magnetic resonance imaging of the peripheral nervedesign of magnetic resonance imaging (mri) systems...

Magnetic Resonance Imagingof the Peripheral Nerve

Roberto Gasparotti and Michela Leali

ContentsAnatomy of Peripheral Nerves . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Magnetic Resonance Neurography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

Normal Versus Pathological Nerves . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

Diffusion Tensor Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8

Ultrasound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Peripheral Nerve Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10Brachial Plexus Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10Lumbosacral Plexus, Sciatic, Peroneal, and Femoral Nerve Injuries . . . . . . . . . . . . . . . . . . . . 11

Entrapment Neuropathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13Carpal Tunnel Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14Ulnar Neuropathy at the Elbow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

This publication is endorsed by: European Society ofNeuroradiology (www.esnr.org).

R. Gasparotti (*)Head of Neuroradiology Unit, University Hospital SpedaliCivili di Brescia, Brescia, Italy

Department of Medical and Surgical Specialties,Radiological Sciences and Public Health, Section ofNeuroradiology, University of Brescia, Brescia, Italye-mail: [email protected]

M. LealiRadiology resident, University of Brescia, Brescia, Italye-mail: [email protected]

# Springer Nature Switzerland AG 2018F. Barkhof et al. (eds.), Clinical Neuroradiology,https://doi.org/10.1007/978-3-319-61423-6_76-1

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Other Entrapments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

Non-traumatic Brachial Plexopathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

Non- traumatic Lumbosacral Plexopathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

Inflammatory Neuropathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23Guillain-Barré Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23Chronic Inflammatory Demyelinating Polyradiculoneuropathy . . . . . . . . . . . . . . . . . . . . . . . . . 25Multifocal Motor Neuropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26

Inherited Neuropathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

Amyloid Neuropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

Diabetic Polyneuropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

Peripheral Nerve Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

Case 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

Case 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34

Reporting Checklist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

AbstractThe diagnostic work-up of peripheral neurop-athies has traditionally relied on the patient’sclinical history, physical examination, andelectrophysiological studies. However, thesediagnostic tools have limitations to displaythe anatomic detail needed for precise locali-zation and treatment planning. Technicaladvances are rapidly changing the clinical andinstrumental approach to peripheral nervediseases, and radiological techniques such asnerve ultrasound and magnetic resonanceneurography are increasingly being used inthe investigation of the peripheral nerve systemin addition to diagnostic modalities such asneurophysiology. The recent progresses in thedesign of magnetic resonance imaging (MRI)systems and image acquisition techniques(e.g., pulse sequences) can provide high-resolution peripheral nerve imaging and excel-lent assessment of nerve size, morphology, andinternal fascicular structure. Clinical neurora-diology plays a crucial role in improving thediagnosis, addressing the treatments, and allo-wing a better prognosis of peripheral nervedamage.

This chapter reviews the new imaging tech-niques and their impact on patients’ diagnosisand treatment strategies in the principal

categories of peripheral nerve diseases, suchas nerve trauma, entrapments, tumors, and dif-fuse neuropathies, and discusses the role ofmost promising research findings with poten-tial applicability to the clinical practice.

KeywordsDiffusion tensor imaging · Entrapment · MRI ·MR neurography · Nerve tumor · Peripheralneuropathy · Traumatic nerve injury

Anatomy of Peripheral Nerves

Peripheral nerves are formed by multiple axons,grouped into fascicles, sustained by three differentconnective tissue sheaths. Each axon issurrounded by the endoneurium, which investsthe Schwann cell-axon complex. Its inner borderis represented by the Schwann cell basementmembrane, and its outer border is the secondconnective tissue sheath, the perineurium.

The endoneurial fluid within each fascicle isisolated from the general extracellular space bytightly adherent epithelial-like cells of the peri-neurium and from the circulating blood by thetight junctions between the endothelial cells ofthe endoneurial capillaries.

2 R. Gasparotti and M. Leali

The epineurium is the outermost connectivetissue sheath, and it consists of dense, irregularconnective tissue, with thick collagen and elastinfibers. It envelops the nerve and has inner exten-sions that encompass each of the perineurial-linedfascicles, providing mechanical support for theaxons. Variable amounts of interfascicular adi-pose tissue are contained within the larger nerves.

