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Overview of Guillain-Barr syndrome in children

Official reprint from UpToDate www.uptodate.com 2013 UpToDate

Overview of Guillain-Barr syndrome in children Author Robert P Cruse, DO Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jan 2013. | This topic last updated: Aug 2, 2012. INTRODUCTION The acute immune-mediated polyneuropathies are classified under the eponym Guillain-Barr syndrome (GBS), after the authors of early descriptions of the disease. Historically, GBS was considered a single disorder, but it is now known to be a heterogeneous syndrome with several variant forms. Most often, GBS presents as an acute monophasic paralyzing illness provoked by a preceding infection. In addition to the demyelinating form, which is the most common type, axonal forms of GBS are well-recognized. This topic will discuss the epidemiology, pathophysiology, clinical features, variants, diagnosis, pathology and prognosis of GBS in children. The treatment of GBS in children is discussed separately. (See "Treatment of Guillain-Barr syndrome in children".) EPIDEMIOLOGY Guillain-Barr syndrome is the most common cause of acute flaccid paralysis in healthy infants and children [1]. It has an annual incidence of 0.6 to 2.4 cases per 100,000 population and occurs at all ages and in both sexes [2]. The incidence is lower in children, 0.38 and 0.91 cases per 100,000 in two reports [3,4]. GBS occurs rarely in children younger than two years of age, but can occur in infants [5,6]. Males are affected approximately 1.5 times more often than females in all age groups. Vaccinations Guillain-Barr syndrome has occurred after patients have received vaccinations, but this danger may be overstated. As an example, in one report of all patients hospitalized for GBS in Finland between 1982 and 1986, measles-mumps-rubella vaccination did not cause an increase above the background incidence of GBS and no clustering of cases occurred at any time after administration of the vaccine [7]. There may be a small increased risk of GBS following immunization with the quadrivalent meningococcal polysaccharide conjugate vaccine (MCV4). The possible association between MCV4 and GBS is discussed separately. (See "Meningococcal vaccines", section on 'Possible association with Guillain-Barr syndrome'.) The available evidence suggests no increased risk of GBS in children from the H1N1 influenza vaccine [8-10]. PATHOPHYSIOLOGY GBS is really a group of disorders rather than a single disease. It is now considered to be a syndrome with a number of variants. Peripheral nerve demyelination in the demyelinating form is believed to be immunologically mediated. A variety of clinical and experimental data have implicated both humoral factors [11] and cell-mediated immune phenomena that damage myelin and/or the myelin-producing Schwann cells [12]. There is no known genetic factor. (See 'Variants of Guillain-Barr syndrome' below.) Approximately two-thirds of patients have a history of an antecedent respiratory tract or gastrointestinal infection [13]. A variety of infectious agents have been associated with GBS, although Campylobacter is the most frequent. Other organisms that commonly precede GBS include cytomegalovirus [14], Epstein-Barr virus, Haemophilus influenzae [15] mycoplasma pneumoniae, the enteroviruses, hepatitis A and B, herpes simplex, and Chlamydophila (formerly Chlamydia) pneumoniae [16]. Campylobacter infection Campylobacter infection is the most commonly identified precipitant of GBS and can
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Section Editors Douglas R Nordli, Jr, MD Sheldon L Kaplan, MD

