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Table of Contents
GUIDELINES
Year : 2011  |  Volume : 14  |  Issue : 5  |  Page : 73-81
 

Treatment guidelines for Guillain-Barré Syndrome


1 Department of Neurology, Nizam's Institute of Medical Sciences, Hyderabad, India
2 Department of Neurology, Grant Medical College, Mumbai, India
3 The Institute of Neurological Sciences, CARE Hospital, Hyderabad, India

Date of Submission26-Jan-2011
Date of Web Publication21-Jul-2011

Correspondence Address:
A K Meena
Professor, Department of Neurology, Nizam's Institute of Medical Sciences, Hyderabad - 500082
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-2327.83087

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How to cite this article:
Meena A K, Khadilkar S V, Murthy J. Treatment guidelines for Guillain-Barré Syndrome. Ann Indian Acad Neurol 2011;14, Suppl S1:73-81

How to cite this URL:
Meena A K, Khadilkar S V, Murthy J. Treatment guidelines for Guillain-Barré Syndrome. Ann Indian Acad Neurol [serial online] 2011 [cited 2018 Dec 12];14, Suppl S1:73-81. Available from: http://www.annalsofian.org/text.asp?2011/14/5/73/83087



   Introduction Top


Guillain-Barré syndrome (GBS) is an acute onset, usually monophasic immune-mediated disorder of the peripheral nervous system. The term GBS is often considered to be synonymous with acute inflammatory demyelinating polyradiculoneuropathy (AIDP), but with the increasing recognition of variants over the past few decades, the number of diseases that fall under the rubric GBS have grown to include axonal variants and more restricted variants, such as Miller Fisher syndrome (MFS) [Table 1]. [1]
Table 1: Guillain– Barré syndrome— clinical variants

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   Epidemiology Top


The reported incidence rates for GBS are 1-2 per 100,000 population. [2],[3],[4] The lifetime likelihood of any individual acquiring GBS is 1:1000. [5] The subtypes of GBS have different incidence rates in different parts of the world. In Europe and North America AIDP is dominant contributing to 90% of the cases. In contrast in China and Japan AMAN being the most common subtype. [6],[7] The picture is intermediate when we look at other population. In Indian series the incidence of AIDP and AMAN are virtually equal although AMAN is more common in younger patients. [8] There seems to be a slight preponderance of AIDP in studies by Gupta et al [9] and by Meena et al (unpublished data from NIMS, Hyderabad). Available Indian literature indicates a peak incidence between June-July and Sept-October. [10] In western countries, GBS is common in the 5 th decade, [11] but in India it occurs more commonly at a younger age. [10],[12] GBS is equally common in men and women and can occur at any age. There is a male preponderance among the hospitalized population. [10],[12]


   Clinical Features Top


Most often an unremarkable infection, such as upper respiratory infection, often predates the onset of GBS by 14 days. [2],[5] Many antecedent infections have been identified, including Campylobacter jejuni, cytomegalovirus (CMV), Mycoplasma pneumonia, Epstein-Barr virus, influenza virus, JEV. [13],[14] Surgery, immunization, and parturition have also been associated with GBS. GBS usually begins abruptly with distal, relatively symmetrical onset of paraesthesias and quickly followed by progressive limb weakness. Progression is rapid, with 50% of patients reaching clinical nadir by 2 weeks and more than 90% by 4 weeks. The current diagnostic criteria include <4 weeks of progression to clinical nadir. Approximately 80%-90% of patients with GBS become nonambulatory during the illness. [15],[16] Pain is prominent in 50% of patients. [16],[17] Neurological examination is characterized by distal and often proximal, relatively symmetrical, weakness. Although GBS is essentially a motor neuropathy, sensory dysfunction is seen in a few patients. It is seen more in a demyelinating form of GBS. [12],[18] Sensory examination is often normal in the early phase of disease. Facial or pharyngeal weakness is commonly seen in GBS. Diaphragmatic weakness due to phrenic nerve involvement is also common. Approximately one third of hospitalized GBS patients require mechanical ventilation due to respiratory muscle or oropharyngeal weakness. [18],[19] Tachycardia is common but more serious autonomic nervous system dysfunction may occur, including life-threatening arrhythmias, hypotension, hypertension, and gastrointestinal dysmotility. The incidence is between 27% and 55% and is more common in demyelinating than axonal form. [12],[20]


   Pathogenesis Top


Major advances have been made in understanding the mechanisms of some of the subtypes. The histological appearance of the AIDP subtype resembles experimental autoimmune neuritis, which is predominantly caused by T cells directed against peptides from the myelin proteins P0, P2, and PMP22. The role of T-cell-mediated immunity in AIDP remains unclear and there is evidence for the involvement of antibodies and complement. Strong evidence now exists that axonal subtypes of Guillain-Barré syndrome, acute motor axonal neuropathy (AMAN), and acute motor and sensory axonal neuropathy (AMSAN), are caused by antibodies to gangliosides on the axolemma that target macrophages to invade the axon at the node of Ranvier. About a quarter of patients with Guillain-Barré syndrome have had a recent C. jejuni infection, and axonal forms of the disease are especially common in these people. The lipo-oligosaccharide from the C. jejuni bacterial wall contains ganglioside-like structures and its injection into rabbits induces a neuropathy that resembles acute motor axonal neuropathy. [21],[22],[23] Antibodies to GM1, GM1b, GD1a, and GalNac-GD1a are in particular implicated in acute motor axonal neuropathy and, with the exception of GalNacGD1a, in acute motor and sensory axonal neuropathy.


