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<ref name="pmid26223336">{{cite journal| author=Modi S, Dharaiya D, Schultz L, Varelas P| title=Neuroleptic Malignant Syndrome: Complications, Outcomes, and Mortality. | journal=Neurocrit Care | year= 2016 | volume= 24 | issue= 1 | pages= 97-103 | pmid=26223336 | doi=10.1007/s12028-015-0162-5 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26223336  }} </ref>
 
Acute Inflammatory Demyelinating Polyradiculoneuropathy
 
 
==Introduction:==
*Classified under the eponym Guillain-Barre syndrome (GBS)
*Other variants of GBS include Acute Motor Axonal Neuropathy (AMAN), Acute Motor and Sensory Axonal Neuropathy (ASMAN), and the Miller Fisher syndrome (MFS).
*AIDP is acute monophasic immune-mediated polyradiculoneuropathy provoked by a preceding infection
 
==Epidemiology:==
*Mean age of onset of 40 years affecting slightly more males than females of all ages, races and nationalities
*Worldwide incidence of GBS ranges from 0.6 to 4.0/100,000 people
 
==Etiology:==
*AIDP is most common form of GBS in North America, Europe and most of the developed world representing about 85% to 90% of cases
*⅔ patients give history of antecedent respiratory tract or GI tract infection
*Campylobacter infection is most commonly observed in upto 30% cases
*Campylobacter associated GBS has worse prognosis, manifests slow recovery and with greater residual neurologic disability.
*Other precipitants include EBV, CMV, mycoplasma, pneumonia, and influenza-like illnesses
*Also has an association with HIV infection; predominantly in those who are not profoundly immunocompromised
 
==Pathogenesis:==
*Molecular Mimicry: auto-antibodies cross-react with peripheral nerve components because of sharing of cross-reactive epitopes
*Immune response can be directed towards myelin or axon of peripheral nerve
*Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP): When directed against epitopes in myelin or schwann cell membrane; cellular + humoral immune responses are involved
*Progression of disease for about two weeks
*Nadir of disease reaches 4 weeks after initial symptoms in 90% patients
*If disease progression is more than 8 weeks, it is classified as chronic inflammatory demyelinating polyradiculoneuropathy or CIDP
 
 
==Clinical Features:==
*Weakness starts in the legs (90%)
*Decreased or absent reflexes in affected arms or legs (90%)
*Paresthesias accompanying weakness (>80%)
*Dysautonomia (~70%)
*Pain due to nerve root inflammation, typically in the back and extremities (two thirds of patients)
*Facial nerve Palsies (>50%)
*Oropharyngeal weakness (50%)
*Severe respiratory muscle weakness requiring ventilatory support (10%-30%)
*Oculomotor weakness (15%)
*Weakness begins in arms and facial muscles (10%)
*SIADH (5%; more in hospitalized patients)
 
 
*Unusual clinical features of GBS include: papilledema, facial myokymia, hearing loss, meningeal signs, vocal cord paralysis, and mental status changes.
*Posterior reversible encephalopathy syndrome, also called reversible posterior leukoencephalopathy syndrome has been associated with GBS in children and adults likely related to acute hypertension from dysautonomia
 
==Electrodiagnostic findings:==
Earliest findings:

Latest revision as of 00:04, 17 July 2019

[1]

  1. Modi S, Dharaiya D, Schultz L, Varelas P (2016). "Neuroleptic Malignant Syndrome: Complications, Outcomes, and Mortality". Neurocrit Care. 24 (1): 97–103. doi:10.1007/s12028-015-0162-5. PMID 26223336.