Deputy Editor John F Dashe, MD, PhD

12/02/13

Overview of Guillain-Barr syndrome in children

be demonstrated in as many as 30 percent of cases [17]. A case-control study involving 103 patients with the disease found that 26 percent of affected individuals had evidence of recent infection with C. jejuni compared with 2 percent of household and 1 percent of age-matched controls [18]. Seventy percent of those infected with C. jejuni reported a diarrheal illness within 12 weeks before the onset of the neurologic illness. Campylobacter-associated GBS had a worse prognosis than other forms of the disease in this series, manifested by slower recovery and greater residual neurologic disability. The risk for developing GBS during the two months after having a symptomatic episode of C. jejuni infection is approximately 100-fold higher than the risk in the general population [19]. The main lesions of GBS are acute inflammatory demyelinating polyradiculoneuropathy and, particularly in patients with Campylobacter-associated disease, acute axonal degeneration. These changes may be caused by crossreacting antibodies to GM1 ganglioside (present in high concentrations in peripheral nerve myelin) formed in response to similar epitopes expressed by the infecting Campylobacter strain [20-23]. In support of this concept, many of the Campylobacter strains associated with GBS belong to serotypes, notably certain O19 and O41 strains, which are seldom isolated from ordinary cases of enteritis [24,25]. Polysaccharides of this serotype resemble human ganglioside found in human peripheral nerve [26,27]. However, mechanisms other than molecular mimicry may be associated with the production of antibodies to GM1 ganglioside [28], and many patients with Campylobacter infection but no neurologic symptoms also form these antibodies [21]. The presence of antibodies to gangliosides, including N-acetylgalactosaminyl GD1a (GalNAc-GD1a), has been associated with a distinctive clinical pattern in GBS. In one study, patients with anti-GalNAc-GD1a antibodies were more likely to have no cranial nerve involvement (87 versus 38 percent), distal-dominant weakness (80 versus 25 percent), and no sensory disturbance (73 versus 22 percent) compared to those without antibodies [20]. In another report, anti-GD1a antibodies were measured in patients with different subtypes of GBS [29]. Antibodies were detected more frequently in acute motor axonal neuropathy, in which the axolemma and nodes of Ranvier (short intervals between successive segments of the myelin sheath of a nerve) are affected, than in acute inflammatory demyelinating polyneuropathy, in which a component of the Schwann cell is targeted. The GBS variant known as Miller Fisher syndrome, in which the cranial nerves are affected, also is associated with Campylobacter infection. Most of these patients have cross-reacting antibodies to GQ1b ganglioside, which is present in cranial nerve myelin [27,28,30,31]. CLINICAL FEATURES In patients with acute inflammatory demyelinating polyradiculopathy (AIDP), the most common form of GBS, two-thirds develop the neurologic symptoms two to four weeks after having what appears to be a benign febrile respiratory or gastrointestinal infection [13,32]. The classic presentation is fine paresthesias in the toes and fingertips followed by lower extremity symmetric weakness that may ascend over hours to days to involve the arms and, in severe cases, the muscles of respiration [33,34]. The predominant symptoms of GBS at presentation in children are pain and gait difficulty [35]. In preschool aged children, the most common symptoms are refusal to walk and pain in the legs [36]. In a prospective series of 95 children with GBS, the most frequent initial symptoms were gait unsteadiness, neuropathic pain, and inability to walk, occurring in 45, 34, and 24 percent, respectively [37]. By the peak of the illness, the frequency of symptoms was as follows: 79 percent 60 percent 51 percent 46 percent 24 percent 13 percent had neuropathic pain could not walk had autonomic dysfunction had cranial nerve involvement could not use their arms required mechanical ventilation

In those with cranial neuropathy, the facial nerve is most commonly affected, resulting in bilateral facial weakness [37]. Pain typically involves the back and the legs [38].

