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Nerve ultrasound and magnetic resonance imaging in the diagnosis of neuropathy

Goedee, H. Stephana; van der Pol, W. Ludoa; Hendrikse, Jeroenb; van den Berg, Leonard H.a

doi: 10.1097/WCO.0000000000000607

Purpose of review This review summarizes the most relevant developments in the fields of nerve ultrasound and MRI in the diagnosis of treatable inflammatory neuropathies over the last 18 months.

Recent findings MRI and nerve ultrasound can accurately identify potentially treatable neuropathies and thereby help to improve diagnosis. Advanced MRI techniques also show potential to dissect pathophysiology. The apparent mismatch between nerve function and morphology is not surprising and reflects different dimensions of the disease process in neuropathies.

Summary MRI and nerve ultrasound have become useful tools in the diagnosis of inflammatory neuropathies.

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aBrain Center Rudolf Magnus, Department of Neurology and Neurosurgery

bDepartment of Radiology, UMC Utrecht, Utrecht, The Netherlands

Correspondence to H. Stephan Goedee, MD, PhD, UMC Utrecht, Department of Neurology and Neurosurgery, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. Tel: +31 88 75 588 60; fax: +31 88 75 55494; e-mail:

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The incidence of (lower) motor neuron syndromes and axonal neuropathies exceeds by far that of chronic inflammatory neuropathies [1,2]. Consensus diagnostic criteria for chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN) primarily rely on clinical features and results from electrodiagnostic studies (Fig. 1) [3–5]. However, accurate identification may be complicated by the clinician's inexperience or the considerable heterogeneity of the clinical phenotype of these rare disorders. Moreover, the execution of electrodiagnostic studies (EDX) is labor intensive and requires appropriate facilities to warm limbs prior to investigation [6,7]. Elaborate testing of multiple limbs is crucial, as is the inclusion of proximal nerve segments, because conduction block and conduction slowing are often focal and patchily distributed. Even in ideal circumstances, securing a diagnosis may remain challenging in a substantial number of patients [8]. Neuroimaging of the peripheral nerves might help and is becoming an important complement to EDX. It allows an additional means of detecting nerve involvement and thereby the identification of patients with treatable neuropathies. This review examines the most prominent developments in the fields of diagnostic nerve ultrasound and MRI of inflammatory neuropathies in the last 18 months.

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The first published case-reports and -series suggested that inflammation and myelin dysfunction led to thickening of nerves in patients with chronic immune-mediated neuropathies that could be detected by both MRI and nerve ultrasound [9–11]. In subsequent studies, MRI was mainly used to explore the frequency of abnormalities in spinal nerve roots, whereas ultrasound studies focused more on large arm and leg nerves [12–16].

An important drawback was the lack of systematic studies addressing the diagnostic properties of imaging techniques in chronic immune- mediated neuropathies. The interpretation and comparison of available studies was complicated by the use of different protocols and patient cohorts with important differences in disease duration and treatment status. Nevertheless, these imaging studies corroborated the initial pilot studies and indicated nerve enlargement along the length of nerves in chronic immune-mediated neuropathies, this in striking contrast to the often focal abnormalities (i.e. conduction block) found during nerve conduction studies (NCS). A subsequent step was to propose several ultrasound scoring-systems in an attempt to further distinguish patterns of nerve enlargement [17–24]. These systems were based on structure (normal, mild, regional, and diffuse enlargement), anatomic sites, and fascicular involvement.

The MRI of the plexus primarily relies on T2-weighted sequences [DIXON or 2D short tau inversion recovery (STIR] that can reveal enlargement and/or hyperintense signal of nerve roots or postgadolinium enhancement [13]. The few studies that described the distribution of plexus abnormalities (normal, symmetric, or focal, root dominant or fusiform) were all retrospective cohort studies with modest sample sizes [15,25,26,27,28▪]. Reported MRI abnormalities in CIDP and MMN showed considerable variation (40–100%). Hyperintense signal is probably the most common abnormality (CIDP: 44–72%; MMN: 44–100%), while enlargement (CIDP: 13–88%; MMN: 22–30%) and postgadolinium enhancement (CIDP: 10–89%; none in MMN) are less frequently documented [9–11]. Symmetric abnormalities on plexus MRI may be associated with generalized, and focal abnormalities with asymmetric clinical weakness, but this relationship remains to be corroborated in prospective studies [28▪].

