AIDP atypical forms and mimics PT I

Levin KH. Variants and mimics ocf Guillian Barre Syndrome.The Neurologist 2004;10:61-74

typical case AIDP: febrile antecedent esp. campylobacter jej, CMV, EBV, infl, mycoplasma, coxsackie, hepatitis virus. Other noninfectious causes include Hodgkins dis, and events such as surgery, childbirth, and immunization. Within 2 weeks, get symmetric leg paresthesiae, tingling, crawling sensations, pain esp in back (50%), ascending weakness. 50 % develop weakness diaphragmand cranial nn. > 50 % have autonomic findings. CSF dissociation acellularity, increased protein, and typical NCS (not detailed here).
Variants: asymmetric; pure motor; prominent sensory loss; preserved DTR's; regional presentations (pharyngeal/brachial/cervical); paraparetic; facial diplegia with paresthesias; pure sensory neuropathy; pure autonomic neuropathy; Miller Fisher variant; axon loss variants (AMAN, AMSAN).
Miller Fisher syndrome-- triad opthalmoplegia, areflexia, ataxia (follows sensory loss). NCS show loss of SNAP amplitude. Course is often benign,maynot require IVIG/Plasmapx. may include facial weakness, dysarthria, dysphagia, abnormal pupils, limb weakness. 95 % have ANTI GQ1B antibodies.
AMAN-- Chinese disease-- NCS show motor amplitude loss without demyelination. High correlation with campylobacter. Antibodies to GD1a and GM1 at node of Ranvier. Involves complement activation and macrophage infiltration.
AMSAN-- cannot differentiate from AMAN until enough time has elapsed to show NCS findings. Typically this does not respond to IVIG/plasmapx.

Mimics:
tick paralysis-- notoriously overlooked in children, esp preadolescent girls. Ticks may infest scalp. Symptoms develop 2-4 days later including paresthesias, gait ataxia, diplopia, dysarthria, rapid weakness. Tick is dermocenter andersonii. Paralysis reverses within 24 hours of tick removal. Australian ticks cause paralysis that lasts longer. NCS show reduced CMAP amplitudes.

marine toxins-- ciguatoxin (diflagellates eaten by algae), tetrodotoxin (pufferfish) and saxitoxin
(dinoflagellates eaten by shellfish)cause paresthesias and weakness within hours. NCS show slow motor/sensory responses (mimics GBS) and dispersed CMAP.

buckthorn berry-- in SW USA and Mexico. Affects children and cattle causing rapid weakness within a few weeks. Limited amt published.

heavy metals (esp arsenic, gold, thallium).
Arsenic-- 7-14 days after ingestion. presents with N/V/D paresthesias, burning, then stocking glove loss small and large fibers. Weakness is distal to proximal and lead to footdrop. Predominant axon loss, Occassional ans dysfunction.
Gold-- usually secondary to RA treatment. PN, with pain, may be sudden or slow, with or without dermatitis and stomatitis.
Thallium-- usually deliberate ingestion (may be accidental in kids) or due to mal intent. Causes dermatitis, alopecia (usually a LATE finding), GI (N/V/D), CNS (ON, confusion, movement disorders, psych), acute and chronic PN. Starts with painful paresthesias and painful joints, ascending weakness, possibly normal DTR's, autonomic dysfunction