurology and neurosurgery 06/2009; 111(7):624-8. DOI:10.1016/j.clineuro.2009.05.003 · 1.13 Impact Factor
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    ABSTRACT: We present the cases of 3 patients with a histidine-to-arginine substitution at position 46 of the Cu/Zn superoxide dismutase gene. Consistent with previous reports, the initial symptom in each patient was unilateral weakness in the distal leg muscles. Remarkably, muscular atrophy in these patients during the early stage of the disease was more specific to the flexor muscle group, with the extensor muscle group remaining intact over long-term observation. More interestingly, biopsy of the affected muscle in the early stage of the disease revealed necrotic and regenerative myofibers with infiltration of lymphocytes, resembling inflammatory myopathy. These novel findings might provide further insights into the pathophysiology of familial amyotrophic lateral sclerosis.
    Journal of the neurological sciences 05/2009; 281(1-2):6-10. DOI:10.1016/j.jns.2009.03.010 · 2.47 Impact Factor

  • Nosotchu 01/2009; 31(4):238-244. DOI:10.3995/jstroke.31.238