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Autonomic dysfunction occurs in approximately one-half of children with GBS, and may include the following [37,39]: A variety of cardiac dysrhythmias (asystole, bradycardia, persistent sinus tachycardia, and atrial and ventricular tachyarrhythmias) Orthostatic hypotension Transient or persistent hypertension Paralytic ileus Bladder dysfunction Abnormal sweating Rare patients have central nervous system involvement [40]. Physical examination Physical examination reveals symmetric weakness with diminished or absent reflexes [33,34]. Minimal loss of sensation occurs, despite paresthesias. Variable initial physical findings can render making an early diagnosis difficult. Examples of less common signs include predominant proximal weakness, hyperreflexia with extensor plantar response, and sphincter disturbances that raise concerns about a spinal cord lesion. Papilledema can occur with [41] or without increased intracranial pressure [42]. Clinical course More than 90 percent of patients reach the nadir of their function within two to four weeks [43], followed by return of function occurring slowly over the course of weeks to months. A chronic (extending beyond two months), slowly progressive or relapsing inflammatory demyelinating polyneuropathy generally is considered a distinct entity from acute GBS. The clinical course of GBS in children is shorter than in adults and recovery is more complete [44-47]. In patients who did not require mechanical ventilation, the median time to recovery of independent walking was 43 to 52 days in children compared to 85 days in adults [48-50]. VARIANTS OF GUILLAIN-BARR SYNDROME Historically, GBS was considered a single disorder. It is now known to be a heterogeneous syndrome with several variant forms [51-56]. In addition to the demyelinating form, which is the most common type, axonal forms of GBS are now well recognized. Each variant of GBS has distinguishing clinical, pathophysiologic and pathologic features. Acute inflammatory demyelinating polyneuropathy Acute inflammatory demyelinating polyneuropathy (AIDP) is the prototype of GBS, and is the most common form in North America, Europe and most of the developed world, where it accounts for about 85 to 90 percent of cases. Acute motor axonal neuropathy Acute motor axonal neuropathy (AMAN) is a pure motor form of GBS. This disorder is distinguished from AIDP by its involvement of predominantly motor nerves and an electrophysiologic pattern suggesting axonal damage. AMAN occurs mainly in northern China, but is also a common form of GBS in other locations, including Japan, Mexico, and South America [53,57-60]. It is more common in developing nations, has a seasonal incidence, and is associated with a preceding Campylobacter jejuni infection. In a series of 31 Japanese children with GBS classified by electrophysiologic criteria, AIDP, AMAN, and unclassified GBS were seen in 11, 15 and 5 children (35, 48 and 16 percent) respectively [59]. The presenting clinical features and recovery are similar to those of AIDP [61]. However, more patients have respiratory failure requiring assisted ventilation. Acute motor-sensory axonal neuropathy Acute motor-sensory axonal neuropathy (AMSAN) resembles the motor axonal variant but has more sensory symptoms. The course tends to be prolonged [51,62]. The pathology is predominantly axonal lesions of both motor and sensory nerve fibers. This form of GBS is recognized infrequently in children. The infrequent diagnosis may be caused in part by the difficulty of performing sensory testing in children and because electrophysiologic studies often are not done.
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Miller Fisher syndrome Patients with Miller Fisher syndrome (MFS) have external ophthalmoplegia, ataxia, and muscle weakness with areflexia [63,64]. CSF and electrophysiologic features are similar to those in AIDP. Brainstem auditory evoked potentials demonstrate peripheral and central conduction defects [47]. Polyneuritis cranialis Patients with polyneuritis cranialis develop acute bilateral multiple cranial nerve involvement and severe peripheral sensory loss. They typically have bilateral facial weakness, dysphagia, and dysphonia with optic nerve sparing. Patients tend to be younger than those with other types. This variant is associated with preceding cytomegalovirus infections [65]. Cerebrospinal fluid findings and electrophysiologic features of polyneuritis cranialis are similar to those of AIDP. Contrast MRI shows enhancement of multiple cranial nerves [66]. More children with this variant require ventilator support than those with the more typical presentation of GBS [67]. However, most recover fully. DIAGNOSIS Electrophysiologic studies are the most specific and sensitive tests for diagnosis of the disease. (See "Overview of electromyography" and "Overview of nerve conduction studies".) They demonstrate a variety of abnormalities indicating evolving multifocal demyelination, including [68]: Partial motor conduction block Slowed nerve conduction velocities Abnormal temporal dispersion Prolonged distal latencies Evidence of conduction block usually is the earliest abnormality. Slowed nerve conduction velocities reflect the segmental demyelination. Absent H reflexes or abnormal prolonged F-waves indicate proximal nerve root involvement. A retrospective study assessed early electrophysiologic changes in 31 patients with GBS [69]. The Hreflex was the single most sensitive test for early GBS, being absent in 97 percent tested within seven days of the onset of neurologic symptoms. Testing for the H-reflex requires electrical stimulation of the sciatic nerve. (See "Nerve conduction studies: Late responses".) A normal nerve conduction study occurring after several days of symptoms, particularly in the setting of severe weakness, renders the diagnosis of GBS unlikely. This finding should prompt a search for alternative explanations for the patient's illness. Electromyogram abnormalities typically are delayed for two to three