   Diagnosis Top


Progressive weakness in both upper and lower extremities within 4 weeks along with areflexia is essential requirement for the diagnosis. Supportive ancillary testing for GBS includes CSF analysis and electrodiagnostic testing, both of which may be normal in the early phase of GBS. The limitations of ancillary testing in the early phase combined with the importance of prompt treatment of GBS mandates that the clinician at times make the diagnosis based solely on history and examination. An elevated CSF protein concentration (with normal cell count) is only found on initial CSF analysis in 50% of patients; elevated CSF protein concentration occurs in more than 90% of patients at the peak of the disease. CSF pleocytosis is an important red flag, which raises the question of infectious (HIV, CMV, Lyme, sarcoid), carcinomatous, or lymphomatous polyradiculoneuropathy [Table 2].
Table 2: Guillian– Barré syndrome— red flags raising other diagnostic possibilities

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   Electrodiagnosis Top


Electrodiagnostic (EDX) testing is performed to support the clinical impression. EDX testing of GBS patients often demonstrates features of demyelination, such as temporal dispersion, significantly slow conduction velocities, and prolonged distal and F-wave latencies. [24] Electrodiagnostic testing features of acquired demyelination (eg, conduction block, temporal dispersion, nonuniform slowing of conduction velocities) are particularly helpful because these findings are characteristic of immune-mediated demyelinating neuropathies. In early GBS, prolonged distal compound muscle action potential (CMAP) latencies and temporal dispersion are more commonly demonstrated than are slow motor conduction velocities and conduction block. [ 27] Another electrodiagnostic testing hallmark of GBS is the "sural sparing" pattern; that is, the finding of a normal sural sensory nerve response in the setting of abnormal upper extremity sensory nerve results. [27] This pattern is very unusual for neuropathies other than GBS. Sural sparing, a marker of demyelinating neuropathy, is more commonly seen in later than in early stages of AIDP. Other electrodiagnostic testing abnormalities are frequently encountered in early GBS but they are less specific to GBS. These include absent H-reflexes, low motor nerve CMAP amplitudes on distal stimulation, and prolonged F-wave responses. [25],[26],[27] It is reported that the H-reflex was absent in 97% of GBS patients within the first week of symptom onset. It should also be pointed out that motor electrodiagnostic testing findings are more often abnormal than sensory nerve results in early GBS. Blink reflex studies are often abnormal when there is facial nerve involvement. [26] Phrenic nerve conduction studies can be used to predict respiratory failure and the need for ventilation. [28] Reduced CMAP amplitudes of 0%-20% of the lower limit of normal carry a poor prognosis. [29]

The diagnostic yield of various neurophysiological criteria may vary in different subforms of Guillain-Barré syndrome, whose prevalence varies in different geographical areas. In a recent study the diagnostic sensitivity of Albers et al, [30] Cornblath, [31] Ho et al, [32] Dutch GBS Study Group, [33] Italian GBS Study Group, [34] and Albers and Kelly criteria [35] were evaluated and correlated with clinical subtypes of GBS, duration, severity, and outcome. [36] The sensitivity of nerve conduction study in the diagnosis of GBS and in different clinical subtypes of GBS was highest using Albers criteria (88.2%) and lowest using Cornblath criteria (39.2%). As per Ho et al, patients could be categorized into AIDP (86.3%), AMAN (7.8%), and AMSAN (5.9%). Electrophysiological findings necessary to diagnose GBS is in [Table 3].
Table 3: Electrodiagnostic findings in Guillain– Barré syndrome[32]

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Incidence of antiganglioside antibodies in GBS has varied widely in different published series. [37],[38] Its much more common in AMAN variant than AIDP. The incidence was found to be 58% in a study of 60 patients of GBS by Meena et al (Unpublished data from NIMS, Hyderabad). Although antiganglioside antibodies have been implicated in the pathogenesis of GBS, assaying antiganglioside values in a patient with GBS other than MFS at the present time has no diagnostic value in routine practice.

Variants of Guillain-Barré syndrome

Commonly recognized variants include those with axonal forms, variants based on particular fiber-type involvement (sensory or autonomic), and MFS. Variants with regional or a markedly asymmetric distribution also occur. [1] There are also differences in abruptness of onset and time to reach nadir, which can complicate diagnosis and decisions about treatment. For example, some patients have clinical features and disease course similar to GBS except for a slower progression (ie, progression that lasts longer than 4 weeks); this disease is sometimes referred to as subacute inflammatory demyelinating polyradiculoneuropathy (SIDP); [39],[40] however, in many respects SIDP is like GBS and often should be treated as such. AMSAN and AMAN are two variants characterized by immune attack directed at axons rather than Schwann cells and myelin. [41],[42],[43],[44]

AMAN occurs in large epidemics during summer in northern China and more sporadically elsewhere. [44] It mostly affects children and young people, usually from rural areas. Onset of motor weakness is abrupt. In addition to acute pure motor paralysis, many patients have transient neck and back stiffness early in the course with resolution within day. Recovery usually begins within 3 weeks and is often complete and may take longer. Mortality rate is roughly 3%-5%. Sensory nerve conduction studies are normal and motor nerve studies are remarkable for low or absent CMAP amplitudes with normal conduction velocities. Denervating potentials are seen on needle electromyography. [6]

AMSAN shares many pathological features with acute motor axonal neuropathy but differs clinically from it in patient age of onset (usually adults rather than children), geographic distribution (can occur anywhere), time of onset (not only summertime), involvement of sensory nerves, course (protracted), and outcome (usually severe residual disability). [40],[41],[42],[43],[44] It has an abrupt onset and rapid progression with most patients requiring mechanical ventilation within a few days of symptom onset. Motor nerves are electrically inexcitable early in the disorder. Sensory nerve conduction studies are also abnormal. Widespread denervation is seen on needle examination. The course is protracted and outcome poor, with only 20% ambulating at 1 year.

MFS: The more recognizable and distinct regional variant of GBS is MFS. [1],[45],[46] Like GBS, the onset of MFS often follows an infection, for example C. jejuni. [47] MFS patients classically present with external ophthalmoparesis, areflexia, and ataxia, [2] although MFS patients often present with fewer components of the classical clinical triad [1],[46],[48],[49] or with additional clinical features (facial weakness, oropharyngeal weakness, internal ophthalmoparesis, central nervous system involvement). Bickerstaffs brainstem encephalitis (BBE) is a related syndrome in which alteration of consciousness or conticospinal tract signs are seen in addition to ophthalmoparesis and ataxia. Many patients with MFS or BBE also have "overlapping GBS" with flaccid quadriparesis. [46],[50] Anti-GQ1b antibodies are present in 95% of patients with acute MFS [51] and in approximately two-thirds of patients with BBE. The recognition of various clinical presentations and the high sensitivity and specificity of anti-GQ1b antibody testing suggest rubric name of "anti-GQ1b antibody syndrome."

