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native or additional diagnosis such as neoplastic meningitis, HIV, or Lyme infection We have been unable to relate pleocytosis in the spinal uid with any of the clinical features of GBS or to the severity of illness Usually, the protein content is normal during the rst few days of symptoms, but then it begins to rise, 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 re ection of the widespread in ammatory disease of the nerve roots, but high values have had no clinical or prognostic signi cance in our material, perhaps 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 It is worth stating that from our experience, among patients with Fisher syndrome and other restricted or axonal forms of GBS, there is a higher proportion with normal or only slightly elevated protein values Abnormalities of nerve conduction are early and dependable diagnostic indicators of GBS In cases with a typical clinical and EMG presentation one can probably dispense with the CSF analysis as a con rmatory test The most frequent early electrodiagnostic ndings 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 45) Prolonged distal latencies (re ecting distal conduction block) and prolonged or absent F-responses (indicating involvement of proximal parts of nerves and roots) are other important diagnostic ndings, all re ecting focal demyelination The H-re ex is almost always very delayed, or more often absent, but this does little more than con rm the loss of ankle re exes Although a limited electrodiagnostic examination may be normal early in the illness, a more thorough study, which includes measurement of late responses, almost invariably shows disordered conduction in an affected limb within days of the rst symptom Early on, features that indicate widespread axonal damage (the axonal GBS discussed earlier) portend a poor and protracted recovery in both young and old patients The clinical, CSF, and electrodiagnostic criteria for GBS have been reassessed by Asbury and Cornblath and are discussed in detail in the monograph by Ropper et al Most patients with acute GBS have shown gadolinium enhancement of the cauda equina roots on magnetic resonance imaging (MRI; 21 of 24 patients in our study), and this may serve as a useful test in complicated cases (Gorson, Ropper, et al) Abnormalities of liver function occur in fewer than 10 percent of patients, probably re ecting a recent or ongoing viral hepatitis, usually due to CMV or EBV infections (rarely one of the hepatitis viruses) T-wave and other electrocardiographic changes of minor degree are reported frequently but are 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 rst week, especially 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 Transient diabetes insipidus is a rare and unexplained complication We are unable to comment on a high rate of proteinuria and glomerulonephritis reported by several groups in cases of GBS, but have found it only infrequently Pathologic Findings These have had a relatively consistent pattern and form Even when the disease is fatal within a few days,.

Paralysis of both lower extremities may occur with diseases of the spinal cord, nerve roots, or, less often, the peripheral nerves If the onset is acute, it may be dif cult to distinguish spinal from neuropathic paralysis because of the element of spinal shock, which results in abolition of re exes and accidity In acute spinal cord diseases with involvement of corticospinal tracts, the paralysis or weakness affects all muscles below a given level; usually, if the white matter is extensively damaged, sensory loss below a partic-

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