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Acute Inflammatory Demyelinating Polyradiculoneuropathy Clinical Presentation

  • Author: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS; Chief Editor: Nicholas Lorenzo, MD, MHA, CPE  more...
 
Updated: Mar 25, 2016
 

History

See the list below:

  • Acute inflammatory demyelinating polyneuropathy typically manifests as an ascending paralysis.
  • Even in these cases, the clinical presentation and course vary. Additionally, many variants exist that differ markedly from classic AIDP in disease onset or course.
  • Progressive weakness
    • The hallmark of classic AIDP is progressive weakness that usually begins in the feet before involving all 4 limbs. At presentation, 60% of patients have weakness in all 4 limbs.
    • Weakness plateaus at 2 weeks after onset in 50% of patients and by 4 weeks in over 90%. It is usually symmetric, although mild asymmetry is not uncommon early in the disease course.
    • In the arms, weakness may be worse proximally than distally. At presentation, half of patients have some facial weakness, although only 5% have varying degrees of ophthalmoplegia.
    • Oropharyngeal or respiratory weakness is a presenting symptom in 40% of patients. Improvement in strength usually begins 1-4 weeks after the plateau. About one third of patients require mechanical ventilation because of respiratory failure.
  • Sensory symptoms
    • Mild to moderately severe paresthesias in the distal limbs are common and often precede the onset of weakness by 1 or more days.
    • Proximal sensory changes are uncommon but may occur in more severe cases of AIDP.
  • Autonomic dysfunction
    • About two thirds of patients have one or more autonomic abnormalities. Sustained sinus tachycardia is the most common dysfunction. Postural hypotension leading to presyncope or syncope can occur.
    • Sweating dysfunction is common but rarely noted by patients. Urinary retention and constipation are more likely to occur later in the course of AIDP. Autonomic dysfunction is more common in intubated patients.
  • Pain
    • Mild lower back and/or hip pain is very common and occasionally precedes the onset of weakness.
    • The pain is severe in about 15% of patients.
  • AIDP may vary early in the course. More than 95% of patients eventually have the classic symptoms; other patients may have one of the characterized variants.
    • The Miller-Fisher variant, appearing with ophthalmoplegia, areflexia, and ataxia, is the most common variant and is seen in as many as 5% of patients with AIDP. Although usually seen in adults, this variant is also common in children. Most patients with the Miller-Fisher variant have antibodies against ganglioside GQ1b.
    • Regional variants of Guillain-Barré syndrome, such as pharyngeal-cervical-brachial weakness or only leg weakness, are rare and resemble AIDP in time course.
    • Pure pandysautonomia with little, if any, weakness parallels classic AIDP in time course and antecedent infections. The difference is that this variant is manifested primarily by autonomic failure. Many of these patients also have areflexia.
    • The AMAN variant is seen in China and in developing countries. It presents with weakness only.
    • Acute motor-sensory axonal neuropathy resembles classic Guillain-Barré syndrome in presentation but is related pathologically to AMAN.
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Physical

A detailed physical examination can help support the diagnosis of acute inflammatory demyelinating polyneuropathy and/or exclude disorders in the differential diagnosis.

