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Background:
?1859- Landry published a report on 10 patients with ascending paralysis
?1916- Guillain, Barre and Strohl described 2 French soldiers with motor weakness, areflexia, and ?albuniocytological dissociation? in the cerebrospinal fluid. They recognized the peripheral nature of the illness
Epidemiology:
?1-3 per 100,000 (US)
?M:F ? 1.5:1
?Ages: bimodal distribution with 2 peaks (15-35 yrs) & (50-75 yrs)
Etiology:
?Post-infectious AI disease
?Cellular and humoral mechanisms
?Association with administration of certain vaccinations, and other systemic illnesses
Auto-immunity In GBS
?Humoral immunity: antibodies formed against capsular antigens cross-react with myelin
?Target: gangliosides and glycolipids, such as GM1 and GD1b, distributed throughout the myelin in the peripheral nervous system
?Lmphocytic infiltration of spinal roots and peripheral nerves, followed by macrophage-mediated multifocal stripping of myelin
?Sub-group: primary immune attack directly against nerve axons
Variants:
?Miller-Fisher syndrome: ataxia, ophthalmoplegia, and areflexia. Anti-GQ1b antibodies (ophthalmoplegia)
?Acute motor axonal neuropathy (AMAN): pure motor axonopathy. Pediatric age groups
?Acute motor-sensory axonal neuropathy (AMSAN): axonal degeneration of motor and sensory nerve
?Pure sensory variant of GBS
?Acute pandysautonomia: postural hypotension, bowel and bladder retention, anhidrosis
Common Infectious Agents:
?Bacteria: C jejuni (60% in north China study), Haemophilus influenzae, Mycoplasma pneumoniae, and Borrelia burgdorferi
?Viruses: cytomegalovirus (13% in Dutch Study), Ebstein-Barr virus and HIV
Other Associations:
?Vaccines: group A streptococci vaccines, the rabies vaccine, and the swine flu vaccine
?Systemic illnesses: systemic lupus erythematosus, sarcoidosis, lymphoma, surgery, renal transplantation (ANECDOTAL)
Presentation:
?History - Antecedent illness
- Weakness (ascending and symmetrical)
- Sensory changes (ascending paraesthesias)
- CN involvement ( Facial droop, Diplopias, Dysarthria, Dysphagia)
- Pain (Back & leg)
- Autonomic changes
- Respiratory involvement
?Preceding illness
?2/3 of patients
?URTI or GI symptoms
?1-3 weeks prior to onset
?C jejuni- can cause both URTI or GI symptoms
?Weakness
?Classic clinical picture is ascending and symmetrical
?Develops over days to weeks
?Can very from mild to tetraplegia
?Peaks 4 weeks after onset
?Recovery 2-4 weeks after peak
?Sensory change
?Frequently ascending as well
?Parasthesia, numbness.
?Usually mild
?Cranial nerve involvement
?45-75% of patients
?Facial drop
?Diplopia
?Dysarthria
?Dysphagia
?Pain
?89% of one study experienced pain
?50% of these severe and distressing
?Back and leg pain
?Autonomic symptoms
?Tachycardia, bradycardia
?Urinary retention
?Sweating
?Respiratory involvement
?40% of patients
?Exertional dyspnea
?SOB
?Slurred speech
?Ventilatory arrest
Physical
?Tachycardia/bradycardia, tachypnea
?BP lability
?Lower extremities first affected
?If marked asymmetry then ???GBS
?Weakness
?Hyporeflexia or absent reflexes
?Normal objective sensory exam
?If marked then ??? GBS
?CN: facial weakness, also VI,III,XII,IX,X
Investigations:
?CSF studies- CSF protein (>0.55 g/L) without an elevation of white blood cells (<10 lymphocytes/mm3)
?EMG / NCV - demyelination: nerve conduction slowing
- Axonal variant: absent or markedly reduced distal compound muscle action potentials (CMAP)
? Pulmonary Function tests- Max Insp. Pressure, VC
Management:
?Constant vigilant monitering
?Rehab
?Physical
?Speech
?Mental
?Respiratory support
?Immune therapy
Monitoring
?Monitor
?RR
?Vitals
?ABG
?PFT
?Pressure sores, DVT prophylaxis
?Enteric/Parenteral feedings
?Requires SCU/ICU admission
Immunotherapy:
Plasmapheresis
?IVIG- blocks macrophage receptors, inhibits antibody production, complement binding, and neutralizes pathologic antibodies
Prognosis:
?Most patients (up to 85%) with GBS achieve a full and functional recovery within 6-12 months
?7-15% of patients have permanent neurologic sequelae
?Mortality rate less than 5%
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