J Clin Neurol.  2016 Oct;12(4):495-501. 10.3988/jcn.2016.12.4.495.

Early Electrodiagnostic Features of Upper Extremity Sensory Nerves Can Differentiate Axonal Guillain-Barré Syndrome from Acute Inflammatory Demyelinating Polyneuropathy

Affiliations
  • 1Department of Neurology, Korea University Medical Center, Seoul, Korea. nukbj@korea.ac.kr
  • 2Department of Neurology, Yonsei University College of Medicine, Seoul, Korea.
  • 3Department of Neurology, Dong-A University College of Medicine, Busan, Korea.
  • 4Department of Neurology, Chonnam National University Medical School, Gwangju, Korea.
  • 5Department of Neurology, Haeundae Paik Hospital, Inje University, Busan, Korea.
  • 6Department of Neurology, College of Medicine, Hallym University, Chunchoen, Korea.
  • 7Department of Neurology, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.
  • 8Department of Neurology, Konkuk University Medical Center, Seoul, Korea.
  • 9Brain Convergence Research Center, Korea University Anam Hospital, Seoul, Korea.

Abstract

BACKGROUND AND PURPOSE
Serial nerve conduction studies (NCSs) are recommended for differentiating axonal and demyelinating Guillain-Barré syndrome (GBS), but this approach is not suitable for early diagnoses. This study was designed to identify possible NCS parameters for differentiating GBS subtypes.
METHODS
We retrospectively reviewed the medical records of 70 patients with GBS who underwent NCS within 10 days of symptom onset. Patients with axonal GBS and acute inflammatory demyelinating polyneuropathy (AIDP) were selected based on clinical characteristics and serial NCSs. An antiganglioside antibody study was used to increase the diagnostic certainty.
RESULTS
The amplitudes of median and ulnar nerve sensory nerve action potentials (SNAPs) were significantly smaller in the AIDP group than in the axonal-GBS group. Classification and regression-tree analysis revealed that the distal ulnar sensory nerve SNAP amplitude was the best predictor of axonal GBS.
CONCLUSIONS
Early upper extremity sensory NCS findings are helpful in differentiating axonal-GBS patients with antiganglioside antibodies from AIDP patients.

Keyword

Guillain-Barré syndrome; acute inflammatory demyelinating polyneuropathy; early diagnosis; electrodiagnosis; neural conduction

MeSH Terms

Action Potentials
Antibodies
Axons*
Classification
Diagnosis
Early Diagnosis
Electrodiagnosis
Guillain-Barre Syndrome*
Humans
Medical Records
Neural Conduction
Retrospective Studies
Ulnar Nerve
Upper Extremity*
Antibodies

Figure

  • Fig. 1 Classification and regression tree (CART) diagram for discriminating acute axonal Guillain-Barré syndrome (GBS) from acute inflammatory demyelinating polyneuropathy (AIDP) using a set of independent variables. A: CART diagram involving a set of independent variables related to both motor and sensory nerves. According to this model, patients in nodes 1 and 2 were classified as AIDP and axonal-GBS patients, respectively. B: CART diagram involving variables for motor nerves only. According to this model, patients in nodes 3 and 4 were classified as axonal GBS, and those in node 2 were classified as AIDP patients. PerMDL: distal latency in peroneal motor nerve, TibMPDur: duration in proximal tibial motor nerve, UlnSDAm: distal amplitude in ulnar sensory nerve.


