872
REVIEW ARTICLE
Rehabilitation of Guillain-Barr
Jay M. Meythaler, MD, JD
ABSTRACT. Meythaler JM. Rehabilitation of Guillain-
Barr6 syndrome. Arch Phys Med Rehabil 1997;78:872-9.
Guillain-Barr6 syndrome (GBS) is the most common cause
of acute neuromuscular paralysis in developed countries. GBS
is a significant cause of new long-term disability for at least
1,000 persons per year in the United States, and more elsewhere.
Given the young age at which GBS sometimes occurs and the
relatively long life expectancies following GBS, it is likely
that at least 25,000 and perhaps 50,000 persons in the US are
experiencing some residual effects of GBS. Approximately 40%
of patients who are hospitalized with GBS will require admis-
sion to inpatient rehabilitation. For GBS persons necessitating
admission to inpatient rehabilitation, the requirement of prior
ventilator support most strongly predicts an extended length of
stay on inpatient rehabilitation. Other issues that affect rehabili-
tation are dysautonomia, cranial nerve involvement, and various
medical complications associated with GBS. Deafferent pain
syndrome is common in the early stages of recovery. Multiple
medical complications, including deep venous thrombosis, joint
contractures, hypercalcemia of immobilization, and decubitii,
may develop in the early stages of recovery and interfere with
the rehabilitation program. Anemia is a frequent finding in the
first few months of illness but does not appear to interfere with
functional recovery. Therapy should not overfatigue the motor
unit, which has been associated with paradoxical weakening.
Little is known of the long-term implications of the disability
caused by GBS. Work similar to that performed for postpolio
syndrome and spinal cord injury should be started in the rehabil-
itation setting.
© 1997 by the American Congress of Rehabilitation Medicine
and the American Academy of Physical Medicine and Rehabili-
tation
UILLAIN-BARRI~ syndrome (GBS) is the most common
G cause of acute nontraumatic neuromuscular paralysis in
developed countries, afflicting 1 to 2 per 100,00 people annu-
ally. 1-3 There is almost a 2:1 preponderance towards males. ~
Approximately 10% of patients die and 20% are left with defi-
cits in ambulation or require ventilator assistance a year later.4-6
There are an approximately 5,000 new cases per year in the
United States, which is half the incidence of spinal cord in-
jury. 1-3 Therefore, GBS is a significant cause of new long-term
disability for at least 1,000 persons per year in the United States.
The prevalence of those who have long-term disability second-
ary to GBS is unknown. Given the young age at which GBS
can occur however, it is likely that at least 25,000 and perhaps
From the Spain Rehabilitation Center, and Department of Rehabilitation Medi-
cine, University of Alabama School of Medicine, Birmingham, AL.
Submitted for publication August 2, 1996. Accepted in revised form January
21, 1997.
No commercial party" having a direct financial interest in the results of the
research supporting this article has or will confer a benefit upon the authors or
upon any organization with which the authors are associated.
Reprint requests to Jay M. Meythaler, MD, JD, Associate Professor, Spain
Rehabilitation Center, Department of Rehabilitation Medicine, University of Ala-
bama School of Medicine, 1717 6th Avenue South, Birmingham, AL 35233-7330.
© 1997 by the American Congress of Rehabilitation Medicine and the American
Academy of Physical Medicine and Rehabilitation
0003-9993/97/7808-419953.00/0
Arch Phys Med Rehabil Vol 78, August 1997
Syndrome
as many as 50,000 persons in the United States have residual
functional deficits of GBS.
Historically, ascending paralytic illness has been recognized
for centuries but it was Osler7 who offered the first reasonable
clinical description. Later, Guillain, Barr6, and Strohl 8published
a report that more adequately described the syndrome of a radic-
uloneuritis associated with elevated protein in the cerebrospinal
fluid without a "cellular reaction." The definition of GBS is
still largely a descriptive one. Most of the literature reviewed
in this article consists of descriptive case reports, sequential
case series, or retrospective reviews unless otherwise specified.
CLINICAL PRESENTATION
Briefly stated, GBS is an immunopathy with an acute, often
fulminate evolution of a demyelinafing inflammatory polyradic-
uloneuropathy.6 The duration of the illness is usually less than
12 weeks in the majority of patients, with most expected to a
have a favorable outcome (generally this is equated to mean
ambulation without assistive devices). 1 With an approximate
5,000 new cases per year and an expected poor outcome of
20% with regard to mobility or pulmonary function in those
who survive, 1-3one can conclude this is a significant and under-
studied cause of disability.
