Cerebrospinal fluid findings in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathies

Research output: Chapter in Book/Report/Conference proceedingBook chapterResearchpeer-review

Abstract

The classic immunologic alteration of the cerebrospinal fluid (CSF) in Guillain-Barré syndrome (GBS), albuminocytologic dissociation, has been known since the original paper by Guillain, Barré, and Strohl. Albuminocytologic dissociation has been also described in other forms of the GBS spectrum, such as axonal motor or motor-sensory forms (AMAN, AMSAN), the anti-GQ1b spectrum of Miller Fisher syndrome, and Bickerstaff brainstem encephalitis. Cytokines, chemokines, antibodies, complement components, and molecules with a putative neuroprotective role or indicating axonal damage have also been examined using different methods. Besides these candidate approaches, proteomics has been recently applied to discover potential biomarkers. The overall results support the immunopathogenesis of GBS, but albuminocytologic dissociation remained the only consistent CSF biomarker supporting the diagnosis of GBS. Chronic inflammatory neuropathies also comprise a heterogeneous group of diseases. Increased protein in the CSF is a supportive factor of chronic inflammatory demyelinating polyneuropathy, especially in the absence of definite electrophysiologic criteria. A number of other markers have also been investigated in the CSF of patients with chronic inflammatory neuropathies, similar to GBS. However, none has been used in supporting diagnosis, differentiating among syndromes, or predicting the clinical course and treatment responses.

Original languageEnglish
Title of host publicationHandbook of Clinical Neurology : Cerebrospinal Fluid in Neurologic Disorders
EditorsFlorian Deisenhammer, Charlotte E. Teunissen, Hayrettin Tumani
Volume146
PublisherElsevier Masson
Publication date1. Jan 2017
Pages125-138
ISBN (Print)9780128042793
DOIs
Publication statusPublished - 1. Jan 2017
SeriesHandbook of Clinical Neurology
Volume146
ISSN0072-9752

Fingerprint

Chronic Inflammatory Demyelinating Polyradiculoneuropathy
Cerebrospinal Fluid
Miller Fisher Syndrome
Cerebrospinal Fluid Proteins

Keywords

  • AMAN
  • AMSAN
  • Bickerstaff brainstem encephalitis
  • CANOMAD
  • CIDP
  • DADS
  • GBS
  • MADSAM
  • MMN
  • Miller Fisher syndrome

Cite this

Illes, Z., & Blaabjerg, M. (2017). Cerebrospinal fluid findings in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathies. In F. Deisenhammer, C. E. Teunissen, & H. Tumani (Eds.), Handbook of Clinical Neurology: Cerebrospinal Fluid in Neurologic Disorders (Vol. 146, pp. 125-138). Elsevier Masson. Handbook of Clinical Neurology, Vol.. 146 https://doi.org/10.1016/B978-0-12-804279-3.00009-5
Illes, Zsolt ; Blaabjerg, Morten. / Cerebrospinal fluid findings in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathies. Handbook of Clinical Neurology: Cerebrospinal Fluid in Neurologic Disorders. editor / Florian Deisenhammer ; Charlotte E. Teunissen ; Hayrettin Tumani. Vol. 146 Elsevier Masson, 2017. pp. 125-138 (Handbook of Clinical Neurology, Vol. 146).
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abstract = "The classic immunologic alteration of the cerebrospinal fluid (CSF) in Guillain-Barr{\'e} syndrome (GBS), albuminocytologic dissociation, has been known since the original paper by Guillain, Barr{\'e}, and Strohl. Albuminocytologic dissociation has been also described in other forms of the GBS spectrum, such as axonal motor or motor-sensory forms (AMAN, AMSAN), the anti-GQ1b spectrum of Miller Fisher syndrome, and Bickerstaff brainstem encephalitis. Cytokines, chemokines, antibodies, complement components, and molecules with a putative neuroprotective role or indicating axonal damage have also been examined using different methods. Besides these candidate approaches, proteomics has been recently applied to discover potential biomarkers. The overall results support the immunopathogenesis of GBS, but albuminocytologic dissociation remained the only consistent CSF biomarker supporting the diagnosis of GBS. Chronic inflammatory neuropathies also comprise a heterogeneous group of diseases. Increased protein in the CSF is a supportive factor of chronic inflammatory demyelinating polyneuropathy, especially in the absence of definite electrophysiologic criteria. A number of other markers have also been investigated in the CSF of patients with chronic inflammatory neuropathies, similar to GBS. However, none has been used in supporting diagnosis, differentiating among syndromes, or predicting the clinical course and treatment responses.",
keywords = "AMAN, AMSAN, Bickerstaff brainstem encephalitis, CANOMAD, CIDP, DADS, GBS, MADSAM, MMN, Miller Fisher syndrome",
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Illes, Z & Blaabjerg, M 2017, Cerebrospinal fluid findings in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathies. in F Deisenhammer, CE Teunissen & H Tumani (eds), Handbook of Clinical Neurology: Cerebrospinal Fluid in Neurologic Disorders. vol. 146, Elsevier Masson, Handbook of Clinical Neurology, vol. 146, pp. 125-138. https://doi.org/10.1016/B978-0-12-804279-3.00009-5

