今日の臨床サポート

しびれ・感覚障害

著者: 綿貫聡1) 東京都立多摩総合医療センター 救急総合診療センター

著者: 漆葉章典2) 東京都立神経病院 脳神経内科

監修: 野口善令 豊田地域医療センター 総合診療科

著者校正/監修レビュー済:2021/03/03
患者向け説明資料

概要・推奨   

  1. 糖尿病性ニューロパチーの治療は、血糖値の正常化が最も重要である。
  1. ギラン・バレー症候群(Guillain-Barré syndrome:GBS)の治療には免疫グロブリン大量療法(IVIG)や血漿浄化療法が有効である。
  1. 小型血管に障害を来す血管炎症候群は多発性単ニューロパチーを来し得るため、鑑別に挙げることが推奨される(推奨度2)。
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約
  1. 感覚障害中心のポリニューロパチーにおいては、耐糖能やビタミンB1、ビタミンB12などの代謝・栄養障害に関する項目、電解質をまず確認すべきである。
薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
綿貫聡 : 特に申告事項無し[2021年]
漆葉章典 : 特に申告事項無し[2021年]
監修:野口善令 : 特に申告事項無し[2021年]

改訂のポイント:
  1. 定期レビューを行った(変更なし)。

病態・疫学・診察

疾患情報(疫学・病態)  
ポイント:
  1. 「しびれ」とは、日常的にはさまざまな意味で用いられる言葉である。したがって、診察の際にはできる限りその意味を把握し、適切な医学カテゴリー(下記参照)に分類することが必要になる。多くの場合は、知覚神経障害を意図することが多いが、一部運動神経障害を意図することもある。
  1. なお、四肢のしびれを訴える患者の割合は人口比で10万人に2,400人、年齢の上昇に伴って8,000人にまで増加するとの報告がある[1]。なお、顔面の神経障害については別項「 顔面神経麻痺(Bell麻痺、Hunt症候群:耳性帯状疱疹) 」を参照にしてほしい。
 
しびれの医学的カテゴリー:
  1. 患者の訴える「しびれ」の内容は、①感覚鈍麻、②異常感覚、③運動麻痺――の3つに大別される。以下のように細かく分類した用語も使われるが、学会(領域)によって定義、訳語が統一されていない。特にdysesthesiaとparesthesiaの区別には混乱がある。さらに、実際にはこれらが混在したり、患者自身にも判別が難しいこともあるので、ピリピリ・ジンジン感じる、触ると痛みを感じるなどの場合は異常感覚として大まかにとらえるのが実用的である。
  1. ① 感覚鈍麻:
  1. 感覚鈍麻(hypesthesia):感覚が鈍くなる
  1. 無感覚、知覚脱失(anesthesia):感覚がまったくなくなる
  1. ② 異常感覚:
  1. 異常感覚、ジセステジア(dysesthesia)
  1. 錯感覚、パレステジア(paresthesia)
  1. 感覚過敏(hyperesthesia):感覚が敏感になる
  1. 日本神経学会の定義:
  1. 錯感覚:外界から与えられた感覚刺激とは異なって感ずること
  1. 異常感覚:外的刺激がないにもかかわらず感受される自発的感覚のうちで、痛み以外の感覚
 
知覚の伝導路:
  1. 「しびれ」の原因評価は知覚の伝導路に沿って考察するとよい。知覚の伝導は、末梢の受容器にて把握された刺激が電気的興奮となって脊髄後根神経を介して脊髄に達することより開始する。その後、位置覚・振動覚は、同側の後索を上昇し内側毛帯となって対側の視床に向かい大脳皮質の知覚野に達する。一方、温痛覚は、後根を介して脊髄に入った後にすぐに対側の外側脊髄視床路になって上行し視床を経て大脳皮質に向かう。大脳では、これらの情報は、中心後回のブロードマン第1-3野が一次中枢となり、その後連合野などにて情報処理がされる。
  1. 「しびれ」の原因は上述の知覚の伝導路のいずれの部位でも生じ得るため、原因疾患として、中枢神経疾患(脳血管障害など)、脊髄・神経根疾患(頚椎症、横断性脊髄炎、椎間板ヘルニアなど)、末梢神経疾患(単神経炎、多発神経炎など)などが考えられる。ほかに、全身疾患として、血管疾患(動脈閉塞など)、精神疾患(パニック発作、過換気症候群など)、産婦人科疾患(更年期障害)、電解質異常(低Ca血症、低Mg血症、アルカローシス、過換気症候群など)なども原因として考慮され、神経内科、脳神経外科、整形外科、内分泌内科、血管外科、精神科など多くの科に専門がまたがっている。
 
