GBS is not only the most frequent acute generalized polyneuropathy seen in general hospitals but also the most rapidly evolving and potentially fatal form. Any polyneuropathy that brings the patient to the brink of death or to respiratory failure within a few days will usually be of this variety. Most cases, however, are of the more limited type with paresthesias, limb weakness, and areflexia. Several other conditions must be considered. The immediate problem is to differentiate GBS from acute spinal cord disease marked by sensorimotor paralysis with a defined spinal level and prominent sphincter disturbances and from several neuromuscular diseases that can simulate GBS. There may be diagnostic difficulty in the case of an acute lesion of the cord in which tendon reflexes are initially lost (spinal shock), or with necrotizing myelopathy, where a permanent loss of tendon reflexes follows extensive destruction of spinal gray matter. Early and transient urinary retention occurs in a proportion of patients with GBS and causes additional diagnostic confusion with spinal disease. Several features are useful in distinguishing GBS from a cervical myelopathy: in GBS, the facial and respiratory muscles are usually involved if there is generalized paralysis; the fingertips should be paresthetic once sensory symptoms have ascended to the level of the midcalves; marked sensory loss proximal to the hands or feet or only of the trunk is unusual early in the illness; and tendon reflexes are almost invariably lost in limbs that are too weak to resist gravity. Of course, careful testing of sensation on the trunk and limbs will expose the cause of paralysis as spinal in origin.
Tick paralysis, a disease of children in the United States but affecting both children and adults in Australia and elsewhere, may be nearly impossible to distinguish from GBS unless one finds the tick (see Chap. 41). In addition to an ascending generalized paralysis, both may cause ataxia and may paralyze eye movements, but sensory loss is not usually a feature of tick paralysis and the CSF protein is normal. Episodes of painful paralytic porphyria also bear a superficial resemblance to GBS. Predominant motor features in comparison to sensory ones is the major characteristic of GBS, for which reason the differential diagnosis also includes poliomyelitis, caused by the West Nile virus and by enteroviruses other than the polio agent. In these infectious cases, the illness is marked by fever, meningoencephalitic symptoms, early pleocytosis in the spinal fluid, and purely motor and usually asymmetrical areflexic paralysis, all unusual in GBS.
Several times we were misled by cases of carcinomatous meningitis with painless polyradiculopathy that caused a subacute, and fairly symmetric but mainly distal weakness, similar to GBS. An irregular distribution of weakness between proximal and distal parts and between sides, the absence of facial weakness, and the appearance of symptoms sequentially in one limb after another suggest the presence of this type of neoplastic polyradiculopathy. Sciatica may occur as an early feature with either process but radicular pain in the arms is unusual in GBS. Examination of the spinal fluid usually settles the matter.