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  • Landry-Guillain-Barré-Strohl syndrome
  • Acute inflammatory demyelinating polyneuropathy
  • Acute demyelinating polyneuritis

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  • 357.0 Acute infective polyneuritis

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  • G61.0 Guillain-Barré syndrome

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Description

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Essentials of Diagnosis

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  • Most common bacteria identified with Guillain-Barré syndrome (GBS) is Campylobacter jejuni; other common infections include cytomegalovirus and Epstein-Barr virus
  • 60% of cases have preceding upper-respiratory illness or vaccination 1 to 3 weeks prior to onset

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General Considerations

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  • Two forms of GBS are common, though several other variants exist
    • Non-axonal form
      • Peripheral nerves undergo demyelination, but no damage to axons
      • High likelihood of regaining full function with appropriate medical and therapeutic intervention
    • Axonal form
      • Axon of the peripheral nerve is damaged, does not re-myelinate
      • Function through that nerve is lost, patient will likely have permanent functional loss of associated muscle
  • Rapid progression from onset to potential respiratory failure; should be identified and treated very quickly
  • Most patients show gradual return of strength beginning 2 to 4 weeks after the point at which progression of the disease stops (“nadir”)
  • Approximately 50% of patients experience dysfunction of the autonomic nervous system, including
    • Low cardiac output
    • Cardiac dysrhythmias
    • Marked fluctuation in blood pressure
    • Poor venous return
    • Bowel and bladder retention

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Demographics

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  • Males and females of all ages susceptible
  • Approximately 4 in 100,000 people afflicted each year

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Signs and Symptoms

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  • Progressive weakness in distal to proximal direction resulting in quadriplegia
    • Decreased muscle strength, recruitment, endurance
    • Decreased active range of motion (AROM)
    • Decreased sensation in stocking/glove pattern
  • Loss of deep tendon reflexes, initially at the calcaneal (Achilles) tendon
  • Deep muscle aching
  • Respiratory failure

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Functional Implications

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  • Bed mobility, transfers, gait, basic and complex ADLs
  • Decreased independence with all self-care
  • Decreased ability to interact with environment physically, verbally, sometimes visually (if cranial nerves controlling vision are affected)

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Possible Contributing Causes

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  • Definitive cause unknown
  • Campylobacter jejuni most common bacterium associated with GBS
  • Pre-morbid respiratory illness (severe cold or flu) is also a common contributing cause

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Differential Diagnosis

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  • Spinal cord compression (myelopathy)
  • Miller-Fisher syndrome (GBS variant)
  • Chronic inflammatory demyelinating polyradiculoneuropathy
  • Acute spinal cord disease
  • Myasthenia gravis
  • Sarcoidosis
  • Upper motor neuron (UMN) disorder
  • Tick paralysis
  • Poliomyelitis
  • Polyarteritis nodosa
  • Polyneuropathy of critical illness
  • Transverse myelitis
  • Cervical stenosis
  • Spinal tumor
  • Diabetic neuropathy

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Laboratory Tests

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  • Test of cerebral spinal fluid (CSF): positive if protein levels elevated

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Imaging

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  • MRI with contrast will show gadolinium enhancement of cauda equina roots

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