In contrast to ultrasound, systematic scoring-systems for MRI brachial plexus abnormalities still need to be developed. This may improve sensitivity and further strengthen the important place that brachial plexus MRI already has in the current diagnostic consensus criteria for MMN, Lewis–Sumner syndrome (LSS), and CIDP [3–5,29]. Specificity of brachial plexus MRI is context dependent. Although there are several other neuropathies that are also associated with nerve (root) abnormalities, including Charcot–Marie–Tooth (CMT) type 1, neuropathy associated with monoclonal immunoglobulin M (IgM) gammopathy, diabetic plexoradiculoneuropathy, neurolymphomatosis, neuralgic amyotrophy, vasculitis syndromes, and neurofibromatosis, most of these disorders, with the possible exception of the occasional atypical presentation of CMT type 1, can be distinguished from CIDP, LSS, and MMN on clinical grounds [3–5,29]. The specificity of MRI and nerve ultrasound to identify inflammatory neuropathies is high in the context of (lower) motor neurone syndromes and axonal neuropathy.

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Last year results that support predefined scoring systems of peripheral nerve imaging were published. In this study, we used a standardized ultrasound protocol in 75 consecutive treatment-naive patients with CIDP and MMN, and 70 clinically relevant mimics [30▪▪]. Enlargement of the median nerve at forearm and upper arm in combination with enlargement of any trunk of the brachial plexus was 99% specific for an inflammatory neuropathy. Two abnormal segments in a relatively short and user-friendly ultrasound protocol of bilateral median nerve assessment in combination with the brachial plexus showed similar high sensitivity and specificity. This study provides Class II evidence that, in the absence of clinical features suggesting a possible demyelinating hereditary neuropathy, sonographic enlargement of proximal median nerve segments and brachial plexus reliably identifies patients with CIDP, LSS, and MMN [30▪▪]. Nerve ultrasound protocols can be shortened for daily practice without losing much of the test characteristics (Fig. 2A). The study also confirmed that nerve size is the most robust sonographic parameter in neuropathies and that other sonographic parameters, such as fascicle size, echogenicity, and vascularization, have no added value for the identification of inflammatory neuropathies.



It was not known whether the diagnostic performance of MRI and sonography were comparable because only a few case-series compared the use of these techniques in CIDP [31,32]. Results from a recent study suggest that the diagnostic yield of brachial plexus sonography and MRI in a treatment-naive cohort [33▪] is comparable, with abnormalities in the 63–73% range. The combination of both imaging modalities further increased diagnostic sensitivity to 83% of patients with CIDP and MMN. Both imaging techniques have their intrinsic advantages and limitations: MRI can produce optimized images for evaluation of abnormal diameter and separately for signal intensity of nerve roots, but lacks objective cut-off values for abnormality [34▪,35,36] and requires neuroradiological expertize; nerve ultrasound is a broadly available bedside tool which is sensitive and has a more flexible field of view (e.g., to include large arm nerves), but it requires training [37▪]. This study also showed that contrast enhancement on MRI, similar to hypervascularization in sonography [14], is probably an indicator of the degree of chronic inflammation rather than a disease-specific parameter.

Another recent development is further refinement of MRI protocols with more advanced T2-based sequences that may improve resolution [27,35,38–41]. It is our experience that this approach is feasible and that this may boost image quality and thereby diagnostic value (Fig. 2B). Nevertheless, more systematic studies in unselected patient populations and controls to define disease-specific cut-off values for abnormality are needed to accurately determine their effect on diagnostic performance. Expanding the field of view with whole body MRI-neurography is another potentially interesting development. This allows screening for nerve enlargement among multiple nerves on MRI [42], but currently has inferior image resolution compared to the dedicated plexus protocols. Similar to the higher diagnostic yield of ultrasound protocols that asses multiple nerves, we expect that whole body MRI-neurography may ultimately prove an important step forward.