The endoneurium and perineurium worktogether to form a functional, relatively imper-meable barrier known as the blood-nerveinterface (BNI) regulating the endoneurial micro-environment and protecting the peripheral ner-vous system against toxic and infectious agents.

The peripheral nerves range from 1 to 20 mmin size and contain a variable number of fascicles(1–100), depending on the size and length of thenerve.

Magnetic Resonance Neurography

Conventional MRI techniques have substantiallimitation with respect to the visualization ofperipheral nerves due to low-contrast resolutionbetween nerves, muscles, and vessels, signalintensity variability, pulsatility artifacts, andsmall tissue size.

These limitations have been overcome by thedevelopment of magnetic resonance neurography(MRN), which amplifies the difference in the sig-nal intensity of intact nerves compared to thesignal intensity of the muscles.

MRN is a tissue-selective imaging technique,based on high-resolution T2-weighted sequenceswith fat suppression, acquired with surface coilsselectively focusing on specific characteristics ofnerve morphology, such as internal fascicular pat-tern, longitudinal variations in signal intensity andcaliber, and connections and relations to othernerves or plexuses (Filler et al. 2004).

The most efficient method of fat suppression iswith T2-weighted short tau inversion recovery(STIR) sequences, which provide a selective sup-pression of the fat signal using an inversion recov-ery pulse (150 ms at 1.5 T or 220 ms at 3 T)(Fig. 1). These sequences, however, have somedisadvantages such as the relatively low signal-to-noise ratio and a higher propensity to pulsation

artifacts caused by vessels. Alternative methodsfor fat suppression are represented by T2 spectraladiabatic inversion recovery imaging (SPAIR) orDIXON-type fat suppression, which are bothcharacterized by a better signal-to-noise ratio,although the contrast ratio is lower (Chhabraet al. 2014).

In order to obtain the best compromisebetween spatial resolution and acquisition time,MRN sequences should be specifically designedaccording to the anatomical region. In particular,this includes the selection of the right echo time inorder to obtain a satisfactory differentiationbetween nerves and muscles, as the signal inten-sity of the nerve is very sensitive to small changes.

Recent technological advances in MR acquisi-tion, such as parallel imaging, new coil design,and new sequences, in combination with anincreasing availability and use of 3 T MR scan-ners, have led to the development of high-resolutionMR peripheral nerve imaging protocolsproviding a significantly improved depiction ofperipheral nerve structures (Fig. 2).

Three-dimensional (3D) MRN, based on 3DT2-weighted sequences with fat suppression, rep-resents a further refinement of conventionalMRN, providing enhanced contrast between

Fig. 1 MRN, axial T2-STIR section of the right arm at themid-humerus in a healthy subject. The median (arrow),ulnar (curved arrow), and radial (arrowhead) nerves aremoderately hyperintense and can be differentiated fromthe adjacent muscles and vessels

Magnetic Resonance Imaging of the Peripheral Nerve 3

nerves and muscle. 3D sequences are typicallyacquired with isotropic voxels, therefore confer-ring the advantage of generating oblique andcurved-planar reformations of nerve roots, periph-eral nerves, and plexuses using both multiplanarreconstructions (MPR) and maximum intensityprojections (MIP algorithms (Viallon et al. 2008)(Figs. 3 and 4).

In order to obtain higher spatial resolutionimages in certain anatomical locations, e.g., car-pal, cubital, or tarsal tunnels, specific jointreceiver coils should be used (Tables 1 and 2).A surface flex coil can be added to evaluatethe nerve over a longer distance. For brachialand lumbosacral plexus imaging, an anteriorbody coil is usually combined with the spine coilto obtain a more homogeneous signal (Tables 3and 4).

Investigation of peripheral nerves with 3 TMRsystems offers advantages compared with 1.5 T

Fig. 2 MRN (3 T), high-resolution axial T2-SPAIR sec-tion at the mid-thigh in a healthy subject. The right sciaticnerve (arrow) is moderately hyperintense compared to theadjacent muscles. The transverse fascicular pattern isclearly identifiable

Fig. 3 3D MRN (3D SPACE T2 STIR sequence) of thebrachial plexus in a normal subject. (a) Single partition ofthe 3D volume, (b) axial reformat used as reference fortracing the brachial plexus, (c) curvilinear reformat withsimultaneous display of the supra and infraclavicular

segments of the brachial plexus (MIP thin 12 mm), (d–e)double oblique reformats showing the superior, medium,and inferior trunks and posterior, lateral, and medial cords(MIP thin)


due to the improved signal-to-noise ratio (SNR)allowing scanning with a higher spatial and/ortemporal resolution.