神経線維の種類:
  1. 神経には有髄のA線維(太い方からα:位置覚、β:触覚・圧覚、γ:位置覚、δ:温痛覚の4群)とB線維(自律神経)、無髄のC線維(交感神経、温痛覚)があり、Aδは 速い痛み(チクッとする痛み:体性痛)と温度覚を、最も細いC線維は遅い痛み(ジーンとする痛み:内臓痛・関連痛)を伝達する。
  1. 末梢で血行障害が発生したときには、まず有髄線維であるAβ線維やAδ線維が障害を受け、次いでC線維が障害を受ける。また、有髄線維が圧迫された場合は、通常知覚障害が常に先に出現し、その後運動障害は遅れて出現することが知られている。
問診・診察のポイント  
問診のポイント:
  1. 問診の際には、しびれという言葉の意味や、しびれの分布、しびれの発症機転、背景因子を確認することが診断に有用である。

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文献 

著者: C N Martyn, R A Hughes
雑誌名: J Neurol Neurosurg Psychiatry. 1997 Apr;62(4):310-8.
Abstract/Text
PMID 9120441  J Neurol Neurosurg Psychiatry. 1997 Apr;62(4):310-8.
著者: A Gordon Smith, J Robinson Singleton
雑誌名: Arch Intern Med. 2004 May 10;164(9):1021-5. doi: 10.1001/archinte.164.9.1021.
Abstract/Text BACKGROUND: Peripheral neuropathy is a common problem that often prompts a lengthy and expensive diagnostic evaluation. A rational, evidence-based diagnostic approach to peripheral neuropathy is desirable. Prior studies have focused on all patients presenting to a tertiary referral center with a diagnosis of unclassified neuropathy. However, most patients with peripheral neuropathy have primarily sensory symptoms. This study focuses on patients with sensory-predominant neuropathy. The goal was to develop a focused diagnostic algorithm that can be easily applied in a general medical setting.
METHODS: Patients referred with predominantly sensory symptoms and no previously defined cause were included and evaluated using a standard diagnostic approach.
RESULTS: Among 138 patients, 25% had at least 1 first-degree relative with symptoms suggestive of neuropathy. Among laboratory studies, a 2-hour oral glucose tolerance test had the highest diagnostic yield (61%) and was more sensitive than other measures of glucose metabolism. Vitamin B(12) deficiency was identified in 2 patients. Results of serum protein electrophoresis, immunofixation, and antinuclear antibody testing were abnormal in less than 5% of patients, and these rates are similar to those found in the general population. Using this approach, only 31% of patients completing the recommended evaluation were found to have an idiopathic neuropathy.
CONCLUSIONS: Patients with sensory-predominant neuropathy should be tested for glucose tolerance and vitamin B(12) concentration. The significance of abnormalities of serum protein electrophoresis and antinuclear antibodies is uncertain. Other tests should be performed only when the clinical scenario is suggestive. Patients with atypical features may benefit from referral to a peripheral neuropathy center.

PMID 15136313  Arch Intern Med. 2004 May 10;164(9):1021-5. doi: 10.100・・・
著者:
雑誌名: Ann Intern Med. 1995 Apr 15;122(8):561-8.
Abstract/Text OBJECTIVE: To examine whether intensive therapy designed to achieve glycemic levels as close to normal as possible prevents or slows the progression of neuropathy when compared with conventional therapy in patients with insulin-dependent diabetes mellitus in the Diabetes Control and Complications Trial.
DESIGN: Multicenter, randomized, controlled clinical trial.
SETTING: 29 U.S. and Canadian clinical centers.
PARTICIPANTS: 1441 patients aged 13 to 39 years, of whom 726 had had insulin-dependent diabetes mellitus for 1 to 5 years and had no retinopathy at baseline (primary prevention cohort); 715 had had diabetes for 1 to 15 years and had minimal to moderate nonproliferative retinopathy at baseline (secondary intervention cohort).
INTERVENTION: Intensive therapy with three or more daily insulin injections or continuous subcutaneous insulin infusion guided by four or more glucose tests per day compared with conventional therapy with one or two daily insulin injections.
RESULTS: Intensive therapy reduced the development of confirmed clinical neuropathy (defined as a history or physical examination consistent with clinical neuropathy confirmed by either abnormal nerve conduction or autonomic nervous system testing) by 64% (95% CI, 45% to 76%) in the combined cohorts after 5 years of follow-up (5% of the intensive therapy group compared with 13% of the conventional therapy group). The prevalence of abnormal nerve conduction and abnormal autonomic nervous system function were reduced by 44% (CI, 34% to 53%) and 53% (CI, 24% to 70%), respectively (26% of the intensive treatment group developed abnormal nerve conduction compared with 46% of the conventional treatment group; 4% of the intensive treatment group had abnormal autonomic nervous system function compared with 9% of the conventional treatment group). Finally, nerve conduction velocities generally remained stable with intensive therapy but decreased significantly with conventional therapy.
CONCLUSION: Intensive diabetes therapy markedly delays or prevents the development of clinically manifest diabetic polyneuropathy as confirmed by objective nerve function testing in patients with insulin-dependent diabetes mellitus.

