Skip to main content
Advertisement
  • Neurology.org
  • Journals
    • Neurology
    • Clinical Practice
    • Genetics
    • Neuroimmunology & Neuroinflammation
    • Education
  • Online Sections
    • COVID-19
    • Inclusion, Diversity, Equity, Anti-racism, & Social Justice (IDEAS)
    • Innovations in Care Delivery
    • Practice Buzz
    • Practice Current
    • Residents & Fellows
    • Without Borders
  • Collections
    • Topics A-Z
    • Disputes & Debates
    • Health Disparities
    • Infographics
    • Patient Pages
    • Null Hypothesis
    • Translations
  • Podcast
  • CME
  • About
    • About the Journals
    • Contact Us
    • Editorial Board
  • Authors
    • Submit a Manuscript
    • Author Center

Advanced Search

Main menu

  • Neurology.org
  • Journals
    • Neurology
    • Clinical Practice
    • Genetics
    • Neuroimmunology & Neuroinflammation
    • Education
  • Online Sections
    • COVID-19
    • Inclusion, Diversity, Equity, Anti-racism, & Social Justice (IDEAS)
    • Innovations in Care Delivery
    • Practice Buzz
    • Practice Current
    • Residents & Fellows
    • Without Borders
  • Collections
    • Topics A-Z
    • Disputes & Debates
    • Health Disparities
    • Infographics
    • Patient Pages
    • Null Hypothesis
    • Translations
  • Podcast
  • CME
  • About
    • About the Journals
    • Contact Us
    • Editorial Board
  • Authors
    • Submit a Manuscript
    • Author Center
  • Home
  • Latest Articles
  • Current Issue
  • Past Issues
  • Residents & Fellows

User menu

  • Subscribe
  • My Alerts
  • Log in
  • Log out

Search

  • Advanced search
Neurology
Home
The most widely read and highly cited peer-reviewed neurology journal
  • Subscribe
  • My Alerts
  • Log in
  • Log out
Site Logo
  • Home
  • Latest Articles
  • Current Issue
  • Past Issues
  • Residents & Fellows

Share

February 01, 1996; 46 (2) BRIEF COMMUNICATIONS

Multifocal motor neuropathy with conduction block and Campylobacter jejuni

James R. White, George M. Sachs, James M. Gilchrist
First published February 1, 1996, DOI: https://doi.org/10.1212/WNL.46.2.562
James R. White
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
George M. Sachs
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
James M. Gilchrist
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Full PDF
Citation
Multifocal motor neuropathy with conduction block and Campylobacter jejuni
James R. White, George M. Sachs, James M. Gilchrist
Neurology Feb 1996, 46 (2) 562-563; DOI: 10.1212/WNL.46.2.562

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Permissions

Make Comment

See Comments

Downloads
311

Share

  • Article
  • Figures & Data
  • Info & Disclosures
Loading

Abstract

We describe a patient with acute multifocal motor neuropathy with conduction block (MMNCB) and high titers of immunoglobulin G anti-GM1 antibodies after Campylobacter jejuni enteritis. Treatment with intravenous immune globulin led to rapid improvement with return of normal function by 6 weeks. This is the first report of C. jejuni enteritis preceding MMNCB.

NEUROLOGY 1996;46: 562-563

Multifocal motor neuropathy with conduction block

(MMNCB) is a clinical syndrome defined by progressive, asymmetric, lower motor neuron-type weakness most often starting in the arms. Diagnostic criteria also include electrophysiologic evidence of motor conduction block with normal sensory evoked responses. [1] The syndrome is often associated with antiglycolipid antibodies in the serum. [2] We report the first case of Campylobacter jejuni associated with acute MMNCB.

Case report.

A 63-year-old man experienced abdominal pain and diarrhea in September 1994. C. jejuni enteritis was diagnosed by stool culture, and he was treated with ciprofloxacin. One week later he noted left hand weakness. Over the subsequent 4 days, he experienced progressive right hand and distal bilateral leg weakness. Six days after onset of symptoms, he was hospitalized. He denied bulbar symptoms or sensory change. The past medical history was significant for myocardial infarction 1 month before admission with left anterior descending artery stent placement. The family history was negative, and he denied alcohol use or toxin exposure.