Anti-GT1a antibody without anti-GQ1b reactivity is found in patients presenting with the pharyngeal-cervical-brachial (PCB) variant of GBS. [52],[53] More than half of MFS patients will have cytoalbuminological dissociation on CSF analysis performed within the first 3 weeks of disease onset. [54] In MFS, motor nerve conduction studies in the limbs are usually normal or only mildly abnormal with slight reductions in compound muscle action potential amplitudes and conduction velocities. [55] Conduction block and temporal dispersion are not a feature of MFS. Sensory nerve action potential amplitudes are usually moderately to severely reduced, more so in the upper extremity sensory nerves (eg, median) than the sural nerve. Blink reflex R1 delayed or absent. MRI of the brain frequently demonstrates cranial nerve enhancement (eg, occulomotor nerves) in MFS [56] and high-intensity abnormalities in the posterior fossa, white matter, or thalami in patients with BBE. [50] MFS is generally a benign, self-limiting conduction. Almost all treated and untreated patients return to normal activities within 6 months of disease onset, usually with resolution of ophthalmoplegia within 1-2 months and ataxia within 3-4 months. [57]

Other regional variants of GBS are those that affect other specific areas of the body, such as only the face or the afferent sensory and autonomic systems. [58]

Management

Patients with GBS who are symptomatic but are able to walk unaided for more than 5 m and who are stable can be managed conservatively at peripheral centers. However, they should be observed for progression of the disease, especially if they are still within the first week of the onset of the disease. Blood pressure and heart rate fluctuations, clinical signs of respiratory failure should be carefully and meticulously monitored. Clinical signs of ileus should be watched. If any of these signs are detected they should be immediately shifted to specialized centers for further management. In the acute phase in bed-bound adult patients require both supportive therapy and immunotherapy can be used taking into consideration the cost factors and the clinical status (staging, complications, and other comorbid conditions) of individual patients.


   Supportive Care Top


Immunotherapy therapy has not reduced the mortality in GBS. Mortality is due to disease-related issues or secondary complications developed in hospital due to prolonged disease course. Meticulous and attentive care of these patients are essential in reducing the mortality. Supportive care consensus guidelines have been published. [59]

Management of respiratory failure

GBS is the most common peripheral neuropathy causing respiratory paralysis. Despite advances in respiratory management and immunotherapy, mortality from GBS is as high as 20% for ventilated patients. Mechanical ventilation is usually required by one third of the patients. [59] Clinical signs like tachypnea, tachycardia, brow sweating asynchronous movements of chest and abdomen and a vital capacity < 20 mL/kg, maximal inspiratory pressures < 30 mm H 2 O, maximal expiratory pressure < 40 cm H 2 O predicts imminent respiratory failure. [59] Time from onset to admission of less than 1 week, facial weakness, bulbar paresis, and neck weakness are other factors associated with respiratory failure. [59],[60],[61] Simple bedside single breath count, which correlates well with vital capacity than phrenic nerve conduction studies is a good predictor of respiratory failure (Unpublished data by Meena et al from NIMS, Hyderabad). Percutaneous dilatational tracheostomy may be advantageous over traditional tracheostomy by allowing less risk of accidental extubation and a better cosmetic outcome. In general it takes 2-6 weeks to wean out of ventilatory support. [62] Tracheostomy may be performed 2 weeks following intubation and should be based on status of an individual. It is comfortable and provides airway safety but is associated at times with life-threatening complications and disfiguration. [59] If pulmonary function is improving, it may be preferable to wait 1 more week to attempt at weaning from ventilator.


   Management of Dysautonomia Top


Acute dysautonomia is a significant cause of death in patients with GBS. Cardiac and hemodynamic disturbance manifesting as hypertension, postural hypotension, and tachycardia occur in a majority of GBS patients. [69] This is due to excessive sympathetic over activity and parasympathetic under activity. Severe dysautonomia occurs usually in severe cases at the peak of the deficit. [69] Tachycardia is most common, usually in the range of 100-120/min, which does not require treatment. Approach to inserting a pacemaker for serious bradycardia or sinus arrest has varied widely because of the uncertainty that exists in anticipating such events at the bed side by different ways. However, the presence of tachycardia, increased daily variation in systolic blood pressure, reduced normal respiratory-induced heart rate variation, and first episode of severe bradyarrhythmia reduce the threshold for insertion of pacemaker. [70],[71] Endotrachial suction may provoke bradycardia or systole, and this can be reduced by hyperoxygenation. Hypertension is seen in one third of patients with GBS and can be labile or be followed by hypotension. [63],[64],[65] If hypertension is severe (mean pressure greater than approximately 125 mmHg) and sustained, specific therapy may be necessary. Antihypertensives with short half-lives (labetolol, esmolol, or nitroprusside infusions) should be considered. [65] Beta-adrenergic or calcium channel blockers should be used with caution, especially if episodes of hypertension alternate with hypotension. Hypotension can be managed by maintaining intravascular volume and avoid using diuretics. Patients with a risk of hypotension should not be left unattended in a sitting or upright position. Pronounced and persistent hypotension should warrant search for other causes, such as sepsis myocardial infarction and pulmonary thromboembolism or use of narcotics or positive pressure ventilation. Gastrointestinal motility disorders occur in 15% of severely affected GBS patients. Ileus is associated with other features of dysautonomia (tachycardia and hypertension). Dysmotility can be effectively managed by suspension of enteral feeds, nasogastric suctioning, and erythromycin or neostigmine. [59],[69]

Hyponatremia is the common electrolyte abnormality in GBS and is due to SIADH (in majority of the cases) and natriuresis. The treatment is different for both. Both require replenishment of sodium but SIADH need fluid restriction and in case of natriuresis requires intravascular volume expansion. The best way to differentiate these two conditions is by measuring central venous pressure.

Deep vein thrombosis prophylaxis

All patients should be given subcutaneous fractionated or unfractionated heparin and support stockings until they are able to walk independently to prevent deep vein thrombosis. [59] If a prolonged bedridden period is anticipated and a tracheostomy has already been performed, institute oral anticoagulant treatment with warfarin coumadin.

Pain and sensory symptoms are reported in majority of patients with GBS and should be treated effectively with opioid analogues. Sedation and bowel hypomotility may become a problem. Other drugs, such as gabapentin, carbamazepine acetaminophen, NSAIDs, and tricyclic antidepressants also can be tried.

Nutrition

Nasogastric or gastric tube feeding should be instituted early and slowly. High energy (40-45 nonprotein kcal) and high protein diet (2-2.5 g/kg) have been recommended so has to reduce muscle wasting and assist respiratory weaning. Continuous enteral feeding seems to be better tolerated than bolus feeding in these patients.

