NEUROLOGICAL REVIEW

SECTION EDITOR: DAVID E. PLEASURE, MD

Supportive Care for Patients With

Guillain-Barré Syndrome
Richard A. C. Hughes, MD; Eelco F. M. Wijdicks, MD; Estelle Benson; David R. Cornblath, MD; Angelika F. Hahn, MD;
Jay M. Meythaler, MD; John T. Sladky, MD; Richard J. Barohn, MD; James C. Stevens, MD

A
multidisciplinary consensus group searched MEDLINE from 1966 to May 2003, ex-
tracted relevant references, and prepared recommendations on supportive care for Guil-
lain-Barré syndrome. In the absence of randomized controlled trials, we agreed on rec-
ommendations by consensus based on observational studies and expert opinion. In
the acute phase in bed-bound adult patients, the group recommended the use of heparin and gradu-
ated pressure stockings to prevent deep vein thrombosis, monitoring for blood pressure, pulse,
autonomic disturbances, and respiratory failure, and the timely institution of artificial ventilation
and tracheostomy. Pain management is difficult, but carbamazepine or gabapentin may help. The
cautious use of narcotic analgesics may be needed. Disabled patients should be treated by a mul-
tidisciplinary rehabilitation team and should receive an assistive exercise program. Persistent fa-
tigue following Guillain-Barré syndrome is common and may be helped by an exercise program.
Because of a very small and possibly only theoretical increase in the risk of recurrence following
immunization, the need for immunization should be reviewed on an individual basis. More re-
search is needed to identify optimal methods for all aspects of supportive care.
Arch Neurol. 2005;62:1194-1198
A recent practice parameter recom- 15% of patients with GBS die from this syn-
mended either intravenous immunoglob- drome2-6 and nearly 20% have a persistent
ulin or plasma exchange, but not cortico- disability.5 Death from GBS occurs mostly
steroids, as appropriate treatments for adults in mechanically ventilated patients. Sup-
and probably children with severe Guillain- portive care remains the mainstay of treat-
Barré syndrome (GBS) within 2 weeks from ment, but the evidence for the methods of
onset.1 Most patients in the trials of these supportive care is inadequate and consen-
treatments have had the demyelinating form sus guidelines for treatment have not been
of the disease, and the benefits of treat- published.
ment in uncommon subgroups, such as
those with axonal disease, cannot be dis- EVIDENCE REVIEW
tinguished. Despite immunotherapy, 4% to
The consensus group of 6 neurologists with
Author Affiliations: Department of Clinical Neuroscience, King’s College, London, a special interest in GBS, 1 physical medi-
England (Dr Hughes); Department of Neurology, Mayo Clinic, Rochester, Minn cine specialist, 1 evidence-based medicine
(Dr Wijdicks); Guillain-Barré Syndrome Foundation International, Wynnewood, specialist, and 1 patient advocate met and
Pa (Mrs Benson); Department of Neurology, Johns Hopkins University School of decided which questions to review.
Medicine, Baltimore, Md (Dr Cornblath); London Health Sciences Center, London, We searched MEDLINE from 1966 on-
Canada (Dr Hahn); Department of Physical Medicine and Rehabilitation, ward (last search in May 2003) for articles
University of Alabama, Birmingham (Dr Meythaler); Division of Neurology, Emory
including the term polyradiculoneuritis, lim-
University School of Medicine, Atlanta, Ga (Dr Sladky); Department of Neurology,
University of Kansas Medical Center, Kansas City (Dr Barohn); and Fort Wayne ited by human and cross-referenced with the
Neurological Center, Fort Wayne, Ind (Dr Stevens). terms therapy, pain, nutrition, diet, pulmo-
Financial Disclosure: Dr Cornblath has consulted for Pfizer Inc, who makes nary ventilation, tracheostomy, artificial res-
Neurontin (gabapentin), and Ortho-McNeil Pharmaceutical Inc, who makes Ultram piration, autonomic nervous system, dysau-
(tramadol). tonomia, arrhythmia, neurogenic bladder,

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urinary incontinence, urination disorders, constipation, physi- by GBS until they have discontinued the ventilatory sup-
cal therapy, occupational therapy, palliative care, support- port and have had their tracheostomy removed or until
ive care, thrombophlebitis, immunization, and recurrence. they have begun to recover without needing either in-
We also searched the Cochrane Library register of ran- tervention. The evidence concerning the method and set-
domized trials (issue 3, 2003) with Guillain-Barré syn- ting of monitoring is insufficient to make specific rec-
drome as the search term. Two members of the group pre- ommendations.