Finally, relatively novel magnetic resonance techniques that are used routinely for imaging of the central nervous tissue [e.g., diffusion tensor imaging (DTI] may be tools to study pathophysiological processes, disease progression, or treatment effects in chronic inflammatory neuropathies [43–45]. In a proof of principle study, diffusivity was reduced in the forearm of patients with MMN compared with healthy individuals and patients’ motor neurone disease [43]. These protocols can and need to be further improved, but DTI apparently can yield qualitative in addition to quantitative data. We need to further explore its usefulness to study pathophysiology of MMN and CIDP or as a biomarker of response to treatment [43–45].

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An important question is whether imaging and nerve conduction abnormalities reflect the same underlying pathophysiological processes. Multiple studies have compared parameters of nerve imaging with those of nerve conduction, but suffer from multiple methodological weaknesses. The lack of standardization of anatomical sites, limb temperature during NCS, and distances complicates the interpretation of the available comparative studies. At present, we think the available data do not suggest a relation between nerve morphology (MRI/ultrasound) and nerve function (EDX) [46–50]. The reports that did suggest such an association did not address important methodological questions how comparisons at nerve level [10,44,51,52] using selected sets of EDX and imaging parameters can be properly performed. Comparison between techniques is for example only possible at the segmental level of arm and leg nerves. It is not possible to reliably compare morphological changes to nerve conduction abnormalities at the level of the plexus. For example, prolonged F-wave latency or conduction block at the level of the shoulder in only one nerve cannot be associated with plexus thickening as other parts of the plexus may well be abnormal without similar associated nerve conduction abnormalities in other (arm) nerves. Future comparative studies also need to address neighboring nerve segments (e.g., include proximal/distal/contralateral segments of same nerve or ipsilateral equivalent in other nerve) as an intraindividual control of their findings on possible associations.

Moreover, the apparent mismatch between function and morphology in neuropathies is not only far from unique but also seen in other neurological conditions (e.g., silent ischemic or pure radiological increase of new multiple sclerosis lesions on brain MRI). In fact, it implies that the underlying pathological processes that lead to functional and morphological disturbances are not necessarily the same (Fig. 3). Inflammation and edema, ischemia, fibrosis, and myelin dysfunction probably all lead to nerve hypertrophy. Routine electrodiagnostic studies only evaluate groups of axons within nerves, i.e., the sum of most fast conducting fibers. Therefore, standard EDX does not appreciate pathological changes that occur in individual axons, such as different degrees of myelin, nodal, and axonal dysfunction between axons within the same nerve. There may be alternatives such as nerve excitability that better reflect function of myelinated axons, such as sodium-pump function, but this remains to be established in more detail [53–55].



Summarizing, nerve imaging and nerve conduction yield complementary sets of information about nerve condition and should be combined rather than compared in neuropathies. Their combined use can help to maximize the diagnostic yield of inflammatory neuropathies.

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Although important advances have been made, there are still several gaps in knowledge on nerve imaging studies, which need to be addressed. Objective and disease-specific cut-off values for MRI parameters and systematic evaluation of their diagnostic yield are warranted to standardize interpretation. This will undoubtedly help to optimize its application in routine clinical practice. Other important remaining questions are comparison of the diagnostic yield of lumbosacral versus brachial plexus MRI, and a thorough evaluation of the added value of more advanced MRI techniques [e.g., further development of STIR, neurography with maximal intensity projection (MIP)].

