1. Steck AJ, Stalder AK, Renaud S. Anti-myelin-associated glycoprotein neuropathy. Curr Opin Neurol 2006;19:458–463. 2. Willison HJ, O’Leary CP, Veitch J, Blumhardt LD, Busby M, Donaghy M, et al. The clinical and laboratory features of chronic sensory ataxic neuropathy with anti-disialosyl IgM antibodies. Brain 2001; 124(Pt 10):1968–1977. 3. van Schaik IN, Bossuyt PM, Brand A, Vermeulen M. Diagnostic value of GM1 antibodies in motor neuron disorders and neuropathies: a meta-analysis. Neurology 1995;45:1570–1577. 4. Van den Berg L, Hays AP, Nobile-Orazio E, Kinsella LJ, Manfredini E, Corbo M, et al. Anti-MAG and anti-SGPG antibodies in neuropathy. Muscle Nerve 1996;19:637–643. 5. Weiss MD, Dalakas MC, Lauter CJ, Willison HJ, Quarles RH. Variability in the binding of anti-MAG and anti-SGPG antibodies to target antigens in demyelinating neuropathy and IgM paraproteinemia. J Neuroimmunol 1999;95:174–184. 6. Kuijf ML, Eurelings M, Tio-Gillen AP, van Doorn PA, van den Berg LH, Hooijkaas H, et al. Detection of anti-MAG antibodies in polyneuropathy associated with IgM monoclonal gammopathy. Neurology 2009;73:688–695. 7. Lopate G, Kornberg AJ, Yue J, Choksi R, Pestronk A. Anti-myelin associated glycoprotein antibodies: variability in patterns of IgM binding to peripheral nerve. J Neurol Sci 2001;188:67–72. 8. Rowland LP, Sherman WL, Hays AP, Lange DJ, Latov N, Trojaborg W, et al. Autopsy-proven amyotrophic lateral sclerosis, Waldenstrom’s macroglobulinemia, and antibodies to sulfated glucuronic acid paragloboside. Neurology 1995;45:827–829. 9. Ben Younes-Chennoufi A, Rozier A, Dib M, Bouche P, Lacomblez L, Mombo N, et al. Anti-sulfoglucuronyl paragloboside IgM antibodies in amyotrophic lateral sclerosis. J Neuroimmunol 1995;57:111–115. 10. Nobile-Orazio E, Vietorisz T, Messito MJ, Sherman WH, Latov N. Anti-MAG IgM antibodies in patients with neuropathy and IgM M proteins: detection by ELISA. Neurology 1983;33:939–942.
Published online 11 September 2014 in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/mus.24456
--------------------------------------------------------THE VALUE OF ULTRASONOGRAPHY VERSUS CLINICAL EXAMINATION IN DIFFERENTIATING ACUTE INFLAMMATORY DEMYELINATING POLYNEUROPATHY FROM ACUTE-ONSET CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY: THE IMPORTANCE OF TIMING We read with interest the article by Kerasnoudis et al., who described a nerve ultrasound score, the Bochum ultrasound score (BUS), as a useful tool that can distinguish acute inflammatory demyelinating polyneuropathy (AIDP) from acute-onset chronic inflammatory demyelinating polyneuropathy (AO-CIDP).1 The authors reviewed the records of 35 patients in the derivative phase of their analysis. The subjects were defined on clinical grounds as having AIDP or AO-CIDP, but they were evaluated at significantly different time-points (AIDP mean 12.5 days, AO-CIDP mean 21.2 days; P 5 0.021). Although this may not be important clinically, this discrepancy matters very much for ultrasonography, as a chronic inflammatory process is more likely to demonstrate morphological changes with time. As a result, a higher BUS would be more likely if ultrasonography is done later. The AO-CIDP patients are thus likely to have demonstrated more abnormalities, as they were evaluated later. In phase 2 of their study, the validation phase, other than the clearly very small total sample size of 10 subjects, they performed studies over an extremely wide time range, from a minimum of 2 days to a maximum of Letters to the Editor