Surveillance for infections with weekly or more frequent sputum and urine cultures and blood count may be useful but the use of these tests should be guided by clinical circumstances.

Immunotherapy

Both plasma exchange and IVIg are effective immunotherapies for adult and pediatric patients with GBS if given during the first few weeks of disease.

Plasmapheresis

In a meta-analysis of 6 class II trails comparing plasma exchange (PE) to supportive care alone for adults with GBS, it was found that PE reduced the risk of developing respiratory failure. [72],[73] Patients treated with PE fared significantly better in the following secondary outcome measures: Time to recover walking without aid, percentage of patients requiring artificial ventilation, duration of ventilation, full muscle strength recovery after 1 year, and severe sequelae after 1 year. Time to onset of motor recovery in mildly affected patients was significantly shortened in the PE group. However, the cost of PE has been shown to be offset by the savings of shorter hospital stay. [74]

The volume of plasma removed and the optimum number of PE has not been established and it varies in different trials, but many physicians use the protocol of North American trial in which a total of 200-250 mL/kg was exchanged over 7-10 days all over the world. [75] There is evidence that the number of PE in GBS should be adjusted to disease severity and that also patients with mild symptoms do benefit from PE. [76]

In mild GBS, two sessions of PE are superior to none. In moderate GBS, 4 sessions are superior to 2. In severe GBS, 6 sessions are no better than 4. In line with these findings, Yuki et al reported that at least 2 PE are needed to significantly reduce the circulating immunoglobulin complexes. [77] In developing countries where cost is the limiting factor, small volume PE may be used. In India small volume PE was used by Tharakan et al with comparable results. [78] They used 15 mL/kg body weight/day to be continued till the progression of the disease got arrested or recovery started. This protocol is still performed in various centers in developing countries with good results.


   Type of Plasma Exchange Top


Continuous flow PE is superior to intermittent flow exchanges. The replacement fluids do not affect the outcome of PE according to the French Study Group. [79] Although albumin was found to be superior to fresh frozen plasma as the exchange fluid.

When to use PE? A better outcome was demonstrated with PE in French Study Group when compared with North American Study Group. [79] This is due to the fact that treatment was initiated within 2 weeks in the former study group and within 4 weeks in the latter. Hence PE is more beneficial when started within 7 days after disease onset rather than later, but was still beneficial in patients treated up to 30 days after disease onset.

Who should be offered PE? All patients with mild, moderate, and severe GBS benefit from treatment. Patients who need even minimum assistance for walking, who are steadily progressing and those who are bed- and ventilator-bound should be advised PE. The value of PE in children younger than 12 years is not known.

AAN in 2003 concluded that PE hastens recovery in nonambulant patients who get treatment within 4 weeks of onset, and PE hastens recovery of ambulant patients with GBS who are examined within 2 weeks. PE is usually administered as one plasma volume, 50 mL/kg, on 5 separate occasions over 1-2 weeks. [72]

Slightly more complications were observed in PE group than the IVIg group. Significant adverse events of PE include hypotension, septicemia, pneumonia, abnormal clotting, and hypocalcemia. Major hemostatic disorders, unstable cardiovascular state, active infection, and pregnancy are contraindications to PE.

Immunoadsorption therapy is an alternative technique to PE. This form of therapy removes Ig from the circulation without the need for replacement with albumin or FFP because of loss of albumin. Evidence says that there is no difference in outcomes between patients treated with immunoadsorption and PE or double filtration plasmapheresis. [80],[81]


   Steroids Top


In a Cochrane systematic review of 6 trials with 587 patients it has been shown that corticosteroid therapy is ineffective for treating GBS. [82]


   Intravenous Immunoglobulins Top


The first RCT on the use of IVIg was published in 1992, and showed that IVIg is as effective as PE. [83] Since the publication of these results, IVIg, in a regimen of 0·4 g/kg bodyweight daily for 5 consecutive days, has replaced PE as the preferred treatment in many centers, mainly because of its greater convenience and availability. The Cochrane review on the use of IVIg in GBS contained 4 additional trials. [84] No difference was found between IVIg and PE with respect to the improvement in disability grade after 4 weeks, the duration of mechanical ventilation, mortality, or residual disability. The combination of PE followed by IVIg was not significantly better than PE or IVIg alone. The combination of IVIg and intravenous methyl prednisolone was not more effective than IVIg alone, although there might be a short-term effect of this combined treatment when a correction is made for known prognostic factors. [85],[86]

In general in patients with renal dysfunction the rate of infusion should be decreased to half of the normal infusion rate.

Timing of treatment


Most RCTs have included only patients who are treated within the first 2 weeks from onset of weakness and who are unable to walk without assistance. If these criteria are met, there is no doubt that patients with GBS should be treated with IVIg or PE. The question remains as to what to do in patients with rapidly progressive limb weakness or impaired pulmonary function but who are still able to walk. Although not proven effective, it seems logical to treat these patients with IVIg.

Treatment of mildly affected patients

These patients are able to walk with some support or no support. A retrospective study showed that these patients often have residual disabilities. [87] RCTs that have assessed the effect of IVIg have not studied the effect in mildly affected patients. It should be kept in mind that no RCTs have assessed the effect of PE or IVIg in these mildly affected patients with GBS.

Miller Fisher syndrome

No RCTs have studied the effect of PE or IVIg in patients with MFS. [88] Observational studies have suggested that the final outcome in patients with MFS is generally good. In a large uncontrolled observational study, [89] IVIg slightly hastened the amelioration of ophthalmoplegia and ataxia. The investigators concluded that IVIg and PE did not influence the outcome of patients with MFS, presumably because of good natural recovery. Patients with mild or uncomplicated MFS may perhaps be treated conservatively. Patients with more severe or complicated anti-GQIB antibody syndrome, an overlapping GBS, should probably receive immunotherapy.

Treatment of patients who deteriorate in spite of therapy

Some patients with GBS continue to deteriorate after PE or a standard course of IVIg. In these cases, the best option is unknown. Whether these patients need PE after they have been treated with IVIg has not been investigated, but the combination of PE followed by IVIg is no better than PE or IVIg alone. PE after IVIg is also not advised, because PE would probably wash out the IVIg previously administered. A study in a small series of patients investigated the effect of a second course of IVIg in severe unresponsive patients with GBS. [90] This uncontrolled study suggested that a repeated course of IVIg could be effective. About 5%-10% of patients with GBS deteriorate after initial improvement or stabilization following IVIg treatment. [91] Although no RCTs have assessed the effect of a repeated IVIg dose in this condition, it is common practice to give a second IVIg course (2 g/kg in 2-5 days). These patients are thought to have a prolonged immune response that causes persistent nerve damage that needs treatment for a longer period of time. [92] A longer interval between onset and treatment and longer time to nadir may be associated with a greater chance of relapse.

