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tral and dorsal roots, and dorsal root ganglia and along the entire length of the peripheral nerves Sparse focal in ltrates of in ammatory cells (lymphocytes and other mononuclear cells) may also be found in lymph nodes, liver, spleen, heart, and other organs 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 of peripheral nerve damage have been observed, each perhaps representing a different immunopathology Rarely, in a clinically typical case, there may be widespread demyelinative changes and only a paucity of perivascular lymphocytes In patients whose electrophysiologic tests display severe axonal damage early in the illness as discussed later, the pathologic ndings corroborate the predominantly axonal nature of the disease with secondary myelin damage and little in ammatory response An occasional case has shown an in ammatory process with primary axonal damage rather than demyelination (Honovar et al)
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Pathogenesis and Etiology Most of the evidence supports a cell-mediated immunologic reaction directed at peripheral nerve Waksman and Adams demonstrated that experimentally induced peripheral nerve disease (experimental allergic neuritis, or C 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 speci c peptide in the P2 protein However, it has become evident that there is no dominant antigen-antibody reaction in GBS and that any number of myelin and axonal elD ements may be involved in inciting the immune reaction The pathologic steps in this proposed reaction are diagrammatically illustrated in Fig 46-3 Figure 46-3 Diagram of probable cellular events in acute in ammatory polyneuropathy Hartung and colleagues have found high levels of (Guillain-Barre syndrome) A Lymphocytes attach to the walls of endoneurial vessels and soluble interleukin (IL)-2 receptors, that is shed migrate through the vessel wall, enlarging and transforming as they do so At this stage no from activated T cells, and IL-2 itself in the serum nerve damage has occurred B More lymphocytes have migrated into the surrounding tissue of patients with acute GBS, re ecting activation of The rst effect on the nerve is breakdown of myelin, the axon being spared (segmental demyelination) This change appears to be mediated by the mononuclear exudate, but the these cells As noted below, complement also seems mechanism is uncertain C The lesion is more intense, polymorphonuclear leukocytes being to be a necessary factor in the initial attack on mypresent as well as lymphocytes There is interruption of the axon in addition to myelin sheath elin Although the transmission of EAN by T cells damage; as a result, the muscle undergoes denervation atrophy and the nerve cell body shows central chromatolysis If the axonal damage is distal, the nerve cell body will survive, and sensitized to myelin is strong evidence of their role regeneration and clinical recovery is likely If, as in D, axonal interruption has occurred in GBS, antimyelin antibodies are probably involved proximally because of a particularly intense root or proximal nerve lesion, the nerve cell body in the initial part in the disease The serum from may die and undergo dissolution In this situation, there is no regeneration, only the possibility patients with GBS causes damage to myelin in tissue of collateral reinnervation of muscle from surviving motor bers (From Asbury et al, 1969, cultures and induces a characteristic ( vesicular ) by permission) form of myelin destruction Subepineural injection of serum from GBS patients into the sciatic nerve of rats leads to local demyelination and electrical conduction block virtually all cases show perivascular (mainly perivenous) lymphoThe studies by Koski and associates of complement-dependent mycytic in ltrates Later, the characteristic in ammatory cell in lelin damage by IgM antimyelin antibodies in GBS provided evitrates and perivenous demyelination are combined with segmental dence that antimyelin antibodies are able to initiate myelin destrucdemyelination and a variable degree of wallerian degeneration The tion even though T cells and that macrophages are the ultimate cellular in ltrates are scattered throughout the cranial nerves, ven-
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