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these latter cases the illness thereafter becomes relapsing or it simply worsens slowly and progressively An antecedent infection is identi ed far less regularly in patients with CIDP than in those with GBS and is probably not a necessary component of the disease Furthermore, CIDP may be distinct immunologically from GBS, insofar as certain HLA antigens occur with greater frequency in patients with CIDP than they do in the normal population, whereas there are no clear HLA propensities in patients with GBS Finally, in contrast to acute GBS, many cases of CIDP respond favorably to the administration of prednisone An ambiguity is introduced here because, as mentioned earlier, Hughes has described a group of patients with polyneuritis in whom weakness progressed steadily for 4 to 12 weeks and who responded to corticosteroids, thus again blurring the distinction between GBS and CIDP The chronic symmetric sensorimotor loss coupled with EMG ndings of demyelination largely de ne the illness The typical EMG ndings are of multifocal conduction block as described in Chap 45, prolonged distal latencies (distal block), nerve conduction slowing to less than 80 percent of normal in several nerves, loss of late responses, and dispersion of the compound muscle action potentials, further re ecting demyelination in motor nerves One or several of these changes have been present in more than three quarters of our patients (Gorson, Ropper, et al) In the early stages of the disease demyelinative features must be carefully sought by testing multiple nerves at several sites along this course After several months there is often some degree of axonal change (30 percent of our series), but the fundamental process continues to be one of multiple foci of demyelination Most dependable is the absence of denervation changes early on despite weakness and reduced amplitude of the motor action potential, indicative of a demyelinating block to conduction at a proximal site Several large series of CIDP cases are available for review Dyck and colleagues (1975) studied 53 patients in whom the neuropathy progressed for more than 6 months The clinical course was monophasic and slowly progressive in about one-third, stepwise and progressive in another third, and relapsing in the remaining third The periods of worsening or improvement were measured in weeks or months Infections and inoculations in the 3 months preceding the onset of CIDP were no more frequent than in the population at large Weakness of the limbs, particularly of the proximal leg muscles, or numbness, paresthesias, and dysesthesias of the hands and feet were the initial symptoms In 45 of the 53 patients, the signs were those of a mixed sensorimotor polyneuropathy with weakness of the shoulder, upper arm, and thigh muscles, in addition to motor and sensory loss in the distal parts of the limbs In 5 patients the neuropathy was purely motor, and in 3, purely sensory Cranial nerve abnormalities were distinctly unusual Enlarged, rm nerves were found in 6 patients Not emphasized in their series is the common occurrence of a cerebellar-like tremor in cases of long-standing In the series reported by McCombe et al comprising 92 patients, two major subgroups were recognized relapsing (corresponding to the relapsing and stepwise progressive cases of Dyck et al) and nonrelapsing ones In our own series of more than 100 patients, we have been impressed with several additional unusual patterns of clinical presentation In 10 percent, numbness and weakness of the hands preceded involvement of the feet, which is unusual in other polyneuropathies A sensory ataxic form, a purely motor form, and mononeuropathies superimposed on a mild generalized polyneuropathy each accounted for approximately 5 percent of the cases As mentioned earlier, a small pro-.

The diagnosis of a vascular lesion rests essentially on recognition of the stroke syndrome; without evidence of this, the diagnosis must always be in doubt The three criteria by which the stroke is identi ed should be re-emphasized: (1) the temporal pro le of the clinical syndrome, (2) evidence of focal brain disease, and (3) the clinical setting De nition of the temporal pro le requires a clear history of the premonitory phenomena, the mode of onset, and the evolution of the neurologic disturbance in relation to the patient s medical status Here, an inadequate history is the most frequent cause of diagnostic error If these data are lacking, the stroke pro le may still be determined by extending the period of observation for a few days or weeks, thus invoking the clinical rule that the physician s best diagnostic tool is a second and third examination There are few categories of neurologic disease whose temporal pro le mimics that of the cerebrovascular disorders Migraine may do so, but the history usually provides the diagnosis A seizure may be followed by a prolonged focal de cit (Todd s paralysis) but is rarely the initial event in a stroke; the setting in which these symptoms occur and their subsequent course clarify the clinical situation Stroke-like episodes appear in the course of certain hereditary metabolic disorders (Fabry disease, homocystinuria, mitochondrial disease) Differentiation is not dif cult because of the associated myopathic and neurologic signs and characteristic metabolic defects Tumor, infection, in ammation, degeneration, and nutritional de ciency are not likely to manifest themselves precipitously, although rarely a brain metastasis produces a focal de cit of abrupt onset (see below) Trauma, of course,

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