GuillainBarr syndrome (GBS)

GBS or acute inflammatory polyradiculoneuropathy (AIP) produces

a variable degree of acute or subacute quadriparesis; this
is frequently severe. GBS affects between 0.75 and 2.0 persons
per 100,000 per year (Ropper, 1992). These incidence figures
have more recently been confirmed in theUK(Rees et al., 1998).
Patients often become unable to walk and there can be associated
respiratory, bulbar, and autonomic failure. Admission to an
intensive therapy unit is sometimes needed and about 20% of
patients require artificial ventilation (Ropper, 1992). In a UK
series prior to the use of immunomodulatory treatment (Winer
et al., 1988), 13% of patients died and, at 12 months, 20% were
left significantly disabled, whereas 67% had recovered completely;
88% lost the ability to walk at the height of the illness.
Plasma exchange (Ropper, 1992) or intravenous IgG (Van Der
Meche et al., 1992) effectively attenuate the severity of GBS
if commenced within 2 weeks of the onset. Such therapy is
indicated in patients who are unable to walk or have significant
bulbar or respiratory weakness. Intravenous IgG infusion is currently
the preferred treatment because of the ease of application
(Hahn, 1998). In a recent UK study, 68% of patients with GBS
had immunomodulatory treatment. At 1 year, 8% of all patients
had died, 62% had made a complete or almost complete recovery,
4% remained bedbound or ventilator dependent, 9% were
unable to walk unaided, and 17% were unable to run (Rees,
1998).
This highlights the fact that a significant minority of patients
remain disabled despite immunomodulatory treatment and
require continuing rehabilitation. However, many aspects of the
management in both the acute and more chronic stages require
a multidisciplinary approach, which is applicable to all patients
with GBS.
At an early stage, various prognostic factors can be used to
predict the likely degree and duration of disability (Winer et al.,
1988). Older age, small compound muscle action potentials on
nerve conduction tests, inability to walk within 4 days, onset
after campylobacter infection (Rees et al., 1995), or the need
for artificial ventilation all predict a poor outcome. Reliable and
reproducible functional measures of severity are useful; a lack
of demonstrable improvement in the first few weeks suggests
a poor outlook with prolonged or permanent disability.
From the outset, high priority must be given to the prevention
of complications if long-term disability is to be minimised. In
severely affected patients, close monitoring of respiratory, cardiovascular,
and bulbar function (on an intensive therapy unit)
is vital to prevent potentially lethal complications. Attention
to positioning, posture, bowel and bladder function, and chest
physiotherapy can prevent pressure ulcers, peripheral nerve
damage, constipation, urinary infection, and chest infections.
Passive limb movements and moulded limb splints can avoid
contractures. In this regard, the use of a tilt table to prevent
contractures should be supervised closely because of
the dangers of severe postural hypotension in patients with
autonomic involvement. Compression stockings (and probably
subcutaneous heparin) are aimed at the prevention of venous
thromboembolism. Pain, perhaps mediated by nervi nervorum in
inflamed nerve roots (Thomas, 1979), can be severe and should
be borne in mind, especially in the ventilated patient. It can be
resistant to all treatments apart from intrathecal opioids. Attention
to positioning and limb support, passive movements, cold
or heat, vibration or transcutaneous neural stimulation (TNS)
can be helpful.
The psychological impact of GBS can be devastating (Rice,
1977) and depression is common (Ropper, 1992). Reassurance,
explanation, and attention to a frequently deranged sleep pattern
are important. Support from ex-patients can be enlisted from the
local branch of the GuillainBarr Support Group (see the section
useful addresses at the end of the chapter). During recovery
a full range of movement should be maintained in all joints.
Muscle strengthening will initially involve movements that are
assisted and can exclude the effect of gravity. Hydrotherapy can
have a place here. Later, active movement against gravity will
target trunk and head control, sitting, unsupported, kneeling,
standing from sitting and walking. In most patients, the use of
special seating (including head support), walking aids, and functional
splinting will be more or less temporary. Activities of daily
living will be gradually reintroduced. Graduated strengthening
exercises, and exercises to improve balance and coordination
will also be started at around this time. The relative value of the
various techniques in use is entirely unexplored.