Classically, GBS has an acute onset (table 1). A devastating
acute course may take a person from being absolutely normal
to bedridden and on a respirator within 2 or 3 days. The progres-
sion usually occurs over 10 to 12 days before a plateau is
reached, followed by gradual recovery. Some patients may have
a stuttering onset, while others may present with a rather slow
progression that can take place over a few weeks. 9 Approxi-
mately 40% to 60% of patients have some antecedent infectious
process. 6'1°In interviews with patients, nonspecific or "flulike"
upper respiratory infections are reported most frequently.1 These
usually occur approximately 2 to 4 weeks before the onset of
weakness. Gastrointestinal illnesses, often relatively mild, are
reported as the second most common type of illness. ~ Viruses
which have been most often implicated are cytomegalovirus
and Epstein-Barr virus. TM Surgical procedures and trauma are
predisposing events in a small percentage of patients, certainly
less than 2% or 3%. 9 Flu vaccines have been implicated in some
cases, 9'a2 and more recently human immunodeficiency virus
(HIV) has been implicated in the development of GBS. 11
Campylobacter jejuni enteritis has recently been recognized as
an important preliminary disease 1° and has been linked to the
more severe axonal variety. 13 Epidural anesthesia, as well as
drugs, including thrombolytic agents and heroin, have been as-
sociated with a few cases.l° Underlying systemic disease such as
lupus erythematosis, sarcoidosis, Hodgkin's disease, and other
neoplasms have been recognized to cause a small number of
"symptomatic" cases of GBS] °'14
Acute GBS typically begins with fine paresthesias in the toes
or fingertips (tables 1, 2) followed within days by the major
clinical manifestation, weakness, which evolves more or less
symmetrically over several days. Leg weakness may make
walking and stair climbing difficult. Variable arm, facial, and
oropharyngeal weakness follows as paresthesias extend proxi-
mally. 14,~5
Early in the illness there are many clinical features that sug-
gest the disease. Initially, the patient will demonstrate approxi-
mately symmetric limb weakness, absent or greatly diminished
 REHABILITATION OF GBS, Meythaler 873

Table 1: Frequency of Features and Clinical Variants of Acute GBS than 20% of normal; (3) summed distal motor amplitude less
% Frequency than 20% of normal.9
Fully
There is described a primary axonal variety of GBS ~7 that
Developed may account for part of the discrepancy between the clinical
Condition Initially Illness diagnostic criteria and the electrodiagnostic criteria.
Features of Syndrome A confirmatory workup should include an examination of
Paresthesia 70 85 cerebrospinal fluid, which usually reveals a normal pressure,
Weakness few or no cells, and a protein concentration of >.55g/L after
Arms 20 90
Legs 60 95 the first week of illness.I°
Face 35 60
Oropharynx 25 50 CLINICAL AND P A T H O P H Y S I O L O G I C MODELS
Ophthalmoparesis 5 15
Sphincter dysfunction 15 5 Pathologically, GBS is an inflammatory polyradiculoneuro-
Ataxia 10 15 pathy that resembles experimental allergic neuritis (EAN) in
Arefiexia 75 90
Pain 25 30 animals) 1 Both EAN and GBS share common histopathologic
Sensory Loss 40 75 features, characterized by the presence of perivascular mononu-
Respiratory failure 10 30 clear cell inflammation, demyelination, and edema. Experiments
CSF protein >0.55 g/liter 50 90 in various animal models have demonstrated that the sensitiza-
Clinical variants*
Fisher's syndrome 5 tion of T-lymphocytes of the CD4 subclass to proteins in the
Weakness without paresthesia or loss 3 myelin sheath is necessary for disease induction.2~The principle
Pha ryngeal-cervical-brachial weakness 3 electrophysiologic finding that accounts for the weakness noted
Paraparesis 2 in GBS, at least early in the disease, is the conduction block
Facial paresis with paresthesia 1
Pure ataxia 1 produced when a portion of the axon fails to transmit impulses
in a segment where myelin has been destroyed or rendered
* Variants are associated with diminished reflexes, demyelinating fea- nonfunctional)2
tures as detected on electrophysiologic studies, and elevated cerebrospi-
nal concentrations of fluid protein. Frequencies shown are those found Recently, the presence of antiganglioside antibodies, such as
in fully developed illness. antiganglioside GM1 antibodies or antiganglioside GQlb anti-
Adapted and reprinted by permission of The New England Journal of bodies, has been associated with axonal damage and a poorer
Medicine, Ropper AH, The Guiilain-Barr6 syndrome, 326:1130-6, copy-
right 1992, Massachusetts Medical Society; and adapted and reprinted
outcome. 23 GMt gangliosides are used clinically to reduce the
from Asbury and Cornblath, 12with permission. amount of neurological injury in SCI. A suggested link between
the use of gangliosides and GBS has not been established.2427
Furthermore, there has been a proposed link between the pres-
tendon reflexes, and minimal loss of sensation despite the pares- ence of IgG anti-GDta and anti-GMt antibodies and a more
thesias. 1° Pain is common, presenting as either a bilateral sciat- severe presentation of GBS. 28'29
ica or aching in large muscles of the upper legs, flanks, or
back. 16 Weakness of the facial muscles occurs in about one DIFFERENTIAL DIAGNOSIS
third of all cases, to In severe cases the disease affects respiration,
and may result in cranial nerve palsies with associated func- GBS as a recognizable entity is based on descriptive criteria.