pared draft statements and recommendations that were
circulated through the entire group repeatedly until con- RESPIRATORY MONITORING
sensus was achieved. Our recommendations are, there- AND AIRWAY PROTECTION
fore, consensus statements based on observational stud-
ies of GBS, inferences from randomized controlled trials
Neuromuscular respiratory function becomes compro-
in other conditions, and expert opinion.
mised in 17% to 30% of patients with GBS.6,16,18-21 In some
patients, bulbar dysfunction causes difficulty with clear-
PROPHYLAXIS FOR DEEP VEIN THROMBOSIS
ing secretions, compromising gas exchange and increas-
ing the risk of aspiration.22-24 Clinical features that indi-
Immobilization owing to GBS is a risk factor for the de-
cate fatigue of respiratory muscles are tachypnea, sweating,
velopment of deep vein thrombosis (DVT).7 Time to de-
tachycardia, asynchronous movements of the chest and
veloping DVT or pulmonary embolus varies from 4 to
abdomen, and episodic use of accessory muscles of res-
67 days after onset.7,8 Children have a very low inci-
piration. In 1 case series,22 rapid disease progression, pres-
dence of DVT.9 There is a lack of clinical studies that ad-
ence of bilateral facial palsy, and autonomic dysfunc-
dress methods of prophylaxis against thrombosis in GBS,
tion increased the likelihood of intubation. A study of
duration of prophylaxis, or monitoring of patients at risk
722 patients, of whom 313 required ventilation, identi-
for thrombosis. Observational studies in orthopedic or
fied 6 predictors of the need for ventilation in a multi-
general surgery patients suggest a benefit from subcuta-
variate analysis: time from onset to admission being less
neous heparin (5000 U, 12-hourly) in preventing DVT.9
than 7 days, inability to cough, inability to stand, inabil-
In acutely ill medical patients, prophylactic treatment with
ity to flex the arms or head, and liver enzyme level in-
subcutaneous enoxaparin (40 mg daily) reduced the in-
creases.25 In 196 of the patients with available vital ca-
cidence of DVT from 15% in the placebo group to ap-
pacity measurements, predictors were time from onset
proximately 5% in the treated patients.10 In a recent meta-
to admission being less than 7 days, inability to lift the
analysis, support stockings reduced the risk by almost
head, and vital capacity of less than 60% of that which
70% in patients at moderate risk for development of post-
was predicted. In many patients, a vital capacity (mea-
operative thromboembolism.11
sured volume with forceful exhalation after maximal in-
halation) below 20 mL/kg, a PImax (maximum inspira-
RECOMMENDATION
tory pressure generated after maximal sucking in through
a mouth piece while occluding the nose) of less than 30
Subcutaneous unfractionated or fractionated heparin
cm H2O or a PEmax (maximum expiratory pressure gen-
and support stockings are recommended for nonam-
erated on maximal blowing out) of less than 40 cm H2O
bulant adult patients until they become able to walk
warns of imminent respiratory arrest.26-28 Rapid decline
independently.
in vital capacity (eg, 50% from baseline) may further in-
dicate impending respiratory failure, but this finding needs
CARDIAC AND HEMODYNAMIC MONITORING
confirmation.26,27 Patients with pulmonary infiltrates or
atelectasis generally require intubation and mechanical
Serious and potentially fatal disturbances of autonomic func-
ventilation. Hypoxemia is also an indicator of neuro-
tion, including arrhythmias and extreme hypertension or
muscular respiratory failure. Hypercarbia appears later.21
hypotension, occur in approximately 20% of patients with
Thus, respiratory failure in GBS is common and life threat-
GBS.12,13 Severe bradycardia may be preceded by wide
ening. Emerging diaphragmatic failure can be detected
swings, exceeding 85 mm Hg, of systolic blood pressure
by serial clinical observation or respiratory function tests.