Patients often fatigue early: both exercise regimes and a
patients daily routine must take this into account. Fatigue can
continue even when power has returned to normal on clinical
testing. This can be shown to be due to residual motor, rather
than psychological, factors by myometry (Nicklin et al., 1987
GUILLAIN-BARRE SYNDROME =--:.~=----=---''-=-..:c:==-- _
Guillain-Barre syndrome (GBS) is the most frequent cause of
acute generalized weakness now that polio is all but eradicated.
It is referred to as a syndrome because it represents a
broad group of demyelinating inflammatory polyradiculoneuropathies.
There are many forms of GBS. The two major forms can be distinguished based on pathologic and
electrophysiologic findings: acquired inflammatory demyelinating
polyradiculoneuropathy (AIDP) and acute axonal
neuropathy (AMAN). Another common variant of CBS is
Miller-Fisher syndrome with cranial nerve involvement,
ataxia, and areflexia. Because the nerve roots (radiculopathy)
and peripheral nerves (polyneuropathy) are aHected, CBS
results in flaccid paralysis. Cranial nerves which are a part of
the peripheral nervous system may also be involved.
Therefore, CBS is a classic lower motor-neuron disorder.
Incidence and Etiology
CBS is rare with an incidence of 1 per 100,000 people. It
occurs in all age groups, including children and adults. The
majority of individuals who acquire CBS experience a respiratory
or gastrointestinal illness prior to the onset ofweakness
and sensory changes. A common cause of gastroenteritis,
Campylabaeter jejuni, is the most frequent infectious agent
(Hahn, 1998). Although certain viruses, bacterium, surgery,
and vaccinations have been linked to CBS, there is no one
causal agent. It is a reactive, self-limited autoimmune disease
with a good overall prognosis.
Pathophysiology
The pathophysiology of CBS is complex because it involves
autoimmune reactions. The immune responses cause a crossreaction
with neural tissue. When myelin is destroyed,
destruction is accompanied by inflammation. These acute
inflammatory lesions are present within several days of the
onset of symptoms. Nerve conduction is slowed and may be
blocked completely. Even though the Schwann cells that produce myelin in the peripheral nervous system are
destroyed, the axons are left intact in all but the most severe
cases. Two to three weeks after the original demyelination, the
Schwann cells begin to proliferate, inflammation subsides,
and remyelination begins (Ropper et aI., 1991).
While CBS is the most common cause of acute paralysis,
the exact pathogenesis is as yet unclear. The progression of
the demyelination appears to be different in the AMAN
type of CBS versus the AIDP type. Patients with the AMAN
type have a more rapid progression and reach nadir earlier.
Nadir is the point of greatest severity. The only way to classify
a patient with CBS as having the axonal or nonaxonal
type is electrodiagnostically (Hiraga et a!', 2003).
Clinical FGatures
CBS is characterized by a symmetrical ascending progressive
loss of motor function that begins distally and progresses
proximally. Distal sensory impairments often present
as paresthesias (burning, tingling) of the toes or hypesthesias
(an abnormal sensitivity to touch). The sensory involvement
varies and is usually not as significant as the motor involvement.
The progression of motor and sensory changes may
be limited to the limbs, or the progression of weakness can
impair the diaphragm and cranial nerves.
The diaphragm is the major muscle of ventilation.
Weakness of shoulder elevators and neck flexion parallels
diaphragmatic weakness. The diaphragm is innervated by
cervical nerve roots 3, 4, and 5. If the diaphragm becomes
involved, the person will need to be placed on mechanical
ventilation. In addition, 50 percent of people with CBS
experience changes in the autonomic nervous system such
as fluctuations of blood pressure and pooling of blood with
poor venous return, tachycardia, and arrhythmias.