At 3 T, the nerves of upper and lower limbsshould be investigated close to the isocenter of themagnetic bore with the aim to reduce ghost arti-facts. For peripheral nerve assessment in the upperand lower extremities, SPAIR is generally favoredfor MRN sequences, because it provides a more

homogenous fat suppression with a better SNRcompared to STIR. Patients should be reminded toremain as still as possible during the acquisition ofMRN, especially at 3 T, because this technique isparticularly sensitive to motion, which results inghosting artifacts.

A standardized MR protocol for investigationof peripheral nerve diseases should include axial2D MRN and T1-weighted sequences, which are

Fig. 4 3D MRN (3D SPACE STIR T2 sequence) of thelumbosacral plexus in a normal subject. (a) Coronal MPRreconstruction: visualization of L3–L5 roots, (b–c) coronal

MIP view, both sciatic nerves are identified with theirtypical longitudinal fascicular pattern (arrows in b) andthe right femoral nerve (arrow in c)

Table 1 MR imaging protocol for upper limbs

Coil Plane TR (ms)TE(ms)

FOV(mm)

Slice thickness(mm)

T2 STIR (T2 SPAIR) Surface bodycoilFlex coil/jointcoil

Axial 4000 70 180–200 3

TSE T1 Axial 500–600 6–10 180–200 3

Optional 3D MRN(SPAIR)

Axial(sagittal)

3000 180 200 1–1.5 isotropic


first directed at identifying and delineating theperipheral nerves from the adjacent blood vessels,arteries, and veins. Arteries are characterized byflow void both in T2- and T1-weighted sequences,and veins are markedly hyperintense onT2-weighted images.

The field of view (FOV) should be kept assmall as possible to maintain high-resolutionimages, depending on the clinical indications.

To maximize T2 signal abnormalities and min-imize the effects of magic angle, echo times lon-ger than 60 ms are recommended.

Pulsation artifacts from vessels can obscure thenerve or make it appear abnormally hyperintense,leading to possible misdiagnosis. Shorter echospacing and reorientation of the phase encodinggradient can help mitigate this artifact.

Radiofrequency saturation pulses are necessaryto reduce the ghosting artifacts caused by adjacentvessels.

For plexus imaging, 3DMRN STIR sequencesare preferred, because they provide a more homo-geneous suppression of fat signal.

Normal nerves do not enhance after gadolin-ium administration due to the blood-nerve barrier(BNB). Therefore, the administration of contrastmedia should be restricted to certain indicationssuch as suspected neoplasm or in inflammatorypolyneuropathies.

Table 3 Brachial plexus MR imaging protocol

Plane TR (ms)TE(ms)

FOV(mm)

Slice thickness(mm)

3D T2 STIR Coronal 3500 180 300–350 Isotropic 0.8

2D T1 TSE Coronal 500–600 6–10 300–350 3

2D T2 STIR Sagittal 4000 70 250 3

Optional 2D T2 STIR Axial 4000 70 250 3

Optional T1 fat-sat (Dixon) post-gadolinium

Coronal 500–700 10 300 3

Table 4 Lumbosacral plexus MR imaging protocol

Plane TR (ms) TE (ms) FOV (mm) Slice thickness

3D T2 STIR Coronal 3500 180 300–350 0.8 isotropic

2D T1 TSE Coronal 500–600 6–10 300–350 3

2D T2 STIR Axial 4000 70 340 3

Optional T1 fat-sat (Dixon) post-gadolinium Coronal 500–700 10 300–350 3

Table 2 MR imaging protocol for lower limbs

Coil Plane TR (ms)TE(ms) FOV (mm)

Slice thickness(mm)

2D T2 SPAIR(T2 STIR)

Surface body coil (thighand leg)Joint coil (knee-ankle)

Axial 4000 70 340(comparative)200 (single)

4 mm

2D T1 TSE Axial 500–600 6–10 340(comparative)200 (single)

4 mm

Optional3D MRN(SPAIR)

Axial(sagittal)

3500 180 250 1–1.5 isotropic


Normal Versus Pathological Nerves

In MRN studies, normal nerves are identifiable asrounded or ovoid structures on axial images; theyare typically isointense to slightly hyperintense onT2-weighted sequences, depending on the size ofthe nerve, on the amount of endoneurial fluid, andon degree of fat suppression, whereas they areisointense to the adjacent muscles on conven-tional T1-weighted images.

