神経治療学
Online ISSN : 2189-7824
Print ISSN : 0916-8443
34 巻 , 4 号
選択された号の論文の71件中1~50を表示しています
第34回日本神経治療学会総会特集2
教育講演
マラソンレクチャー
  • 吉良 潤一
    2018 年 34 巻 4 号 p. 358
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー
  • 目崎 高広
    2018 年 34 巻 4 号 p. 359-362
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー

    Botulinum toxin has been widely applied to therapeutic and cosmetic uses since 1980's. In Japan two formulations, one type A and one type B, are available under strict official regulations. Off–label use is prohibited, and the reimbursement of national insurance is too much restrictive to encourage clinicians of the next generation to launch the practice of this highly effective treatment. Moreover, many of the doctors in Japan are too busy to learn and perform this relatively time–consuming but financially unrewarded procedure. These hardships may regrettably result in the future decline, both quantitative and qualitative, of practice in the clinical setting, as far as Japan is concerned.

    For injection, the author prefers 27–30 gauge thin needles to thicker ones, to minimize patient's agony, and whenever possible tries to accurately identify target muscles under the monitoring with electromyography, electrical stimulation, or ultrasonography, for the treatment of the limb or deep cervical muscles. Especially for the obliquus capitis inferior and semispinalis cervicis muscles, the ultrasound is superior to other monitoring techniques.

    In spasticity many patients have anticoagulant or antiplatelet drugs for the secondary prevention of cardio– or cerebro–vascular diseases, and special care should be taken to avoid massive intramuscular bleeding in these patients. The consensus about the adequate use of these drugs still remains to be confirmed.

    Antitoxin antibody may abolish the toxin effect, but significant number of patients may show apparent secondary resistance to the therapy due to another reasons than neutralizing antibody. Target sites, dose, and technical issues should be re–assessed before abandoning treatment whenever the toxin effect appears to have diminished.

  • 平田 幸一
    2018 年 34 巻 4 号 p. 363
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー
  • 中村 雄作
    2018 年 34 巻 4 号 p. 364-367
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー

    Essential tremor (ET) is most frequent movement disorder in individuals above 40 years old. The prevalence of ET increases steeply with increasing ages. ET is slowly progressive disorder which is sometimes causing severe disability but is not life–limiting.

    Diagnosis of ET is based on clinical examination and neurological history, as a specific biological marker or diagnostic test is not available. Differences among tremor disorders are important in published clinical criteria for ET. In pharmacotherapy, Propranolol and Primidone have level A recommendations. And Topiramate and Gabapentin have level B recommendations. However, drugs for ET is not enough reduction of tremor and side–effects is common. Botulinum toxin is possibly effective. Vim thalamotomy is highly effective but side–effects of surgery should be considered. Noninvasive functional neurosurgery using transcranial MRI guided focus ultrasound is a novel treatment and will become a new option near future.

  • 城倉 健
    2018 年 34 巻 4 号 p. 368
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー
  • 森 悦朗
    2018 年 34 巻 4 号 p. 369
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー
  • 梶 龍兒
    2018 年 34 巻 4 号 p. 370
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー
  • 桑原 聡
    2018 年 34 巻 4 号 p. 371-372
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー

    Guillain–Barré syndrome (GBS) is currently classified into the two major categories ; classical demyelinating form, and axonal form termed acute motor axonal neuropathy (AMAN). AMAN is a pure motor axonal subtype of GBS that was identified in the late 1990s. In Asia and Central and South America, it is the major subtype of GBS, seen in 30–65% of patients. One of the main causes is molecular mimicry of human gangliosides by Campylobacter jejuni lipo–oligosaccharides. In addition to axonal degeneration, electrophysiology shows rapidly reversible nerve conduction blockade or slowing, presumably due to pathological changes at the nodes or paranodes. Autoantibodies that bind to GM1 or GD1a gangliosides at the nodes of Ranvier activate complement and disrupt sodium–channel clusters and axoglial junctions, which leads to nerve conduction failure. Improved understanding of the disease mechanism and pathophysiology might lead to new treatment options. Currently eculizumab (anti–complement C5 monocloncal antibody) is a promising agent, and the phase 2 trial has been finished in Japan.

    Fisher syndrome has been regarded peculiar inflammatory neuropathy with ophthalmoplegia, ataxia, and areflexia, whereas Bickerstaff brainstem encephalitis has been considered pure central nervous system disease characterized with ophthalmoplegia, ataxia, and consciousness disturbance. Both disorder share common features including preceding infection, albumin–cytological dissociation, and association with Guillain–Barré syndrome. The discovery of anti–GQ1b IgG antibodies further supports the view that the two disorder represent a single disease spectrum. The lesions in Fisher syndrome and Bickerstaff brainstem encephalitis are presumably determined by expression of ganglioside GQ1b in the human nervous system, either peripheral or central. Bickerstaff brainstem encephalitis is likely to represent a variant of Fisher syndrome with central nervous system involvement.