Pain is reported by patients as being muscular in nature
(myalgia). Pain can be an early symptom and requires constant
intervention. Hypesthesias may make using a bed sheet
uncomfortable. Pain can be difficult to manage and add to
the person's fear and anxiety. The cause of pain is often
unclear but it may result from spontaneous transmissions
from demyelinated nerves (Sulton, 2002).
Half of the patients with GBS have oral-motor involvement
in the form of weakness that causes difficulty speaking
(dysarthria) and swallowing (dysphagia). Alternative means of
communication may need to be explored as well as measures
taken to prevent aspiration. The facial nerve (cranial nerve
VII) is frequently involved, and bilateral facial weakness is
common. Double vision (diplopia) can result from eye muscle
weakness secondary to cranial nerves III, IV, and VI involvement.
Paralysis ofcranial nerves is termed bulbarpalsy. Cranial
nerve involvement is referred to as bulbar because the majority
of cranial nerves exit the bulb or brainstem. Deep tendon
reflexes are absent because of the demyelination of the
peripheral nerves, therefore making areflexia a core feature of
this lower motor-neuron disorder.
Medicai Management
The mainstay of medical management of patients with GBS
is plasmapheresis or Infusion of immunoglobulins. In plasmapheresis,
blood is removed from the body, the red and white
blood cells are separated from the plasma, and only the blood
cells are returned to the patient. The patient makes more
plasma to replace what has been removed. It is thought that
removing the plasma eliminates some of the immune factors
that are responsible for the disease progression. Studies have
shown that the use of plasmapheresis reduced the length of
the illness as well as shortened times on mechanical ventilation
and led to earlier ambulation (Dada and Kaplan, 2004).
Immunoglobulins given intravenously have also had a positive
impact on speed of recovery. One study showed IV
immunoglobulins (IVIG) to be at least as effective as plasma
exchange. In addition, IVIG is less likely to transmit infection
and has fewer side effects (Sulton, 2002; Gilroy, 2000). Both
of these interventions need to be initiated within the first
week or two ofsymptom onset in order to shorten the course
of the disease (Pascuzzi and Fleck, 1997).
There are three phases of GBS: acute, plateau, and recovery.
The first stage lasts up to four weeks. During this time,
symptoms appear: 80 percent of individuals present with
paresthesias, 70 percent with areflexia, and 60 percent with
weakness in all limbs. Gradually the percentages of patients
exhibiting the core symptoms increase to close to 100 percent.
The plateau phase is defined by the stabilization of
symptoms. While symptoms are present, they are not progressing
or getting worse. This phase can also last up to four
weeks. Lastly, the recovery phase is evident when the patient
begins to improve. Eighty percent of patients recover within
a year (Sulton, 2002) but may have some neurologic sequel
or residual deficits. The recovery phase can last a few
months to several years. Patients who tend to have a poorer
outcome include those who needed ventilatory support,
had a rapid progression of demyelination, and demonstrated
low distal motor amplitudes on EMG (Ropper et al.,
1991). The latter finding is reflective of the amount of
axonal damage incurred.
PT TREATMENT
ACUTE PHASE
Supportive care during the acute stage is a necessity. Because
of the possibility of respiratory involvement, people with
GBS are hospitalized and may spend a long time in intensive
care. During the acute phase, it is most appropriate for the
physical therapist to treat the patient as symptoms are usually
progressing. If a patient's respiratory musculature becomes
involved, he will likely require ventilatory support and be in
an intensive care unit (ICU). Physical therapy goals during
the acute stage include minimizing the acute signs and symptoms;
supporting pulmonary function, preventing skin breakdown
and contracture formation; and managing pain.
If the PTA is providing passive ROM and positioning
under the supervision of the physical therapist, the therapist
needs to provide information about oxygen saturation and
vital capacity parameters in order for the assistant to be alert
to changes in the patient's respiratory status. The physical
therapist assistant may also provide postural drainage with
percussion to maintain airway clearance. Gentle stretching of
the chest wall and trunk rotation may be done while the
patient is still on a ventilator (Hallum, 2001). The patient is
positioned to decrease potential contractures with hand and
foot splints. Extra care should be taken when performing
ROM because denervated muscles can easily be damaged.
