Guillain-Barre Syndrome (GBS)
Background
- Rapid-onset polyneuropathy that manifests most often with ascending weakness and numbness that can involve the respiratory and facial musculature
- Usually preceded by infectious illness a few weeks prior (Campylobacter, CMV, Flu, HIV, etc)
- Pts are much more likely to get GBS from an infection than any vaccine, weak vaccine links to GBS are an additional 1-2 cases per million flu vaccines
Presentation
- Most common form is acute inflammatory demyelinating polyneuropathy (AIDP)
- Progressive extremity weakness, weak or absent reflexes, and potentially subjective sensatory changes, especially back pain, with nadir being reached within 4 weeks
- Sensory loss is common in an ascending pattern too
- There are many variants of GBS
- Miller-Fischer Syndrome: ophthalmoplegia, ataxia
- Bickerstaff brainstem encephalitis: encephalopathy, ophthalmoplegia, ataxia
- Pure Sensory GBS: sensory loss with only mild motor involvement
- Do not use lack of classic ascending weakness to dismiss the idea of GBS
Evaluation
- LP: albuminocytologic dissociation = high protein with normal cell count
- One exception is HIV, which can cause AIDP but also have a high cell count and high protein count
- EMG/NCV: usually normal early in course, so typically performed at least 2 weeks after symptom onset
- MRI L-Spine w/wo: Assess for spinal cord lesions, can demonstrate nerve root enhancement
- Ddx: Spinal cord lesions, LEMS, MG, acute HIV or HCV, viral myelitis (enterovirus/WNV)
Management
- ABCs! Ensure adequate respiratory status with baseline NIF/VC, then Q4-6H
- NIF > -30 with good effort, generally warrants ICU monitoring
- IVIG or PLEX
- Avoid steroids as they can worsen symptoms