Neurologic examination revealed no cranial nerve abnormalities. Muscle bulk and tone were normal. Strength was decreased asymmetrically in the following muscles (Medical Research Council scale): finger extensors (3 on the right, 4 on the left), interossei (3 on the right, 4 minus on the left), wrist extensors (4 minus on the right, 4 plus on the left), deltoids (4 on the right, 5 on the left). There was symmetric weakness in the extensor hallucis longus (4 minus), tibialis anterior (4), and biceps (4 plus). Strength was normal bilaterally in triceps, illiopsoas, quadriceps femoris, hamstrings, and gastrocnemius. Reflexes and sensory functions were normal.

CBC, electrolytes, serum protein electrophoresis, repeat stool cultures, pulmonary function tests, and CT of the cervical spine were within normal limits. Lumbar puncture was not performed because the patient was on warfarin.

The titer of immunoglobulin IgG anti-GM1 antibodies was 6,400, which is highly elevated. The following were all within normal limits: IgM anti-GM1 antibodies, IgA anti-GM1 antibodies, anti-sialo GM1 antibodies, anti-GD1A antibodies, anti-GD1B antibodies, anti-sulfated glucuronyl paragloboside (anti-SGPG) antibodies, and anti-myelin associated glycoprotein (anti-MAG) antibodies.

Initial left median and bilateral ulnar motor nerve conduction studies showed normal compound muscle action potential amplitudes (CMAP) and latencies with stimulation at the wrist. Stimulation at the elbow revealed conduction block with CMAP amplitude reductions of 91% in the left ulnar, 89% in the right ulnar, and 83% in the left median nerves Figure 1. Motor nerve conduction velocity (52 m/s in median and 58 m/s in ulnar nerves) was normal. Left median and ulnar antidromic sensory nerve conduction studies were normal, including conduction across segments with motor conduction block. EMG examination 8 days after onset of symptoms showed markedly reduced motor unit recruitment without abnormal spontaneous activity in the intrinsic muscles of the left hand.

Figure
  • Download figure
  • Open in new tab
  • Download powerpoint

Figure 1. Motor conduction studies of the left ulnar nerve before, 10 days after, and 6 weeks after human immune globulin therapy. The resolution of conduction block is demonstrated by marked increase in amplitude/area of hypothenar CMAP evoked from stimulation at the elbow Scale 2 mv, 3 msec.

The patient was treated with IVIg (0.4 g/kg/d for 5 consecutive days) and his strength began to improve subjectively by day 3 of treatment. By 6 weeks, the patient believed he had regained normal function of both hands, which has continued through our latest assessment at 5 months. As shown in the Figure 1, there was a marked recovery in conduction block underlying the improvement in strength. EMG repeated at 6 weeks showed improved motor unit recruitment with 1 plus fibrillations in the left abductor pollicis brevis muscle but no spontaneous activity in ulnar intrinsic muscles of either hand.

Discussion.

The patient presented with a neuropathy that fulfilled the strictest suggested criteria for MMNCB [1] but with an unusually acute course. We believe that a number of clinical features are more consistent with MMNCB than previously reported cases of Guillain-Barre Syndrome (GBS). [3] Asymmetric distal upper extremity weakness is the most common presentation of MMNCB but is rarely seen in GBS. Normal tendon reflexes have been reported in a number of cases of MMNCB, particularly when the relevant muscles are not profoundly weakened. On the other hand, hyporeflexia is a widely accepted cardinal feature of GBS, including cases of ``pure motor'' GBS. Although C. jejuni is the most commonly identified bacterial infection preceding GBS, [4] there are no previous descriptions in association with MMNCB. In addition to classic GBS, C. jejuni has been reported in association with the acute axonal form of GBS, which is clinically similar to classic GBS except for particularly rapid evolution of disease, poor recovery, severe axonal degeneration, and no physiologic evidence of demyelination. [5] C jejuni has also been associated with Chinese acute motor neuropathy. [6] Thus, this case of MMNCB may be viewed as part of a continuum of acute neuropathies associated with C. jejuni.

There is evidence suggesting C. jejuni may be involved in the pathogenesis of some acute neuropathies. A lipopolysaccharide from C. jejuni has the terminal structure [GalB1-3GalNAcB1-4(NeuAca2-3)GalB], which is identical to the terminal tetrasaccharide of GM1 ganglioside, [7] a component of peripheral nerve concentrated at nodes of Ranvier and motor axon terminals. Immune cross-reactivity has been suggested between a GM1-like structure of C. jejuni and peripheral nerve. The combination of a preceding C. jejuni enteritis and high titers of IgG antibodies to GM1 has been most frequently noted in cases of axonal GBS that generally afford a poor prognosis. [8] The present case suggests that similar mechanisms of immunopathogenesis may be operative in MMNCB.

  • Copyright 1996 by the Advanstar Communication Inc.

