The most common form of Guillain–Barre syndrome (GBS), acute inflammatory demyelinating polyradiculoneurolopathy (AIDP) is an immune-mediated disorder that targets the peripheral nerves and accounts for up to 90% of all cases of GBS. Patients with AIDP present with subacute symmetrical progressive weakness and paresthesias, along with significantly decreased or absent tendon reflexes. Though patients commonly complain of an ascending pattern of lower extremity weakness and sensory changes, this is not always the case. In over half of these patients, neurological symptoms are preceded by a nonspecific febrile illness, or gastrointestinal or respiratory infections days to weeks prior to symptom onset. The most common preceding infectious cause is Campylobacter jejuni gastroenteritis. However, many other antecedent infections have been associated with the later development of AIDP, including Epstein–Barr virus, hepatitis virus, Mycoplasma pneumonia, cytomegalovirus, and HIV. Additionally, metabolically stressful events have been known to precede the onset of AIDP symptoms, such as pregnancy, surgery, extreme emotional and physical stress, vaccination, and development of another autoimmune disease.