The epineurium appears as a thinhypointense rim.

Peripheral nerves usually follow a straightcourse, do not branch, do not exhibit flow voids,and are surrounded by a peripheral hyperintensehalo in T1-weighted images, representingepineurial fat.

In larger nerves, such as the sciatic nerve or themedian nerve at the level of the carpal tunnel,prominent fascicles can be easily identified asthey are characterized by a slightly higher signalintensity than the surrounding perineurial andepineurial tissue, due to the presence of endo-neurial fluid.

The signal intensity of normal nerves isstrongly influenced by the amount of collagenfibers contained in the perineurium and endo-neurium and their magnetic properties, whichdepend on the angle with the principal vector ofthe magnetic field.

To minimize artificial signal increase related tothe so-called magic angle effect, the longitudinalaxis of the investigated segment should be aligned

at an angle of less than or equal to 10� relative tothe B0 field direction (Chappell et al. 2004).

Affected nerves become hyperintense relativeto muscles and look focally or globally enlarged(Table 5). Irrespective of the underlying etiology,the change in signal intensity results fromincreased water content in the epineurial spaceas a consequence of blood-nerve barrier damage,blockade of axoplasmic flow, inflammation, anddistal Wallerian degeneration (Stoll et al. 2009)(Fig. 5).

Neuropathies with different etiologies cannotbe routinely distinguished on the basis of signalintensity changes, as no reliable quantitativemethods for evaluating the signal intensity ofnormal versus abnormal nerves have beenestablished and validated so far. However, simplemethods may be used to estimate relative signalintensity abnormalities of peripheral nerves,based on manually drawn ROIs in reference mus-cles according to different anatomical locations,e.g., triceps muscle, sterno-cleido-mastoid mus-cle, or quadriceps muscle: a) nerve-to-musclecontrast-to-noise ratio = SInerve�SImuscle/SDbackground noise.

MRN has the advantage of a simultaneousexploration of nerves and adjacent muscles; there-fore muscle denervation leading to muscle celledema represents a useful MR sign of peripheralnerve disease.

In the acute phase of muscle denervation,increased signal intensity can be observed onT2-weigthed sequences as early as 24 h afternerve injury and lasting for more than 2 months

Table 5 MR findings in normal and diseased nerves

Normal nerve Diseased nerve Pathophysiology

Iso- to slightly hyperintensein T2W images

Hyperintense to muscles Increased water content in epineurialspaceBlood-nerve barrier damageBlockade of axoplasmic flow

Hypointense rim(epineurium)Fascicular structure (larger

nerves)

Fascicular hypertrophy, diffuse or sparseLoss of fascicular pattern

Size comparable to theadjacent artery

Focal or global enlargement Edema, fibrosis, axonaldegeneration, and myelin loss

No contrast enhancement Contrast enhancement (inflammatorypolyneuropathies and tumors)

Blood-nerve barrier disruption


(Bendszus et al. 2002) (Fig. 5a). Thesedenervation-related signal abnormalities arereversible and represent enlargement of the capil-lary bed and shift of fluid to the extracellularspace. In the subacute phase, a progressivedecrease of signal intensity is associated with aninitial fat replacement, and in chronic phase, mus-cles show atrophy and sever fat replacement,which is better displayed by T1-weighted images.

The observed MR changes precede the earliestEMG findings of denervation, which are notdetectable until the second week; thus MRimaging may be useful in narrowing thisdiagnostic gap.

A comprehensive MRI protocol for the inves-tigation of peripheral nerves should includeMRN, which provide both structural and func-tional information on the nerves and muscledenervation, T1-weighted sequences that arehelpful for a precise anatomical identification ofnerves and for the identification of muscular atro-phy, and T1-weighted sequences after contrastmedia administration for the evaluation of theblood-nerve barrier integrity.