Reference

1. Kim JK, Bae JS, Kim DS, Kusunoki S, Kim JE, Kim JS, et al. Prevalence of anti-ganglioside antibodies and their clinical correlates with guillain-barré syndrome in Korea: a nationwide multicenter study. J Clin Neurol. 2014; 10:94–100.
Article
2. Uncini A, Manzoli C, Notturno F, Capasso M. Pitfalls in electrodiagnosis of Guillain-Barré syndrome subtypes. J Neurol Neurosurg Psychiatry. 2010; 81:1157–1163.
3. Hadden RD, Cornblath DR, Hughes RA, Zielasek J, Hartung HP, Toyka KV, et al. Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group. Electrophysiological classification of Guillain-Barré syndrome: clinical associations and outcome. Ann Neurol. 1998; 44:780–788.
Article
4. Ho TW, Mishu B, Li CY, Gao CY, Cornblath DR, Griffin JW, et al. Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies. Brain. 1995; 118(Pt 3):597–605.
Article
5. Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barré syndrome. Ann Neurol. 1990; 27:Suppl. S21–S24.
Article
6. Arcila-Londono X, Lewis RA. Guillain-Barré syndrome. Semin Neurol. 2012; 32:179–186.
Article
7. Kusunoki S, Chiba A, Kon K, Ando S, Arisawa K, Tate A, et al. N-acetylgalactosaminyl GD1a is a target molecule for serum antibody in Guillain-Barré syndrome. Ann Neurol. 1994; 35:570–576.
Article
8. Koo YS, Cho CS, Kim BJ. Pitfalls in using electrophysiological studies to diagnose neuromuscular disorders. J Clin Neurol. 2012; 8:1–14.
Article
9. Ogawara K, Kuwabara S, Mori M, Hattori T, Koga M, Yuki N. Axonal Guillain-Barré syndrome: relation to anti-ganglioside antibodies and Campylobacter jejuni infection in Japan. Ann Neurol. 2000; 48:624–631.
Article
10. Drenthen J, Yuki N, Meulstee J, Maathuis EM, van Doorn PA, Visser GH, et al. Guillain-Barré syndrome subtypes related to Campylobacter infection. J Neurol Neurosurg Psychiatry. 2011; 82:300–305.
11. Neisser A, Schwerer B, Bernheimer H, Moran AP. Ganglioside-induced antiganglioside antibodies from a neuropathy patient crossreact with lipopolysaccharides of Campylobacter jejuni associated with Guillain-Barré syndrome. J Neuroimmunol. 2000; 102:85–88.
Article
12. Susuki K, Baba H, Tohyama K, Kanai K, Kuwabara S, Hirata K, et al. Gangliosides contribute to stability of paranodal junctions and ion channel clusters in myelinated nerve fibers. Glia. 2007; 55:746–757.
Article
13. Uncini A, Susuki K, Yuki N. Nodo-paranodopathy: beyond the demyelinating and axonal classification in anti-ganglioside antibody-mediated neuropathies. Clin Neurophysiol. 2013; 124:1928–1934.
Article
14. Willison HJ. The immunobiology of Guillain-Barré syndromes. J Peripher Nerv Syst. 2005; 10:94–112.
15. Hiraga A, Kuwabara S, Ogawara K, Misawa S, Kanesaka T, Koga M, et al. Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain-Barré syndrome. Neurology. 2005; 64:856–860.
Article
16. Kokubun N, Nishibayashi M, Uncini A, Odaka M, Hirata K, Yuki N. Conduction block in acute motor axonal neuropathy. Brain. 2010; 133:2897–2908.
Article
17. Sekiguchi Y, Uncini A, Yuki N, Misawa S, Notturno F, Nasu S, et al. Antiganglioside antibodies are associated with axonal Guillain-Barré syndrome: a Japanese-Italian collaborative study. J Neurol Neurosurg Psychiatry. 2012; 83:23–28.
Article
18. Rajabally YA, Durand MC, Mitchell J, Orlikowski D, Nicolas G. Electrophysiological diagnosis of Guillain-Barré syndrome subtype: could a single study suffice? J Neurol Neurosurg Psychiatry. 2015; 86:115–119.
Article
19. Albers JW, Kelly JJ Jr. Acquired inflammatory demyelinating polyneuropathies: clinical and electrodiagnostic features. Muscle Nerve. 1989; 12:435–451.
Article
20. Gordon PH, Wilbourn AJ. Early electrodiagnostic findings in Guillain-Barré syndrome. Arch Neurol. 2001; 58:913–917.
Article
21. Chanson JB, Echaniz-Laguna A. Early electrodiagnostic abnormalities in acute inflammatory demyelinating polyneuropathy: a retrospective study of 58 patients. Clin Neurophysiol. 2014; 125:1900–1905.
Article
22. Albertí MA, Alentorn A, Martínez-Yelamos S, Martínez-Matos JA, Povedano M, Montero J, et al. Very early electrodiagnostic findings in Guillain-Barré syndrome. J Peripher Nerv Syst. 2011; 16:136–142.
Article
23. Derksen A, Ritter C, Athar P, Kieseier BC, Mancias P, Hartung HP, et al. Sural sparing pattern discriminates Guillain-Barré syndrome from its mimics. Muscle Nerve. 2014; 50:780–784.
Article
24. Kuwabara S, Yuki N, Koga M, Hattori T, Matsuura D, Miyake M, et al. IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barré syndrome. Ann Neurol. 1998; 44:202–208.
Article
25. Kuwabara S, Ogawara K, Misawa S, Mizobuchi K, Sung JY, Kitano Y, et al. Sensory nerve conduction in demyelinating and axonal Guillain-Barré syndromes. Eur Neurol. 2004; 51:196–198.
Article
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