from day to day.14 Bradycardia may be so severe as to cause
Patients who require ventilation are at high risk of suf-
asystole, which may require a cardiac pacemaker.12 Endo-
fering major complications including pneumonia, sep-
tracheal suction or pharmaceutical agents may provoke these
sis, gastrointestinal tract bleeding, pulmonary embolus,
changes.14,15 Other significant autonomic disturbances in
and others. In a series of 114 patients, 60% admitted to
GBS are adynamic ileus, hyponatremia, and deficiencies in
an intensive care unit had major complications in 1 of
bronchial mucosal function. Most, but not all, dysauto-
these categories.29
nomic complications occur among patients with ad-
vanced generalized weakness and respiratory failure.16 In
1 prospective study,17 a reduction in beat-to-beat varia- RECOMMENDATION
tion in heart rate predicted subsequent dysautonomia.
Respiratory function should be monitored in patients with
RECOMMENDATION GBS, but there is insufficient evidence to recommend spe-
cific methods. Weaning from the ventilator should be
Monitoring of pulse and blood pressure is recom- guided by improvement in strength and serial pulmo-
mended in patients who are becoming severely affected nary function tests.

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 TIMING AND METHOD OF TRACHEOSTOMY
The mean duration of ventilation in various treatment trials
has ranged between 15 and 43 days, suggesting that a pro-
portion of patients can be spared from receiving a trache-
ostomy.28,30-32 Early tracheostomy increases patient com-
fort and airway safety and may help weaning. On the other
hand, surgical tracheostomy results in permanent disfig-
urement and has sometimes been associated with life-
threatening hemorrhage, infection, accidental dislodge-
ment of the tube, fatal procedure-related necrotizing
mediastinitis, chyle fistula due to a thoracic duct perfora-
tion, and a cosmetically unacceptable, hypertrophic ke-
loid tracheostomy scar. More recently, percutaneous di-
latational tracheostomy has been introduced, but this
technique has not been compared with traditional trache-
ostomy in GBS. In a randomized trial in patients selected
for elective tracheostomy, percutaneous dilatational tra-
cheostomy was superior.33 The procedure involves a small
skin incision and then insertion of a cannula into the tra-
chea, followed by dilators of gradually increasing size un-
til the desired tracheostomy tube can be accommodated.
Percutaneous tracheostomy may reduce the risk of acci-
dental extubation owing to the fact that it fits more snugly
around the stoma. A better cosmetic outcome may result
from a smaller skin incision.34-36
A newly introduced pulmonary function ratio has been
used to predict the need for tracheostomy.37 Daily vital
capacity and maximal inspiratory and expiratory pres-
sures were summed to create an integrated pulmonary
function score. A pulmonary function ratio was calcu-
lated, which represents the pulmonary function score at
day 12 after intubation divided by the pulmonary func-
tion score at the day of intubation. This study found that
at day 12 with a pulmonary function ratio of less than 1,
it is highly unlikely that patients will be weaned from the
ventilator within 3 weeks and tracheostomy should be
performed. The sensitivity of a pulmonary function ra-
tio of less than 1 for predicting that the duration of ven-
tilation would be more than 3 weeks was 70%, and the
specificity and positive predictive value were 100%.
RECOMMENDATION
The decision to place a tracheostomy may be postponed
for 2 weeks. If after 2 weeks the pulmonary function tests
do not show any significant improvement from baseline,
tracheostomy should be performed. If the pulmonary func-
tion test tends to improve above baseline, tracheostomy
could be deferred for an additional week, allowing the pa-
tient to attempt to be weaned from the ventilator. Percu-
taneous tracheostomy may be preferred in centers with
adequate experience in using the technique.