tional losses in eye movements and deglutition.1° Disturbances The features required for diagnosis are a progressive motor
of autonomic function (sinus tachycardia and, less often, brady- weakness of more than one limb and areflexia. 1° The current
cardia and facial flushing, fluctuating hypertension and hypoten- proposed electrodiagnostic criteria for GBS are for the demy-
sion, loss of sweating or episodic profuse diaphoresis) are com- elinating versions of the disease and do not cover the primary
mon, but in the majority of patients these abnormalities do not axonal variety. 3°
persist for more than a week or two. t°
There are many variants of GBS that may cause diagnostic Table 2: Diagnostic Criteria for Typical GBS
difficulty, including Fisher's syndrome, which involves ophthal-
moplegia, ataxia and areflexia with little weakness and accounts Features required for diagnosis
Progressive weakness in both arms and both legs
for approximately 5% of the cases14'17; weakness without pares- Areflexia
thesias or sensory loss; isolated weakness of the arm and oro- Features strongly supporting the diagnosis
pharynx, or of the leg~8; bilateral weakness of facial muscles Progression of symptoms over days to 4 wks
with distal paresthesias; severe ataxia and sensory loss; acute Relative symmetry of symptoms
Mild sensory symptoms or signs
pandysantonomia, an autonomic polyneuropathy often com- Cranial-nerve involvement, especially bilateral weakness
bined with sensory featurest9; and "axonal" GBS with rapid, of facial muscles
almost complete paralysis and electrically inexcitable motor Recovery beginning 2 to 4 weeks after progression ceases
nerves.2° The effect of these many "subtypes" on the ultimate Autonomic dysfunction
Absence of fever at the onset
functional outcome or disability of the afflicted patients is not Elevated concentration of protein in cerebrospinal fluid,
sufficiently known (table 2). with fewer than 10 cells per cubic millimeter
Typical electrodiagnostic features
Features making the diagnosis doubtful
E M G and Laboratory Findings
Diagnosis of botulism, myasthenia, poliomyelitis,
Abnormalities of nerve conduction, reflecting demyelination, or toxic neuropathy
are the most sensitive and specific laboratory findings in GBS, Abnormal porphyrin metabolism
Recent diphtheria
and there are proposed diagnostic criteria for the demyelinating Purely sensory syndrome, without weakness
versions of the disease t2 (table 3).
Adapted and reprinted by permission of The New England Journal of
Electrodiagnostic and physiologic parameters associated with Medicine, Ropper AH, The Guillain-Barre syndrome, 326:1130-6, copy-
a poor outcome include (1) summed motor velocity less than right 1992, Massachusetts Medical Society; and adapted and reprinted
80% of normal, (2) summed proximal motor amplitude less from Asbury and Cornblath, 1=with permission.

Arch Phys Med Rehabil Vol 78, August 1997

874 REHABILITATION OF GBS, Meythaler

Table 3: Proposed Electrodiagnostic Criteria for Demyelination of Peripheral Nerve

These criteria concern nerve conduction studies (including proximal nerve segments) in which the predominant process is demyelination.
Must have three of the following four features:
1. Reduction in conduction velocity in two or more motor nerves.
a. <80% of lower limit of normal (LLN) if amplitude >80% of LLN.
b. <70% of LLN if amplitude <80% of LLN.
2. Conduction block or abnormal temporal dispersion in one or more motor nerves: either peroneal nerve between ankle and below fibular head,
median nerve between wrist and elbow, or ulnar nerve between wrist and below elbow,
Criteria for partial conduction block:
a. <15% change in duration between proximal and distal sites and >20% drop in negative-peak area of peak-to-peak amplitude between
proximal and distal sites.
Criteria for abnormal temporal dispersion and possible conduction block:
a. >15% change in duration between proximal and distal sites and >20% drop in negative-peak area or peak-to-peak amplitude between
proximal and distal sites.
3. Prolonged distal latencies in two or more nerves,
a. >125% of upper limit or normal (ULN) if amplitude >80% of LLN.
b. >150% of ULN if amplitude <80% of LLN.
4. Absent F-waves or prolonged minimum F-wave latencies (10-15 trials) in two or more motor nerves.
a. >120% of ULN if amplitude >80% of LLN,
b. >150% of ULN if amplitude <80% of LLN.
Adapted and reprinted from Annals of Neurology V27 (Suppl), $21-$24, 1990, by permission of Little, Brown and Company (Inc.).

The differential diagnosis is generally determined by the clin-
ical course and the pattern of weakness and includes spinal cord
compression, transverse myelitis, myasthenia gravis, basilar ar-
tery occlusion, neoplastic meningitis, vasculitic neuropathy,
polymyositis, metabolic myopathies, and paraneoplastic neu-
ropathy. I° Other diagnoses that can be confused with GBS in-
clude hypophosphatemia, heavy-metal intoxication, neurotoxic
fish poisoning, botulism, poliomyelitis, and tick paralysis. 1°
Various syndromes present with many of the same clinical
and diagnostic findings of GBS, including chronic immune de-
myetinating polyneuropathy, autoimmnne neuropathies caused
by connective tissue diseases, cancer, toxic neuropathies, and
hormonal and metabolic neuropathies. 10 ' 12' 14'31 The greatest diag-
nostic controversy surrounds chronic inflammatory demyelinat-
ing polyneuropathy (CIDP) and relapsing inflammatory poly-
neuropathy, which are considered by some to be separable from
GBS. 1° This separation may indeed be arbitrary or logically
defensible as separating the various clinical presentations of
multiple sclerosis. What is important from a rehabilitation stand-
point is that the clinical course may vary considerably in these
other presentations from those of classically described GBS, so
an accurate diagnosis and prognosis is important.