  • Weakness
    • Although patients often report only weakness in the legs, careful examination usually demonstrates arm weakness (proximally and distally).
    • Some patients with Miller-Fisher or other regional variants may have weakness of cranial muscles only.
  • Deep tendon reflexes
    • Hyporeflexia or areflexia is seen in 70% of patients at presentation and eventually in all patients.
    • A progressive decrease in reflexes is a useful finding that may precede electromyographic (EMG) changes.
  • Autonomic dysfunction
    • Fluctuations in heart rate, specifically a sustained sinus tachycardia, are seen often.
    • Some intubated patients also may have bradycardia, especially after vagal stimulation with Valsalva and/or tracheal suctioning maneuvers.
    • Orthostatic hypotension can occur and is likely due to dysfunction of the baroreceptor reflex.
    • At times, the labile blood pressure is observed with severe hypertension that may be due to dysfunction of the afferent limb of the baroreceptor reflex.
    • Urinary retention is common, especially in intubated patients. The rare patient may even develop an ileus.
  • Findings that are inconsistent with a diagnosis of AIDP
    • Weakness that remains markedly asymmetric
    • Sharp sensory level
    • Severe bladder or bowel dysfunction at onset
  • Diagnostic criteria for Guillain-Barré syndrome include the presence of progressive weakness and areflexia, relative symmetry, mild sensory involvement, cranial nerve involvement, at least partial recovery, autonomic dysfunction, and absence of fever. Cerebrospinal fluid features that strongly support the diagnosis are an increase in protein beyond the first week, cell count < 10 (albuminocytological dissociation). Electrophysiologic evidence of conduction slowing, block, prolonged distal latency or F-wave latencies are also strongly supportive (80% of the case), though these abnormalities may be delayed for several weeks. Marked persistent asymmetry of weakness, the presence of a sensory level, bowel/bladder involvement at onset, and a prominent pleocytosis, often cast doubt on the diagnosis, so is the presence of another cause for the neuropathy.
  • In 1986, Ropper described 3 patients who experienced acute progression of oropharyngeal, neck, and shoulder weakness. Clinically, they had facial palsy, blepharoptosis, absence of sensory disturbance, and preserved tendon jerk in the legs. Based on elevated CSF protein levels and electrophysiological findings (a denervation pattern and decreased conduction velocity in peripheral nerves), he speculated that these patients had a Guillain-Barré syndrome variant, which he called pharyngeal-cervical-brachial weakness (PCB).[5]
  • Since then, PCB is considered a rare variant of Guillain-Barré syndrome. Nagashima et al identified the clinical profiles of PCB. They feel that the clinical overlapping, frequent Campylobacter jejuni infection, and common antiganglioside antibodies present in PCB, Guillain-Barré syndrome, Fisher syndrome, and Bickerstaff brainstem encephalitis provide conclusive evidence that PCB and these conditions form a continuous spectrum.[6]
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Causes

Acute inflammatory demyelinating polyneuropathy is thought to be caused by a dysregulated immune response against myelin. This response may be triggered by several illnesses and conditions. Two thirds of patients with AIDP recall an antecedent upper respiratory or gastrointestinal infection or syndrome from 1-6 weeks prior to the onset of weakness.