The assistant should be careful to support the limb to prevent
overstretching. This includes always checking to be sure
that the anlde is in a subtalar neutral position prior to stretching
the heel cord. The subtalar neutral position in which the
talus is equally prominent when palpated anteriorly can be
seen in Figure 13-2. ROM should be performed at least twice
a day. The schedule of positioning, splinting, and the ROM
program should be posted bedside (Hallum, 2001).
Pain is one of the most difficult symptoms to treat in
patients with GBS. Medications are not always effective.
Passive ROM, massage, and transcutaneous electrical nerve
stimulation may be helpful. If the patient demonstrates an
increased sensitivity to light touch, a cradle can be used to
keep the bed sheet away from the skin. Low-pressure wrapping
or a snug-fitting garment may provide a way to avoid
light moving touch on the limbs. Pain may be heightened
by the patient's fear about what has happened. Reassurance
and an explanation about what to expect may help alleviate
anxiety that could compound the pain (Karni et aI., 1984).

PLATEAU PHASE
When respiratory and autonomic functions stabilize, a program
to increase tolerance to upright can be begun. This must be initiated very gradually because the patient may
still be on a ventilator. Physical therapy goals during the
plateau phase include acclimation to upright, maintenance
of ROM, improvement in pulmonary function, and avoidance
of fatigue and overexertion. The patient is acclimated
to sitting upright with appropriate postural alignment and
support of the trunk since it may still have minimal innervation.
Pressure relief is still provided by changing positions
on a regular basis. If the patient continues to experience
pain, it may lead to holding limbs in potentially contracture-
prone positions. Heat may be used prior to stretching if
there is no sensory loss. Return of oral musculature may signal
the need for additional team members to work on the
movement patterns needed for swallowing, eating, and
speaking. The physical therapist assistant may provide postural
support for the patient during these sessions. At the
very least the assistant needs to be aware of any precautions
regarding potential aspiration and any requirement for
maintaining an upright upper-body posture after any oral
intake of food or fluids.
RECOVERY PHASE

Muscle strength is gradually recovered two to four weeks
after the condition has reached a plateau. The muscles
return in the reverse order or descending pattern. This is
opposite from the ascending order of loss. As the neck and
trunk muscles recover, the patient may begin to use a tilt
table for continued acclimation to upright and weight bearing
on the lower extremities. Positioning splints may be
needed for the lower extremities as well as thromboemolic
stockings to decrease venous pooling. Muscles of respiration
can be weak if the person required ventilatory assistance,
and this weakness may limit tolerance to upright.
Physical therapy goals at this time now encompass
strengthening and maximizing functional abilities in addition
to carrying over any goals from the previous phases.
Strengthening activities and exercise prescription for these
individuals is challenging. Depending on the number of
intact motor units present in any given muscle, the same
amount of exercise can be harmful or beneficial. If there are
too few motor units, working the muscle may be detrimental
to its recovery. Unfortunately, there is no easy way to ascertain
how many motor units are present in a patient recovering
from GBS.
Once the patient has stabilized or reached a plateau,
active exercise can begin. Bensman (1970) recommends the
following four guidelines for exercise:
1. Use short periods of nonfiltiguing exercise matched to
the patient's strength.
2. Increase the difficulty of an activity or level of exercise
only if the patient improves or if there is no deterioration
in status after a week.
3. Return the patient to bed rest if a decrease in strength
or function occurs.
4. Direct the strengthening exercises at improving function,
not merely at improving strength.