PMID 7887548  Ann Intern Med. 1995 Apr 15;122(8):561-8.
著者: J C Raphaël, S Chevret, R A Hughes, D Annane
雑誌名: Cochrane Database Syst Rev. 2002;(2):CD001798. doi: 10.1002/14651858.CD001798.
Abstract/Text BACKGROUND: Guillain-Barré syndrome is an acute symmetric, usually ascending and usually paralysing illness, due to inflammation of peripheral nerves. It is thought to be caused by autoimmune factors, such as antibodies. Plasma exchange removes antibodies and other potentially injurious factors from the blood stream. It involves connecting the patient's blood circulation to a machine which exchanges the plasma for a substitute solution, usually albumin. Several studies have evaluated plasma exchange for Guillain-Barré syndrome.
OBJECTIVES: To systematically review the evidence concerning the efficacy of plasma exchange for treating Guillain-Barré syndrome.
SEARCH STRATEGY: Search of the Cochrane Neuromuscular Disease Trial Register for randomised trials concerning plasma exchange in Guillain-Barré syndrome, search of the bibliographies of identified papers and enquiry from the authors of the papers.
SELECTION CRITERIA: Randomised and quasi-randomised trials of plasma exchange versus sham exchange or supportive treatment.
DATA COLLECTION AND ANALYSIS: Potentially relevant papers were scrutinised by two reviewers and the selection of eligible studies was agreed by them and a third reviewer. Data were extracted by one reviewer and checked by a second reviewer. Some missing data were obtained from the authors of studies.
MAIN RESULTS: Six eligible trials concerning 649 patients were identified, all comparing plasma exchange versus supportive treatment alone. Primary outcome measures ~bullet~Time to recover walking with aid In the only two trials for which this measure was reported, the median time to recover this ability was faster in the plasma exchange than the control group. ~bullet~Time to onset of motor recovery in mildly affected patients In the one trial for which this measure was available, the time was significantly shortened in the plasma exchange group. Secondary outcome measures ~bullet~Improvement in disability grade at four weeks In five trials, there were significantly more patients who had improved by one disability grade or more in the plasma exchange group as compared to the control group. Patients treated with plasma exchange fared significantly better in the following secondary outcome measures: time to recover walking without aid, percentage of patients requiring artificial ventilation, duration of ventilation, full muscle strength recovery after one year, and severe sequelae after one year. There were less patients with infectious events and cardiac arrhythmias in the plasma exchange than the control group. Subgroup analyses Plasma exchange was beneficial in patients with mild, moderate and severe (needing ventilation) Guillain-Barré syndrome. It was beneficial in patients with a disease duration of seven or less days and also in those with disease lasting more than seven days. However, in the only trial that enrolled patients up to 30 days from disease onset, the benefit of plasma exchange in patients treated after seven days was less apparent. Type of treatment Single studies showed that two plasma exchanges were significantly superior to none for mild Guillain-Barré syndrome and four to two for moderate Guillain-Barré syndrome, but that six were not superior to four for severe Guillain-Barré syndrome requiring ventilation. One study suggested that continuous flow plasma exchange was significantly superior to intermittent flow. Another study found no significant difference between the two techniques. The same study found a significantly higher rate of adverse events with fresh frozen plasma as the replacement fluid than albumin. Plasma exchange compared with cerebrospinal fluid filtration A single trial comparing these two treatments did not show any difference in outcomes but was too small to demonstrate equivalence.
REVIEWER'S CONCLUSIONS: Plasma exchange is the first and only treatment that has been proven to be superior to supportive treatment alone in Guillain-Barré syndrome. Consequently, plasma exchange should be regarded as the treatment against which new treatments, such as intravenous immunoglobulin, should be judged. In mild Guillain-Barré syndrome two sessions of plasma exchange are superior to none. In moderate Guillain-Barré syndrome four sessions are superior to two. In severe Guillain-Barré syndrome six sessions are no better than four. Continuous flow plasma exchange machines may be superior to intermittent flow machines and albumin to fresh frozen plasma as the exchange fluid. Plasma exchange is more beneficial when started within seven days after disease onset rather than later, but was still beneficial in patients treated up to 30 days after disease onset. The value of plasma exchange in children less than 12 years old is not known. There is insufficient evidence to determine whether cerebrospinal fluid filtration is equivalent to plasma exchange.