  • Viral
    • Infection with influenza, coxsackie, Epstein-Barr virus, or cytomegalovirus can cause upper respiratory infection. Immunoglobulin M (IgM) antibodies to each have been identified in some individuals.
    • In the winter of 2015-2016 a Zika viral infection outbreak was noted by the WHO and CDC. This outbreak was primarily centered in South and Central America and the Caribbean regions.
      • Zika virus disease is spread primarily by a bite from an Aedes species mosquito and typically causes a mild viral syndrome clinical picture.
      • However, in pregnant women Zika infection has been associated with microcephaly and other congenital abnormalities in their subsequently born children.
      • Additionally, in rare cases (approximately 0.03% risk) Zika viral infection can be associated with AIDP.[7]
    • Acute infection with either herpes simplex virus or human immunodeficiency virus (HIV) also has been associated with AIDP in some individuals.
      • Patients with HIV-associated AIDP often have a pleocytosis with up to 200 WBC/µL CSF.
      • Rare cases also have been reported after infection with rubella, measles, varicella-zoster, hepatitis B, Q fever, and Hantavirus.[8]
      • Wagner at al presented a case of acute motor axonal neuropathy in a patient with previously unrecognized human immunodeficiency virus (HIV) infection. To their knowledge, this is the first case of acute motor axonal neuropathy in HIV outside of a seroconversion reaction.[9]
  • Bacterial
    • Strains of C jejuni that cause enteritis are associated closely with the subsequent development of AMAN.
    • Molecular mimicry between gangliosidelike epitopes of the C jejuni lipopolysaccharide and peripheral nerve gangliosides in nerve is a proposed mechanism.
    • In children, an association exists between AIDP and Mycoplasma pneumoniae infection.
  • Other: Rare cases of AIDP in individuals infected with toxoplasma, malaria, or filaria have been reported.
  • Vaccination
    • Many cases of AIDP were reported after vaccination for swine influenza (especially in 1976).
    • Several cases have been reported after immunization against rabies, influenza, measles, mumps, or rubella.
  • Malignancies and systemic illnesses
    • Case reports document patients with AIDP associated with Hodgkin lymphoma, acute myelogenous lymphoma, Castleman disease, systemic lupus erythematosus, and hypothyroidism.
    • The rarity of these combinations raises doubts on the significance of these associations.
  • Pregnancy: Most cases occur during the last trimester or during the first 2 weeks of the postpartum period.
  • Bone marrow transplantation
  • Surgery: Most patients also had an infection or blood transfusion.
  • Other problems to be considered
    • Poliomyelitis: Classic poliomyelitis is very rare. However, coxsackievirus and echovirus can cause a similar, milder paralysis, especially in children.
    • Buckthorn shrub poisoning: This plant is found in the southwestern United States and Central America and bears a fruit that causes paralysis by an unknown mechanism. The CSF is usually normal.
    • Critical illness polyneuropathy: Weakness is more common in the setting of sepsis and/or multiorgan failure.
    • Diphtheria: Weakness may follow the pharyngeal infection by 2-3 weeks, beginning with palatal paralysis and, often, paralysis of accommodation. Limb weakness is not common.
    • Hypophosphatemia: An acute areflexic paralysis may follow hypophosphatemia in the setting of total parenteral nutrition, alcohol abuse, or rapid refeeding after starvation. The weakness rapidly responds to phosphate replacement.
    • Malingering and conversion reaction: Bizarre or nonphysiologic abnormalities may be seen on neurologic examination.
    • The antidepressant drug zimeldine, a serotonin reuptake blocker, was reported to be associated with Guillain-Barré syndrome and the drug has been withdrawn.
  • Variants
    • A number of entities are related to acute demyelinating neuropathy. Although they are acute, likely inflammatory, and immune mediated, they are not necessarily demyelinating. The acute panautonomic neuropathy is characterized by widespread and severe sympathetic and parasympathetic failure. Acute motor axonal neuropathy (AMAN) results in motor axonal degeneration, with little or no demyelination or inflammation. Many follow C jejuni infection. Axonal Guillain-Barré syndrome is at the other end of the spectrum, where the illness predominantly involves the axis cylinder of the somatic nervous system, and is fairly common. Hyperacute axonal polyradiculoneuropathy has a hyperacute course with onset to respiratory failure within 48 hours. These patients have a high mortality rate. Recovery when it occurs, is delayed, very prolonged, and characteristically quite incomplete.
    • Critical illness polyneuropathy has an uncertain relationship to the acute inflammatory neuropathies. Sensory Guillain-Barré syndrome, where sensory symptoms occur in isolation, are rare.
    • The Fisher syndrome is an uncommon variant of AIDP (about 5% of the cases) characterized by the triad of ophthalmoplegia, ataxia, and areflexia. Occasionally papillary abnormalities occur, and many cases are associated with some evidence of more widespread motor involvement. Miller-Fisher variant may be associated with a particular serotype of C jejuni.
    • Other unusual variants include the pharyngeal-cervical brachial variant, with deficits limited to these regions alone, and the paraparetic variant, where the weakness is confined to the lower extremities only, as the name implies. Acute sensory neuronopathy is usually associated with autonomic failure. It is likely inflammatory-immune-mediated. The brunt of the attack is borne on the dorsal root ganglia cells.
    • The demonstration in some studies of demyelination in excess of control sera when injected into peripheral nerve, and the demonstration of IgM antibodies that bind to carbohydrate residues of peripheral nerve in 90% of Guillain-Barré syndrome patients at the onset of the disease, support of an antibody as the mechanism of Guillain-Barré syndrome.
    • Over the past decade, great progress has been made in Guillain-Barré syndrome research, and the highlights include (1) the emerging correlations between antiganglioside antibodies and specific clinical phenotypes, notably between anti-GM1/anti-GD1a antibodies and the acute motor axonal variant and anti-GQ1b/anti-GT1a antibodies and the Miller Fisher syndrome; (2) the identification of molecular mimicry between Guillain-Barré syndrome–associated C jejuni oligosaccharides and GM1, GD1a, and GT1a gangliosides as a mechanism for antiganglioside antibody induction; and (3) the development of rodent models of Guillain-Barré syndrome with sensory ataxic or motor phenotypes induced by immunization with GD1b or GM1 gangliosides, respectively.[10]
  • Comparison of clinical features of Guillain-Barré syndrome with CIDP
    • Patients with CIDP have a more slowly progressive weakness and a protracted course either monophasic or relapsing, and relapses are much more common with CIDP. While a history of viral infection is often obtained with Guillain-Barré syndrome, this is rather uncommon in CIDP. Occurrence of respiratory failure is very uncommon with CIDP. Both conditions are associated with areflexia, typical CSF findings of increased protein, abnormal nerve conduction studies (patchy conduction slowing with Guillain-Barré syndrome and diffuse slowing with CIDP). While prednisone therapy on its own has no proven role in Guillain-Barré syndrome, CIDP patients are sensitive to prednisone therapy.
    • Guillain-Barré syndrome and CIDP have been associated with HIV-1 infection. They are most common in infected patients who are otherwise asymptomatic. In certain cases, Guillain-Barré syndrome may occur with seroconversion. The clinical features of Guillain-Barré syndrome and CIDP in HIV-1 infected patients are similar to patients without HIV-1 infection.
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Contributor Information and Disclosures
Author

Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital

Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS is a member of the following medical societies: American College of International Physicians, American Heart Association, American Stroke Association, American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners Institute, National Association of Managed Care Physicians, American College of Physicians, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, Royal Society of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Richard A Sater, MD, PhD, MD, PhD 

Richard A Sater, MD, PhD, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Medical Association, American Society of Neuroradiology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Glenn Lopate, MD Associate Professor, Department of Neurology, Division of Neuromuscular Diseases, Washington University School of Medicine; Consulting Staff, Department of Neurology, Barnes-Jewish Hospital

Glenn Lopate, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Nicholas Lorenzo, MD, MHA, CPE Founding Editor-in-Chief, eMedicine Neurology; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc

Nicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Association for Physician Leadership, American Academy of Neurology

Disclosure: Nothing to disclose.

References
  1. HAYMAKER WE, KERNOHAN JW. The Landry-Guillain-Barré syndrome; a clinicopathologic report of 50 fatal cases and a critique of the literature. Medicine (Baltimore). 1949 Feb. 28(1):59-141. [Medline].

  2. Krucke W. Die primar-entzundliche polyneuritis unbekannter ursache. Handbuch des speziellen pathologischen anatomie und histologie. 1955. Berlin, Springer-Verlag:

  3. WAKSMAN BH, ADAMS RD. Allergic neuritis: an experimental disease of rabbits induced by the injection of peripheral nervous tissue and adjuvants. J Exp Med. 1955 Aug 1. 102(2):213-36. [Medline].

  4. Nachamkin I, Barbosa PA, Ung H, Lobato C, Rivera AG, Rodriguez P. Patterns of Guillain-Barre syndrome in children: results from a Mexican population. Neurology. 2007 Oct 23. 69(17):1665-71. [Medline].

  5. Ropper AH. Unusual clinical variants and signs in Guillain-Barre syndrome. Arch Neurol. 1986 Nov. 43(11):1150-2. [Medline].

  6. Nagashima T, Koga M, Odaka M, Hirata K, Yuki N. Continuous spectrum of pharyngeal-cervical-brachial variant of Guillain-Barré syndrome. Arch Neurol. 2007 Oct. 64(10):1519-23. [Medline].

  7. Ladhani SN, O'Connor C, Kirkbride H, Brooks T, Morgan D. Outbreak of Zika virus disease in the Americas and the association with microcephaly, congenital malformations and Guillain-Barré syndrome. Arch Dis Child. 2016 Mar 14. [Medline].

  8. Tse AC, Cheung RT, Ho SL, Chan KH. Guillain-Barré syndrome associated with acute hepatitis E infection. J Clin Neurosci. 2012 Jan 26. [Medline].

  9. Wagner JC, Bromberg MB. HIV infection presenting with motor axonal variant of Guillain-Barré Syndrome. J Clin Neuromuscul Dis. 2007 Dec. 9(2):303-5. [Medline].

  10. Willison HJ. The immunobiology of Guillain-Barre syndromes. J Peripher Nerv Syst. 2005 Jun. 10(2):94-112. [Medline].

  11. Park SJ, Pai KS, Kim JH, Shin JI. The role of interleukin 6 in the pathogenesis of hyponatremia associated with Guillain-Barré syndrome. Nefrologia. 2012 Jan 27. 32(1):114. [Medline].

  12. Kaida K, Kamakura K, Ogawa G, Ueda M, Motoyoshi K, Arita M. GD1b-specific antibody induces ataxia in Guillain-Barre syndrome. Neurology. 2008 Jul 15. 71(3):196-201. [Medline].

  13. Cornblath DR. Electrophysiology in Guillain-Barré syndrome. Ann Neurol. 1990. 27 Suppl:S17-20. [Medline].

  14. Matsumoto H, Hanajima R, Terao Y, Hashida H, Ugawa Y. Cauda equina conduction time in Guillain-Barre syndrome. J Neurol Sci. 2015 Apr. 15. 351(1-2):187-90.

  15. Umapathi T. Li Z, Verma K, Yuki N. Sural-sparing is seen in axonal as well as demyelinating forms of Guillain-Barre syndrome. Clin Neurophysiol. 2015 Feb. 9. pii S1388-2457(15):00072-3.