Ove17fJork weakness is a term first used in conjunction with
polio in the late 1950s. The term continues to be used when
describing the hazards of overworking partially denervated
muscles. Overworking a partially denervated muscle produces
a profound decrease in that muscle's ability to demonstrate
strength and endurance. Signs ofoveruse weakness are delayed
onset of muscle soreness, which gets worse one to five days
after exercising, and a reduction in the maximum amount of
force the muscle is able to generate (Clarkson et al., 1992;
Faulkner et al., 1993). Bassile (1996) recommends training
muscles that are at a 2/5 muscle strength in a gravity-eliminated
plane using only the weight of the limb. Once the person
can move the limb against a resistance equal to the mass
of the limb, the person can perform antigravity exercise.
Hallum (2001) views exercise progression in this population asa pyramid with passive ROM on the bottom, functionally
specific resistive exercise on the middle tier, and coordinated
functional movement at the top.
Regardless of the terminology, everyone agrees that it is
best to start with low repetitions and short, frequent bouts of
exercise matched to the patient's muscular abilities, that is,
muscle strength. For example, someone who has poor (2/5)
deltoid muscle strength could exercise in a pool, or with an
overhead sling apparatus or a powder board. All of these situations
are gravity-eliminated. Facilitation techniques such
as stroking, brushing, vibration, and tapping of the muscle
can be combined with gravity-eliminated exercise. The
patient is restricted from moving against gravity until the
deltoid muscles' strength is a 3/5. The lower extremities are
going to recovery after the upper extremities. Most people
walk within six months of the onset of symptoms (Hallum,
2001). The dilemma comes as to whether to attempt
ambulation with a patient before the muscles of the lower
extremities have at least a fair grade (3/5) (Bassile, 1996).
Adaptive equipment needs change as the patient recovers.
Once acclimated to upright, mobility may initially be limited
to a wheelchair. When ambulation is achieved, a walker,
forearm crutches, or a cane may be needed as an assistive
device. Orthotic assistance needs to be lightweight. A plastic
AFO or even an air stirrup splint can provide support for
weak anldes. Residual weakness is most often apparent in the
distal muscles of the hands and feet such as the wrist extensors,
finger intrinsics, ankle dorsiflexors, and foot intrinsics.
The gluteal and quadriceps may also remain weak.
Endurance is often lacking and may be a major obstacle even
if the person is strong enough to return to work. Endurance
training should be included in the patient's home exercise
program; otherwise the patient may continue to be minimally
active despite adequate strength. Pitetti and associates
(1993) studied a 54-year-old man three years post GBS. He
was able to improve leg strength and total work capacity after
a three-times-a-week aerobic exercise program using a bike
ergometer. He was even able to return to gardening.
SAFEGUARDING THE MUSCULOSKELETAL AND CARDIO PULMLNARY SYSTEM
The prognosis for a person with Guillain-Barre Syndrome is
usually very good. Fortunately, the muscle weakness is
reversed as the peripheral nervous system recovers.
However, patients with GBS are often immobilized for
lengthy periods of time due to the slow nature of the recovery
process. The health care team's role during that time is
to safeguard the musculoskeletal and cardiopulmonary systems
so that when recovery occurs, the patient is able to
make the most of the changes. The role of exercise in this
neuromuscular disease is to improve function without causing
overuse damage. The use of nonfatiguing exercise protocols
is indicated. These protocols will be discussed further
in the section on postpolio syndrome.
Acute inflammatory demyelinating
polyradiculopathy
Acute inflammatory demyelinating polyradiculopathy, also
known as Guillain-Barre syndrome, was first described by
Landry in the 1860s, but derived its eponym from a description
in 1916 by Georges Guillain and Jean Alexander Barre. Guillain
and Barre recognized that this was a paralyzing condition associated
with an increased concentration of protein, but not cells,
in the cerebrospinal fluid. This laboratory finding was termed
cytoalbuminologic disassociation, and distinguished the condition
from other causes of acquired acute paralysis such as poliomyelitis.
Since their original description, other related disorders
have been identified. These include a relapsing-remitting form,
the Miller-Fisher variant, in which there is ataxia, ophthalmoplegia,
and depressed MSRs but preserved strength,SO and a
slowly progressive (chronic) steroid-responsive form.