PMID 12076424  Cochrane Database Syst Rev. 2002;(2):CD001798. doi: 10.・・・
著者: R A C Hughes, J C Raphaël, A V Swan, P A Doorn
雑誌名: Cochrane Database Syst Rev. 2004;(1):CD002063. doi: 10.1002/14651858.CD002063.pub2.
Abstract/Text BACKGROUND: Guillain-Barré syndrome is an acute, paralysing, inflammatory peripheral nerve disease. Intravenous immunoglobulin purified from donated blood is beneficial in other autoimmune diseases.
OBJECTIVES: We aimed to determine the efficacy of intravenous immunoglobulin for treating Guillain-Barré syndrome.
SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group register (search updated 11 February 2003), MEDLINE and EMBASE (from January 2000 to February 2003) using Guillain-Barré syndrome and acute polyradiculoneuritis as the search terms. We also searched bibliographies of trials and made contact with their authors and other experts.
SELECTION CRITERIA: We included all randomised and quasi-randomised trials.
DATA COLLECTION AND ANALYSIS: Two reviewers examined the titles and abstracts of all the papers retrieved by the search, extracted the data and assessed the quality of the trials independently.
MAIN RESULTS: Two trials comparing intravenous immunoglobulin with supportive treatment were inadequate to establish its value. Another Cochrane systematic review has shown that plasma exchange hastens recovery. We found six randomised trials that compared intravenous immunoglobulin with plasma exchange. In a meta-analysis of five trials involving 536, mostly adult, participants who were unable to walk unaided and had been ill for less than two weeks. The primary outcome measure in this review was the change in a seven grade disability scale four weeks after randomisation. The weighted mean difference of this measure was not statistically significant, being only 0.04 (95% CI -0.26 to 0.19) of a disability grade more improvement in the intravenous immunoglobulin group than the plasma exchange group. There were also no statistically significant differences in time to walk unaided, mortality, and proportion of participants unable to walk without aid after a year. One trial involving 249 participants compared plasma exchange followed by intravenous immunoglobulin with plasma exchange alone, and another involving 37 participants compared immunoabsorption followed by intravenous immunoglobulin with immunoabsorption alone. Neither revealed significant extra benefit from intravenous immunoglobulin. One study of only 39 participants showed a trend towards more improvement with high-dose compared with low-dose intravenous immunoglobulin.
REVIEWER'S CONCLUSIONS: Although there are no adequate comparisons with placebo, intravenous immunoglobulin hastens recovery from Guillain-Barré syndrome as much as plasma exchange. Giving intravenous immunoglobulin after plasma exchange is not significantly better than plasma exchange alone. Randomised trials are needed to decide the effect of intravenous immunoglobulin in children, in adults with mild disease and in adults who start treatment after more than two weeks.