Nerve ultrasound is an important addition to the repertoire of ancillary investigations that complements EDX and MRI. The available evidence supports combined EDX and nerve imaging in the diagnostic work-up of patients who may have an inflammatory neuropathy. Although nerve imaging clearly improves detection of treatment-responsive neuropathies, the balance of extra yield and false positives is unknown. Prospective studies are needed in large unbiased patient cohorts that apply nerve imaging alongside standardized EDX to all cases in a routine clinical setting. For the time being, both nerve ultrasound and MRI should be considered as ‘imaging’ modalities and eventually be included in future revisions of diagnostic consensus criteria for chronic inflammatory neuropathies. In Fig. 4 , we present an outline of what revised diagnostic criteria could look like after addition of ultrasound based on a synthesis of the current European Federation of Neurological Societies (currently the Academy of Neurology (EAN))/Peripheral Nerve Society criteria and Utrecht criteria [3–5], with clinical (core, supportive, and exclusion), EDX (definite, probable, and possible), and supportive criteria. The relevance of ultrasound clearly lies in its promising test characteristics that allows the clinician to identify patients with CIDP and MMN, even when EDX is inconclusive or negative [31,32,56,57]. On the contrary, it is unlikely that imaging modalities can replace EDX.





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MRI and nerve ultrasound have become adjunctive diagnostic tools for potentially treatable neuropathies. Future MRI studies are needed to provide objective and disease-specific cut-off values for abnormality, particularly for spinal nerve roots, whereas ongoing prospective sonography studies will determine the diagnostic yield and frequencies of false positive findings.

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The authors would like to thank Prof. L.H. Visser, Dr J.T.H. van Asseldonk, I.J.T. Herraets, and J. Telleman for the collaborative efforts and helpful discussion that helped to shape the content of this manuscript.

H.S.G. helped in review of literature and selection of published articles, analysis and interpretation of data, and drafting/revision of the manuscript. Whereas W.L. van der P., J.H., and L.H. van den B. contributed to selection of published articles, analysis and interpretation of data, and drafting/revision of the manuscript.

H.S.G. received research support from the Prinses Beatrix Spierfonds; travel grant from Shire.

L.H. van den B. served on scientific advisory boards for the Biogen Idec, Cytokinetics, and Sarepta; received an educational grant from Shire; served on the editorial boards of Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, the Journal of Neurology, Neurosurgery and Psychiatry, and the Journal of Neuromuscular Diseases; and received research support from the Prinses Beatrix Spierfonds, Netherlands ALS Foundation, The European Community's Health Seventh Framework Programme (grant agreement no. 259867), and The Netherlands Organization for Health Research and Development (Vici Scheme, JPND (SOPHIA, STRENGTH,NETCALS, ALSCare)).

W.L. van der P. received research support from the Prinses Beatrix Spierfonds; Stichting Spieren voor Spieren.

J.H. received research support from the Netherlands Organization for Scientific Research (NWO) under grant no. 91712322, the European Research Council under grant agreement no. 37024.

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Financial support and sponsorship


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Conflicts of interest

There are no conflicts of interest.

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Papers of particular interest, published within the annual period of review, have been highlighted as:

