Abnormalities of liver function occur in fewer than 10 percent of patients, probably reflecting a recent or ongoing viral hepatitis, usually as a result of CMV or EBV infections (rarely one of the hepatitis viruses). T-wave and other electrocardiographic changes of minor degree are reported frequently but tend to be evanescent. The sedimentation rate is normal unless there is an additional process of infectious, neoplastic, or autoimmune nature, any of which can occasionally coexist with GBS. Hyponatremia occurs in a proportion of cases after the first week, but particularly in ventilated patients. This is usually attributable to the syndrome of inappropriate antidiuretic hormone secretion (SIADH), but a natriuretic type also occurs, from an excess of atrial natriuretic factor (Wijdicks et al). Transient diabetes insipidus is a rare and unexplained complication. With regard to proteinuria due to glomerulonephritis reported by several groups in cases of GBS, we have found it infrequently.
These have had a relatively consistent pattern and form. Even when the disease is fatal within a few days, most cases show endoneural perivascular (mainly perivenous) lymphocytic infiltrates. Later, there is segmental demyelination and a variable degree of wallerian degeneration. The cellular infiltrates are scattered throughout the cranial nerves, ventral and dorsal spinal roots, dorsal root ganglia, and along the entire length of the peripheral nerves. Swelling of nerve roots at the site of their dural exit has been emphasized by some authors and theorized to cause root damage.
Variations of this pattern have been observed, each perhaps representing a different immunopathology. For example, there may be widespread demyelinative changes and only a paucity of perivascular lymphocytes (Ropper and Adelman). In patients whose electrophysiologic tests display severe axonal damage early in the illness as discussed earlier the pathologic findings corroborate the predominantly axonal nature of the disease with secondary myelin damage and usually little inflammatory response. An occasional case has shown an inflammatory process with primary axonal damage rather than demyelination (Honovar et al).
Most evidence supports a cell-mediated immunologic reaction directed at peripheral nerves but the humoral immune system is clearly implicated as well. Waksman and Adams demonstrated that experimentally induced peripheral nerve disease (experimental allergic neuritis [EAN]), clinically and pathologically indistinguishable from GBS, develops in animals 2 weeks after immunization with peripheral nerve homogenates. Brostoff and colleagues suggested that the antigen in this reaction is a basic protein, designated P2, found only in peripheral nerve myelin. Subsequent investigations by these authors indicated that the neuritogenic factor might be a specific peptide in the P2 protein. However, it has become evident that there is no dominant antigen–antibody reaction in GBS and it is likely that any number of myelin and axonal elements may be involved in inciting the immune reaction. Figure 43-3 diagrammatically illustrates the pathologic steps in this proposed reaction. As noted further on, complement also seems to be a necessary factor in the initial attack on myelin.