4.5 weeks. The authors did not provide these ranges for the 2 subgroups separately. From the clinical point of view, we believe the results cannot be conclusive in these circumstances. For example, inclusion of a subject with AIDP without early autonomic failure who develops it soon after evaluation would result in obvious bias, as he/ she would be categorized as not having this particular clinical feature. This in turn could lead, as may have happened here, to the erroneous conclusion that autonomic dysfunction is not helpful to distinguish between the 2 disorders. Similarly, delayed appearance of ultrasonographic changes could have led to further errors of interpretation, as may have occurred if most/all AO-CIDP patients were evaluated late. A wide range of assessment timings in such a small sample size makes any attempt at meaningful conclusions hazardous in our opinion. Nerve excitability studies have also been reported recently to be useful in separating these 2 entities.2 In that study, however, there was no difference between the time of symptom onset and the nerve excitability test between cohorts. The main interest in distinguishing AIDP from AO-CIDP early is to plan subsequent therapeutic monitoring and management. It could be argued that this becomes clinically obvious with time anyway. Previous studies have demonstrated important early clinical pointers to differentiate the 2 disorders.3,4 Some of these clinical features have been confirmed by Kerasnoudis et al.1 For that reason also, the need for alternative methods appears debatable. Additional early prognostic information is always welcome, both by patients and their treating physicians, but it needs to be reliable. If ultrasonography is to become a practical and dependable diagnostic/prognostic tool in this setting, further larger studies will be required to justify its usefulness versus simple rigorous clinical evaluation. Yusuf A. Rajabally, MD, FRCP Fu Liong Hiew, MBBS, MRCP Regional Neuromuscular Clinic, Queen Elizabeth Neurosciences Centre, University Hospitals of Birmingham, Birmingham, UK 1. Kerasnoudis A, Pitarokoili K, Behrendt V, Gold R, Yoon MS. Bochum ultrasound score versus clinical and electrophysiological parameters in distinguishing acute-onset chronic from acute inflammatory demyelinating polyneuropathy. Muscle Nerve 2014 (Epub ahead of print). doi: 10.1002/mus.24484. 2. Sung J-Y, Tani J, Park SB, Kiernan MC, Lin CS. Early identification of “acute-onset” chronic inflammatory demyelinating polyneuropathy. Brain 2014;137:2155–2163. 3. Dionne A, Nicolle MW, Hahn AF. Clinical and electrophysiological parameters distinguishing acute-onset chronic inflammatory demyelinating polyneuropathy from acute inflammatory demyelinating polyneuropathy. Muscle Nerve 2010;41:202–207. 4. Ruts L, Drenthen J, Jacobs BC, van Doorn PA. Dutch GBS Study Group. Distinguishing acute-onset CIDP from fluctuating Guillain– Barr e syndrome: a prospective study. Neurology 2010;74:1680–1686.