TREATMENT
Progress is being made in the treatment of GBS. It has been
suggested that improved rates of survival are related to the
special care units staffed by personnel who are experienced in
handling the complications of the disease. 1° Most of these spe-
cial care units are located in regional medical centers that treat
the majority of cases. Many GBS patients die of avoidable
medical complications such as sepsis, adult respiratory distress
syndrome, pulmonary emboli (usually secondary to deep venous
thrombosis), or cardiac arrest perhaps related to dysautonomia.
With appropriate medical supportive care, the rate of mortality
could be reduced to less than 5%. w
Plasmapheresis and Intravenous Immunoglobulin
Plasmapheresis and intravenous immunoglobulin (IVIg) are
the accepted therapy for GBS. The North American and French
prospective, randomized clinical trials clearly demonstrate that
plasmapheresis shortens the time required to achieve indepen-
dent walking and the time a patient stays on a respiratory sup-
port. In addition, plasmapheresis is reported to improve func-
tional improvement of mobility at 6 months. 32~34
Besides plasmapheresis, another alternative treatment is the
use of infused immunoglobulins (IVIg). 35 Infusion of immuno-
globulin has been associated with a beneficial outcome in other
immunologically mediated diseases. 9'22Results from a prospec-
tive, randomized Dutch trial of 100 GBS patients treated with
IVIg compared to plasmapheresis suggests that IVIg is as good,
if not better, than plasmapheresis. 36 There have been reports,
however, of a high incidence of relapses following IVIg. 23 Al-
though treatment with plasma exchange and immunoglobulins
has decreased the duration of mechanical ventilation by half,
GBS still remains the most common cause of acute neuromuscu-
lar ventilatory failure. 37
Steroids
The use of steroids in treatment of acute GBS has been con-
troversial.38 Their use was based on promising trials with EAN
in animals,39 and in early clinical trials with humans it was
suggested that steroids were useful in decreasing the severity
of illness.38 However, in a large randomized prospective study
of 242 patients treated with 500mg methylprednisolone, it was
concluded that steroids were ineffective.2
CLINICAL COURSE
The course of illness may be more prolonged in adults, partic-
ularly older adults, than in children.9 Persons who have suffered
GBS may continue to improve for up to 2 years after injury,4°'41
although there is little information other than general descrip-
tions on the rate or variability of the neurological recovery.
Prognostic factors with regard to a poor outcome recently identi-
fied in a North American study9'42 were older age, requirement
for respiratory support, rate of progression, abnormal physiolog-
ical characteristics of peripheral nerve function, or if no plasma-
pheresis was performed. 9'42 There has been no correlation be-
tween recovery from GBS and sex, occupation, the presence of
diabetes mellitus, previous steroid use, or prior immuniza-
tion.9,43
The point of maximal neurologic dysfunction is reported as
the "disease nadir."9 The average period from the clinical onset
symptoms to nadir of illness is 8 days. 1The point of time before
or at disease nadir has frequently has been considered critical
with regard to the success of therapeutic interventions utilizing
plasmapheresis or IVIg, 9 but this has never been established
and in one study did not correlate with outcome. 44 Yet many
institutions will not intervene with plasmapheresis or IVIg if
the patient has already begun neurological recovery or has not
deteriorated neurologically for several days. More work is nec-
essary to delineate whether late intervention after the point of
disease nadir is useful.

Arch Phys Med Rehabil Vol 78, August 1997

 REHABILITATION OF GBB, Meythaler
In our experience, patients with GBS who were so severely
involved as to require admission to inpatient rehabilitation had
an extended period to disease nadir. Clearly, patients with GBS
requiring inpatient rehabilitation are the more severely involved.
The development of relapses may be related to a more extended
course of the disease in these patients. Frequent neurologic
evaluations will detect the development of relapses, and inter-
vention with plasmapheresis and/or IVIg may be of therapeutic
benefit.
There are multiple medical complications that may develop
from GBS. Many of these complications may persist for some
time, interfering with rehabilitation or even leading to perma-
nent functional deficits.