Cerebrospinal fluid findings in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathies. / Illes, Zsolt; Blaabjerg, Morten.

Handbook of Clinical Neurology: Cerebrospinal Fluid in Neurologic Disorders. ed. / Florian Deisenhammer; Charlotte E. Teunissen; Hayrettin Tumani. Vol. 146 Elsevier Masson, 2017. p. 125-138 (Handbook of Clinical Neurology, Vol. 146).

Research output: Chapter in Book/Report/Conference proceedingBook chapterResearchpeer-review

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AU - Illes, Zsolt

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PY - 2017/1/1

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N2 - The classic immunologic alteration of the cerebrospinal fluid (CSF) in Guillain-Barré syndrome (GBS), albuminocytologic dissociation, has been known since the original paper by Guillain, Barré, and Strohl. Albuminocytologic dissociation has been also described in other forms of the GBS spectrum, such as axonal motor or motor-sensory forms (AMAN, AMSAN), the anti-GQ1b spectrum of Miller Fisher syndrome, and Bickerstaff brainstem encephalitis. Cytokines, chemokines, antibodies, complement components, and molecules with a putative neuroprotective role or indicating axonal damage have also been examined using different methods. Besides these candidate approaches, proteomics has been recently applied to discover potential biomarkers. The overall results support the immunopathogenesis of GBS, but albuminocytologic dissociation remained the only consistent CSF biomarker supporting the diagnosis of GBS. Chronic inflammatory neuropathies also comprise a heterogeneous group of diseases. Increased protein in the CSF is a supportive factor of chronic inflammatory demyelinating polyneuropathy, especially in the absence of definite electrophysiologic criteria. A number of other markers have also been investigated in the CSF of patients with chronic inflammatory neuropathies, similar to GBS. However, none has been used in supporting diagnosis, differentiating among syndromes, or predicting the clinical course and treatment responses.

AB - The classic immunologic alteration of the cerebrospinal fluid (CSF) in Guillain-Barré syndrome (GBS), albuminocytologic dissociation, has been known since the original paper by Guillain, Barré, and Strohl. Albuminocytologic dissociation has been also described in other forms of the GBS spectrum, such as axonal motor or motor-sensory forms (AMAN, AMSAN), the anti-GQ1b spectrum of Miller Fisher syndrome, and Bickerstaff brainstem encephalitis. Cytokines, chemokines, antibodies, complement components, and molecules with a putative neuroprotective role or indicating axonal damage have also been examined using different methods. Besides these candidate approaches, proteomics has been recently applied to discover potential biomarkers. The overall results support the immunopathogenesis of GBS, but albuminocytologic dissociation remained the only consistent CSF biomarker supporting the diagnosis of GBS. Chronic inflammatory neuropathies also comprise a heterogeneous group of diseases. Increased protein in the CSF is a supportive factor of chronic inflammatory demyelinating polyneuropathy, especially in the absence of definite electrophysiologic criteria. A number of other markers have also been investigated in the CSF of patients with chronic inflammatory neuropathies, similar to GBS. However, none has been used in supporting diagnosis, differentiating among syndromes, or predicting the clinical course and treatment responses.

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Illes Z, Blaabjerg M. Cerebrospinal fluid findings in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathies. In Deisenhammer F, Teunissen CE, Tumani H, editors, Handbook of Clinical Neurology: Cerebrospinal Fluid in Neurologic Disorders. Vol. 146. Elsevier Masson. 2017. p. 125-138. (Handbook of Clinical Neurology, Vol. 146). https://doi.org/10.1016/B978-0-12-804279-3.00009-5