  • 砂田 芳秀
    2018 年 34 巻 4 号 p. 373
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー
メディカルスタッフレクチャー5
シンポジウム6:神経治療薬開発を促進するための手がかり:他学会,他領域から学ぶ
シンポジウム7:日内リズムによる問題症状とその対応
  • 平田 幸一
    2018 年 34 巻 4 号 p. 405
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー
  • 神林 崇, 大森 佑貴, 今西 彩, 高木 学, 佐川 洋平, 筒井 幸, 竹島 正浩, 小野 太輔, 塩見 利明, 清水 徹男
    2018 年 34 巻 4 号 p. 406-410
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー

    Delayed sleep phase disorder (DSPD) comprises a persistent or recurrent pattern of sleep disturbances, sleep disruption that leads to insomnia and/or excessive daytime sleepiness, and impaired functioning in social, occupational, or other spheres. Three techniques are typically used to treat DSPD : chronotherapy, phototherapy, and exogenous melatonin administration. Antipsychotics have not been reported in the treatment of DSPD, aripiprazole (APZ), which is a second generation antipsychotic, manifests a novel mechanism of action by serving as a partial agonist of D2 receptors. Depression is reported to be the most common psychopathology associated with DSPD, and APZ is reported to be effective in major depressive disorder as adjunctive therapy. Therefore, we speculated that APZ might be effective to treat DSPD, and we observed how APZ works for the treatment of DSPD.

    Methods : 18 subjects (including 7 women) who are 14–48–year–old (the average is 31.6) were included. The patients were prescribed 0.75–4.5mg APZ at once a day.

    Results : We prescribed 1.5–3.0mg/day of APZ, all subject reduced total sleep time (9.6 +/− 2.3h → 7.8 +/− 2.0h, p=0.03), many cases got up earlier (9.1 +/− 1.9h → 6.7 +/− 1.4h, p=0.005) in the morning and advanced their sleep phase within one week. The sleep onset was not significantly changed (23.5 +/− 2.0h → 22.9 +/− 1.9h, n.s.).

    Conclusion : Low dose of APZ would reduce nocturnal sleep time in the subjects who had prolonged sleep time and DSPD symptoms. The mechanism of action would be dopaminergic up regulation due to dopamine D3 agonistic activity. Since it is difficult for physicians to treat prolonged sleep time and DSPD symptoms, this medication would become a new therapeutic tool for these patients.

  • 井上 雄一
    2018 年 34 巻 4 号 p. 411
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー
  • 榊原 隆次
    2018 年 34 巻 4 号 p. 412-417
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー

    Parkinson's disease (PD) is a common neurodegenerative disorder, and lower urinary tract (LUT) dysfunction is one of the most common autonomic disorders, and nocturia is the major LUTS in PD with an estimated incidence rate of 70%. We review the pathophysiology of bladder dysfunction in PD, lower urinary tract symptoms (LUTS), objective assessment, and treatment options. In patients with PD, disruption of the dopamine D1–GABAergic direct pathway may lead to LUTS. Overactive bladder (OAB) is the most common LUT symptom in PD patients, and an objective assessment using urodynamics commonly shows detrusor overactivity (DO) in these patients. The post–void residual (PVR) volume is minimal in PD, which differs significantly from multiple system atrophy (MSA) patients who have a more progressive disease that leads to urinary retention. However, subclinical detrusor weakness during voiding may also occur in PD. Regarding bladder management, there are no large, double–blind, prospective studies in this area. It is well recognised that dopaminergic drugs can improve or worsen LUTS in PD patients. Therefore, an add–on therapy with anticholinergics is required. Beta–3 adrenergic agonists are a potential treatment option because there are little to no central cognitive events. Newer interventions, such as deep brain stimulation (DBS), are expected to improve bladder dysfunction in PD. Botulinum toxin injections can be used to treat intractable urinary incontinence in PD. Transurethral resection of the prostate gland (TURP) for comorbid BPH in PD is now recognised to be not contraindicated if MSA is excluded. Collaboration of urologists with neurologists is highly recommended to maximise a patients' bladder–associated QOL.

  • 岡 靖哲
    2018 年 34 巻 4 号 p. 418
    発行日: 2018年
    公開日: 2018/02/20
    ジャーナル フリー
シンポジウム8:脳卒中における診療連携の課題
シンポジウム9:慢性神経疾患におけるケア
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