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effectors of the damage Indeed, the very earliest change that could be detected by Hafer-Macko and colleagues was the deposition of complement on the inner layer of myelin A number of autoantibodies directed at components of nerve ganglioside are detected inconsistently in patients with GBS, the most important being anti-GQ1b, which is found in almost all patients with ophthalmoplegia Approximately one-third of patients have anti-GM1 antibodies early in their course, corresponding in most instances to a predominantly motor presentation and to axonal damage, the highest titers usually being associated with cases that follow Campylobacter infections Antibodies directed against GD1a or GT1b have been associated in some cases with the pharyngeal-brachial-cervical variant It would therefore seem that casting GBS exclusively as a humoral or as a cellular immune process is an oversimpli cation An unanswered question is how the immune reaction is initiated in humans All attempts to isolate a virus or microbial agent from nerves or to demonstrate one by electron microscopy have failed, and it is more likely that a variety of agents viral, bacterial (particularly C jejuni), certain vaccines, and perhaps neural injury itself are all capable, in susceptible individuals, of precipitating an immune response against components of autologous peripheral myelin The occurrence of GBS in patients with acquired immune de ciency syndrome (AIDS) or with EBV or CMV infections simply indicates that these agents, too, induce such an autoimmune response without implicating a direct viral infection of nerve The observation that only one of many individuals who are infected with a particular pathogen go on to develop GBS suggests that host factors are signi cant (there is, however, little consistency among HLA types in GBS patients) Whether the aforementioned antibodies against various gangliosides of peripheral nerve are pathogenically active is also uncertain Several animal diseases namely coonhound paralysis of dogs, Marek s disease of chickens (a viral neuritis), and cauda equina neuritis of horses all resemble GBS super cially but do not share its main clinical or pathologic features Differential Diagnosis GBS is not only the most frequent type of acute generalized polyneuropathy seen in a general hospital but also the most rapidly evolving and potentially fatal form Any polyneuropathy that brings the patient to the brink of death or to respiratory failure within a few days will usually be of this variety However, several other neurologic conditions must be considered The immediate problem is to differentiate GBS from acute spinal cord disease marked by sensorimotor paralysis below a de ned level and a marked sphincteric disturbance There may be particular dif culty in the case of an acute lesion of the cord in which tendon re exes are initially lost (spinal shock), or with necrotizing myelopathy, where a permanent loss of tendon re exes follows extensive destruction of spinal gray matter (pages 781 and 1064) Also confusing is early and transient urinary retention in a proportion of patients with GBS Several rules of thumb are useful in distinguishing the disease from a cervical myelopathy: in GBS, the facial and respiratory muscles are usually involved if there is generalized paralysis; the ngertips should be paresthetic once sensory symptoms have ascended to the level of the midcalves; marked sensory loss proximal to the hands or feet or only of the trunk is unusual early in the illness; and tendon re exes are almost invariably lost in limbs that are too weak to resist gravity A predominantly motor paralysis is the major characteristic of GBS, for which reason the differential diagnosis also includes po-. birt pdf 417 Eclipse BIRT PDF417 Barcode Maker add-in makes PDF417 ...
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