  16. Jin K, Takeda A, Shiga Y, Sato S, Ohnuma A, Nomura H. CSF tau protein: a new prognostic marker for Guillain-Barré syndrome. Neurology. 2006 Oct 24. 67(8):1470-2. [Medline].

  17. Alshekhlee A, Hussain Z, Sultan B, Katirji B. Immunotherapy for Guillain-Barré syndrome in the US hospitals. J Clin Neuromuscul Dis. 2008 Sep. 10(1):4-10. [Medline].

  18. Hou HQ, Miao J, Feng XD, Han M, Song XJ, Guo L. Changes in lymphocyte subsets in patients with Guillain-Barre syndrome treated with immunoglobulin. BMC Neurol. 2014 Oct. 15. 14:202.

  19. Grand'Maison F, Feasby TE, Hahn AF, Koopman WJ. Recurrent Guillain-Barré syndrome. Clinical and laboratory features. Brain. 1992 Aug. 115 ( Pt 4):1093-106. [Medline].

  20. Wijdicks EF, Ropper AH. Acute relapsing Guillain-Barré syndrome after long asymptomatic intervals. Arch Neurol. 1990 Jan. 47(1):82-4. [Medline].

  21. Martic V, Lepic T. Recurrence of childhood Guillain-Barré syndrome after a long asymptomatic interval: a case report. J Clin Neuromuscul Dis. 2007 Sep. 9(1):256-61. [Medline].

  22. Souayah N, Nasar A, Suri MFK, Qureshi A. National Trends in Hospital Outcomes Among Patients with Guillain-Barre Syndrome Requiring Mechanical Ventilation. Journal of Clinical Neuromuscular Disease. 2008. 10(1):24-28.

  23. Frenzen PD. Economic cost of Guillain-Barré syndrome in the United States. Neurology. 2008 Jul 1. 71(1):21-7. [Medline].

  24. Asbury AK. Diagnostic considerations in Guillain-Barre syndrome. Ann Neurol. 1981. 9 Suppl:1-5. [Medline].

  25. Ascherio A, Bermudez CS, Garcia D. Outbreak of buckthorn paralysis in Nicaragua. J Trop Pediatr. 1992 Apr. 38(2):87-9. [Medline].

  26. Berlit P, Rakicky J. The Miller Fisher syndrome. Review of the literature. J Clin Neuroophthalmol. 1992 Mar. 12(1):57-63. [Medline].

  27. Chiba A, Kusunoki S, Obata H. Serum anti-GQ1b IgG antibody is associated with ophthalmoplegia in Miller Fisher syndrome and Guillain-Barre syndrome: clinical and immunohistochemical studies. Neurology. 1993 Oct. 43(10):1911-7. [Medline].

  28. Crino PB, Zimmerman R, Laskowitz D. Magnetic resonance imaging of the cauda equina in Guillain-Barre syndrome. Neurology. 1994 Jul. 44(7):1334-6. [Medline].

  29. Dwyer JM. Manipulating the immune system with immune globulin. N Engl J Med. 1992 Jan 9. 326(2):107-16. [Medline].

  30. Feasby TE. Axonal Guillain-Barre syndrome. Muscle Nerve. 1994 Jun. 17(6):678-9. [Medline].

  31. FISHER M. An unusual variant of acute idiopathic polyneuritis (syndrome of ophthalmoplegia, ataxia and areflexia). N Engl J Med. 1956 Jul 12. 255(2):57-65. [Medline].

  32. French Cooperative Group on Plasma Exchange in Guillain-Barre syndrome. Efficiency of plasma exchange in Guillain-Barre syndrome: role of replacement fluids. French Cooperative Group on Plasma Exchange in Guillain-Barre syndrome. Ann Neurol. 1987 Dec. 22(6):753-61. [Medline].

  33. Guillain G, Barre JA, Strohl A. Sur un syndrome de radiculo-nevrite avec hyperalbuminose du liquide cephalo-rachidien sans reaction cellulaire. Bulletins et memories de la Societe Medicale des Hopitaux de Paris. 1916. 40:1462.

  34. Guillain-Barré Syndrome Study Group. Plasmapheresis and acute Guillain-Barre syndrome. Neurology. 1985 Aug. 35(8):1096-104. [Medline].

  35. Hughes RAC. Guillain-Barre Syndrome. 1990.

  36. Irani DN, Cornblath DR, Chaudhry V. Relapse in Guillain-Barre syndrome after treatment with human immune globulin. Neurology. 1993 May. 43(5):872-5. [Medline].

