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be appreciated in areas of segmental demyelination (Fig 11 1) Polymorphonuclear cells, in addition to monocytes, may be associated with axonal degeneration in severe cases During the recovery phase, remyelination is appreciated Myelin thickness is reduced and the number of internodes is increased compared to normal peripheral nerve Autopsy studies of patients in China who died early in the course of their illness have shed light on the pathology of GBS, including AIDP, AMSAN, and AMAN52 55 In two patients who died at 7 and 9 days after onset of the neuropathy, autopsies revealed completely demyelinated peripheral nerves accompanied by extensive lymphocytic in ltrate54 However, in a patient who died only 3 days after symptom onset, the peripheral nerves had only scant in ammatory in ltrate and just a few of the nerves were completely demyelinated Markers of complement activation were demonstrated on the outermost surface of the Schwann cells, and early vesicular changes in the myelin sheaths, beginning in the outer lamellae, were appreciated on electron microscopy

If gHeadPtr is NULL, the list must be empty. If so, make gHeadPtr point to the new struct:

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moral arm of the immune system has been implicated by the demonstration of ganglioside antibodies in many patients and the clinical improvement following plasmapheresis57,58 Further, injection of serum from patients with AIDP into nerves of animal models induces complement-dependent demyelination and conduction block60 Buchwald et al investigated the effect of serum from 10 patients with GBS on mouse hemidiaphragm using a macro-patch-clamp technique and observed depressed presynaptic transmitter release and, in some cases, the activation of postsynaptic channels61 The neuromuscular blockade was independent of complement, and there was no link to the presence (in six patients) or absence (in four patients) of antibodies to GM1 or GQ1B One study revealed that 56 out of 233 (23%) of GBS patients with GBS had circulating immunoglobulin G autoantibodies against proliferating, nonmyelinating human Schwann cells62 Immuno uorescence was localized at the distal tips (leading lamella) of the Schwann cell processes and of nerve-growth cones Serum immunoreactivity was also observed in teased nerve ber preparations The observer speculated that the immune attack may be directed against nonmyelin proteins and epitopes possibly involved in Schwann cell axon interaction62 The nature of the epitope is not known but probably is a glycolipid Molecular similarity between the myelin epitope(s) and glycolipids expressed on Campylobacter, Mycoplasma, and other infectious agents, which precede attacks of AIDP, may be the underlying trigger for the immune attack (Fig 11 2)54 Antibodies directed against these infectious agents may cross-react with speci c antigens on the Schwann cell because of this molecular mimicry These autoantibodies may bind to the Schwann cells and then activate the complement cascade, leading to lysis of myelin sheaths (Fig 11 3) In ammatory cells are subsequently recruited to complete the demyelinating process

PE63 65 and IVIG27,66 have proven effective treatments of AIDP (Table 11 4)67,68 In the North American trial, PE reduced the time necessary to improve one clinical grade, time to walk unaided, time on a ventilator, and the percentages of patients improving after 1 and 6 months compared to the control group64 The French Plasmapheresis Group con rmed that PE was ef cacious in GBS63 The exact mechanism is unclear but is likely that PE removes autoantibodies, immune complexes, complement, or other humoral factors involved in the pathogenesis of AIDP The standard course of PE is 200 250 mL/kg of patient body weight over 10 14 days Thus, a 70-kg patient would receive 14,000 17,500 mL (14 175 L) total exchange, which can be accomplished by 4 6 alternate day exchanges of 2 4 L each

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A T-cell-mediated process may play a role, given the in ammation apparent in the nerves, markers of T-cell activation (eg, soluble interleukin-2 receptor and interferon- ) in the serum, and the resemblance to experimental allergic neuritis9,56 59 The hu-

Figure 11 2 Structures of gangliosides and galactocerebroside and Guillain Barre syndrome subtype associations (With permission from Hughes RA, Cornblath DR Guillain Barre syndrome Lancet 2005;366(9497):1653 1666, Fig 4, p 1659)

If gHeadPtr is not NULL, the linked list contains at least one element. In that case, make the next field of the very last element on the list point to the new struct:

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