Guillain-Barre syndrome is an acquired symmetric polyneuropathy
that usually affects the lower extremities initially. It
often begins with paresthesias in the toes or fingertips, followed
shortly by weakness, which begins distally and then ascends
proximally. Pain is a less common symptom but can be present
in the form of a deep backache, or less commonly as painful
limb paresthesias. The weakness progresses over days to about
4 weeks and can, in severe cases, produce total body paresis,
including of the muscles of respiration. GBS can involve somatic,
cranial, and autonomic nerves. The extraocular muscles and
sphincters are generally spared.
The etiology of GBS is not fully established, but the condition
often begins several weeks following a viral or bacterial
infection, immunization, or surgery9 Diagnostic criteria llH for
typical GBS include the required features of areflexia and
acquired, progressive weakness in all extremities. Features that
strongly support the diagnosis include progression over a period
of up to 4 weeks, relative symmetry, mild sensory symptoms,
cranial nerve involvement, recovery beginning 2-4 weeks after
progression ceases, autonomic dysfunction, elevated concentration
of protein in the cerebrospinal fluid with <10 cells
per mm3, and typical electrodiagnostic features.
On physical examination, GBS shows symmetric limb weakness.
Bilateral facial weakness is also present in one-third of the
patients. The MSRs are absent. Sensory deficits are usually
mild. If respiratory muscles are involved, the vital capacity is
usually one-half the predicted value. The vital capacity should
be carefully monitored, because weakness can progress rapidly
and the patient might require ventilatory support. Autonomic
function is often affected (71 %) S9 and can produce abnormalities
in heart rate, heart rhythm, and blood pressure. A period
of observation in an intensive care unit is necessary. Patients
who require ventilatory support generally have a longer period
of recovery that can extend over months.99
The damage to the nerve in GBS appears to be primarily of
a demyelinating type, but in more severe cases there can also
be prominent axonalloss.39 Histologic examination of the nerves
reveals lymphocytes and macrophages surrounding the endoneurial
vessels.s The neuropathy is thought to be produced by
a cell-mediated attack on the myelin sheath, although in some
cases the axons appear to be the target instead. In general,
antibodies have not 'been shown to be causative of the nerve
dysfunction. The role of other humoral mediators, such as
cytokines, has also not been established thus far.
The nerves are affected earliest at the root leve1.9 Shortly
thereafter, the most distal part of the nerve becomes involved,
with the intervening segments being affected last.
Electrodiagnostic findings in Guillain-Barre syndrome
Because the earliest involvement of GBS is at the nerve root
level, the earliest electrodiagnostic abnormalities are prolongation
or absence of the late responses (F wave and H reflex).
A few days later, there can be a prolongation of distal
latency, and then slowing of motor nerve conduction velocity.
Temporal dispersion of the evoked responses and partial conduction
block between distal and proximal stimulus sites can
also be seen. The EMG in patients with weakness tends to show
a reduction in the number of motor units firing on maximal
effort.
If serial studies are performed, the electrodiagnostic findings
frequently lag behind the clinical course, both during worsening
and recovery phases.s EMG signs of denervation indicate that
the patient has a component ofaxonopathy rather than just
demyelination. A poorer short-tern1 outcome is suggested when
axonal change is seen with the amplitude of the distal compound
muscle action potential < 10% of normal.
Management of Guillain-Barre syndrome
Patients with acute GBS should be hospitalized for observation
and monitoring of the progression of the disease. It is particularly
important to serially monitor the pulmonary and cardiovascular
systems. If the vital capacity is rapidly declining,
especially if it is <18 mUkg of body weight, liS or .if there is
cardiovascular dysautonomia, the patient should be monitored
in an intensive care unit. Mechanical ventilation might become
necessary.
