The most important laboratory aids are the electrodiagnostic studies and CSF examination. The CSF is under normal pressure and is acellular or contains only a few lymphocytes in all but 10 percent of patients; in the latter group, 10 to 50 cells (rarely more) per cubic millimeter, predominantly lymphocytes, may be found. The number of cells then decreases in a matter of 2 to 3 days; persistent pleocytosis suggests an alternative or additional process producing aseptic meningitis such as neoplastic infiltration, HIV, sarcoidosis, or Lyme infection. We have been unable to relate pleocytosis in the spinal fluid with any of the clinical features of GBS or to the severity of illness. The protein content is usually normal during the first few days of illness, but then it rises, reaching a peak in 4 to 6 weeks and persisting at a variably elevated level for many weeks. The increase in CSF protein is probably a reflection of widespread inflammatory disease of the nerve roots, but high values have had no clinical or prognostic significance in our material, apart from a few exceptional cases of pseudotumor cerebri (Ropper and Marmarou). In a few patients (fewer than 10 percent), the CSF protein values remain normal throughout the illness. From our experience, there is a higher proportion of patients with normal or only slightly elevated protein values among those with Fisher syndrome and other restricted or axonal forms of GBS.
Abnormalities of nerve conduction are early and dependable diagnostic indicators of GBS. In cases with a typical clinical and EMG/NCS presentation, one can probably dispense with the CSF analysis as a confirmatory test. The most frequent early electrodiagnostic findings are a reduction in the amplitude of muscle action potentials, slowed conduction velocity, and conduction block in motor nerves, singly or in combination (see Chap. 2). Prolonged distal latencies and reduced distal amplitudes (reflecting distal conduction block) and prolonged or absent F responses (indicating involvement of proximal parts of motor nerves and roots) are other important diagnostic findings, all reflecting focal areas of demyelination. The H reflex is almost always much delayed, or more often absent, but this does little more than confirm the loss of ankle reflexes. Although a limited electrodiagnostic examination may be normal early in the illness, a thorough study, which includes measurement of late responses, invariably shows disordered conduction in an affected limb within days of the first symptom. Features that indicate widespread axonal damage portend a poor and protracted recovery in both young and old patients as discussed above.
The clinical, CSF, and electrodiagnostic criteria for GBS were assessed by Asbury and Cornblath and are discussed in detail in the monograph by Ropper and colleagues. Many patients with acute GBS have shown gadolinium enhancement of the cauda equina roots on magnetic resonance imaging (21 of 24 patients in our study) and this may serve as a useful test in complicated cases (Gorson et al, 1996).
Beyond the close association between autoantibodies to GQ 1b and Fisher syndrome or other variants that include ophthalmoplegia as mentioned previously other anti-ganglioside antibodies have become of interest in GBS. The acute motor axonal variety has a tendency to be associated with antibodies to GM1 or GD1a and the pharyngeal-cervical-brachial syndrome, to GT1a. Much of this work comes from the laboratory of Yuki, and his review article with Hartung is recommended for further explanations of potential autoimmune mechanisms.