Requirement of Ventilatory Support
Little is known regarding the predisposing factors that result
in the need for support. It has been noted that autonomic dys-
function is related to the requirement of ventilatory support. 14'is
In epidemiologic studies it is estimated that 10% to 30% of
patients will require mechanical ventilation, 5% to 10% will
remain seriously disabled, and 3% to 8% will die. 37 Intubation
should be considered when the vital capacity decreases to
<lSmL/kg. 1° The need for-ventilatory support correlates with
outcome as evaluated by ambulatory function. 15 More recently,
ventilatory support has been correlated with longer lengths of
stay and increased costs for inpatient rehabilitation.43
Respiratory failure and pneumonia may occur in 30% of
patients in the acute phases of illness (first 12 weeks), but many
will have adequate recovery of their respiratory function]° As
many as 25 % of these patients will develop pneumonia.I° Those
who do not have full respiratory recovery may have complica-
tions leading to long-term morbidity secondary to antecedent
chronic obstructive disease, restrictive pulmonary disease from
pulmonary scarring secondary to pneumonia, tracheitis from
chronic intubation, or respiratory musculature insufficiencyY
Deep Venous Thrombosis
Deep venous thrombosis (DVT) is considered to be common
in GBSY The incidence of DVT in GBS is unknown because
it has never been systematically studied. In one early study,46
pulmonary embolus (PE) was believed to occur in up to one
third of patients who suffered from GBS. However, predispos-
ing factors such as the severity of disease or the length of
immobilization have not been well delineated.46 While prophy-
lactic treatment for DVT is recommended by some authors, 1°'45
without knowing the incidence or risk factors for the develop-
ment of DVT, it is hard to make informed judgments regarding
the type and length of prophylaxis necessary.
Dysautonomia
Dysautonomia in GBS is indicated by orthostatic hypoten-
sion, unstable blood pressure, or abnormal heart rates. This
definition has recently been expanded to include bowel and
bladder dysfunction.47 Autonomic dysfunction without bladder
and bowel dysfunction is related to the need for ventilatory
support. 14A5'48'49Dysautonomia has been found in particularly
severe versions of GBS, extending the acute care length of stay
in previous epidemiological studies,48'49 and is believed to be
clinically related to life-threatening cardiac arrhythmias.47 Uro-
logic dysfunction may develop early in the disease process but
it is believed to resolve in most cases; however, this conclusion
appears to be based totally on anecdotal evidence, m2 Some
men will develop residual impotence, l° Dysautonomia has been
linked to cardiac arrhythmias, cardiovascular collapse, and
death in various case reports of GBS. 47 In one case series of
875
100 patients, 11 developed cardiac arrhythmias sufficient to
compromise their circulation and 7 of the 1 1 died. 48 Despite
the recent attention to dysautonomia and its relevance to both
morbidity and mortality,48 there have been no prospective stud-
ies on predicting its onset or evaluating various interventions
to limit its impact.
Pain and Sensory Involvement
Most reports of GBS describe pain as a prominent clinical
feature of the diagnosis, and it has been reported to be the sole
initial presenting symptom in some cases. 5° The types of pain
described include paraesthesia, dysaesthesia, axial and radicular
pain, meningism, myalgia, joint pain, and visceral discomfortfi
In one small prospective study 16early pain was reported in 55%
of the patients and in 72% of the patients throughout the whole
course of illness. Symptoms of mild depression that continues
long after the initial onset, indicated by persistent mental fa-
tigue, are common. I° This may be exacerbated by deafferent
pain syndromes.
Immobilization
GBS patients are usually hypotonic or flaccid as well as
immobilized. They develop complications of decubitis ulcers,
tendon shortening, joint contractures, and malalignment, as well
as peroneal nerve palsies. 1° Yet the treatment approach has been
similar to that used for many patients who have an upper motor
neuron lesion such as spinal cord injury or traumatic brain
injury. How these medical complications and functional deficits
affect the final disability of these patients is unknown. The
incidence of immobilization on the development of functional
deficits is not well understood in GBS. Can the same treatment
milieu be utilized in this lower motor neuron disease when the
predisposing factors and impact of these therapies are not well
delineated?