PAIN MANAGEMENT
Retrospective observational analyses of GBS case series
have documented pain as an early symptom, with an in-
cidence ranging from 33% to 71%.38-43 One study exam-
ined incidence and intensity of pain prospectively and
quantified the response to medical pain intervention.41
Pain was reported by 89% of the patients and was severe
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in half. First-line drugs that were used were acetamino-
phen and nonsteroidal anti-inflammatory drugs. How-
ever, 75% of the patients additionally required oral or par-
enteral opioids and 30% of the patients were treated with
intravenous morphine infusions (range, 1-7 mg/h). Ten
percent of the patients received tricyclic antidepres-
sants and a further 10% received carbamazepine as ad-
juvant treatments for neuropathic pain during the later
course of the illness. In a randomized, double-blind, cross-
over trial involving 18 participants, gabapentin (15 mg/kg
daily) or placebo was given by a nasogastric tube for 7
days before switching to the alternate treatment.44 There
was prompt substantial and significant relief of pain and
reduction in the need for rescue medication. In a similar
study45 of 12 patients, greater pain relief was obtained
from carbamazepine (300 mg daily for 3 days) than from
placebo. Excellent relief of intractable and severe pain
by epidural infusions of morphine (1- to 4-mg morphine
bolus injections every 8-24 hours) has been reported in
a single case study.46 Opioid analgesics may aggravate au-
tonomic gut dysmotility and bladder distention.47,48
RECOMMENDATION
Simple analgesics or nonsteroidal anti-inflammatory drugs
may be tried but often do not provide adequate pain re-
lief. Single small randomized controlled trials support the
use of gabapentin or carbamazepine in the intensive care
unit for the treatment of pain in the acute phase of GBS.
Appropriate narcotic analgesics may be used but re-
quire careful monitoring of adverse effects in the setting
of autonomic denervation. Adjuvant therapy with tricy-
clic antidepressant medication, tramadol, gabapentin, car-
bamazepine, or mexilitene may aid in the long-term man-
agement of neuropathic pain.
MANAGEMENT OF BLADDER
AND BOWEL DYSFUNCTION
Constipation occurs frequently in bed-bound patients.
Approximately half of the patients develop adynamic il-
eus in the acute phase, often but not invariably in con-
junction with other features of dysautonomia.47 In other
instances, the risk is increased by long-term immobili-
zation, incremental doses of opiates for pain control, or
preexisting causes such as prior abdominal procedures.
Bladder function has only been studied infrequently
in the acute phase of GBS, partly because most patients
are catheterized as part of their general nursing care to
maintain bodily hygiene and to avoid bladder disten-
tion. Voiding is more frequently compromised with axo-
nal types of GBS. Urodynamic studies have documented
bladder areflexia and disturbed bladder sensation.49
RECOMMENDATION
Daily abdominal auscultation for development of gut si-
lence and monitoring of opioid administration are rec-
ommended. In addition to suspension of gut-feeding na-
sogastric and rectal tubes, erythromycin or neostigmine
may be effective in treating adynamic ileus.50 Promotil-
ity agents are contraindicated in patients with dysauto-
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nomia. Bladder catheterization is often needed as part of
the intensive care of severely affected patients. A sterile,
closed urinary drainage system should be used with avoid-
ance of breaking the seal to obtain urinary samples and
irrigation of the bladder.
REHABILITATION
Although most patients with GBS need rehabilitation, there
are no long-term rehabilitation outcome studies or com-
parisons of different methods.51 In neuromuscular dis-
ease, overfatiguing the affected motor unit in therapy may
impede recovery and cause paradoxical weakening.52,53 At-
tention needs to be paid to many details that cannot be
summarized briefly. There is a danger of muscle shorten-
ing and joint contractures.51 Prolonged immobilization
leads to a reduction of blood volume and increased epi-
sodes of postural hypotension.54 For some immobilized pa-
tients, a tilt table has been useful.51 Weight loss and sig-
nificant sensory loss make patients susceptible to peripheral
nerve compression and the development of decubitus ul-
cers, requiring proper bed positioning with frequent pos-
tural changes.51 In patients noted to have immobilization
hypercalcemia, early mobilization was correlated with a
therapeutic drop in the serum calcium levels.55 In the acute
stage, patients lose weight. During recovery, they regain
weight owing to reduced activity levels.55,56
RECOMMENDATION
Treatment in the acute phase should include an indi-
vidual program of gentle strengthening involving iso-
metric, isotonic, isokinetic, and manual resistive and pro-
gressive resistive exercises. Rehabilitation should be
focused on proper limb positioning, posture, orthotics,
and nutrition.