Cost-effectiveness of PE and IVIg in GBS

When faced with restrictions in financial resources, especially in developing countries cost-effectiveness of any treatment becomes a major issue in treatment decision making. This is very true in GBS in which the currently approved treatment has shown equal efficacy. There are a few available cost analysis studies addressing this issue and the results are controversial. [93],[94] However, in developing countries use of small volume PE may bring down the cost when compared to IVIg. Hence the decision to use PE or IVIg must be based on multiple factors. The main limitations for use of PE would be availability of the technical expertise and support. Lack of these, ease of administration, and fewer side effects with IVIg may dictate use of IVIg as the first line of therapy.


   Prognosis Top


GBS has a serious long-term impact on the patients' work and private life, even 3-6 years after the onset of illness. Recovery can be slow and take years. . Persistent disability is seen in 20%-30% of adult patients but is less common in children. [2],[95] Severe fatigue is a sequel of GBS in two thirds of adult patients. In an RCT of amantidine, it was not superior to placebo. [96] Twelve weeks bicycle extensive training program had positive effects on fatigue, anxiety, depression, and functional outcome. [97]


   Conclusions Top


GBS is a monophasic immune-mediated neuropathy characterized by acute onset of predominantly motor weakness and is a common cause of respiratory paralysis. There are many variants described with different prognosis and manifestations. Electrodiagnosis aids in the diagnosis. Immunotherapy definitely makes a difference in the recovery of GBS patients and both PE and IVIg are equally effective. IVIg may be preferred because of its low side-effect profile and ease of administration. However, small volume PE can be used with equal efficacy due to cost constraints. Attentive anticipatory supportive treatment is equally important in reducing the morbidity and mortality in GBS.

 
   References Top

1.Levin KH. Variants and mimics of Guillain-Barré syndrome. Neurologist 2004;10:61-74.  Back to cited text no. 1
    
2.Chiò A, Cocito D, Leone M, Giordana MT, Mora G, Mutani R. Guillain-Barré syndrome: A prospective, population based incidence and outcome survey. Neurology 2003;60:1146-50.  Back to cited text no. 2
    
3.Hughes RA, Rees JH. Clinical and epidemiologic features of Guillain-Barré syndrome. J Infect Dis 1997;176:S92-8.  Back to cited text no. 3
    
4.Alter M. The epidemiology of Guillain-Barré syndrome. Ann Neurol 1990;27:S7-12.  Back to cited text no. 4
    
5.Willison HJ. The immunobiology of Guillain-Barré syndromes. J Peripher Nerv Syst 2005;10:94-112.  Back to cited text no. 5
    
6.McKhann GM, Cornblath DR, Griffin JW, Ho TW, Li CY, Jiang Z, et al. Acute motor axonal neuropathy: A frequent cause of acute flaccid paralysis in China. Ann Neurol 1993;33:333-42.  Back to cited text no. 6
    
7.Ogawara K, Kuwabara S, Mori M, Hattori T, Koga M, Yuki N. Axonal Guillain-Barré syndrome: Relation to antiganglioside antibodies and Campylobacter jejuni infection in Japan. Ann Neurol 2000;48:624-31.  Back to cited text no. 7
    
8.Sinha S, Prasad KN, Jain D, Pandey CM, Jha S, Pradhan S. Preceding infections and gangliosides antibodies in patients with Guillain-Barré syndrome: A single center prospective case-control study. Clin Microbial Infect 2007;13:334-7.  Back to cited text no. 8
    
9.Gupta D, Nair M, Baheti NN, Sarma PS, Kuruvilla A. Electrodiagnostic and clinical aspects of Guillain-Barré syndrome: An analysis of 142 cases. J Clin Neuromuscul Dis 2008;10:42-51.  Back to cited text no. 9
    
10.Kaur U, Chopra JS, Prabhakar S, Radhakrishnan K, Rana S. Guillain-Barré syndrome - a clinical electrophysiological and biochemical study. Acta Neurol Scand 1986;73:394-402.  Back to cited text no. 10
    
11.Alter M . The epidemiology of Guillain-Barré syndrome. Ann Neurol 1990;27:7-12.  Back to cited text no. 11
    
12.Gupta SK, Taly AB, Suresh TG, Rao S, Nagaraja D. Acute idiopathic axonal neuropathy (AIAN) - a clinical and electrophysiology observation. Acta Neurol Scand 1994;89:220-4.  Back to cited text no. 12
    
13.Jacobs BC, Rothbarth PH, van der Meché FG, Herbrink P, Schmitz PI, de Klerk MA, et al. The spectrum of antecedent infections in Guillain-Barré syndrome: A case control study. Neurology 1998;51:1110-5.  Back to cited text no. 13
    
14.Ravi V, Taly AB, Shankar SK, Shenoy PK, Desai A, Nagaraja D, et al. Association of Japanese encephalitis virus infection with Guillain-Barré syndrome in endemic areas of south-India. Acta Neurol Scand 1994;90:67-72.  Back to cited text no. 14
    
15.Green DM, Ropper AH, Mild Guillain-Barré syndrome. Arch Neurol 2001;58:1098-101.  Back to cited text no. 15
    
16.Winer JB, Hughes RA, Osmond C. A prospective study of acute idiopathic neuropathy. I. clinical features and their prognostic value. J Neurol Neurosurg Psychiatry 1988;51:605-12.  Back to cited text no. 16
    
17.Moulin DE, Hagen N, Feasby TE, Amireh R, Hahn A. Pain in Guillain-Barré syndrome. Neurology 1997;48:328-31.  Back to cited text no. 17
    
18.Ropper AH. The Guillain-Barré syndrome. N Engl J Med 1992;326:1130-6.  Back to cited text no. 18
    
19.Lawn ND, Fletcher DD, Henderson RD, Wolter TD, Wijdicks EF. Anticipating mechanical ventilation in Guillain-Barré Syndrome. Arch Neurol 2001;58:893-8.  Back to cited text no. 19
    