Dysfunction of bone and calcium metabolism can occur in
GBS. Heterotopic ossification has been reported in GBS. 52's3
Hypercalcemia of immobilization of such a severe nature as to
require aggressive medical intervention has been noted in a few
case reports of GBS. 52'54 Both of these conditions are fairly
common in spinal cord injury, but the incidences of both have
not been well defined in GBS and are believed to be the result
of prolonged immobilization.52
Anemia
Anemia in persons with GBS with such severe involvement
as to require inpatient rehabilitation is more common than that
found in the corresponding spinal cord population.5s'56The ane-
mia may in part be related to immobilization. In a retrospective
study, 79% of persons admitted to acute inpatient rehabilitation
from GBS had anemia with hematocrits and hemoglobin two
standard deviations below the mean.55 Patients with a history
of receiving plasmapheresis had a higher mean hemoglobin and
hematocritY A study on the effects of immobilization in healthy
male subjects who were confined to bed rest found that the
red cell count and reticulocyte count declined slowly over 5
weeks. 57'~8All these changes reversed with mobilization. Plas-
mapheresis may be a factor, by reducing inflammatory immuno-
globulins that may interact with bone marrow precursorsY It
has been suggested that correcting anemia may aid in the treat-
ment of orthostatic hypotension in persons with GBS 9 Anemia
appears not to relate to rehabilitation outcome or length of stay
for those persons with such severe involvement as to require
inpatient rehabilitation.55
Arch Phys Med Rehabil Vol 78, August 1997
876 REHABILITATION OF GBS, Meythaler
Cranial Nerve Involvement
Crania/ nerve involvement has been described in the more
severe cases of GBS.14'~5In one study cranial nerve involvement
was associated with an increased total length of hospital stay
(acute and rehabilitation combined) for persons with such severe
involvement as to require inpatient rehabilitation.43In a previous
study, cranial nerve involvement was associated with a pro-
longed duration to reach the plateau phase of illness, but did
not aid in predicting future motor deficitJ 5 Cranial nerve
involvement may result in dysphagia, bilateral vocal cord paral-
ysis, optic neuritis, and hearing loss. I4'15'60-63
REHABILITATION
Approximately 40% of the patients who are hospitalized with
GBS will require inpatient rehabilitation.4°'43They are generally
considered the more severely involved patients. One study4°
described an incidence of persistent plegia in 54% of these
patients, ranging from monoplegia to tetraplegia of 54%. Reha-
bilitation requires an organized program with defined end
points, yet no long-term rehabilitation outcome studies have
been done. The lack of systematic studies on rehabilitation out-
come has been noted in the literature recently. 1° Consequently,
most rehabilitation approaches for measuring functional out-
come in GBS have been adopted on the basis of experience
with other diseases. The only studies reported are largely de-
scriptive with no well-defined functional outcomes except for
physical findings regarding weakness or alterations in gait. 4°'41'44
There are patients who will have a relapse of the disease;
these relapses are believed to be more frequent with the current
treatments, particularly IVIg. 23 Since the course of GBS remains
clinically unpredictable at its onset, and patients are in general
being transferred to rehabilitation more quickly, close supervi-
sion on an inpatient rehabilitation service is warranted. This
evaluation should include detailed daily physical examinations,
documenting motor and sensory tests, to evaluate for relapses
and/or complications.
Functional motor gain and recovery on inpatient rehabilita-
tion as measured by the admit motor and discharge FIM Rasch
motor converted score on admission to rehabilitation correlate
strongly with the requirement for ventilatory support, 43 and
agree with other epidemiologie studies which generally evalu-
ated outcome by ambulatory function.4'15
Poor proprioceptive function has been associated with a
longer length of stay on inpatient rehabilitation.43 There was,
however, no association with propfioceptive changes and func-
tional status as measured by the admit motor and discharge FIM
Rasch motor converted score on admission to rehabilitation, so
the connection is unclear.43 Also, there appears to be no relation
between the presence of relapses and rehabilitation outcome
except for lower FIM Rasch-converted motor discharge scores
from in-patient rehabilitation.43 This relation may be related to
the more extended course of the disease in these patients, but
requires further study.
GBS is a disease that often leads to a functional deficit. Little
is known about the true incidence of disability in GBS patients.
The absence of deep tendon reflexes in upper or lower extremi-
ties, as well as severe distal upper extremity weakness or lower
extremity weakness, are all indicative of incomplete recovery. 44
This may lead to an impairment, which is defined as "any
loss or abnormality of psychological, physical, or anatomical
structure or function. ''64 Disability, as defined by the World
Health Organization exists when an impairment prohibits one
from accomplishing a task required for personal independence.64
Assessment of disability in GBS has usually been on a crude
6-point ordinal scale, or some modification thereof2'28'32'65'66:0,
Arch Phys Med Rehabil Vol 78, August 1997
healthy; 1, minor symptoms or signs; 2, able to walk 5m without
assistance; 3, able to walk 5m with assistance; 4, chair-bound
or bed-bound; 5, requiring assisted ventilation for at least part
of the day or night; 6, dead. One problem with this scale is that
the length of time patients are followed varies between 6 months
and 12 months, while recovery may continue for up to 18
months, nor has this 6-point functional scale ever been corre-
lated with more traditional, and more frequently employed,
scales that measure function and aid in the assessment of disabil-
ity. More importantly, this scale may not be sensitive enough to
detect subtle changes in function with various treatment options.
Furthermore, the interrater reliability and reproducibility of this
scale has never been established. Consequently, the validity and
reliability of studies regarding the effectiveness of therapeutic
interventions such as plasmapheresis,4z IVIg, 36 or steroids 2 may
be in question. The usefulness of this scale in relation to the
more traditional scales used to measure outcome in rehabilita-
tion has yet to be established.
Another important issue that needs to be addressed by rehabil-
itation research is how GBS patients age with a functional defi-
cit. The extent of muscle strength recovery after GBS may be
a major determinant of the patient's ultimate functional poten-
tial.2.a0.28
REHABILITATION THERAPEUTICS
Motor Recovery and Musculoskeletal Complications
There have been no systematic studies on the efficacy of
physical therapy in GBS. l° Generally, therapy approaches have
been adapted from experiences with other neuromuscular ill-
nesses and diseases. GBS patients may present with such diverse
findings as significant involvement with quadriparesis, or iso-
lated weakness of the arm, leg, facial muscles, or oropharynx.