MRN has been reported to be effective on thediagnostic work-up of traumatic nerve injuries,nerve entrapment syndromes, and nerve tumors.More recently, MRN has been proposed for theevaluation of hereditary and immune-mediateddisorders of peripheral nerves.

Diffusion Tensor Imaging

Diffusion tensor imaging (DTI) is a novel tech-nique which has been recently applied to theinvestigation of peripheral nerve disorders.Nerves are characterized by greater water diffu-sion anisotropy compared to the surrounding tis-sues, due to the presence of a barrier to waterdiffusion, formed by the myelin sheath of axons.Bundle of axons provide a pathway for diffusionalong the fibers, whereas diffusion is restrictedacross the fibers.

The technique is sensitive to subtle changes intissue microstructure and enables measurement ofnerve integrity based on quantitative parameterssuch as fractional anisotropy (FA), apparent dif-fusion coefficient (ADC), and mean (MD), axial(AD), and radial diffusivity (RD) (Jeon et al.2017). In peripheral nerve DTI, the most signifi-cant artifacts include magnetic field inhomogene-ity, motion, incomplete fat suppression, aliasing,and distortion.

Diffusion tensor tractography (DTT) isincreasingly used for selective visualization ofperipheral nerves. DTI datasets can bereconstructed as a 3D representation of aniso-tropic nerve fibers. In DTT, adjacent voxels withsimilar principal fiber orientation fields are

Fig. 5 MRN findings in pathological nerves. Comparablesciatic nerve hyperintensity and enlargement (arrows) intwo different underlying diseases: (a) sciatic nerve traumawith denervation-related muscle cell edema involving the

muscles of the posterior compartment of the thigh (aster-isks), (b) chronic inflammatory demyelinating poly-radiculoneuropathy (CIDP). In both cases diffusefascicular hypertrophy is identifiable


connected to follow anisotropic structures in anautomated way.

Using the same approach as deterministictractography of the brain white matter bundles,seed points manually drawn along the course ofa peripheral nerve, with the aid of an overlaidreference anatomical image, allow successfultracking of the major peripheral nerves (Fig. 6).

Visualization with DTTand characterization ofFA and ADC may allow for evaluation of periph-eral nerve lesions, entrapments, degeneration, andregeneration.

DTI has been extensively applied to study themedian nerve at the carpal tunnel and morerecently to assess brachial, lumbar plexus, andsciatic nerves, although its overall diagnosticvalue in clinical routine is still to be ascertained.

Ultrasound

Ultrasound has become a valuable diagnostic toolin the management of peripheral neuropathiesowing to technical advances and the developmentof affordable high-frequency probes. The highspatial resolution, currently below 1 mm, enablesthe evaluation of anatomical details on nerve

morphology, size, and echotexture, including fas-cicles, epineurium, and perineurium, and on thesurrounding structures, such as muscles, soft tis-sues, and vessels, providing accurate identifica-tion also of smaller nerves like the digital nerves(Gallardo et al. 2015).

The most important US measure is the nervecross-sectional area (CSA) that is calculatedinside the hyperechoic rim of the epineuriumusing the “ellipse method” or the “tracingmethod” when the nerve has an irregular shape(Patel et al. 2014) Another measure that is usuallyassessed is the ratio between the cross-sectionalarea of nerve tracts that are involved in thepathological damage and those that are spared,particularly useful in entrapment syndromes, intraumatic injuries, and in acquired and hereditaryneuropathies (Padua et al. 2012).

Besides the conventional US visualization ofthe nerve, the assessment of intraneural vascularflow is an emerging complementary technique. Itis based on Doppler and power Doppler tech-niques (the latter particularly effective to showsmall vessel flow) and allows depiction of nervecirculatory system and its abnormalities (Borireet al. 2017). Usually, in healthy nerves, vascular-ization is not depicted with the current probes,

Fig. 6 DTI tractography (3 T) of left sciatic nerve at themid-thigh in a normal subject. (a) FAmap overlaid on axialT2 STIR section: sciatic nerve fibers (arrow) are displayedwith blue color coding according to the preferential

diffusion of water molecules along the cranio-caudal direc-tion, (b) 3D visualization of sciatic nerve tract, with axialand sagittal planes displayed as reference


whereas increased intraneural vascularizationmay be seen in entrapment or inflammatoryneuropathies.