20.Taly AB, Arunodaya GR, Rao S. Sympathetic skin response in Guillain-Barré syndrome. Clin Auton Res 1995;5:215-20.  Back to cited text no. 20
    
21.Willison HJ. Ganglioside complexes as targets for antibodies in Miller Fisher syndrome. J Neurol Neurosurg Psychiatry 2006;77:1002-3.  Back to cited text no. 21
    
22.Sheikh KA, Nachamkin I, Ho TW, Willison HJ, Veitch J, Ung H, et al. Campylobacter jejuni lipopolysaccharides in Guillain-Barré syndrome: Molecular mimicry and host susceptibility. Neurology 1998;51:371-8.  Back to cited text no. 22
    
23.Vriesendorp FJ, Mishu B, Blaser MJ, Koski CL. Serum antibodies to GM1, GD1b, peripheral nerve myelin, and Campylobacter jejuni in patients with Guillain-Barré syndrome and controls: Correlation and prognosis. Ann Neurol 1993;34:130-5.  Back to cited text no. 23
    
24.Albers JW, Kelly JJ Jr. Acquired inflammatory demyelinating polyneuropathies: Clinical and electrodiagnostic features. Muscle Nerve 1989;12:435-51.  Back to cited text no. 24
    
25.Albers JW, Donofrio PD, McGonagle TK. Sequential electrodiagnostic abnormalities in acute inflammatory demyelinating polyradiculoneuropathy. Muscle Nerve 1985;8:528- 39.  Back to cited text no. 25
    
26.Ropper AH, Wijdicks EF, Shahani BT. Electrodiagnostic abnormalities in 113 consecutive patients with Guillain-Barré syndrome. Arch Neurol 1990;47:881-7.  Back to cited text no. 26
    
27.Gordon PH, Wilbourn AJ. Early electrodiagnostic findings in Guillain-Barré syndrome. Arch Neurol 2001;58:913-7.  Back to cited text no. 27
    
28.Durand MC, Lofaso F, Lefaucheur JP, Chevret S, Gajdos P, Raphaël JC, et al. Electrophysiology to predict mechanical ventilation in Guillain-Barré syndrome. Eur J Neurol 2003;10:39- 44.  Back to cited text no. 28
    
29.Cornblath DR, Mellits ED, Griffin JW, McKhann GM, Albers JW, Miller RG, et al. Motor conduction studies in Guillain-Barré syndrome: Description and prognostic value. Ann Neurol 1988;23:354-9 .  Back to cited text no. 29
    
30.Albers JW, Donofrio PD, McGonagle TK. Sequential electrodiagnostic abnormalities in acute inflammatory demyelinating polyradiculoneuropathy. Muscle Nerve 1985;8:528- 39.  Back to cited text no. 30
    
31.Cornblath DR. Electrophysiology in Guillain-Barré syndrome. Ann Neurol 1990;27:S17-20.  Back to cited text no. 31
    
32.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 antiglycolipid antibodies. Brain 1995;118:597-605.  Back to cited text no. 32
    
33.Meulstee J, van der Meché FG. Electrodiagnostic criteria for polyneuropathy and demyelination: Application in 135 patients with Guillain-Barré syndrome. Dutch Guillain Barré Study Group. J Neurol Neurosurg Psychiatry 1995;59:482-6.  Back to cited text no. 33
    
34.Italian Guillain Barré Study Group. The prognosis and main prognostic indicators of Guillain-Barré syndrome. Brain 1996;119:2053-61.  Back to cited text no. 34
    
35.Albers JW, Kelly JJ. Acquired inflammatory demyelinating polyneuropathies: Clinical and electrodiagnostic features. Muscle Nerve 1989;12:435-51.  Back to cited text no. 35
    
36.Kalita J, Misra UK, Das M. Neurophysiological criteria in the diagnosis of different clinical types of Guillain-Barré syndrome. J Neurol Neurosurg Psychiatry 2008;79:289-93.  Back to cited text no. 36
    
37.Ylyas AA, Willison HJ, Quarles RH, Jugalwala FB, Cornblath DR, Trapp BD, et al. Serum antibodies to gangoliosides in GB Syndrome. Ann Neurol 1988;23:440-7.  Back to cited text no. 37
    
38.Menon A, Patil AS, Taly AB, Vasanth A. Anti-Ganglioside antibodies in GB syndrome: Do they indicate prognosis. Ann Indian Acad Neurol 2003;6;11-6.  Back to cited text no. 38
    
39.Hughes R, Sanders E, Hall S, Atkinson P, Colchester A, Payan P. Subacute idiopathic demyelinating polyradiculoneuropathy. Arch Neurol 1992;49:612-6.  Back to cited text no. 39
    
40.Oh SJ, Kurokawa K, de Almeida DF, Ryan HF Jr, Claussen GC. Subacute inflammatory demyelinating polyneuropathy. Neurology 2003;61:1507-12.  Back to cited text no. 40
    
41.Feasby TE, Gilbert JJ, Brown WF, Bolton CF, Hahn AF, Koopman WF, et al. An acute axonal form of Guillain-Barré polyneuropathy. Brain 1986;109:1115-26.  Back to cited text no. 41
    
42.Feasby TE, Hahn AF, Brown WF, Bolton CF, Gilbert JJ, Koopman WJ. Severe axonal degeneration in acute Guillain-Barré syndrome: Evidence of two different mechanisms? J Neurol Sci 1993;116:185-92.  Back to cited text no. 42
    
43.Griffin JW, Li CY, Ho TW, Tian M, Gao CY, Xue P, et al. Pathology of the motor-sensory axonal Guillain-Barré syndrome. Ann Neurol 1996;39:17-28.  Back to cited text no. 43
    
44.Griffin JW, Li CY, Macko C, Ho TW, Hsieh ST, Xue P, et al. Early nodal changes in the acute motor axonal neuropathy pattern of the Guillain-Barré syndrome. J Neurocytol 1996;25:33-51.  Back to cited text no. 44
    
45.Fisher M. An unusual variant of acute idiopathic polyneuritis (syndrome of opthalmoplegia, ataxia and areflexia). N Engl J Med 1956;255:57-65.  Back to cited text no. 45
    
46.Overell JR, Willison HJ. Recent developments in Miller Fisher syndrome and related disorders. Curr Opin Neurol 2005;18:562-6.  Back to cited text no. 46
    
47.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;36:791-3.  Back to cited text no. 47
    
