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Guillain-Barré Syndrome (GBS) Guillain-Barré Syndrome ANNE D. WALLING, MD, ChB, and GRETCHEN DICKSON, MD, MBA University of Kansas School of Medicine, Wichita, Kansas Guillain-Barré syndrome consists of a group of neuropathic conditions characterized by pro- gressive weakness and diminished or absent myotatic reflexes. The estimated annual incidence in the United States is 1.65 to 1.79 per 100,000 persons. Guillain-Barré syndrome is believed to result from an aberrant immune response that attacks nerve tissue. This response may be triggered by surgery, immunizations, or infections. The most common form of the disease, acute inflammatory demyelinating polyradiculoneuropathy, presents as progressive motor weakness, usually beginning in the legs and advancing proximally. Symptoms typically peak within four weeks, then plateau before resolving. More than one-half of patients experience severe pain, and about two-thirds have autonomic symptoms, such as cardiac arrhythmias, blood pressure instability, or urinary retention. Advancing symptoms may compromise respi- ration and vital functions. Diagnosis is based on clinical features, cerebrospinal fluid testing, and nerve conduction studies. Cerebrospinal fluid testing shows increased protein levels but a normal white blood cell count. Nerve conduction studies show a slowing, or possible block- age, of conduction. Patients should be hospitalized for multidisciplinary supportive care and disease-modifying therapy. Supportive therapy includes controlling pain with nonsteroidal anti-inflammatory drugs, carbamazepine, or gabapentin; monitoring for respiratory and auto- nomic complications; and preventing venous thrombosis, skin breakdown, and decondition- ing. Plasma exchange therapy has been shown to improve short-term and long-term outcomes, and intravenous immune globulin has been shown to hasten recovery in adults and children. Other therapies, including corticosteroids, have not demonstrated benefit. About 3 percent of patients with Guillain-Barré syndrome die. Neurologic problems persist in up to 20 percent of patients with the disease, and one-half of these patients are severely disabled. (Am Fam Physi- cian. 2013;87(3):191-197. Copyright © 2013 American Academy of Family Physicians.) ▲ See related Close-ups uillain-Barré syndrome (GBS) ing polyradiculoneuropathy (AIDP) is the on page 166. consists of a group of neuro- most common subtype in the United States.3 pathic conditions characterized by progressive weakness and Epidemiology G diminished or absent reflexes.1,2 Although The estimated overall annual incidence of GBS is uncommon, early diagnosis by family GBS in the United States is 1.65 to 1.79 per physicians and prompt referral for aggressive 100,000 persons.10 The incidence increases therapy may significantly improve outcomes. steadily from 0.62 per 100,000 persons in those younger than nine years to 2.66 per Definitions 100,000 persons in those 80 to 89 years of The diagnostic criteria for GBS include age.4 The male-to-female ratio is 3:2.4 progressive, relatively symmetrical weak- Several infections have been implicated in ness with decreased or absent myotatic the development of GBS. About two-thirds of reflexes. For diagnosis, symptoms must patients with the disease report respiratory reach maximal intensity within four weeks or gastrointestinal symptoms in the three of onset and other possible causes must be weeks before the onset of GBS symptoms.4 excluded.1,2 Table 1 includes features nec- The strongest evidence implicates Campylo- essary for the diagnosis, and features that bacter jejuni infection, but GBS also has been make the diagnosis unlikely or exclude it.2-9 reported following infection with Myco- This syndrome has several distinct subtypes plasma pneumoniae, Haemophilus influ- (Table 2).4,5 Acute inflammatory demyelinat- enzae, cytomegalovirus, and Epstein-Barr Downloaded from the American Family Physician Web site at www.aafp.org/afp. Copyright © 2013 American Academy of Family Physicians. For the private, noncommer- Februarycial 1, use 2013 of one◆ Volume individual 87, user Number of the Web 3 site. All other rights reserved.www.aafp.org/afp Contact [email protected] for copyright questionsAmerican and/or permission Family Physician requests. 