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GBS and may be associated with increased protein in the CSF [179]
Other inflammatory diseases may mimic GBS Chronic inflammatory
demyelinating polyneuropa thy (CIDP) resembles GBs in its symmetry, increased
CSF protein level, and demyelinating changes on NCV/EMG [180]. It generally
progresses more slowly and is less severe, however, Treatment for GBS is usually
effective in CIDP. Myasthenia gravis usually presents with extraocular weakness,
and pharyngeal, neck, and respiratory muscle involvement is common [181].
DTRs are usually preserved. Myasthenia gravis can easily be confused with the
Fisher and pharyngeal-cervical brachial variants of GBS.
Some drugs, chemicals, and nonbacterial toxin: cause paralytic illnesses.
An axonal neuropathy that causes an ascending paralysis with areflexia that
begins with paresthesias occurs after exposure io nhexane or to methyl-butyl-
ketone [182]. Despite quadriparesis, cranial nerve-innervated and respiratory
muscles are not involved. Thallium, arsenic and lead can cause axonal
neuropathies that superficially resemble GBS [183]. Non-neurologic signs and
symptoms such as gastrointestinal distress alopecia, and rash help to differentiate
these syndromes from GBS. Paralysis is common in acute organophosphate
poisoning [184]. A delayed syndrome with weakness, early respiratory failure, an
ophthalmoplegia might mimic GBS but usually presents with normal nerve
conduction velocities. The fruit of the buckthorn shrub, found in the south western
United States and in Central America causes a syndrome indistinguishable from
GBS through an unknown mechanism [185]. The CSF of these patients is usually
normal.
Metabolic derangements can also cause a flaccid paralysis. Standard
laboratory tests can often delineate these disorders. Hypokalemic periodic
paralysis causes a flaccid paralysis with electrically unexcitable skeletal muscle
[186]. Simple laboratory tests, a history of prior attacks, and rapid evolution of
weakness serve to differentiate this disease from GBS. Hypophosphatemia, often
caused by total parenteral nutrition, ethanol abuse, and rapic refeeding after
starvation, causes an acute flaccid, areflexic paralysis evolving over several days
[187]. The weakness responds to phosphate replacement. A motor neuropathy
occurs in acute intermittent porphyria and hereditary coproporphyria [188].
Unlike GBS, mental status is frequently impaired and episodes of weakness are
usually preceded by severe abdominal pain. EMG studies show evidence of
denervation.
Miscellancous imitators of GBS include hysteria, malingering, and
conversion reaction. Bizarre examination findings and normal reflexes are often
seen. Malingering or conversion should always be a diagnosis of exclusion and an
overnight admission is often warranted, Critical illness polyneuropathy occurs in
intensive care unit patients, frequently in the setting of sepsis or multiorgan failure
[189]. Often, the neuropathy follows acute respiratory failure [190]. The cause is
an axonal sensorimotor neuropathy of unknown etiology. Clinically, severe cases
are difficult to discern from GBS, but NCV/EMG studies consistent with an
axonal polyneuropathy are often diagnostic.

Treatment and Prognosis

Treatment of GBS is directed across two fronts: supportive care and
immunomodulation. Although specific immunomodulatory treatments favorably
alter the course of GBS, they do not change mortality. Meanwhile, advances in
ventilation, intensive care medicine, and skilled nursing have more prominently
decreased the mortality and the long term morbidity.

Supportive Care
Supportive care continues to be the most important factor in improved survival
rates and decreased morbidity rates in GBS. Respiratory failure is common in
GBS. with about one-third of patients requiring mechanical ventilation at some
point during their course. Patients on ventilators require an average of 49 days of
assisted respiration. New patients should have vital capacities and negative
inspiratory pressures determined every 8 hours and more frequently if the vital
capacity is decreasing. Consistency in position and method is required for
meaningful comparisons of respiratory measurements. Positive pressure
ventilation should be initiated when vital capacities have dropped to about 15
ml/kg and negative inspiratory pressures are less than -25 cm H 2O. Intermittent
mandatory ventila-