weeks. The motor units show denervation potentials, reflecting secondary axonal degeneration. In the motor and motor-sensory variants of GBS, nerve conduction velocities are normal. In both forms, motor amplitudes in nerve conduction studies are less than 10 percent of normal, with severe denervation evident on follow-up needle examination [70]. In the motor-sensory variant, sensory amplitudes also are decreased. Cerebrospinal fluid After the first week of symptoms, analysis of the cerebrospinal fluid (CSF) by lumbar puncture typically reveals a normal pressure, fewer than 10 cells (typically mononuclear), and an elevated protein concentration (> 45 mg/dL). These findings may be delayed and a repeat lumbar puncture may be required. The protein may not rise for one to two weeks, but only rarely does it remain persistently normal. Maximum protein values may not be seen for four to five weeks. An initial pleocytosis of less than 100 lymphocytes may occur. If this is noted, other diseases associated with GBS (such as HIV infection, Lyme disease, and malignancy) should be considered [32]. In addition, other diseases, including inflammatory (infectious or autoimmune disorders) and demyelinating diseases, may be associated with leg weakness and CSF pleocytosis. Magnetic resonance imaging Spinal MRI with administration of gadolinium frequently shows enhancement of the spinal nerve roots and cauda equina during the first weeks after the onset of GBS in children [71-73]. The enhancement may be diffuse or predominantly involve the ventral (anterior) nerve roots, and less often the dorsal (posterior) roots. In some cases, nerve root enhancement may be delayed and observed only on a repeat MRI. Evidence from uncontrolled retrospective studies suggests that the sensitivity of contrast-enhanced spinal MRI for
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the diagnosis of GBS is >90 percent [71-73]. Nevertheless, spinal nerve root enhancement is a nonspecific finding that can be seen in a variety of disorders including polyradiculopathy related to HIV or cytomegalovirus infection, chronic inflammatory demyelinating polyneuropathy, arachnoiditis, sarcoidosis, carcinomatous or lymphomatous meningitis, and certain metabolic diseases. Thus, the diagnosis of GBS cannot be made by MRI alone. Enhancement of the cranial nerves on contrast MRI has also been reported [66,73]. (See 'Polyneuritis cranialis' above.) Differential diagnosis Disorders of the central nervous system, peripheral nerve, neuromuscular junction, and muscle may have features that initially resemble GBS (table 1). However, consideration of the neurologic examination, clinical course, cerebrospinal fluid profile, and electrophysiologic findings usually establish the diagnosis of GBS [43]. PATHOLOGY The pathologic changes depend upon the form of GBS. In acute inflammatory demyelinating polyneuropathy and the Miller Fisher variant, a focal inflammatory response develops against myelin-producing Schwann cells or peripheral myelin. Infiltration of the epineural and endoneural small vessels (mostly veins) by lymphocytes and monocytes causes segmental myelin degeneration throughout the nerve. The inflammation is more intense at the junction of the dorsal and ventral roots. The demyelination blocks electrical conduction along the nerve. Axonal degeneration occurs as a secondary response; the extent relates to the intensity of the inflammatory response. All myelinated nerves (motor, sensory, cranial, sympathetic) can be affected. The breakdown of the blood-nerve barrier at the dural attachment allows transudation of plasma proteins into the cerebrospinal fluid. In the motor and motor sensory variants, the axon is affected without an inflammatory response [74,75]. The primary immune process is directed at the nodes of Ranvier (short intervals between successive segments of the myelin sheath of a nerve). Macrophages infiltrate at the nodes and extend into the periaxonal spaces, resulting in axonal degeneration [75]. The motor nerves are involved at the ventral roots, peripheral nerve, and the preterminal intramuscular motor twigs [76]. In the motor sensory variant, sensory nerves also are affected. In a study of 29 children with GBS in China, electrophysiologic studies correlated with sural nerve biopsies [77]. Patients classified as having acute inflammatory demyelinating polyneuropathy based upon a physiologic pattern consistent with demyelination commonly had macrophage-mediated demyelination and lymphocytic infiltration. Sural nerves were normal or had few degenerating fibers without lymphocytic infiltration or complement activation in children with acute motor axonal neuropathy. TREATMENT The main modalities of therapy for GBS include plasmapheresis and administration of intravenous immune globulin. Even before initiating specific therapy, common problems are when and whether to admit the patient to the intensive care unit (ICU) and when to consider mechanical ventilation. This topic is discussed separately. (See "Treatment of Guillain-Barr syndrome in children".) PROGNOSIS The severity of GBS in children does not correlate with long-term outcome. As many as 85 percent of children can be expected to have an excellent recovery. Approximately one-half of patients are ambulatory by six months, and 70 percent walk within a year after onset [33,78]. A better prognosis is associated with a gradual evolution of weakness [45,46]. Mortality is approximately 3 to 4 percent, and usually is secondary to respiratory failure or cardiac complications [33,79]. Therapy with IVIG does not appear to improve the prognosis of GBS. In the only report since the introduction of this therapy, the long term outcome of GBS was evaluated in 31 children available for follow-up at an average age of 5.3 years after their illness [80]. Most were treated with IVIG (24 of 31 patients); seven with a milder presentation received supportive therapy alone. Mild weakness in at least one muscle group persisted in 23 percent of children, although this had minimal impact on function. Long term weakness was associated with age younger than nine years at onset and a rapid progression (<10 days) to maximal weakness. In general, the prognosis in affected children is better than adults. In one study, pediatric patients with