PMID 14973982  Cochrane Database Syst Rev. 2004;(1):CD002063. doi: 10.・・・
著者: L Chia, A Fernandez, C Lacroix, D Adams, V Planté, G Said
雑誌名: Brain. 1996 Aug;119 ( Pt 4):1091-8.
Abstract/Text Peripheral neuropathy is an important factor of disability in the elderly. In order to learn more on the usefulness of intensive evaluation of patients over 65 years of age with subacute or chronic disabling peripheral neuropathy, we reviewed the clinical and nerve biopsy findings of the last 100 patients of this age group who suffered from a peripheral neuropathy severe enough to justify performance of a nerve biopsy for a diagnostic or prognostic purpose. Normal nerve biopsy findings led to the diagnosis of lower motor neuron disease in three patients and pointed to lesions of the spinal roots in six other patients. Necrotizing arteritis was demonstrated in the biopsy specimens of 23 patients, and non-necrotizing vasculitis in five. In five additional patients the diagnosis of vasculitic neuropathy was kept in spite of non-contributive biopsy findings. In two diabetic patients who had a multifocal neuropathy the biopsy also revealed the presence of vasculitis. Thus 35% of the patients included in this series had one form or another of vasculitic neuropathy. Fourteen patients had a chronic inflammatory demyelinating polyneuropathy. In 11 patients the neuropathy was associated with monoclonal gammopathy, which was benign in nine and associated with malignant plasma cell dyscrasia in two. Among the six patients with diabetes mellitus, two patients who presented with a multifocal neuropathy were found to have vasculitis in the nerve specimen; in the others the biopsy was performed because of uncommonly severe pains or motor involvement due to an extremely severe diabetic neuropathy. Six patients suffered from a long-lasting disability secondary to a drug-induced neuropathy. The remaining 15% had neuropathies of different origin, including amyloidosis, lepromatous leprosy, carcinomatous neuropathy and alcoholic neuropathy. Six patients had a mild, non-progressive or slowly progressive axonopathy of unknown origin, ageing of the peripheral nervous system may have played a role in its development. Our findings show that vasculitis is an important and treatable cause of disabling neuropathy in the elderly and that the proportion of patients with severe neuropathy of unknown origin is small.

PMID 8813273  Brain. 1996 Aug;119 ( Pt 4):1091-8.
著者: J Finsterer
雑誌名: Acta Neurol Belg. 2009 Jun;109(2):100-13.
Abstract/Text Vasculitis affecting the peripheral nerves predominantly manifests as subacute, progressive, asymmetric sensorimotor polyneuropathy or mononeuritis multiplex, and more rarely as painful mononeuropathy, pure sensory neuropathy, neuropathy of the cranial nerves, plexopathy, or as autonomic neuropathy. Vasculitic neuropathy may occur isolated or non-isolated (systemic) together with involvement of other organs. Systemic vasculitis with involvement of the peripheral nerves is further subdivided into primary (Takayasu syndrome, giant cell arteritis, classical panarteritis nodosa, thrombangitis obliterans, Kawasaki disease, Churg-Strauss syndrome, Wegener granulomatosis, cryoglobulinemic vasculitis, Behcet disease, microscopic polyangitis, Schoenlein Henoch purpura) or secondary systemic vasculitis (autoimmune connective tissue diseases, vasculitis from infection, sarcoidosis, malignancy, drugs, radiation, or diabetes). In addition to routine laboratory investigations and nerve conduction studies, nerve biopsy is essential for diagnosing the condition and to delineate it from differentials, although its sensitivity is only approximately 60%. Therapy of non-viral vasculitic neuropathy is based on corticosteroids and cyclophosphamide alone or in combination. Additional options include azathioprine, methotrexate, mycophenolate mofetil, or rituximab. In single cases immunoglobulins, immunoadsorbtion, or plasma exchange have been successfully applied. In case of virus-associated vasculitis interferon-alpha plus lamivudine or ribaverin may be beneficial.

PMID 19681441  Acta Neurol Belg. 2009 Jun;109(2):100-13.
著者: David Lacomis, Sasa A Zivković
雑誌名: J Clin Neuromuscul Dis. 2007 Sep;9(1):265-76. doi: 10.1097/CND.0b013e31815202b3.
Abstract/Text Since vasculitic neuropathy is treatable and potentially debilitating, clinicians should develop an approach to neuropathy that increases the likelihood of uncovering existing systemic or nonsystemic vasculitis. The presence of a connective tissue disease, systemic vasculitis, asymmetric or non--length-dependent axonal polyneuropathy, or multiple axonal mononeuropathies should heighten suspicion, but vasculitic neuropathy can also present as a distal symmetric polyneuropathy with or without other organ involvement. Electrodiagnostic testing utilizing extensive nerve conductions may be helpful in identifying features suggestive of vasculitic neuropathy and in selecting an abnormal nerve and muscle for biopsy confirmation. An array of laboratory tests may lead to identification of a systemic disorder that is either characterized by or predisposes to vasculitic neuropathy. The mainstays of treatment are corticosteroids and cyclophosphamide, but other drugs are used in specific conditions. With early diagnosis and careful monitoring of treatment regimens, the prognosis is usually good.