It has been suggested that overfatiguing the affected motor unit
in therapy may impede recovery. 67'6sClearly, overworking mus-
cle groups in patients with peripheral nerve involvement has
been clinically associated with paradoxical weakening.68
Motor weakness has been associated with muscle shortening
and resultant joint contractures. These complications can be
prevented with daily range-of-motion exercises. 69Depending on
the amount of weakness, exercise can be passive, active-as-
sistive, or active. Proper positioning in patients is necessary.
Initial exercise, even in the acute phases, may include a program
of gentle strengthening involving isometric, isotonic, isokinetic,
manual-resistive, and progressive resistive exercises carefully
tailored to the clinical condition of the patient.69 Orthotics
should be prescribed for proper positioning and optimizing re-
sidual motor function.
Sensory Dysfunction and Pain
The treatment of pain has generally been directed clinically,
noted by the prominent use of antidepressants and, in some
cases, the use of carbamazepine. More recently, there have been
verbal reports on the use of topical capsaicin and/or transeutane-
ous electrical stimulation to the specific well-localized anatomic
areas of deafferent pain. Pain in the limbs and axial skeleton
has been linked in one report to impaired joint mobility in
GBS. 7° GBS patients with severe pain may have a poor tolerance
for activity resulting in a longer lengths of stay. Various desensi-
tization techniques utilized in the therapies may be clinically
useful. At our institution medical intervention usually starts with
tricyclic antidepressants, capsaicin, and transeutaneous nerve
stimulation. Second-line agents include anticonvulsants (carba-
mazepine, gabapentin) that are reported to be possibly effective
in neurogenic pain. 71'72 Occasionally, in patients who have unre-
mitting pain, pain medications such as tramad01 or narcotics
 REHABILITATION OF GBS, Nleythaler
are indicated in the early stages of treatment to give relief
until the above measures have time to become effective. Many
patients will relate a history of severe pain in the early stages
of recovery from GBS, yet there are few studies on the nature or
duration of this pain. There are no significant studies regarding
interventions for deafferent pain syndrome in GBS.
There are patients with significant involvement in vibratory
sensation and joint position. Proprioceptive losses cause ataxia
and incoordination, resulting in functional deficits. For these
patients, therapy should include techniques of sensory reintegra-
tion and repetitive exercises to redevelop coordination. These
techniques will aid in developing motor engrams that are based
on the altered sensory perception.
Dysautonomia
Any suggestion that dysautonomia is uncommon, and insig-
nificant clinically, is incorrect. Most patients who come to inpa-
tient rehabilitation are probably not as threatened by cardiac
an-hythmias; however, because these patients are the more se-
verely involved, they may still have problems with postural
hypotension, hypertension, and excessive sympathetic outflow,
or bladder and bowel dysfunction. Postural hypotension, which
can be disruptive to therapy, is frequently found in those patients
who are so severely involved as to require inpatient rehabilita-
tion. A recent review of the literature involving dysautonomia
estimates that between 19% to 50% of all GBS patients in a
hospital setting will have evidence of postural hypotension. 47
Patients who have excessive sympathetic outflow and hyperten-
sion appear to have extreme sensitivity to vasoactive drags. 47'73
These patients are particularly likely to develop these episodes
of hypotension or hypertension with suctioning. 74 This is of
concern because some patients are prone to cardiac arrhyth-
mias. 75 Treatment should be directed toward physical modalities
such as compression hose, abdominal binders, and proper hydra-
tion.
Bowel and bladder dysfunction is generally of the lower mo-
tor neuron variety. Urological dysfunction may develop early
in the disease process but is believed to resolve in most
cases. 1°'~2Initial management of the bladder should be directed
toward avoiding overdistention of the bladder with consequent
bladder wall disruption. Furthermore, up to 30% of patients
acquire urinary tract infections, x°
Immobilization
The incidence of DVT in GBS in the rehabilitation setting is
unknown because it has never been studied. Predisposing factors
for DVT development, such as the severity of disease or the
length of immobilization, have not been well delineated.46 Since
the most severely involved patients are those referred to inpa-
tient rehabilitation, most rehabilitation physicians utilize pro-
phylaxis for DVT. Judgments regarding the type and length of
prophylaxis are difficult without knowing the incidence of, or
risk factors for, DVT development. Early mobilization appears
to be beneficial in similar patient groups.
Clearly, prolonged immobilization leads to a reduction of
blood volume 76'v7 and increased episodes of postural hypoten-
sion in the rehabilitation setting. 43 In other immobilized patients,
a tilt table has been a useful therapeutic tool.
These patients tend to lose a significant amount of body mass
because of immobilization, particularly muscle mass. When this
is combined with a significant sensory loss, patients are suscep-
tible to the development of decubitis ulcers from immobiliza-
tion. Proper bed positioning with frequent postural changes is
required to prevent the development of decubitii.