MANAGEMENT OF FATIGUE
A large proportion of patients with GBS remain seriously
affected in their psychosocial functioning even when their
physical recovery was complete or when they were left with
only mild residual signs.57,58 Severe fatigue persists in 80%
of patients and is unrelated to age, duration, or severity of
the initial illness.59 Frequency and severity of fatigue in GBS
were comparable with that encountered in other immune-
mediated neuropathies.59,60 The cause and contributing fac-
tors are not fully known, but fatigue appears in part to be
a sequel of forced inactivity and general muscle decondi-
tioning. Both fatigue and functional abilities were measur-
ably improved with a supervised exercise program in 2 single
case studies.52,61 Pharmacological approaches are being
evaluated.62,63
RECOMMENDATION
An exercise program may be beneficial for persistent
fatigue.
FUTURE IMMUNIZATIONS
Recurrence of GBS after immunization is rare.64 In re-
sponse to a questionnaire, 11 (3.5%) of 311 patients re-
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ported recurrent symptoms within 6 weeks after immu-
nization, but it was possible to deduce with 95% confidence
that the chance of developing GBS severe enough to re-
quire hospital admission was less than 1.2%.65 In 2 pre-
viously reported cases, recurrence occurred following swine
influenza vaccine.66 Recurrent attacks of chronic inflam-
matory demyelinating polyradiculoneuropathy have fol-
lowed tetanus toxoid immunization.67,68
RECOMMENDATION
Immunizations are not recommended during the acute
phase of GBS and probably not during a period, possi-
bly of 1 year, after the onset of the disease. After that,
immunizations need not be withheld, but the need for
the immunization should be reviewed on an individual
basis. If GBS occurs within 6 weeks after a particular im-
munization, consideration should be given to avoiding
that immunization in that individual in the future.
CONCLUSION
This review has highlighted the need for more research
into all aspects of supportive care for GBS.
Accepted for Publication: June 15, 2004.
Correspondence: Richard A. C. Hughes, MD, Depart-
ment of Clinical Neuroscience, King’s College, Guy’s Hos-
pital, London SE1 1UL, England (richard.a.hughes@kcl
.ac.uk).
Author Contributions: Study concept and design: Hughes,
Wijdicks, Benson, Cornblath, Hahn, Barohn, and Stevens.
Acquisition of data: Hughes, Wijdicks, Hahn, Meythaler,
Sladky, and Stevens. Analysis and interpretation of data:
Hughes, Wijdicks, Cornblath, Hahn, Meythaler, and
Stevens. Drafting of the manuscript: Hughes, Wijdicks,
Cornblath, Meythaler, and Sladky. Critical revision of the
manuscript for important intellectual content: Hughes,
Wijdicks, Benson, Cornblath, Hahn, Meythaler, Barohn, and
Stevens. Statistical analysis: Stevens. Administrative, tech-
nical, and material support: Hughes, Wijdicks, Benson, and
Stevens. Study supervision: Hughes and Wijdicks.
Disclaimer: Our recommendations must be interpreted
in relation to the needs of the individual patient and the
capacity of the individual institution.
REFERENCES
1. Hughes RAC, Wijdicks E, Barohn RJ, et al. Practice parameter: immunotherapy
for Guillain-Barré syndrome: report of the Quality Standards Subcommittee of
the American Academy of Neurology. Neurology. 2003;61:736-740.
2. Prevots DR, Sutter RW. Assessment of Guillain-Barré syndrome mortality and
morbidity in the United States: implications for acute flaccid paralysis surveillance.
J Infect Dis. 1997;175(suppl 1):S151-S155.
3. Raphael JC, Masson C, Morice V, Bronel D, Goulon M. Le syndrome de Guillain-
Barré: étude retrospective de 233 observations. Sem Hop Paris. 1984;60:2543-
2546.
4. Rees JH, Thompson RD, Smeeton NC, Hughes RAC. An epidemiological study
of Guillain-Barré syndrome in South East England. J Neurol Neurosurg Psychiatry.
1998;64:74-77.