  37. Landry O. Note sur la paralysis ascendante aigue. Gazette Hebdomadaire. 1859. 6:472.

  38. Leong H, Stachnik J, Bonk ME, Matuszewski KA. Unlabeled uses of intravenous immune globulin. Am J Health Syst Pharm. 2008 Oct 1. 65(19):1815-24. [Medline].

  39. McGrogan A, Madle GC, Seaman HE, de Vries CS. The Epidemiology of Guillain-Barré Syndrome Worldwide. A Systematic Literature Review. Neuroepidemiology. 2008 Dec 17. 32(2):150-163. [Medline].

  40. McKhann GM, Cornblath DR, Griffin JW. Acute motor axonal neuropathy: a frequent cause of acute flaccid paralysis in China. Ann Neurol. 1993 Apr. 33(4):333-42. [Medline].

  41. Osterman PO, Fagius J, Safwenberg J. Early relapse of acute inflammatory polyradiculoneuropathy after successful treatment with plasma exchange. Acta Neurol Scand. 1988 Apr. 77(4):273-7. [Medline].

  42. Plasma Exchange/Sandoglobulin Guillain-Barre Syndrome Trial Group. Randomised trial of plasma exchange, intravenous immunoglobulin, and combined treatments in Guillain-Barre syndrome. Lancet. 1997 Jan 25. 349(9047):225-30. [Medline].

  43. Prineas JW. Acute idiopathic polyneuritis. An electron microscope study. Lab Invest. 1972 Feb. 26(2):133-47. [Medline].

  44. Ropper AH. Further regional variants of acute immune polyneuropathy. Bifacial weakness or sixth nerve paresis with paresthesias, lumbar polyradiculopathy, and ataxia with pharyngeal-cervical-brachial weakness. Arch Neurol. 1994 Jul. 51(7):671-5. [Medline].

  45. Ropper AH, Wijdicks EFM, Truax BT. Guillain-Barre Syndrome. Contemporary Neurology Series. 1991.

  46. Rostami AM, Sater RA. Guillain-Barre Syndrome. Neuroimmunology for the Clinician. 1997. 205-228.

  47. Sater RA, Rostami A. Treatment of Guillain-Barre syndrome with intravenous immunoglobulin. Neurology. 1998 Dec. 51(6 Suppl 5):S9-15. [Medline].

  48. van der Meche FG, Schmitz PI. A randomized trial comparing intravenous immune globulin and plasma exchange in Guillain-Barre syndrome. Dutch Guillain-Barre Study Group. N Engl J Med. 1992 Apr 23. 326(17):1123-9. [Medline].

  49. Vriesendorp FJ, Mishu B, Blaser MJ. Serum antibodies to GM1, GD1b, peripheral nerve myelin, and Campylobacter jejuni in patients with Guillain-Barre syndrome and controls: correlation and prognosis. Ann Neurol. 1993 Aug. 34(2):130-5. [Medline].

  50. Vriesendorp FJ, Triggs WJ, Mayer RF. Electrophysiological studies in Guillain-Barre syndrome: correlation with antibodies to GM1, GD1B and Campylobacter jejuni. J Neurol. 1995 Jul. 242(7):460-5. [Medline].

  51. Willison HJ, Winer JB. Clinical evaluation and investigation of neuropathy. J Neurol Neurosurg Psychiatry. 2003 Jun. 74 Suppl 2:ii3-ii8. [Medline].

  52. Young RR, Asbury AK, Corbett JL. Pure pandysautonomia with recovery. Description and discussion of diagnostic criteria. Brain. 1975 Dec. 98(4):613-36. [Medline].

  53. Yuki N, Taki T, Inagaki F. A bacterium lipopolysaccharide that elicits Guillain-Barre syndrome has a GM1 ganglioside-like structure. J Exp Med. 1993 Nov 1. 178(5):1771-5. [Medline].

  54. Yuki N, Taki T, Takahashi M, Saito K, Yoshino H, Tai T, et al. Molecular mimicry between GQ1b ganglioside and lipopolysaccharides of Campylobacter jejuni isolated from patients with Fisher's syndrome. Ann Neurol. 1994 Nov. 36(5):791-3. [Medline].

  55. Ubogu ee. Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention. Acta Neuropathol. Epub 2015 Aug 12 - 2015 Oct. 130(4):445-68. [Full Text].

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