Comparison of Electrodiagnostic Abnormalities and Criteria in a Cohort of Patients With Chronic Inflammatory Demyelinating Polyneuropathy

Magda, Paul; Latov, Norman; Brannagan, Thomas H.; Weimer, Louis H.; Chin, Russell L.; Sander, Howard W.

doi:10.1001/archneur.60.12.1755

Cited by 96 publications

(81 citation statements)

References 21 publications

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“…The observation that the AAN electrophysiologic criteria 5 only identified 54% of our cases validates our concern and is in keeping with the experience of other authors. [25][26][27] Nonetheless, we believe all our cases clinically had CIDP demonstrated by the typical clinical features, disease course, supportive laboratory and pathologic findings, response to immune modulating treatment, and demyelinating characteristics on electrophysiologic testing (table).…”

Section: Discussionmentioning

confidence: 99%

Incidence and prevalence of CIDP and the association of diabetes mellitus

Laughlin¹,

Melton²,

Leibson³

et al. 2009

Neurology

270

181

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Section: Discussionmentioning

confidence: 99%

Incidence and prevalence of CIDP and the association of diabetes mellitus

Laughlin¹,

Melton²,

Leibson³

et al. 2009

Neurology

270

181

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“…These studies, including the most recent, have used the AAN criteria, which have, for their electrophysiologic component, been shown to be of poor sensitivity in several reports. 10,18,19 The EFNS/PNS criteria have been shown to be of better diagnostic value, 17 but they have not been used for epidemiologic purposes. In the present study, the EFNS/PNS criteria produced a significantly larger number of CIDP diagnoses than the AAN criteria, allowing identification of 27 additional patients (McNemar's exact test; P Ͻ 0.0001).…”

Section: Discussionmentioning

confidence: 99%

Epidemiologic variability of chronic inflammatory demyelinating polyneuropathy with different diagnostic criteria: Study of a UK population

et al. 2009

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Epidemiologic data on chronic inflammatory demyelinating polyneuropathy (CIDP) is limited, and previous studies have shown variable results. The frequencies of CIDP subtypes remain unknown. Variations due to use of different diagnostic criteria have not been studied. We examined the prevalence and incidence of CIDP in Leicestershire and Rutland, UK (population 963,600). Prevalence day was 1 May 2008. The prevalence of CIDP fulfilling the 2006 clinical and electrophysiologic European Federation of Neurological Societies/Peripheral Nerve Society (EFNS/PNS) criteria was 4.77 per 100,000 (95% confidence interval [CI] 3.49-6.37). Using the 1991 American Academy of Neurology (AAN) criteria, the prevalence was 1.97 per 100,000 in this population (95% CI 1.19-3.08). Lewis-Sumner syndrome was diagnosed in 15.2% of patients, and 23.9% had pure sensory onset. Over 40% required no immunotherapy, and 84.6% of those treated responded. More than 80% of the AAN criteria-negative but EFNS/PNS criteria-positive patients were responsive to treatment. Both sets of criteria were equally likely to identify patients who required therapy. The mean annual incidence rate over the 3 years preceding the prevalence day was 0.70 per 100,000/year using EFNS/PNS criteria (95% CI 0.43-1.08), and 0.35 per 100,000/year using AAN criteria (95% CI 0.17-0.64). We conclude that the AAN criteria may underestimate prevalence and incidence of the disease. The EFNS/PNS criteria provide higher diagnostic sensitivity and are of greater clinical relevance, and they also offer a useful breakdown of the epidemiologic data for CIDP subtypes.

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“…There is also a large group of patients with presumed CIDP, who do not fulfill any of the proposed electrodiagnostic criteria. 26 Examples of some confounding diagnoses include:…”

Section: Differential Diagnosismentioning

confidence: 99%

Chronic Inflammatory Demyelinating Polyradiculoneuropathy 101—Pitfalls and Pearls of Diagnosis and Treatment

Beydoun¹,

Brannagan²,

Donofrio³

et al. 2017

US Neurology

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Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), which is caused by demyelination of the peripheral nerves, is characterized by progressive weakness and impaired sensory function in the arms and legs. CIDP is a treatable condition in which early diagnosis is crucial to limit chronic disability. CIDP can mimic other neuropathies and it is important to identify these in order to ensure prompt treatment. Patients with other causes of neuropathy should be suspected of having CIDP if there is rapid progress or proximal weakness. Intravenous immunoglobulin (IVIG), corticosteroids, and plasma exchange are first-line therapies. The IVIG CIDP Efficacy (ICE) trial, the largest trial reported of any CIDP treatment, demonstrated that IVIG therapy reduced disability and functional impairment, as well as improved quality of life. Autoantibodies against membrane proteins of the peripheral nerve axons or the myelin sheath have been reported recently, and an improved understanding of antibody responses in CIDP may enable the development of future targeted therapeutic interventions.

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Comparison of Electrodiagnostic Abnormalities and Criteria in a Cohort of Patients With Chronic Inflammatory Demyelinating Polyneuropathy

Abstract: Current electrodiagnostic criteria for CIDP are insensitive and may fail to diagnose the condition in a substantial number of patients. More inclusive criteria that allow identification of patients in routine clinical practice are needed.

Cited by 96 publications

References 21 publications

Incidence and prevalence of CIDP and the association of diabetes mellitus

Incidence and prevalence of CIDP and the association of diabetes mellitus

Epidemiologic variability of chronic inflammatory demyelinating polyneuropathy with different diagnostic criteria: Study of a UK population

Chronic Inflammatory Demyelinating Polyradiculoneuropathy 101—Pitfalls and Pearls of Diagnosis and Treatment

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