GBS
-There are multiple variants of GBS!

-AIDP (Acute inflammatory demyelinating polyneuropathy)- 85-95 % of GBS
-Miller Fisher Variant (5 % US but up to 25 % in Japan)
-AMAN (Acute motor axonal neuropathy)
-AMSAN (Acute sensorimotor axonal neuropathy)

Timing

Acute (<4 weeks)

Pathophysiology

Due to molecular mimicry from immune response to preceding infection that cross reacts with components of the peripheral nerve.

Most common infectious triggers?
-Campylobacter Jejuni (most common), CMV, EBV, HIV, VZV, Mycoplasma, and even Zika virus

Most sensitive physical exam findings in GBS

-Absent/Depressed DTR (90 %)
-Ascending extremity weakness (90 %)
-Paresthesias (80 %)
-Dysautonomia (70 %)
-Facial weakness or bulbar signs (55 %)
-Back/extremity pain, respiratory failure, oculomotor weakness

What do you see on LP?

Albumino-cytologic dissociation (normal WBC with high protein)

HOWEVER, only 50 % of patients with GBS have it at one week, with >75 % of patients have it at 3 weeks so make sure you interpret it in the right clinical setting

Miller Fisher variant TRIAD (don’t need to see all three)

-Ophthalmoplegia
-Ataxia
-Areflexia
Antibodies against GQ1b (anti-ganglioside) present in 85-90 % of patients- however, this will take a long time to come back and won’t change your initial management.

Treatment

-Supportive treatment
-IVIG 
-Plasma Exchange

Remember that steroids are not effective!