PMID 17989592  J Clin Neuromuscul Dis. 2007 Sep;9(1):265-76. doi: 10.1・・・
著者: Gérard Said, Catherine Lacroix
雑誌名: J Neurol. 2005 Jun;252(6):633-41. doi: 10.1007/s00415-005-0833-9. Epub 2005 Apr 5.
Abstract/Text Necrotizing vasculitis occurs as a primary phenomenon in connective tissue disorders and cognate fields, including polyarteritis nodosa and the Churg and Strauss syndrome variant, rheumatoid arthritis, systemic lupus and Wegener's granulomatosis. In all these conditions focal and multifocal neuropathy occur as a consequence of destruction of the arterial wall and occlusion of the lumen of small epineurial arteries. Vasculitis may also complicate the course of other conditions ranging from infection with the HIV and with the B and C hepatitis viruses to diabetes and sarcoidosis. Pathologically polymorphonuclear cells are present in the infiltrates of the vessel wall in primary necrotizing vasculitis, while in secondary vasculitis the inflammatory infiltrate is mainly composed of mononuclear cells. In all instances symptomatic vasculitis requires corticosteroid to control the inflammatory process and prevent further ischemic nerve lesions.

PMID 15806339  J Neurol. 2005 Jun;252(6):633-41. doi: 10.1007/s00415-0・・・
著者: James R Overell
雑誌名: Pract Neurol. 2011 Apr;11(2):62-70. doi: 10.1136/jnnp.2011.241612.
Abstract/Text Long lists of causes of peripheral neuropathy make peripheral nerve disease a dry and uninspiring subject. A simple scheme based on the answers to just six questions should enable the clinician to recognise characteristic patterns, investigate relevant subgroups appropriately, and identify treatable disorders quickly: which systems are involved? What is the distribution of weakness? What is the nature of the sensory involvement? Is there any evidence of upper motor neuron involvement? What is the temporal evolution? Is there any evidence for a hereditary neuropathy? Standard screening investigations suffice for the common length dependent axonal neuropathies while complex presentations need more detailed investigations targeted to their clinical phenotype.

PMID 21385962  Pract Neurol. 2011 Apr;11(2):62-70. doi: 10.1136/jnnp.2・・・
著者: M Camerlingo, R Nemni, B Ferraro, L Casto, T Partziguian, B Censori, A Mamoli
雑誌名: Arch Neurol. 1998 Jul;55(7):981-4.
Abstract/Text OBJECTIVE: To investigate the frequency of cancer developing in patients with peripheral sensory neuropathy of unexplained cause.
DESIGN: Prospective study.
SETTING: A neurologic unit in a general hospital.
METHODS: Following the diagnosis of neuropathy, we searched for occult malignancy. This search was repeated together with neurologic evaluations every 6 months thereafter. Patient recruitment began January 1, 1988, and ended December 31, 1995. The end point of the study was December 31, 1996.
RESULTS: In the study period, we observed 363 patients with peripheral sensory neuropathy. Of these, 53 patients without any identified cause of neuropathy were invited to participate in the study. Of the 53, 2 patients refused. Thus, we examined and followed up 51 patients, 42 men and 9 women, with a mean age of 64.5 years (range, 19-80 years). The range between the onset of neurologic symptoms and the diagnosis of neuropathy was 2 to 72 months (mean, 13.9 months). The follow-up period ranged from 14 to 94 months (mean, 51.4 months). In 18 patients (35.3%) (16 men and 2 women) whose mean age at diagnosis of neuropathy was 66.5 years. malignant growths were found 3 to 72 months (mean, 27.4 months) after the onset of the neuropathy. The cancer was in the liver in 4 patients (all had a primary hepatoma), the bladder in 3, the lymph nodes in 3 (all with non-Hodgkin lymphoma), the prostate gland in 2, the lungs in 2 (small cell lung cancer in both), the breast in 1, the pancreas in 1, the sublingual gland in 1, and the bone in 1 (a metastatic sarcoma).
CONCLUSIONS: More than one third of the patients with peripheral sensory neuropathy of unexplained cause developed cancer without any predominating type of malignancy.

PMID 9678316  Arch Neurol. 1998 Jul;55(7):981-4.
著者: John D England, Arthur K Asbury
雑誌名: Lancet. 2004 Jun 26;363(9427):2151-61. doi: 10.1016/S0140-6736(04)16508-2.
Abstract/Text
PMID 15220040  Lancet. 2004 Jun 26;363(9427):2151-61. doi: 10.1016/S01・・・

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