Published online 19 December 2014 in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/mus.24548
--------------------------------------------------------REPLY: We thank Drs. Rajabally and Hiew for their interest and comments on our study. They have raised some concerns about the impact of the timing of evaluation on MUSCLE & NERVE
March 2015
459
Published online 11 September 2014 in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/mus.24456
--------------------------------------------------------THE VALUE OF ULTRASONOGRAPHY VERSUS CLINICAL EXAMINATION IN DIFFERENTIATING ACUTE INFLAMMATORY DEMYELINATING POLYNEUROPATHY FROM ACUTE-ONSET CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY: THE IMPORTANCE OF TIMING We read with interest the article by Kerasnoudis et al., who described a nerve ultrasound score, the Bochum ultrasound score (BUS), as a useful tool that can distinguish acute inflammatory demyelinating polyneuropathy (AIDP) from acute-onset chronic inflammatory demyelinating polyneuropathy (AO-CIDP).1 The authors reviewed the records of 35 patients in the derivative phase of their analysis. The subjects were defined on clinical grounds as having AIDP or AO-CIDP, but they were evaluated at significantly different time-points (AIDP mean 12.5 days, AO-CIDP mean 21.2 days; P 5 0.021). Although this may not be important clinically, this discrepancy matters very much for ultrasonography, as a chronic inflammatory process is more likely to demonstrate morphological changes with time. As a result, a higher BUS would be more likely if ultrasonography is done later. The AO-CIDP patients are thus likely to have demonstrated more abnormalities, as they were evaluated later. In phase 2 of their study, the validation phase, other than the clearly very small total sample size of 10 subjects, they performed studies over an extremely wide time range, from a minimum of 2 days to a maximum of Letters to the Editor
4.5 weeks. The authors did not provide these ranges for the 2 subgroups separately. From the clinical point of view, we believe the results cannot be conclusive in these circumstances. For example, inclusion of a subject with AIDP without early autonomic failure who develops it soon after evaluation would result in obvious bias, as he/ she would be categorized as not having this particular clinical feature. This in turn could lead, as may have happened here, to the erroneous conclusion that autonomic dysfunction is not helpful to distinguish between the 2 disorders. Similarly, delayed appearance of ultrasonographic changes could have led to further errors of interpretation, as may have occurred if most/all AO-CIDP patients were evaluated late. A wide range of assessment timings in such a small sample size makes any attempt at meaningful conclusions hazardous in our opinion. Nerve excitability studies have also been reported recently to be useful in separating these 2 entities.2 In that study, however, there was no difference between the time of symptom onset and the nerve excitability test between cohorts. The main interest in distinguishing AIDP from AO-CIDP early is to plan subsequent therapeutic monitoring and management. It could be argued that this becomes clinically obvious with time anyway. Previous studies have demonstrated important early clinical pointers to differentiate the 2 disorders.3,4 Some of these clinical features have been confirmed by Kerasnoudis et al.1 For that reason also, the need for alternative methods appears debatable. Additional early prognostic information is always welcome, both by patients and their treating physicians, but it needs to be reliable. If ultrasonography is to become a practical and dependable diagnostic/prognostic tool in this setting, further larger studies will be required to justify its usefulness versus simple rigorous clinical evaluation. Yusuf A. Rajabally, MD, FRCP Fu Liong Hiew, MBBS, MRCP Regional Neuromuscular Clinic, Queen Elizabeth Neurosciences Centre, University Hospitals of Birmingham, Birmingham, UK 1. Kerasnoudis A, Pitarokoili K, Behrendt V, Gold R, Yoon MS. Bochum ultrasound score versus clinical and electrophysiological parameters in distinguishing acute-onset chronic from acute inflammatory demyelinating polyneuropathy. Muscle Nerve 2014 (Epub ahead of print). doi: 10.1002/mus.24484. 2. Sung J-Y, Tani J, Park SB, Kiernan MC, Lin CS. Early identification of “acute-onset” chronic inflammatory demyelinating polyneuropathy. Brain 2014;137:2155–2163. 3. Dionne A, Nicolle MW, Hahn AF. Clinical and electrophysiological parameters distinguishing acute-onset chronic inflammatory demyelinating polyneuropathy from acute inflammatory demyelinating polyneuropathy. Muscle Nerve 2010;41:202–207. 4. Ruts L, Drenthen J, Jacobs BC, van Doorn PA. Dutch GBS Study Group. Distinguishing acute-onset CIDP from fluctuating Guillain– Barr e syndrome: a prospective study. Neurology 2010;74:1680–1686.
Published online 19 December 2014 in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/mus.24548
--------------------------------------------------------REPLY: We thank Drs. Rajabally and Hiew for their interest and comments on our study. They have raised some concerns about the impact of the timing of evaluation on MUSCLE & NERVE
March 2015
459