5. Italian Guillain-Barré Study Group. The prognosis and main prognostic indica-
tors of Guillain-Barré syndrome: a multicentre prospective study of 297 patients.
Brain. 1996;119:2053-2061.
6. Chio A, Cocito D, Leone M, Giordana MT, Mora G, Mutani R. Guillain-Barré syn-
WWW.ARCHNEUROL.COM
 drome: a prospective, population-based incidence and outcome survey. Neurology.
2003;60:1146-1150.
7. Lawn ND, Wijdicks EF. Fatal Guillain-Barré syndrome. Neurology. 1999;52:635-
638.
8. Legere BM, Dweik RA, Arroliga AC. Venous thromboembolism in the intensive
care unit. Clin Chest Med. 1999;20:367-384.
9. Collins R, Scrimgeour A, Yusuf S, Peto R. Reduction in fatal pulmonary embo-
lism and venous thrombosis by perioperative administration of subcutaneous
heparin: overview of results of randomized trials in general, orthopedic, and uro-
logic surgery. N Engl J Med. 1988;318:1162-1173.
10. Samama MM, Cohen AT, Darmon JY, et al. A comparison of enoxaparin with
placebo for the prevention of venous thromboembolism in acutely ill medical
patients. N Engl J Med. 1999;341:793-800.
11. Clagett GP, Reisch JS. Prevention of venous thromboembolism in general sur-
gical patients: results of meta-analysis. Ann Surg. 1988;208:227-240.
12. Hughes RAC. Guillain-Barré Syndrome. Heidelberg, Germany: Springer-Verlag;
1990.
13. Ropper AH, Wijdicks EFM, Truax BT. Guillain-Barré Syndrome. Philadelphia, Pa:
FA Davis Co; 1991.
14. Pfeiffer G, Schiller B, Kruse J, Netzer J. Indicators of dysautonomia in severe
Guillain-Barré syndrome. J Neurol. 1999;246:1015-1022.
15. Hughes RAC, Bihari D. Acute neuromuscular respiratory paralysis. J Neurol Neu-
rosurg Psychiatry. 1993;56:334-343.
16. Ng KKP, Howard RS, Fish DR, et al. Management and outcome of severe Guillain-
Barré syndrome. QJM. 1995;88:243-250.
17. Flachenecker P, Hartung HP, Reiners K. Power spectrum analysis of heart rate
variability in Guillain-Barré syndrome: a longitudinal study. Brain. 1997;120:
1885-1894.
18. Gracey DR, McMichan JC, Divertie MB, Howard FM Jr. Respiratory failure in Guillain-
Barré syndrome: a 6-year experience. Mayo Clin Proc. 1982;57:742-746.
19. Massam M, Jones RS. Ventilatory failure in the Guillain-Barré syndrome. Thorax.
1980;35:557-558.
20. Moore P, James O. Guillain-Barré syndrome: incidence, management, and out-
come of major complications. Crit Care Med. 1981;9:549-555.
21. Newton-John H. Prevention of pulmonary complications in severe Guillain-
Barré syndrome by early assisted ventilation. Med J Aust. 1985;142:444-445.
22. Lawn ND, Fletcher DD, Henderson RD, Wolter TD, Wijdicks EFM. Anticipating
mechanical ventilation in Guillain-Barré syndrome. Arch Neurol. 2001;58:893-
898.
23. Ropper AH, Kehne SM. Guillain-Barré syndrome: management of respiratory failure.
Neurology. 1985;35:1662-1665.
24. Chevrolet JC, Deleamont P. Repeated vital capacity measurements as predictive
parameters for mechanical ventilation need and weaning success in the Guillain-
Barré syndrome. Am Rev Respir Dis. 1991;144:814-818.
25. Sharshar T, Chevret S, Bourdain F, Raphael JC. Early predictors of mechanical
ventilation in Guillain-Barré syndrome. Crit Care Med. 2003;31:278-283.
26. Sunderrajan EV, Davenport J. The Guillain-Barré syndrome: pulmonary-
neurologic correlations. Medicine. 1995;64:333-341.
27. Pontoppidan H, Geffin B, Lowenstein E. Acute respiratory failure in the adult, 2.
N Engl J Med. 1972;287:743-752.
