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I Required for diagnosis 1 Progressive weakness of variable degree from mild paresis to complete paralysis 2 Generalized hypo- or are exia II Supportive of diagnosis 1 Clinical features a Symptom progression: Motor weakness rapidly progresses initially but ceases by 4 weeks Nadir attained by 2 weeks in 50%, 3 weeks in 80%, and 4 weeks in 90% b Demonstration of relative limb symmetry regarding paresis c Mild to moderate sensory signs d Frequent cranial nerve involvement: Facial (cranial nerve VII) 50% and typically bilateral but asymmetric; occasional involvement of cranial nerves XII, X, and occasionally III, IV, and VI as well as XI e Recovery typically begins 2 4 weeks following plateau phase f Autonomic dysfunction can include tachycardia, other arrhythmias, postural hypotension, hypertension, and other vasomotor symptoms g A preceding gastrointestinal illness (eg, diarrhea) or upper respiratory tract infection is common 2 Cerebrospinal uid features supporting diagnosis a Elevated or serial elevation of CSF protein b CSF cell counts are <10 mononuclear cell/mm3 3 Electrodiagnostic medicine ndings supportive of diagnosis a 80% of patients have evidence of NCV slowing/conduction block at some time during disease process b Patchy reduction in NCV attaining values less than 60% of normal c Distal motor latency increase may reach three times normal values d F-waves indicate proximal NCV slowing e About 15 20% of patients have normal NCV ndings f No abnormalities on nerve conduction studies may be seen for several weeks III Findings reducing possibility of diagnosis 1 Asymmetric weakness 2 Failure of bowel/bladder symptoms to resolve 3 Severe bowel/bladder dysfunction at initiation of disease 4 Greater than 50 mononuclear cells/mm3 in CSF 5 Well-demarcated sensory level IV Exclusionary criteria 1 Diagnosis of other causes of acute neuromuscular weakness (eg, myasthenia gravis, botulism, poliomyelitis, and toxic neuropathy) 2 Abnormal CSF cytology suggesting carcinomatous invasion of the nerve roots.

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With permission from Amato AA, Dumitru D Acquired Neuropathies In Dumitru D,Amato AA, Swartz MJ (eds) Electrodiagnostic Medicine, 2nd edn Philadelphia: Hanley & Belfus, 2002, pp 937 1041,Table 23 1, p 938

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is common in AIDP with hypotension or hypertension and occasionally cardiac arrhythmias The neuropathy usually progresses over the course of 2 4 weeks Approximately 50% of patients reach their nadir by 2 weeks, 80% by 3 weeks, and 90% by 4 weeks7,11 Progression of symptoms and signs for over 8 weeks excludes GBS and suggests the diagnosis of chronic in ammatory demyelinating polyneuropathy Subacute onset with progression of the disease over 4 8 weeks has been termed subacute in ammatory demyelinating polyneuropathy Patients with subacute in ammatory demyelinating polyneuropathy may have a monophasic illness like AIDP or may behave like chronic in ammatory demyelinating polyneuropathy and continue to progress unless treated with immunosuppressive or immunomodulating agents Approximately 30% of patients with AIDP develop respiratory failure Because the immune attack of AIDP has an early predilection for the nerve roots, neck exors and extensors and shoulder abductors, which are innervated by cervical roots close to the phrenic nerve (C3C4), correlate well with diaphragmatic strength and are thus important to closely follow Once the disease nadir is reached, there is a plateau phase of several days to weeks followed by gradual recovery over several months However, 50 85% of patients have some degree of residual de cits as many as 7 years after disease onset, with 5 10% of patients having disabling motor or sensory symptoms including severe fatigue7,11,21 23 The mortality rate is about 5%, with patients dying as a result of respiratory distress syndrome, aspiration pneumonia, pulmonary embolism, cardiac arrhythmias, and sepsis related to secondarily acquired infections7,11 Risk factors for a poor prognosis (slower and incomplete recovery) are age greater than 50 60 years, abrupt onset of profound weakness, the need for mechanical ventilation, and distal compound muscle action potential (CMAP) amplitudes less than 10 20% of normal19,24 31

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an error message and exits if we don t read exactly one item. This is a pretty simplistic error strategy, but it does make a point. Pay attention to error conditions and to function return values.

Antiganglioside antibodies, particularly GM1 IgG antibodies, are found in some patients and correlate with recent C jejuni infection16,17,20,33 Serological evidence of recent antecedent C jejuni infection is evident in 15 45% of patients7,11 17,19,20,34 Molecular mimicry between gangliosides expressed on nerve bers and glycolipids present on C jejuni may account for their association with AIDP and may play a role in the pathogenesis of the disorder Various electrophysiologic criteria for demyelination have been developed to aid in the diagnosis of AIDP (Table 11 3)8 The electrophysiological hallmarks of demyelination include prolonged distal

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