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Landry described a condition characterized by acute ascending paralysis in 1859. Later, Guillain, Barré, and Strohl noted the areflexia and the albuminocytologic dissociation in the cerebral spinal fluid (CSF) associated with this neuropathy.1 The contributions of Landry and Strohl have been neglected, and the neuropathy has been most commonly referred to as Guillain–Barré syndrome (GBS). In 1949, Haymaker and Kernohan detailed the histopathologic features seen in 50 fatal cases of GBS. The earliest features noted were edema of the proximal nerves and the subsequent degeneration of the myelin sheaths within the first week of the illness. They did not appreciate inflammatory cell infiltrate until later in the course of the illness.2 However, another group reported prominent perivascular inflammation in the spinal roots, dorsal root ganglia, cranial nerves, and randomly along the whole length of peripheral nerves, along with segmental demyelination adjacent to the areas of inflammation, in 19 autopsy cases of GBS.3 Thus, the term acute inflammatory demyelinating polyradiculoneuropathy (AIDP), which is quite descriptive of the disease process, has been historically used synonymously with GBS.47 It is now appreciated that GBS is not a single disorder but again a syndrome of several types of acute immune-mediated polyneuropathies (Table 13-1).811 In addition to AIDP, there are two axonal forms of GBS: acute motor–sensory axonal neuropathy (AMSAN) and acute motor axonal neuropathy (AMAN). Further, some disorders that appear clinically different from AIDP (e.g., the Miller Fisher syndrome [MFS] and acute autonomic neuropathy) may share similar pathogenesis and can be considered variants of GBS.




AIDP is the most common cause of acute generalized weakness, with an annual incidence ranging from 0.9 to 4 per 100,000 population.7,1013 The neuropathy can occur at any age, with a peak age of onset of approximately 38–40 years. There may be a slight male predominance.

Approximately 60–70% of patients with AIDP have a history of a recent infection a few weeks prior to the onset of the neuropathy.7,10,11 A control study of 154 patients with GBS revealed serologic evidence of recent Campylobacter jejuni (32%), cytomegalovirus (13%), Epstein–Barr virus (10%), and Mycoplasma pneumoniae (5%) infection.14 The serologic signatures of these infections were more prevalent than in the control population. Other studies have also reported that 15–45% of patients with AIDP have serologic evidence of recent Campylobacter...

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