GUILLAIN BARRE SYNDROME

• Guillain-Barré syndrome (GBS) may be described as a collection of clinical syndromes manifested by an acute inflammatory polyradiculoneuropathy with resultant weakness and diminished reflexes.
• GBS is considered to be a postinfectious immune-mediated disease targeting peripheral nerves. Up to two thirds of patients report an antecedent illness prior to the onset of neurologic symptoms. Respiratory infections are reported most frequently, followed by gastrointestinal infections.
• Campylobacter jejuni is the most common pathogen isolated in several studies.
• Both gastrointestinal and upper respiratory tract symptoms can be observed with C jejuni infections.
• Pathological findings in GBS include lymphocytic infiltration of spinal roots and peripheral nerves, followed by macrophage-mediated multifocal stripping of myelin. This phenomenon results in defects in the propagation of electrical nerve impulses with eventual conduction block and flaccid paralysis.

Symptoms

Antecedent illness

• Up to two thirds of patients with GBS report an antecedent illness or event 1-3 weeks prior to the onset of weakness.
• Upper respiratory and gastrointestinal illnesses are the most commonly reported conditions. Symptoms generally have resolved by the time of medical presentation for the neurologic condition.

Weakness

• The classic clinical picture of weakness is ascending and symmetrical in nature.
• The lower limbs usually are involved before the upper limbs.
• Proximal muscles may be involved earlier than the more distal ones.
• Trunk, bulbar, and respiratory muscles can be affected as well.
• Weakness develops acutely and progresses over days to weeks. Severity may range from mild weakness to complete tetraplegia with ventilatory failure.
• Peak deficits are reached by 4 weeks after initial development of symptoms. Recovery usually begins 2-4 weeks after progression ceases.

Sensory changes

• Most patients complain of paresthesias, numbness, or similar sensory changes.
• Sensory symptoms often precede the weakness.
• Sensory symptoms frequently are ascending in nature and are more pronounced in a distal distribution.
• Sensory symptoms are usually mild. Objective findings of sensory loss tend to be minimal and variable in most cases.

Reflex changes

• Reflexes are absent or hyporeflexic early in the disease course and represent a major clinical finding on examination of the patient with GBS.
• Pathologic reflexes, such as Babinski, are absent.
• Hypotonia can be observed with significant weakness.

Pain

The mechanism of pain is uncertain and may be a product of several factors. Pain can be due to direct nerve injury or the paralysis and prolonged immobilization.

• Most patients complain of back and leg pain, often described as aching or throbbing in nature. The mechanism of pain is thought to be inflamed nerve roots.
• Dysesthetic symptoms are observed in approximately 50% of patients during the course of their illness. Dysesthesias frequently are described as burning, tingling, or shocklike sensations and are often more prevalent in the lower extremities than in the upper extremities.
• Other pain syndromes in GBS can include myalgic complaints with cramping and local muscle tenderness, visceral pain, and pain associated with conditions of immobility (eg, pressure nerve palsies, decubitus ulcers).

Autonomic changes

• Autonomic nervous system involvement with dysfunction in the sympathetic and parasympathetic systems can be observed in patients with GBS.
• Autonomic changes can include the following:
• Tachycardia
• Bradycardia
• Facial flushing
• Orthostatic hypotension
• Autonomic changes rarely persist in the patient with GBS.

Respiratory involvement

• Upon presentation, 40% of patients have respiratory or oropharyngeal weakness.
• Typical complaints may include the following:
• Dyspnea on exertion
• Shortness of breath
• Difficulty swallowing
• Ventilatory failure with required respiratory support is observed in up to one third of patients at some time during the course of their disease.
• GBS-related deaths usually occur in ventilator-dependent patients due to complications such as pneumonia, sepsis, etc.

Treatment Principles

• The goals of the therapy programs are reducing the functional deficits and targeting the impairments and disabilities resulting from GBS.
• Early in the acute phase of the disease course, patients may not be able to participate fully in an active therapy program.
• At that stage, patients benefit from daily range of motion (ROM) exercises and proper positioning to prevent muscle shortening and joint contractures.
• Addressing upright tolerance and endurance also may be a significant issue during the early part of rehabilitation.
• Active muscle strengthening then can be introduced slowly and may include isometric, isotonic, or progressive resistive exercises.
• Mobility skills, such as bed mobility, transfers, and ambulation, are targeted functions.
• Patients should be monitored for hemodynamic instability and cardiac arrhythmias, especially upon initiation of the rehabilitation program.
• The intensity of the exercise program also should be monitored, as overworking the muscles, paradoxically, may lead to worsening weakness.
• Energy conservation techniques and work simplification also may be helpful, especially if the patient demonstrates poor strength and endurance.