28. McKhann GM, Griffin JW, Cornblath DR, et al. Plasmapheresis and Guillain-
Barré syndrome: analysis of prognostic factors and the effect of plasmapheresis.
Ann Neurol. 1988;23:347-353.
29. Henderson RD, Lawn ND, Fletcher MD, McClelland RL, Wijdicks EFM. The mor-
bidity of Guillain-Barré syndrome admitted to the intensive care unit. Neurology.
2003;60:17-21.
30. 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.
31. French Cooperative Group in Plasma Exchange in Guillain-Barré Syndrome.
Efficiency of plasma exchange in Guillain-Barré syndrome: role of replacement
fluids. Ann Neurol. 1987;22:753-761.
32. Guillain-Barré Syndrome Steroid Trial Group. Double-blind trial of intravenous
methylprednisolone in Guillain-Barré syndrome. Lancet. 1993;341:586-590.
33. Holdgaard HO, Pedersen J, Jensen RH, et al. Percutaneous dilatational trache-
ostomy versus conventional surgical tracheostomy: a clinical randomised study.
Acta Anaesthesiol Scand. 1998;42:545-550.
34. Dulguerov P, Gysin C, Perneger TV, Chevrolet JC. Percutaneous or surgical tra-
cheostomy: a meta-analysis. Crit Care Med. 1999;27:1617-1625.
35. Griggs WM, Myburgh JA, Worthley LI. A prospective comparison of a percuta-
neous tracheostomy technique with standard surgical tracheostomy. Intensive
Care Med. 1991;17:261-263.
36. Heffner JE. Percutaneous tracheotomy: novel technique or technical novelty? In-
tensive Care Med. 1991;17:252-253.
37. Lawn ND, Wijdicks EF. Post-intubation pulmonary function test in Guillain-
Barré syndrome. Muscle Nerve. 2000;23:613-616.
(REPRINTED) ARCH NEUROL / VOL 62, AUG 2005
1198
Downloaded from www.archneurol.com on August 9, 2010
38. Haymaker W, Kernohan JW. The Landry-Guillain-Barré syndrome: a clinico-
pathologic report of fifty fatal cases and a critique of the literature. Medicine
(Baltimore). 1949;28:59-141.
39. Marshall J. The Landry-Guillain-Barré syndrome. Brain. 1963;86:55-66.
40. McFarland HR, Heller GL. Guillain-Barré disease complex. Arch Neurol. 1966;14:
196-201.
41. Moulin DE, Hagen N, Feasby TE, Amireh R, Hahn A. Pain in Guillain-Barré syndrome.
Neurology. 1997;48:328-331.
42. Ravn H. The Landry-Guillain-Barré syndrome: a survey and clinical report of 127
cases. Acta Neurol Scand. 1967;43(suppl 30):1-64.
43. Winer JB, Hughes RAC, Osmond C. A prospective study of acute idiopathic neu-
ropathy, I: clinical features and their prognostic value. J Neurol Neurosurg
Psychiatry. 1988;51:605-612.
44. Pandey CK, Bose N, Garg G, et al. Gabapentin for the treatment of pain in Guillain-
Barré syndrome: a double-blinded, placebo-controlled, crossover study. Anesth
Analg. 2002;95:1719-1723.
45. Tripathi M, Kaushik S. Carbamezapine for pain management in Guillain-Barré syn-
drome patients in the intensive care unit. Crit Care Med. 2000;28:655-658.
46. Rosenfeld B, Borel C, Hanley D. Epidural morphine treatment of pain in Guillain-
Barré syndrome. Arch Neurol. 1986;43:1194-1196.
47. Burns TM, Lawn ND, Low PA, Camilleri M, Wijdicks EF. Adynamic ileus in se-
vere Guillain-Barré syndrome. Muscle Nerve. 2001;24:963-965.
48. Zochodne DW. Autonomic involvement in Guillain-Barré syndrome: a review.Muscle
Nerve. 1994;17:1145-1155.
49. Sakakibara R, Hattori T, Kuwabara S, Yamanishi T, Yasuda K. Micturitional dis-
turbance in patients with Guillain-Barré syndrome. J Neurol Neurosurg Psychiatry.