  • ▪ of special interest
  • ▪▪ of outstanding interest
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1. Visser NA, Notermans NC, Linssen RS, et al. Incidence of polyneuropathy in Utrecht, the Netherlands. Neurology 2015; 84:259–264.
2. Simon NG, Ayer G, Lomen-Hoerth C. Is IVIg therapy warranted in progressive lower motor neuron syndromes without conduction block? Neurology 2013; 81:2116–2120.
3. Joint Task Force of the E, the PNS. European Federation of Neurological Societies/Peripheral Nerve Society Guideline on management of chronic inflammatory demyelinating polyradiculoneuropathy: report of a joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society–First Revision. J Peripher Nerv Syst 2010; 15:1–9.
4. Joint Task Force of the E, the PNS. European Federation of Neurological Societies/Peripheral Nerve Society guideline on management of multifocal motor neuropathy. Report of a joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society–first revision. J Peripher Nerv Syst 2010; 15:295–301.
5. Vlam L, van der Pol WL, Cats EA, et al. Multifocal motor neuropathy: diagnosis, pathogenesis and treatment strategies. Nat Rev Neurol 2011; 8:48–58.
6. Franssen H, Wieneke GH. Nerve conduction and temperature: necessary warming time. Muscle Nerve 1994; 17:336–344.
7. Franssen H, Wieneke GH, Wokke JH. The influence of temperature on conduction block. Muscle Nerve 1999; 22:166–173.
8. Allen JA, Lewis RA. CIDP diagnostic pitfalls and perception of treatment benefit. Neurology 2015; 85:498–504.
9. Duggins AJ, McLeod JG, Pollard JD, et al. Spinal root and plexus hypertrophy in chronic inflammatory demyelinating polyneuropathy. Brain 1999; 122:1383–1390.
10. Kuwabara S, Nakajima M, Matsuda S, Hattori T. Magnetic resonance imaging at the demyelinative foci in chronic inflammatory demyelinating polyneuropathy. Neurology 1997; 48:874–877.
11. Taniguchi N, Itoh K, Wang Y, et al. Sonographic detection of diffuse peripheral nerve hypertrophy in chronic inflammatory demyelinating polyradiculoneuropathy. J Clin Ultrasound 2000; 28:488–491.
12. Goedee HS, Brekelmans GJ, van Asseldonk JT, et al. High resolution sonography in the evaluation of the peripheral nervous system in polyneuropathy: a review of the literature. Eur J Neurol 2013; 20:1342–1351.
13. van Es HW. MRI of the brachial plexus. Eur Radiol 2001; 11:325–336.
14. Goedee HS, Brekelmans GJ, Visser LH. Multifocal enlargement and increased vascularization of peripheral nerves detected by sonography in CIDP: a pilot study. Clin Neurophysiol 2014; 125:154–159.
15. Van Es HW, Van den Berg LH, Franssen H, et al. Magnetic resonance imaging of the brachial plexus in patients with multifocal motor neuropathy. Neurology 1997; 48:1218–1224.
16. Eurelings M, Notermans NC, Franssen H, et al. MRI of the brachial plexus in polyneuropathy associated with monoclonal gammopathy. Muscle Nerve 2001; 24:1312–1318.
17. Zaidman CM, Harms MB, Pestronk A. Ultrasound of inherited vs. acquired demyelinating polyneuropathies. J Neurol 2013; 260:3115–3121.
18. Padua L, Martinoli C, Pazzaglia C, et al. Intra- and internerve cross-sectional area variability: new ultrasound measures. Muscle Nerve 2012; 45:730–733.
19. Padua L, Granata G, Sabatelli M, et al. Heterogeneity of root and nerve ultrasound pattern in CIDP patients. Clin Neurophysiol 2014; 125:160–165.
20. Kerasnoudis A, Pitarokoili K, Behrendt V, et al. Nerve ultrasound score in distinguishing chronic from acute inflammatory demyelinating polyneuropathy. Clin Neurophysiol 2014; 125:635–641.
21. Kerasnoudis A, Pitarokoili K, Gold R, Yoon MS. Bochum ultrasound score allows distinction of chronic inflammatory from multifocal acquired demyelinating polyneuropathies. J Neurol Sci 2015; 348:211–215.
22. Kerasnoudis A, Pitarokoili K, Haghikia A, et al. Nerve ultrasound protocol in differentiating chronic immune-mediated neuropathies. Muscle Nerve 2016; 54:864–871.
23. Grimm A, Decard BF, Axer H, Fuhr P. The Ultrasound pattern sum score - UPSS. A new method to differentiate acute and subacute neuropathies using ultrasound of the peripheral nerves. Clin Neurophysiol 2015; 126:2216–2225.
24. Grimm A, Vittore D, Schubert V, et al. Ultrasound pattern sum score, homogeneity score and regional nerve enlargement index for differentiation of demyelinating inflammatory and hereditary neuropathies. Clin Neurophysiol 2016; 127:2618–2624.
25. Van den Berg-Vos RM, Van den Berg LH, Franssen H, et al. Multifocal inflammatory demyelinating neuropathy: a distinct clinical entity? Neurology 2000; 54:26–32.
26. Rajabally YA, Knopp MJ, Martin-Lamb D, Morlese J. Diagnostic value of MR imaging in the Lewis-Sumner syndrome: a case series. J Neurol Sci 2014; 342:182–185.
27. Shibuya K, Sugiyama A, Ito S, et al. Reconstruction magnetic resonance neurography in chronic inflammatory demyelinating polyneuropathy. Ann Neurol 2015; 77:333–337.
28▪. Jongbloed BA, Bos JW, Rutgers D, et al. Brachial plexus magnetic resonance imaging differentiates between inflammatory neuropathies and does not predict disease course. Brain Behav 2017; 7:e00632.