In ultrasonographic images, healthy nervesappear as cable-like structures that consistof hypoechoic fascicles and hyperechoic sur-rounding epineurium. On a transverse scan, theyhave an approximately round shape and a typicalhoneycomb appearance, with small dark areas(the fascicles) on a hyperechoic background (theperineurium). On a longitudinal scan, they appearas parallel hypoechoic (fascicles) and hyperechoic(perineurium and epineurium) lines.

Peripheral Nerve Injuries

In traumatic nerve lesions, essential diagnosticinformation for addressing appropriate treatmentsand defining the prognosis includes the localiza-tion of the site, type and cause of nerve injury, andthe quantification of the degree of axonal loss.EMG and NCS provide information on nervefunction but cannot differentiate betweenneurotmesis and axonotmesis. Additionally, theextent of axonal damage may not be evident upto 1 month after injury, as denervation signs onneedle electromyography appear only after3–4 weeks, and changes in NCS may take10 days to occur.

US may provide relevant information for thetherapeutic strategy, based on the ability to earlydifferentiate axonotmesis from neurotmesis, andto identify the exact site of the lesion, particularlyuseful in the case of loss of nerve continuity whichrequires surgical repair.

MRI can also be used to differentiateneurapraxia from axonotmesis and neurotmesisthrough a combined evaluation of the features ofthe injured nerve (Table 6), typically represented

by nerve swelling with longitudinal variationsin size and increased signal intensity, alongwith signal intensity abnormalities of thecorresponding muscles, reflecting acute or sub-acute denervation.

The contribution of MRI is relevant in thediagnostic assessment of brachial plexus and sci-atic nerve injuries, as it provided useful informa-tion on patients’ prognosis.

Brachial Plexus Injuries

Neuroimaging is important to locate the level of theinjury, as prognosis and treatment planning greatlydepend on differentiating complete (preganglionic)nerve root avulsion from lesions distal to the sen-sory ganglion (postganglionic). The underlyingmechanisms for the injury are stretching and tear-ing of the nerve root and surrounding meninges.Subsequently, cerebrospinal fluid leaks into theadjacent tissue and is surrounded by a membrane,giving rise to a pseudomeningocele. If the nerve istraumatically transected distal to the dorsal rootganglion, nerve repair using sural nerve graftsremains a viable option for restoration of motorfunction. In contrast, if the lesion is proximal tothe dorsal root ganglion, nerve repair is uncom-mon, and nerve transfer (neurotization) becomesthe more useful strategy. Complete or partial cervi-cal nerve root avulsions with or without formationof pseudomeningocele complicate more than 70%of traumatic brachial plexus injuries and can bewell depicted by 3D MR myelography (Table 7).

The diagnostic accuracy can be increasedusing reformatted axial sections from the 3D MRmyelography dataset in order to optimally depicttheir attachment to the spinal cord.

Nerve rootlets should be identified on severalsections and compared with intact rootlets of the

Table 6 MR imaging findings in peripheral nerve injuries according to Seddon’s classification

MR findings

Neurapraxia T2 nerve hyperintensity (within 24 h of trauma)No muscle denervation

Axonotmesis T2 nerve hyperintensity with prominent fascicles, with or without neuroma in continuityMuscle denervation

Neurotmesis Nerve discontinuity with end-bulb neuromaMuscle denervation


uninjured contralateral side to avoid false-positivefindings caused by abnormal postures resulting fromshoulder trauma. Partial avulsions are characterizedby absent ventral or dorsal roots with only minimalor no abnormalities of the nerve root sleeves.

In stretch injuries, edema and fibrosis of thebrachial plexus can manifest as swelling ofthe injured nerves, which develop a tortuousappearance with diffuse increases in nerve signalintensities over considerable lengths, as readilydemonstrated on 3D MRN.

In postganglionic lesions, post-traumatic neu-romas can also be identified along the course oftrunks as a round, resected margin of the distallyretracted nerve forming the “nerve retractionball.”

