Clinical and electrophysiological parameters distinguishing acute‐onset chronic inflammatory demyelinating polyneuropathy from acute inflammatory demyelinating polyneuropathy

Abstract

Up to 16% of chronic inflammatory demyelinating polyneuropathy (CIDP) patients may present acutely. We performed a retrospective chart review on 30 acute inflammatory demyelinating polyneuropathy (AIDP) and 15 acute-onset CIDP (A-CIDP) patients looking for any clinical or electrophysiological parameters that might differentiate AIDP from acutely presenting CIDP. A-CIDP patients were significantly more likely to have prominent sensory signs. They were significantly less likely to have autonomic nervous system involvement, facial weakness, a preceding infectious illness, or need for mechanical ventilation. With regard to electrophysiological features, neither sural-sparing pattern, sensory ratio >1, nor the presence of A-waves was different between the two groups. This study suggests that patients presenting acutely with a demyelinating polyneuropathy and the aforementioned clinical features should be closely monitored as they may be more likely to have CIDP at follow-up.

The Application of Clinical, Electrophysiological and Nerve Ultrasound Parameters in Distinguishing Acute-onset Chronic from Acute Inflammatory Demyelinating Polyneuropathy

“…[16][17][18] ANS dysfunction or the presence of preceding infections seem not to differ statistically among the acute-onset CIDP and the AIDP patients. 16,17 On the other hand, the median time to reach nadir during first exacerbation seems to be significantly longer in the acute-onset CIDP group than in the AIDP group. 16 In contrast to patients having acute-onset CIDP, none of the patients having AIDP, or even treatment-related fluctuations, seemed to deteriorate after 8 weeks.…”

“…On the other hand, subacute CIDP can be diagnosed when patients present acutely within 4 weeks of onset of symptoms but continue to deteriorate beyond 8 weeks, relapse three times or more after initial improvement or resolution of symptoms or require maintenance therapy with more than one additional course of plasma exchange, IVIg and/or immunosuppressive medication. 16,17 In view of recent literature reports, it seems that only the presence of sensory symptoms or signs and the absence of bulbar palsy or respiratory muscle weakness/need for mechanical ventilation are the only clinical parameters that are significantly more frequent in acuteonset CIDP than in AIDP patients. [16][17][18] ANS dysfunction or the presence of preceding infections seem not to differ statistically among the acute-onset CIDP and the AIDP patients.…”

“…16,17 In view of recent literature reports, it seems that only the presence of sensory symptoms or signs and the absence of bulbar palsy or respiratory muscle weakness/need for mechanical ventilation are the only clinical parameters that are significantly more frequent in acuteonset CIDP than in AIDP patients. [16][17][18] ANS dysfunction or the presence of preceding infections seem not to differ statistically among the acute-onset CIDP and the AIDP patients. 16,17 On the other hand, the median time to reach nadir during first exacerbation seems to be significantly longer in the acute-onset CIDP group than in the AIDP group.…”

“…25 According to literature reports, the later electrophysiological parameters do not seem to be statistically different between the acute-onset CIDP and the AIDP patients. [16][17][18] Although the sural-sparing pattern or the elevated sensory ratio might be useful to differentiate an acquired demyelinating polyneuropathy from a length-dependent axonal polyneuropathy, recent studies show that these patterns occur equally in both AIDP and CIDP. 16,[23][24][25] On the other hand, the A-wave is attributed to either sprouting phenomena or ephaptic/ectopic discharges.…”

“…26 The later findings show that despite the use of motor conduction studies at the early phase of a polyradiculoneuropathy as a useful prognostic marker of functional outcome, 27 early sensory studies may not be helpful in distinguishing these two immune-mediated polyradiculoneuropathies. 16,17 Recently, nerve excitability tests have been introduced in the literature as a possible diagnostic biomarker of CIDP. In the nerve excitability test, threshold tracking is used to measure peripheral nerve function.…”