The first systematic study on distribution of MRI abnormalities in relation to different types of chronic inflammatory neuropathy.

29. Rajabally YA, Chavada G. Lewis-sumner syndrome of pure upper-limb onset: diagnostic, prognostic, and therapeutic features. Muscle Nerve 2009; 39:206–220.
30▪▪. Goedee HS, van der Pol WL, van Asseldonk JH, et al. Diagnostic value of sonography in treatment-naive chronic inflammatory neuropathies. Neurology 2017; 88:143–151.

A large systematic nerve ultrasound study that used an elaborate and standardized ultrasound protocol in consecutive treatment-naive patients with CIDP and MMN, and a random sample of clinically relevant mimics, This study provides Class II evidence that, in the absence of clinical features suggesting a possible demyelinating hereditary neuropathy, sonographic enlargement of proximal median nerve segments and brachial plexus reliably identifies patients with CIDP, LSS and MMN. Nerve thickness is the most robust parameter and ultrasound protocols could, therefore, be reduced to a short sonographic test.

31. Viala K. Diagnosis of atypical forms of chronic inflammatory demyelinating polyradiculoneuropathy: a practical overview based on some case studies. Int J Neurosci 2016; 126:777–785.
32. Lozeron P, Lacour MC, Vandendries C, et al. Contribution of plexus MRI in the diagnosis of atypical chronic inflammatory demyelinating polyneuropathies. J Neurol Sci 2016; 360:170–175.
33▪. Goedee HS, Jongbloed BA, van Asseldonk JH, et al. A comparative study of brachial plexus sonography and magnetic resonance imaging in chronic inflammatory demyelinating neuropathy and multifocal motor neuropathy. Eur J Neurol 2017; 24:1307–1313.

First comparative study of MRI and nerve ultrasound in treatment-naive chronic inflammatory neuropathies.

34▪. Chaves H, Bendersky M, Goni R, et al. Lumbosacral plexus root thickening: establishing normal root dimensions using magnetic resonance neurography. Clin Anat 2018; doi: 10.1002/ca.23073. [Epub ahead of print].

First MRI study to report normal values of lumbosacral nerve roots based on healthy controls and correlation with dissection of cadaver specimens.