191 Guillain-Barre´ Syndrome Table 1. Diagnostic Features to Assist in the Evaluation of Suspected Guillain-Barré Syndrome Feature Comments virus.11 The reported associations of GBS Required for diagnosis with age, location, and season probably Bilateral symptoms Usually begins in the legs reflect the epidemiology of the precipitating Decreased myotatic Complete areflexia often occurs in affected conditions. Stressful events and surgeries reflexes limbs also have been shown to trigger the disease. Subacute, weakness Peaks within four weeks: peaks by two and diminished/absent weeks in 50 percent of cases, and by three Despite case reports of GBS develop- reflexes weeks in 80 percent of cases2-4 ing after immunization for tetanus, hepa- Supportive of diagnosis titis, and influenza, studies show that Clinical these immunizations lead to no or very Autonomic involvement Cardiac arrhythmias, orthostasis, blood little increased risk.12,13 The most recent pressure instability, urinary retention, study estimated that the attributable risk slowing of gastrointestinal motility; absent with 2009 pandemic influenza A (H1N1) in some subtypes immunization is up to two cases per Cranial nerve Facial weakness occurs in 30 to 50 percent of 1 million doses, mainly in older persons.14 involvement cases5,6; ophthalmoplegia is common with the Miller Fisher subtype; rarely an initial feature Etiology and Pathophysiology Relatively symmetrical Symptoms may not be absolutely symmetrical in affected limbs or face The mechanism of GBS is believed to be an Sensory involvement Usually mild; absent in some subtypes, inflammatory neuropathy due to cross reac- prominent in others (i.e., acute motor- tivity between neural antigens and antibod- sensory axonal neuropathy) ies that is induced by specific infections. Symptom pattern over Peak by two to four weeks, with variable Infectious organisms, such as C. jejuni, time plateau followed by recovery; permanent express lipooligosaccharides in the bacterial sequelae are possible wall similar to gangliosides. This molecular Cerebrospinal fluid findings mimicry creates antiganglioside antibod- Elevated protein levels Levels may be normal early, but they are elevated by the end of the second week of ies that attack nerves. The specific antibody symptoms in 90 percent of cases7 that is stimulated and its target area in the Normal white blood Less than 10 per mm3 (10 × 106 per L) nerve may explain the different subtypes of cell count GBS. Fewer than one per 1,000 patients with Slowing (< 60 percent Slowing of nerve conduction occurs in C. jejuni infection develops GBS, suggesting normal velocity) or 80 percent of cases, but this may take that host factors play a significant role in the blockage of nerve weeks to develop8,9 pathologic process. However, research has conduction not yet identified factors that increase an Rules out diagnosis individual’s risk of developing GBS. Evidence of neurotoxic Porphyria, diphtheria, botulism, toxic GBS has been shown to cause symptoms conditions neuropathy through multifocal areas of mononuclear Hexacarbon or lead Solvent abuse, exposure to some paints and exposure vapors, occupational exposure cell infiltration in the peripheral nerves. The Only sensory symptoms Sensory symptoms are predominant in the location and severity of the inflammation very rare form of acute motor-sensory correspond to the clinical manifestations. axonal neuropathy, but other neurologic In AIDP, the myelin is predominantly dam- symptoms are also present aged, whereas in acute motor axonal neu- Raises doubt about diagnosis ropathy, the nodes of Ranvier are targeted.5,15 Cerebrospinal fluid Polymorphonuclear leukocyte or monocytes leukocytosis Clinical Features Delineated level of — PRECEDING OR TRIGGERING CONDITIONS sensory dysfunction The most common symptoms reported Persistent and significant — asymmetry of symptoms before onset of GBS are fever, cough, sore Prominent bowel or Occurring at onset or persistent symptoms throat, and other upper respiratory symp- 16 bladder symptoms toms. Infection with Epstein-Barr virus has been linked to milder forms of GBS.17 Gas- Information from references 2 through 9. trointestinal symptoms may be more likely to precede the acute motor or motor-sensory 192 American Family Physician www.aafp.org/afp Volume 87, Number 3 ◆ February 1, 2013 Guillain-Barre´ Syndrome axonal neuropathy subtypes that are related to slower symptoms, upper limb weakness, autonomic dysfunc- recovery and higher risk of residual disability.18 A timely tion, or bulbar palsy. The weakness typically reaches its diagnosis of GBS depends on a high index of suspicion peak by the second week, followed by a plateau of vari- for the condition. able duration before resolution or stabilization with residual disability.19 CLINICAL PRESENTATION Facial, oropharyngeal, and oculomotor muscles may Initial symptoms typically include weakness, numb- be affected because of cranial neuropathy, especially in ness, tingling, and pain in the limbs. The extent, pro- the less common subtypes. Paresthesia in the feet and gression, and severity of symptoms vary greatly among hands is common, but sensory symptoms are generally individual patients. The most prominent symptom in mild, except for in those patients with the acute motor- patients
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