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electrodiagnostic criteria associated with poor outcome in adults (low mean compound muscle action potential amplitude and fibrillation potentials) recovered without residual disability [79]. In an observational study of Japanese children with GBS, outcomes were generally favorable in both AIDP and AMAN subtypes, although delayed recovery was more frequent with AMAN [59]. All 11 children with AIDP and 12 of 15 (80 percent) with AMAN regained the ability to walk independently at six months; 14 of 15 children (93 percent) with AMAN walked independently at two years. Differences in clinical recovery between children with AIDP and AMAN were not statistically significant. INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and Beyond the Basics. The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the keyword(s) of interest.) Basics topics (see "Patient information: Guillain-Barr syndrome (The Basics)") SUMMARY Guillain-Barr syndrome (GBS) is the most common cause of acute flaccid paralysis in healthy infants and children. (See 'Epidemiology' above.) GBS is really a group of disorders rather than a single disease. Peripheral nerve demyelination in the demyelinating form is believed to be immunologically mediated. Approximately two-thirds of patients have a history of an antecedent respiratory tract or gastrointestinal infection. Campylobacter infection is the most commonly identified precipitant of GBS and can be demonstrated in as many as 30 percent of cases. (See 'Pathophysiology' above.) In patients with acute inflammatory demyelinating polyradiculopathy (AIDP), the most common form of GBS, two-thirds develop the neurologic symptoms two to four weeks after having what appears to be a benign febrile respiratory or gastrointestinal infection. The predominant symptoms of GBS at presentation in children are pain and gait difficulty. Lower extremity symmetric weakness may ascend over hours to days to involve the arms and the muscles of respiration in severe cases. In those with cranial neuropathy, the facial nerve is most commonly affected, resulting in bilateral facial weakness. Autonomic dysfunction occurs in approximately one-half of children with GBS. Physical examination reveals symmetric weakness with diminished or absent reflexes. Most patients reach the nadir of their function within two to four weeks, followed by return of function occurring slowly over the course of weeks to months. (See 'Clinical features' above.) Guillain-Barr syndrome is a heterogeneous syndrome with several variant forms. Each has distinguishing clinical, pathophysiologic and pathologic features. These include (see 'Variants of Guillain-Barr syndrome' above): Acute inflammatory demyelinating polyneuropathy, the prototype of GBS (see 'Acute inflammatory demyelinating polyneuropathy' above) Acute motor axonal neuropathy (see 'Acute motor axonal neuropathy' above)
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Acute motor-sensory axonal neuropathy (see 'Acute motor-sensory axonal neuropathy' above) Miller Fisher syndrome (see 'Miller Fisher syndrome' above) Polyneuritis cranialis (see 'Polyneuritis cranialis' above) Electrophysiologic studies are the most specific and sensitive tests for diagnosis of GBS. They demonstrate a variety of abnormalities indicating evolving multifocal demyelination, including partial motor conduction block, slowed nerve conduction velocities, abnormal temporal dispersion, and prolonged distal latencies. With lumbar puncture, characteristic cerebrospinal fluid findings include normal pressure, fewer than 10 cells (typically mononuclear), and an elevated protein concentration (>45 mg/dL). Spinal MRI with administration of gadolinium frequently shows enhancement of the spinal nerve roots and cauda equina during the first weeks after the onset. (See 'Diagnosis' above.) The main modalities of therapy for GBS are plasmapheresis and intravenous immune globulin. Even before initiating specific therapy, common problems are when and whether to admit the patient to the intensive care unit and when to consider mechanical ventilation. These issues are discussed separately. (See "Treatment of Guillain-Barr syndrome in children".) The severity of GBS in children does not correlate with long-term outcome. As many as 85 percent of children can be expected to have an excellent recovery. Approximately one-half of patients are ambulatory by six months, and 70 percent walk within a year after onset. Mortality is approximately 3 to 4 percent, and usually is secondary to respiratory failure or cardiac complications. (See 'Prognosis' above.)

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GRAPHICS
Differential diagnosis of Guillain-Barr syndrome
Differential diagnosis
Cerebral Bilateral strokes Psychogenic symptoms Cerebellar Acute cerebellar ataxia syndromes Posterior fossa structural lesion Spinal Compressive myelopathy Transverse myelitis Anterior spinal artery syndrome Poliomyelitis Other infectious causes of acute myelitis (eg, West Nile virus, coxsackieviruses, echoviruses) Peripheral nervous system Toxic neuropathy
Drugs Toxins

Critical care neuropathy Diphtheria Tick paralysis Porphyria Lyme disease Vasculitis Neuromuscular junction Botulism Myasthenia gravis Neuromuscular blocking agents Muscle disease Acute viral myositis Acute inflammatory myopathies Metabolic myopathies (eg, hypokalemic, hyperkalemic) Periodic paralysis Data from:
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1. Evans OB. Guillain-Barr syndrome in children. Pediatr Rev 1986; 8:69. 2. Jones HR. Childhood Guillain-Barr syndrome: clinical presentation, diagnosis, and therapy. J Child Neurol 1996; 11:4. 3. Yuki N, Hartung HP. Guillain-Barr syndrome. N Engl J Med 2012; 366:2294.

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