35. Hiwatashi A, Togao O, Yamashita K, et al. Evaluation of chronic inflammatory demyelinating polyneuropathy: 3D nerve-sheath signal increased with inked rest-tissue rapid acquisition of relaxation enhancement imaging (3D SHINKEI). Eur Radiol 2017; 27:447–453.
36. Tanaka K, Mori N, Yokota Y, Suenaga T. MRI of the cervical nerve roots in the diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy: a single-institution, retrospective case-control study. BMJ Open 2013; 3: e003443. doi:10.1136/bmjopen-2013- 003443.
37▪. Garcia-Santibanez R, Dietz AR, Bucelli RC, Zaidman CM. Nerve ultrasound reliability of upper limbs: effects of examiner training. Muscle Nerve 2018; 57:189–192.
38. Cejas C, Rollan C, Michelin G, Nogues M. High resolution neurography of the brachial plexus by 3 Tesla magnetic resonance imaging. Radiologia 2016; 58:88–100.
39. Hiwatashi A, Togao O, Yamashita K, et al. Lumbar plexus in patients with chronic inflammatory demyelinating polyneuropathy: evaluation with 3D nerve-sheath signal increased with inked rest-tissue rapid acquisition of relaxation enhancement imaging (3D SHINKEI). Eur J Radiol 2017; 93:95–99.
40. Wang X, Harrison C, Mariappan YK, et al. MR neurography of brachial plexus at 3.0 t with robust fat and blood suppression. Radiology 2017; 283:538–546.
41. Sollmann N, Weidlich D, Cervantes B, et al. High isotropic resolution T2 mapping of the lumbosacral plexus with T2-prepared 3D turbo spin echo. Clin Neuroradiol 2018; doi: 10.1007/s00062-017-0658-9.
42. Ishikawa T, Asakura K, Mizutani Y, et al. MR neurography for the evaluation of CIDP. Muscle Nerve 2017; 55:483–489.
43. Haakma W, Jongbloed BA, Froeling M, et al. MRI shows thickening and altered diffusion in the median and ulnar nerves in multifocal motor neuropathy. Eur Radiol 2017; 27:2216–2224.
44. Kronlage M, Pitarokoili K, Schwarz D, et al. Diffusion tensor imaging in chronic inflammatory demyelinating polyneuropathy: diagnostic accuracy and correlation with electrophysiology. Invest Radiol 2017; 52:701–707.
45. Markvardsen LH, Vaeggemose M, Ringgaard S, Andersen H. Diffusion tensor imaging can be used to detect lesions in peripheral nerves in patients with chronic inflammatory demyelinating polyneuropathy treated with subcutaneous immunoglobulin. Neuroradiology 2016; 58:745–752.
46. Beekman R, van den Berg LH, Franssen H, et al. Ultrasonography shows extensive nerve enlargements in multifocal motor neuropathy. Neurology 2005; 65:305–307.
47. Rajabally YA, Morlese J, Kathuria D, Khan A. Median nerve ultrasonography in distinguishing neuropathy sub-types: a pilot study. Acta Neurol Scand 2012; 125:254–259.
48. Kerasnoudis A, Pitarokoili K, Behrendt V, et al. Correlation of nerve ultrasound, electrophysiological and clinical findings in chronic inflammatory demyelinating polyneuropathy. J Neuroimaging 2015; 25:207–216.
49. Grimm A, Decard BF, Athanasopoulou I, et al. Nerve ultrasound for differentiation between amyotrophic lateral sclerosis and multifocal motor neuropathy. J Neurol 2015; 262:870–880.
50. Kerasnoudis A, Pitarokoili K, Behrendt V, et al. Multifocal motor neuropathy: correlation of nerve ultrasound, electrophysiological, and clinical findings. J Peripher Nerv Syst 2014; 19:165–174.
51. Di Pasquale A, Morino S, Loreti S, et al. Peripheral nerve ultrasound changes in CIDP and correlations with nerve conduction velocity. Neurology 2015; 84:803–809.
52. Simon NG, Kiernan MC. Precise correlation between structural and electrophysiological disturbances in MADSAM neuropathy. Neuromuscul Disord 2015; 25:904–907.
53. Franssen H, Straver DC. Pathophysiology of immune-mediated demyelinating neuropathies-part I: neuroscience. Muscle Nerve 2013; 48:851–864.
54. Kovalchuk MO, Franssen H, Van Schelven LJ, Sleutjes B. Comparing excitability at 37 degrees C versus at 20 degrees C: differences between motor and sensory axons. Muscle Nerve 2018; 57:574–580.
55. Hageman S, Kovalchuk MO, Sleutjes B, et al. Sodium-potassium pump assessment by submaximal electrical nerve stimulation. Clin Neurophysiol 2018; 129:809–814.
56. Gasparotti R, Lucchetta M, Cacciavillani M, et al. Neuroimaging in diagnosis of atypical polyradiculoneuropathies: report of three cases and review of the literature. J Neurol 2015; 262:1714–1723.
57. Hobson-Webb LD, Donahue SN, Bey RD. Multifocal motor neuropathy: 30 years from onset to diagnosis. Muscle Nerve 2016; 53:490–491.

diagnostic value; MRI; neuropathy; ultrasound

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