REFERENCES

  1. 1.↵
    Lange DJ, Trojaborg W, Latov N, et al. Multifocal motor neuropathy with conduction block: is it a distinct entity? Neurology 1992;42:497-505.
    OpenUrl
  2. 2.↵
    Pestronk A, Cornblath DR, Ilyas AA, et al. A treatable multifocal motor neuropathy with antibodies to GM1 ganglioside. Ann Neurol 1988;24:73-78.
    OpenUrl
  3. 3.↵
    Asbury A Diagnostic considerations in Guillain-Barre syndrome. Ann Neurol 1981;9(suppl):1-5.
  4. 4.↵
    Rhodes KM, Tattersfield AE. Guillain-Barre syndrome associated with Campylobacter infection. BMJ 1982;285:173-174.
    OpenUrlFREE Full Text
  5. 5.↵
    Ropper AH, Wijdics EF, Truax BT. Guillain-Barre syndrome Philadelphia: F.A. Davis, 1991.
  6. 6.↵
    McKann GM, Cornblath DR, Griffin JW, et al. Acute motor axonal neuropathy: a frequent cause of acute flaccid paralysis in China. Ann Neurol 1993;33:333-342.
    OpenUrl
  7. 7.↵
    Yuki N, Handa S, Taki T, et al. Cross-reactive antigen between nervous tissue and a bacterium elicits Guillain-Barre syndrome: molecular mimicry between ganglioside Gm1 and lipopolysaccharide from Penner's serotype 19 of Campylobacter jejuni. Biomed Res 1992;13:451-453.
    OpenUrl
  8. 8.↵
    Pestronk A. Invited review: motor neuropathies, motor neuron disorders, and antiglycolipid antibodies. Muscle Nerve 1991;14:927-936.
    OpenUrl

Disputes & Debates: Rapid online correspondence

No comments have been published for this article.
Comment

REQUIREMENTS

If you are uploading a letter concerning an article:
You must have updated your disclosures within six months: http://submit.neurology.org

Your co-authors must send a completed Publishing Agreement Form to Neurology Staff (not necessary for the lead/corresponding author as the form below will suffice) before you upload your comment.

If you are responding to a comment that was written about an article you originally authored:
You (and co-authors) do not need to fill out forms or check disclosures as author forms are still valid
and apply to letter.

Submission specifications:

  • Submissions must be < 200 words with < 5 references. Reference 1 must be the article on which you are commenting.
  • Submissions should not have more than 5 authors. (Exception: original author replies can include all original authors of the article)
  • Submit only on articles published within 6 months of issue date.
  • Do not be redundant. Read any comments already posted on the article prior to submission.
  • Submitted comments are subject to editing and editor review prior to posting.

More guidelines and information on Disputes & Debates

Compose Comment

More information about text formats

Plain text

  • No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
NOTE: The first author must also be the corresponding author of the comment.
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g. higgs-boson@gmail.com
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Publishing Agreement
NOTE: All authors, besides the first/corresponding author, must complete a separate Publishing Agreement Form and provide via email to the editorial office before comments can be posted.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.

Vertical Tabs

You May Also be Interested in

Back to top
  • Article
    • Abstract
    • Multifocal motor neuropathy with conduction block
    • Case report.
    • Discussion.
    • REFERENCES
  • Figures & Data
  • Info & Disclosures
Advertisement

Related Articles

  • No related articles found.

Alert Me

  • Alert me when eletters are published
Neurology: 98 (21)

Articles

  • Ahead of Print
  • Current Issue
  • Past Issues
  • Popular Articles
  • Translations

About

  • About the Journals
  • Ethics Policies
  • Editors & Editorial Board
  • Contact Us
  • Advertise

Submit

  • Author Center
  • Submit a Manuscript
  • Information for Reviewers
  • AAN Guidelines
  • Permissions

Subscribers

  • Subscribe
  • Activate a Subscription
  • Sign up for eAlerts
  • RSS Feed
Site Logo
  • Visit neurology Template on Facebook
  • Follow neurology Template on Twitter
  • Visit Neurology on YouTube
  • Neurology
  • Neurology: Clinical Practice
  • Neurology: Genetics
  • Neurology: Neuroimmunology & Neuroinflammation
  • Neurology: Education
  • AAN.com
  • AANnews
  • Continuum
  • Brain & Life
  • Neurology Today

Wolters Kluwer Logo

Neurology | Print ISSN:0028-3878
Online ISSN:1526-632X

© 2022 American Academy of Neurology

  • Privacy Policy
  • Feedback
  • Advertise