1997;63:649-653.
50. Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute
colonic pseudo-obstruction. N Engl J Med. 1999;341:137-141.
51. Meythaler JM. Rehabilitation of Guillain-Barré syndrome. Arch Phys Med Rehabil.
1997;78:872-879.
52. Pitetti KH, Barrett PJ, Abbas D. Endurance exercise training in Guillain-Barré
syndrome. Arch Phys Med Rehabil. 1993;74:761-765.
53. Herbison GJ, Jaweed M, Ditunno JF. Exercise therapies in peripheral neuropathies.
Arch Phys Med Rehabil. 1983;64:201-205.
54. Johnson PC, Fisher CL, Leach C. Hematological implications of hypodynamic states.
In: Murray RH, McCally M, eds. Hypogravic and Hypodynamic Environments. Wash-
ington, DC: National Aeronautics and Space Administration; 1971:27-34.
55. Meythaler JM, Korkor AB, Kumar NA, Nanda T, Fallon M. Immobilization hyper-
calcemia associated with Landry-Guillain-Barré syndrome: successful therapy with
combined calcitonin and etidronate. Arch Intern Med. 1986;146:1567-1571.
56. Meythaler JM, DeVivo MJ, Braswell WC. Rehabilitation outcomes of patients who
have developed Guillain-Barré syndrome. Am J Phys Med Rehabil. 1997;76:
411-419.
57. Bernsen RAJAM, Jacobs HM, De Jager AEJ, van der Meché FGA. Residual health
status after Guillain-Barré syndrome. J Neurol Neurosurg Psychiatry. 1997;
62:637-640.
58. Bernsen RAJAM, De Jager AEJ, Schmitz PIM, van der Meché FGA. Residual physi-
cal outcome and daily living 3 to 6 years after Guillain-Barré syndrome. Neurology.
1999;53:409-410.
59. Merkies IS, Schmitz PI, Samijn JP, van der Meché FG, van Doorn PA; European
Inflammatory Neuropathy Cause and Treatment (INCAT) Group. Fatigue in immune-
mediated polyneuropathies. Neurology. 1999;53:1648-1654.
60. Krupp LB, LaRocca NG, Muir-Nash J, Steinberg AD. The fatigue severity scale:
application to patients with multiple sclerosis and systemic lupus erythematosus.
Arch Neurol. 1989;46:1121-1123.
61. Karper WB. Effects of low-intensity aerobic exercise on one subject with chronic-
relapsing Guillain-Barré syndrome. Rehabil Nurs. 1991;16:96-98.
62. Murray TJ. Amantadine therapy for fatigue in multiple sclerosis. Can J Neurol
Sci. 1985;12:251-254.
63. Garssen MPJ, Schmitz PIM, van der Meché FGA, Merkies ISJ, van Doorn PA.
Amantadine for treatment of fatigue after the Guillain-Barré syndrome (GBS), a
double-blind, randomized, placebo controlled, cross-over trial. Neuromuscul Disord.
2002;12:759 . Abstract.
64. Wijdicks EFM, Fletcher DD, Lawn DD. Influenza vaccine and the risk of relapse
of Guillain-Barré syndrome. Neurology. 2000;55:452-453.
65. Pritchard J, Mukherjee R, Hughes RAC. The risk of relapse of Guillain-Barré syn-
drome or chronic inflammatory demyelinating polyradiculoneuropathy follow-
ing immunisation. J Neurol Neurosurg Psychiatry. 2002;73:348-349.
66. Seyal M, Ziegler DK, Couch JR. Recurrent Guillain-Barré syndrome following in-
fluenza vaccine. Neurology. 1978;28:725-726.
67. Hughes RAC, Choudhary PP, Osborn M, Rees JH, Sanders EACM. Immunisa-
tion and risk of relapse of Guillain-Barré syndrome or chronic inflammatory de-
myelinating polyradiculoneuropathy. Muscle Nerve. 1996;19:1230-1231.
68. Pollard JD, Selby G. Relapsing neuropathy due to tetanus toxoid. J Neurol Sci.
1978;37:113-125.
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