Acute demyelinating polyneuropathy (AIDP), which closely resembles Guillain-Barré syndrome (GBS) is a rare but well recognised disease in PLWH. The pathogenesis of HIV associated AIDP is unknown. Proposed mechanisms include cell-mediated macrophage demyelination, perivascular T cell lymphocytic infiltration, antibody mediated neuronal damage secondary to molecular mimicry, and HIV neurotoxic proteins ​(75)​. AIDP most commonly occurs in early HIV disease associated with seroconversion, early asymptomatic HIV or as an immune reconstitution disorder one to two months post cART commencement ​(75)​. Chronic inflammatory demyelinating polyneuropathy (CIDP) may occur during any stage of HIV disease though it is exceedingly uncommon with advanced immunosuppression (CD4 count < 200 cm/mm3) where CMV is more likely as it can cause a radiculomyelopathy that can mimic AIDP/CIDP ​(75)​.  

AIDP and CIDP are characterised by progressive, ascending weakness with early loss of reflexes. HIV associated AIDP is generally monophasic with symptoms peaking at 4 weeks with recovery over months to years. Diagnosis is confirmed with nerve conduction studies demonstrating a demyelinating process, and CSF examination which may show classical albuminocytologic dissociation (elevated protein, total white cell count < 50 cells/uL) as in non-HIV associated AIDP/GBS or a mild mononuclear pleocytosis and elevated protein. CSF should also be investigated for opportunistic infection with CMV, VZV, and HSV in those cases where there is a radiculomyelopathy mimicking AIDP/CIDP.  

The response to immune based therapies in HIV associated AIDP/CIDP is similar to non-HIV associated AIDP/CIDP, with early initiation of plasmapheresis and IVIG associated with improvement, and the addition of commencement cART with good CNS penetration (Table 2) ​(75)​.  Unlike in non-HIV associated AIDP, steroids should be considered if AIDP occurs in context of IRIS ​(75)​.