48.Ogawara K, Kuwabara S, Yuki N. Fisher syndrome or Bickerstaff brainstem encephalitis? Anti-GQ1b IgG anti-body syndrome involving both the peripheral and central nervous systems. Muscle Nerve 2002;26:845-9.  Back to cited text no. 48
    
49.Radziwill AJ, Steck AJ, Borruat FX, Bogousslavsky J. Isolated internal opthalmoplegia associated with IgG anti-GQ1b antibody. Neurology 1998;50:307.  Back to cited text no. 49
    
50.Odaka M, Yuki N, Yamada M, Koga M, Takemi T, Hirata K, et al. Bickerstaff's brainstem encephalitis: Clinical features of 62 cases and a subgroup associated with Guillain-Barré syndrome. Brain 2003;126:2279-90.  Back to cited text no. 50
    
51.Chiba A, Kusunoki S, Obata H, Machinami R, Kanazawa I. Serum anti-gq1b IgG antibody is associated with ophthalmoplegia in Miller Fisher syndrome and Guillain-Barré syndrome: Clinical and immunohistochemical studies. Neurology 1993;43:1911-7.  Back to cited text no. 51
    
52.Kashihara K, Shiro Y, Koga M, Yuki N. IgG anti-GT1a antibodies which do not cross react with GQ1b ganglioside in a pharyngeal-cervical-brachial variant of Guillain-Barré syndrome. J Neurol Neurosurg Psychiatry 1998;65:799.  Back to cited text no. 52
    
53.Nagashima T, Koga M, Odaka M, Hirata K, Yuki N. Clinical correlates of serum anti-GT1A IgG antibodies. J Neurol Sci 2004;219:139-45.  Back to cited text no. 53
    
54.Nishimoto Y, Odaka M, Hirata K, Yuki N. Usefulness of anti-GQ1b IgG antibody testing in Fisher syndrome compared with cerebrospinal fluid examination. J Neuroimmunol 2004;148:200-5.  Back to cited text no. 54
    
55.Fross RD, Daube JR. Neuropathy in the Miller Fisher syndrome: Clinical and electrophysiologic findings. Neurology 1987;37:1493- 8.  Back to cited text no. 55
    
56.Nagaoka U, Kato T, Kurita K, Arawaka S, Hosoya T, Yuki N, et al. Cranial nerve enhancement on three-dimensional MRI in Miller Fisher syndrome. Neurology 1996;47:1601-2.  Back to cited text no. 56
    
57.Mori M, Kuwabara S, Fukutake T, Yuki N, Hattori T. Clinical features and prognosis of Miller Fisher syndrome. Neurology 2001;56:1104-6.  Back to cited text no. 57
    
58.Willison HJ. Ganglioside complexes as targets for antibodies in Miller Fisher syndrome. J Neurol Neurosurg Psychiatry 2006;77:1002-3.  Back to cited text no. 58
    
59.Hughes RA, Wijdicks EF, Benson E, Cornblath DR, Hahn AF, Meythaler JM, et al. Supportive care for patients with Guillain-Barré syndrome: Multidisciplinary Consensus Group. Arch Neurol 2005;62:1194-8.  Back to cited text no. 59
    
60.Durand MC, Porcher R, Orlikowski D, Aboab J, Devaux C, Clair B, et al. Clinical and electrophysiological predictors of respiratory failure in Guillain-Barré syndrome: A prospective study. Lancet Neurol 2006;5:1021-8.  Back to cited text no. 60
    
61.Sharshar T, Chevret S, Bourdain F, Raphael JC. French Cooperative Group on Plasma Exchange in Guillain-Barré syndrome. Early predictors of mechanical ventilation in Guillain-Barré syndrome. Crit Care Med 2003;31:278-83.  Back to cited text no. 61
    
62.Lawn ND, Wijdicks EF. Post-intubation pulmonary function test in Guillain-Barré syndrome. Muscle Nerve 2000;23:613-6.  Back to cited text no. 62
    
63.Lichtenfeld P. Autonomic dysfunction in the Guillain-Barré syndrome. Am J Med 1971;50:772-80.  Back to cited text no. 63
    
64.Zochodne DW. Autonomic involvement in Guillain-Barré syndrome: A review. Muscle Nerve 1994;17:1145-55.  Back to cited text no. 64
    
65.Truax BT. Autonomic disturbances in the Guillain-Barré syndrome. Semin Neurol 1984;4:462-8.  Back to cited text no. 65
    
66.Tuck RR, McLeod JG. Autonomic dysfunction in Guillain-Barré syndrome. J Neurol Psychiatry 1981;44:983-90.  Back to cited text no. 66
    
67.Flachenecker P, Hartung HP, Reiners K. Power spectrum analysis of heart rate variability in Guillain-Barré syndrome. A longitudinal study. Brain 1997;120:1885-94.  Back to cited text no. 67
    
68.Flachenecker P, Wermuth P, Hartung HP, Reiners K. Quantitative assessment of cardiovascular autonomic function in Guillain-Barré syndrome. Ann Neurol 1997:42:171-9.  Back to cited text no. 68
    
69.Burns TM, Lawn ND, Low PA, Camilleri M, Wijdicks EF. Adynamic Ileus in severe Guillain-Barré syndrome. Muscle Nerve 2001;24:963-5.  Back to cited text no. 69
    
70.Emmons PR, Blume WT, DuShane JW. Cardiac monitoring and demand pacemaker in Guillain-Barré syndrome. Arch Neurol 1975;32:59-61.  Back to cited text no. 70
    
71.Favre H, Foex P, Guggisberg M. Use of demand pacemaker in a case of Guillain-Barré syndrome. Lancet 1970;1:1062-3.  Back to cited text no. 71
    
72.Hughes RA, Wijdicks EF, Barohn R, Benson E, Cornblath DR, Hahn AF, et al. Practice parameter: Immunotherapy for Guillain-Barré syndrome: Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2003;61:736-40.  Back to cited text no. 72
    
73.Raphaël JC, Chevret S, Hughes RA, Annane D. Plasma exchange for Guillain-Barré syndrome. Cochrane Database Syst Rev. 2001;2:CD001798.   Back to cited text no. 73
    
74.Espérou H, Jars-Guincestre MC, Bolgert F, Raphaël JC, Durand-Zaleski I. Cost analysis of plasma-exchange therapy for the treatment of Guillain-Barré syndrome. French Cooperative Group on Plasma Exchange in Guillain-Barré Syndrome. Intensive Care Med 2000;26:1094-100.  Back to cited text no. 74
    