The loss of body mass, coupled with an already compromised
877
peripheral nervous system, makes proper positioning a necessity
to protect peripheral nerves that may be compressed between
body prominences and the bed. 69 The nerves most frequently
involved are the ulnar, peroneal, and the lateral femoral cuta-
neous sensory nerves.
In patients with immobilization hypercalcemia, early mobili-
zation, even in a therapeutic pool, was correlated with a thera-
peutic decrease in the serum calcium level. 52 The use of aggres-
sive range of motion may also impede the effects of heterotopic
ossification on joint mobility and function.
No studies have been performed on the nutritional needs
of these patients. In our clinical experience, close nutritional
monitoring is warranted as patients tend to lose weight in the
acute stage of illness. Interestingly, with immobilization and
reduced activity, many patients who can eat tend to gain weight
after the first few weeks of illness. The consequent weight gain
impedes the potential functional gains in transfers and mobility
one would expect with motor recovery.
Psychological and Social Issues
Psychosocial variables affect outcome in the rehabilitation of
many other diagnoses. Symptoms of mild depression long after
the initial onset, indicated by persistent mental fatigue, are com-
mon, although GBS itself does not result in chronic fatigue
syndromeY Clearly, an extended period in the intensive care
setting, due to ventilatory support, can affect cognitive function.
Research could establish whether severely involved GBS pa-
tients have many of the same psychological and social issues
that spinal cord injury patients have. This could then result in
the use of already established interventions.
Respiratory Complications
Respiratory failure and pneumonia may be found in 30% of
the acute cases in the first 12 weeks. 44 Aggressive respiratory
therapy with pulmonary toilet is necessary in the early stages
of disease, including acute inpatient rehabilitation, as it would
be with any patient with a neuromuscular disease affecting pul-
monary function. Because this issue appears to be the strongest
predictor of hospital length of stay~ 43'48 close monitoring is nec-
essary. Patients with cranial nerve involvement are particularly
susceptible to pulmonary infections, due to aspiration. Perhaps
this is why cranial nerve involvement has been so closely linked
to ventilatory dependence and severity of GBS. 43'48
GBS leads to restrictive pulmonary function that may persist
for some time after ventilatory assistance is discontinued. Re-
strictive pulmonary conditions in other diseases have been asso-
ciated with sleep hypercapnea and hypoxia during rapid eye
movement (REM) sleep, because within the central nervous
system, the centrally mediated ventilatory response to hypoxia
and hypercapnia are diminished during sleep, ys-sl Many patients
may be assessed on the floor by the use of frequent nighttime
observations using a pulse oximeter. Treatment with bilevel
positive airway pressure (BiPAP) may be indicated for patients
who develop sleep hypoxia or hypercapnia. More recently it
has been suggested that theophylline may benefit patients who
present with reduced hypercapnia or hypoxia at night due to
central respiratory control mechanisms accommodating to pro-
longed blood gas alterations. 82
Clearance of secretions to reduce the work of breathing is
necessary, s3 Often this will require the use of resistive inspira-
tory training. Since many of these patients will initially have a
tracheostomy, a proper tracheostomy tube capping protocol with
fl'equent rest periods needs to be instituted. One must be careful
not to overfatigue the muscles of respiration during the initial
period of motor unit recovery, because this may push the patient
into respiratory failure.
Arch Phys Med Rehabil Vo178, August 1997
878 REHABILITATION OF GBS, Meythaler
OUTPATIENT AND LONG-TERM FOLLOW-UP
The extent and duration of physically disabling sequelae with
GBS, including the incidence of secondary medical complica-
tions, has never been adequately described. With regard to mo-
tor function, poliomyelitis and GBS have many similar clinical
issues. It is not known whether the same long-term problems
will develop in this population because of loss in the number
of active motor units. Furthermore, there have been no long-
term studies on aging in patients who have GBS. It is likely
that these patients will have a loss of function as they age,
similar to patients with postpoliomyelitis. 84 One can assume
that there are outpatient therapy programs that can aid in the
maintenance of functional capacity. Until studies are performed,
much of the rehabilitation of GBS will be based on the experi-
ence gleaned from similarly presenting conditions.
The incidence of GBS, which is half that of SCI, is the most
prevalent cause of acute nontranmatic neuromuscular paralysis
in the US. Undoubtedly, a significant number of the patients
discharged directly to home could benefit from outpatient reha-
bilitative services. Furthermore, vocational and psychosocial
outcomes have not been addressed in any studies. The services
for patients disabled by GBS, however, are as fragmented as
those originally described two decades ago for TBI and SCI.
This fragmentation led to the creation of model systems of
care, which developed a comprehensive continuum of care to
improve the lives of patients with TBI or SCI. In GBS, there
is a similar need for research to estimate the needs of this
population and obtain more accurate data on functional out-
comes. Currently, there is negligible federally-funded rehabilita-
tion research into GBS. Considering that GBS research could
be utilized as a model for other disabling peripheral neuropa-
thies and deafferent syndromes, it is an area worth exploring.
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