MRI should not be performed prior to 1 monthfrom injury, because acute hemorrhage can com-promise visualization of the thecal sac andpseudomeningoceles take time to develop.

DTI tractography can also be used for theassessment of brachial plexus injuries, becauseof its high diagnostic accuracy in the identificationof nerve root avulsion (Gasparotti et al. 2013)(Fig. 7). However, this technique needs furtherevaluation before being included in routine imag-ing protocols.

Computed tomographic (CT) myelographycan be reserved for patients with contraindicationsto MRI.

US provides limited information in brachialplexus injuries because of the blind area behindthe clavicle and within the spine. However, it canbe useful for the early identification of

postganglionic traction injuries, although it can-not replace MRI in the assessment of cervical rootavulsion.

Lumbosacral Plexus, Sciatic, Peroneal,and Femoral Nerve Injuries

LS plexus nerve root avulsions are uncommoncomplications of major trauma. Most patientshave pelvis or hip fractures and dislocation, typi-cally causing stretch-related or traction-relatedpartial plexopathy and, less commonly, nerveavulsions. As in brachial plexus injuries, the com-bination of 3D MR myelography and 3D MRneurography provides excellent informationabout the type of injuries, which is relevant fortherapeutic planning.

Lumbosacral nerve root avulsions typicallyinvolve the L4, L5, and S1 roots, which are tornoutside the spinal cord but proximal to the dorsalroot ganglion. Since the lumbosacral nerve rootsare protected against extreme stretching by thepelvis and lumbar spine, traumatic avulsion ismuch less frequent than in the brachial plexusand typically occurs in association with fracturesor dislocations of the pelvic girdle (Fig. 8).

Traumatic injuries of the sciatic nerve canoccur as a complication of hip replacement sur-gery, and the motor distribution of the peronealdivision is the most frequently involved. High-resolution MRN can localize the level of the

Table 7 MR findings in brachial plexus injuries

Brachial plexusinjuries MR findings

Complete avulsion Traumatic pseudomeningocelesAbsent ventral and dorsal rootletsDenervation edema of posterior paraspinal muscles

Partial avulsion Reduced number of rootlets on MIP projectionsAbsent ventral or dorsal rootlets on axial sections with mild abnormalities of the nerve rootsleeves

Postganglioniclesions

Swelling and increased signal intensity of the injured roots, trunk and cords of the brachialplexusTortuousity and increased signal intensity of the infraclavicular brachial plexusPost-traumatic neuromas along the course of primary trunks


injury and provide information on the distributionof the fascicular lesion and denervation of targetmuscles. The therapeutic options depend on thetype of lesion: nerves can be compressed,surrounded by scar, or lacerated. Neurolysis isperformed for a nerve injury in continuity(Fig. 9), nerve repair, and grafting for a laceratednerve.

US has a limited role in the evaluation of thesciatic nerve, due to its deep location and to thebone shadow.

Peroneal nerve can be injured in peroneal frac-tures and knee dislocation as well as in habitual

leg crossing or repetitive exercise in athletes. Bothhigh-resolution MRN and US are helpful in dif-ferentiating mild-to-moderate nerve abnormalities(e.g., neurapraxia-axonotmesis) from severenerve injury (e.g., neurotmesis) that may requiresurgical treatment. Multiplanar reconstructionsobtained from 3D MRN are particularly usefulfor assessing nerve continuity and the extent offascicular abnormalities and can address the ther-apeutic decisions (Fig. 10).

Femoral nerve is commonly injured in theiliacus compartment, secondary to an iliopsoasmuscular disorder, such as hematoma or abscess,

Fig. 7 MR investigation of the brachial plexus in a33-year-old patient with inferior traumatic right brachialplexus palsy. (a–b) 3D MR myelography, MIP coronalview (a) and MPR axial reformats along the course ofcervical nerve roots (b), (c) 3DMRN, (d) DTI tractographyoverlaid on 3D MRN. Two traumatic pseudomeningocelesare identifiable along with complete avulsion of right C7,

C8, and T1 nerve roots (preganglionic lesions, arrows inb). Postganglionic traction injuries of right C5 and C6nerve roots (arrow in c). DTI tractography of the spinalcord and the BP confirms complete avulsion of the rightC7, C8, and T1 nerve roots and reduced conspicuity of theright C5 and C6 nerve roots (arrows in d) (compared withthe contralateral normal BP)


or at the groin. Iatrogenic causes are most com-mon and include femoral artery puncture for cath-eterization or bypass surgery, with compression ofthe nerve by hematoma or pseudoaneurysm orpelvic, hip, and gynecologic surgery.

