Marieke van Rosmalen

Quantitative MRI characteristics of chronic inflammatory neuropathies 105 6 (inter)nodal regions in patients with CIDP. 3–5,38–41 The mechanism of paranodal myelin detachment is present in some patients with CIDP, as described in earlier electrophysiological studies. 42–44 Taken together, the changes in FA, MD and RD in our CIDP group most likely reflect the loss of myelin. The absence of increased RD values in patients with MMN indicates that the underlying pathophysiological mechanism is different from that in CIDP and that demyelination is probably not the dominant pathophysiological process. Patients with MMN seem to have comparable quantitative MRI parameters as healthy controls. Scarce histological reports describe normal myelin sheets. 6–8 Electrophysiological studies may support the idea of changed axon structure with largely intact myelin sheets. 44 However, it is rather remarkable that such different DTI profiles are found between patients with MMN and CIDP while diagnostic tools used in clinical practice, such as nerve conduction studies, nerve ultrasound and qualitative MRI of the brachial plexus may show similar abnormalities, e.g. conduction blocks and thickening of the nerves. The differences in DTI profiles indicate that these abnormalities are more likely to present common endpoints of different pathophysiological mechanisms rather than comparable etiologies. In a previous study we found lower AD in the median and ulnar nerves in the forearm of patients with MMN compared to healthy controls and patients with ALS. 18 It is assumed that AD correlates with axonal loss, e.g. due to axonal swelling due to the breakdown or change in the permeability of the axolemma, which is an important feature of MMN. 11,45,46 We did not detect differences in AD between groups at the brachial plexus in this study, which can be explained by the fact that longer axons and distal parts of axons are more susceptible to injury than short and proximal parts of axons. Consequently, AD may remain relatively unchanged in the proximal spinal nerve roots of the brachial plexus. In the previous study we did not find a significant difference in FA between patients with MMN and ALS, although absolute values of FA were higher in patients with MMN. 18 We found a significantly higher FA in patients with MMN compared to patients with MND in this study, which can be explained by the larger sample size and higher statical power in the current study. Correlations between clinical data and quantitative MRI parameters were weak. We refrained from studying correlations of nerve conduction studies and imaging results since the measurement sites did not match. More in general, imaging and electrophysiological studies may reveal different pathophysiological dimensions. Previous studies found that imaging results did not correlate with nerve conduction study results in cohorts of patients with inflammatory neuropathies. 47–51 A limitation of our study is the effect of partial volume, which may lead to an underestimation of diffusion parameters and fat fraction, and varying SNR which may lead to higher FA and lower RD in case of lower SNRs. 52 However, the influence of partial volume effects and different SNR values were probably small as our results in DTI analysis, T2 mapping and fat fraction analysis are consistent with each other, and scans were performed in random order with the same software