75.Plasmapheresis and acute Guillain-Barré syndrome. The Guillain-Barré Syndrome Study Group. Neurology 1985;35:1096-104.  Back to cited text no. 75
    
76.French Cooperative Group on Plasma Exchange in Guillain-Barré syndrome. Appropriate number of plasma exchanges in Guillain-Barré syndrome. Ann Neurol 1997;41:298-306.  Back to cited text no. 76
    
77.Yuki N, Tagawa Y, Hirata K. Minimal number of plasma exchanges needed to reduce immunoglobulin in Guillain-Barré syndrome. Neurology 1998;51:875-7.  Back to cited text no. 77
    
78.Tharakan J, Jayaprakash PA, Iyer VP. Small volume plasma exchange in Guillain-Barré syndrome: Experience in 25 patients. J Assoc Physicians India 1990;38:550-3.  Back to cited text no. 78
    
79.Efficacy of plasma exchange in Guillain-Barré syndrome: Role of replacement fluids. French Cooperative Group on Plasma Exchange in Guillain-Barré syndrome. Ann Neurol 1987;22:753- 61.  Back to cited text no. 79
    
80.Okamiya S, Ogino M, Ogino Y, Irie S, Kanazawa N, Saito T, et al. Tryptophanimmobilized column-based immunoadsorption as the choice method for plasmapheresis in Guillain-Barré syndrome. Ther Apher Dial 2004;8:248-53.  Back to cited text no. 80
    
81.Haupt WF, Rosenow F, van der Ven C, Borberg H, Pawlik G. Sequential treatment of Guillain-Barré syndrome with extracorporeal elimination and intravenous immunoglobulin. J Neurol Sci 1996;137:145-9.  Back to cited text no. 81
    
82.Hughes RA, Swan AV, van Koningsveld R, van Doorn PA. Corticosteroids for Guillain-Barré syndrome. Cochrane Database Syst Rev 2006;2:CD001446.  Back to cited text no. 82
    
83.van der Meché FG, Schmitz PI. A randomized trial comparing intravenous immune globulin and plasma exchange in Guillain-Barré syndrome. Dutch Guillain-Barré Study Group. N Engl J Med 1992;326:1123-9.  Back to cited text no. 83
    
84.Hughes RA, Raphael JC, Swan AV, van Doorn PA. Intravenous immunoglobulin for Guillain-Barré syndrome. Cochrane Database Syst Rev 2006;1:CD002063.  Back to cited text no. 84
    
85.Susuki K, Yuki N. Effect of methylprednisolone in patients with Guillain-Barré syndrome. Lancet 2004;363:1236-7.  Back to cited text no. 85
    
86.van Koningsveld R, Schmitz PI, van der Meche FG, Visser LH, Meulstee J, van Doorn PA. Effect of methylprednisolone when added to standard treatment with intravenous immunoglobulin for Guillain-Barré syndrome: Randomised trial. Lancet 2004;363:192- 6.  Back to cited text no. 86
    
87.Van Koningsveld R, Schmitz PI, Ang CW, Groen J, Osterhaus AD, Van der Meché FG, et al. Infections and course of disease in mild forms of Guillain-Barré syndrome. Neurology 2002;58:610-4.  Back to cited text no. 87
    
88.Overell JR, Hsieh ST, Odaka M, Yuki N, Willison HJ. Treatment for Fisher syndrome, Bickerstaff 's brainstem encephalitis and related disorders. Cochrane Database Syst Rev 2007;1:CD004761.  Back to cited text no. 88
    
89.Mori M, Kuwabara S, Fukutake T, Hattori T. Intravenous immunoglobulin therapy for Miller Fisher syndrome. Neurology 2007;68:1144-6.  Back to cited text no. 89
    
90.Farcas P, Avnun L, Frisher S, Herishanu YO, Wirguin I. Efficacy of repeated intravenous immunoglobulin in severe unresponsive Guillain-Barré syndrome. Lancet 1997;350:1747.  Back to cited text no. 90
    
91.van Koningsveld R, Steyerberg EW, Hughes RA, Swan AV, van Doorn PA, Jacobs BC. A clinical prognostic scoring system for Guillain-Barré syndrome. Lancet Neurol 2007;6:589-94.  Back to cited text no. 91
    
92.Visser LH, van der Meché FG, Meulstee J, van Doorn PA. Risk factors for treatment related clinical fluctuations in Guillain-Barré syndrome. Dutch Guillain-Barré Study Group. J Neurol Neurosurg Psychiatry 1998;64:242-4.  Back to cited text no. 92
    
93.Nagpal S, Benstead T, Shumak K, Rock G, Brown M, Anderson DR. Treatment of Guillain-Barré syndrome: A cost -effectiveness analysis. J Clin Apher 1999;14:107-13.  Back to cited text no. 93
    
94.Tsai CP, Wang KC, Liu CY, Sheng WY, Lee TC. Pharmacoeconomics of therapy for Guillain-Barré syndrome: Plasma exchange and intravenous immunoglobulin. J Clin Neurosci 2007;14:625-9.  Back to cited text no. 94
    
95.Bradshaw DY, Jones HR Jr. Guillain-Barré syndrome in children: Clinical course, electrodiagnosis, and prognosis. Muscle Nerve 1992;15:500-6.   Back to cited text no. 95
    
96.Garssen MP, Schmitz PI, Merkies IS, Jacobs BC, van der Meché FG, van Doorn PA. Amantadine for treatment of fatigue in Guillain-Barré syndrome: A randomised, double blind, placebo controlled, crossover trial. J Neurol Neurosurg Psychiatry 2006;77:61-5.  Back to cited text no. 96
    
97.Garssen MP, Bussmann JB, Schmitz PI, Zandbergen A, Welter TG, Merkies IS, et al. Physical training and fatigue, fitness, and quality of life in Guillain-Barré syndrome and CIDP. Neurology 2004;63:2393-5.  Back to cited text no. 97
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]


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   Introduction
   Epidemiology
   Clinical Features
   Pathogenesis
   Diagnosis
   Electrodiagnosis
   Supportive Care
    Management of Dy...
    Type of Plasma E...
   Steroids
    Intravenous Immu...
   Prognosis
   Conclusions
    References
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