Due to their immobility, these patients are at risk for developing
deep venous thrombosis, pressure ulcers, and other complications
of immobility. Appropriate preventive and treatment
measures should be undertaken. Treatment with plasmapheresis
or high-dose intravenous immunoglobulin (IVIg) is effective
in shortening the course of an attack of GBS.97 Plasmapheresis
is done in a series of three to five plasma exchanges, performed
on an approximately every other day schedule.6s Intravenous
gamma globulin is usually administered daily at 0.4 g/kg of body
weight for five consecutive days. lOS
Intravenous immunoglobulin has som~ advantages over plasmapheresis.
It is easier to administer, has fewer complications,
and is more comfortable for the patient. lOS IVIg can cause selflimited
flu-like symptoms such as fever, myalgia, headache,
nausea, and vomiting.92 It should be used cautiously in patients
with congestive heart failure and renal failure, due to the resulting
increased plasma volume. Los
Contraindications to plasma exchange include recent myocardial
infarction, angina, sepsis, or cardiovascular dysautonomia.
IIB A rare complication of plasmapheresis is sepsis, thought
to be secondary to immunoglobulin depletion.53 There is a
risk of acquiring viral infections, such as hepatitis or HIV,
if fresh frozen plasma is used. GBS does not respond to
corticosteroids. 71
Rehabilitation methods In the early stages of GBS, the
patient can be bedridden due to weakness and even tetraplegia.
During this time, it is important to prevent contractures
with range of motion exercise, positioning, and the use of static
splints. Careful positioning and turning are necessary to prevent
peripheral nerve compression and pressure ulcer formation.
Meticulous pulmonary care is indicated to prevent atelectasis
.and pneumonia.
The rehabilitation program is gradually advanced in intensity
as the patient improves. Because the patient with GBS is susceptible
to overwork weakness, the strengthening program
should initially be non-fatiguing. When muscles regain greater
than antigravity strength, they can generally be stressed with
more aggressive strengthening exercises. If the exercises are
advanced too quickly, however, there can be a regression of
strength (the so-called overwork weakness). 10 This occurrence should alert the clinician and therapist to reduce the
activity
level.
During recovery, patients with GBS often benefit from the
use of orthoses and assistive devices. Rocker feeders are helpful,
as are clothing adaptations and other assistive devices (see Ch.
27). Ankle-foot and wrist orthoses can be useful in preventing
contractures and enhancing function. It is more common for
GBS patients to develop tightness of two-joint muscles than
joint contractures. Stretching of these muscles alleviates this
problem, and should include the hamstrings, tensor fascia lata,
and gastrocnemius muscles.
Gait retraining typically begins with the use of the tilt table.
The tilt table is actually valuable well before gait training is
possible, as it helps prevent orthostatic intolerance. Tilt table
training can be instituted as soon as the patient is medically
. stable. This can also be started by elevating the head of the bed
and having the patient sit upright for extended periods as tolerated.
Cardiovascular and autonomic adaptation occur as the
patient is gradually elevated to the upright position. Patients
are eventually allowed to stand in a standing table, which
improves their muscular endurance and permits them to work
on other tasks. When muscle strength improves sufficiently, the
patient is advanced to the parallel bars. This is done with the
close assistance of a therapist to assist in movement and to
prevent falls. As gait skills improve, the patient can be advanced
to an assistive device for ambulation, such as a walker, and then
to crutches or canes. The patient is ultimately advanced to
ambulation without assistance or with assistive devices. Lowerextremity orthoses are used as indicated throughout the
course
of treatment (see Ch. 16).
In addition to progressive ambulation training, patients
develop upper limb strength and endurance through a combinalion of functional and weight-training exercises. The goal is
to
achieve independent self-care using assistive devices as needed
(only temporarily, it is hoped). Most patients tolerate such a
rehabilitation program and go on to an essentially complete
recovery. Approximately 85% of patients with GBS achieve a
full and functional recovery within 6-12 months. 105 The 7-15%
or so who do not recover completely from GBS"8 benefit from
the long-term use of assistive devices and rehabilitation strategies.
Relapse of GBS can occur, but only at a rate of 3_5~o.67