Femoral nerve injury results in weakness ofknee extension (quadriceps muscle) and hip flex-ion (iliopsoas muscle) as well as sensory loss ofthe anteromedial knee, medial leg, and foot.

On MR imaging, the intrapelvic femoral nervemay show increased signal and size and coursedeviation caused by mass effect. Abnormalities ofthe nerve at the thigh are more difficult to detect.

The iliopsoas muscle may show denervationsignal alterations following injury of theintrapelvic femoral nerve, whereas the pectineus,sartorius, and quadriceps muscles may be affectedif injury occurs distal to the inguinal ligament(Fig. 11).

Entrapment Neuropathies

Although nerves can be injured anywhere alongtheir course, peripheral nerve compression orentrapment occurs at specific anatomic locations,often close to limb joints, such as in sites wherea nerve courses through fibro-osseous orfibromuscular tunnels or penetrates muscles(Table 8). MRN and high-resolution US can pro-vide the direct anatomic visualization of theentrapped nerves and sometimes the identificationof the cause of compression.

Compared to MRN, US has the advantage toprovide a dynamic evaluation, crucial for thestudy of nerve entrapment, which causes typicalfindings as fusiform swelling of the nerve that ismaximum proximal to the compression site,where the nerve suddenly flattens, sometimeswith the loss of the normal fascicular pattern andreduced echogenicity.

MRN has the ability to demonstrate intrinsicsignal abnormalities within the nerve itself, show-ing a variable degree of signal intensity change

Fig. 8 A 32-year-old male with traumatic pelvic girdlefracture and severe motor deficit of the left lower limb,treated with orthopedic surgery. Sagittal (a) and axial (d)T2 images show a left L4 pseudomeningocele with

complete nerve root avulsion (arrows). Axial MRN (b–c)show acute denervation edema of left great adductor, exter-nal obturator, and iliopsoas muscles (arrows)


that is commonly higher proximal to the site ofentrapment and the associated signs of muscledenervation. Proximal nerve enlargement andfascicular hypertrophy together with distal flatten-ing can develop with increasing severity ofneuropathy.

Carpal Tunnel Syndrome

Carpal tunnel syndrome is the most commonperipheral nerve entrapment syndrome, with anannual incidence of 50–150 cases/100000. Mostcases are idiopathic, and patients may experienceburning wrist pain and paresthesia or numbness inthe 1st through 3rd fingers and the radial aspect ofthe 4th finger. It may result from a wide variety ofetiologies, including repetitive trauma, conditions

related to metabolic and hormonal changes, andganglion cysts.

US has been widely applied to investigate thecompression of the median nerve in the carpaltunnel, providing standards for the diagnosticapplication of US in nerve entrapments. A meta-analysis concluded that US has 77.6% of sensitiv-ity and 86.8% of specificity in diagnosing carpaltunnel syndrome (CTS) (Fowler et al. 2011),whereas the sensitivity of MRN has been reportedto be above 90%, the length of abnormal nervesignal and the CSA at the distal radioulnar jointbeing the best predictors of the severity (Jarviket al. 2002). Nevertheless, its relatively lowerspecificity and the higher sensitivity and specific-ity of US have limited the use of MRN in themanagement of CTS patients. MRN can play arole in the evaluation of atypical CTS, whenspace-occupying tissue is suspected or in patients

Fig. 9 A 62-year-old male with recent hip replacementsurgery and motor deficit of plantar and dorsal flexion ofthe left foot. (a) 3D MRN, coronal MIP view, (b–d) axial2D MRN. Paramagnetic artifacts are recognizable in a andb (empty arrow). Left sciatic nerve enlargement, withhyperintensity and fascicular hypertrophy (arrows) at the

level of the gluteal region (a–b) and at the mid-thigh (c).Increased signal intensity due to denervation edema of themuscles (asterisks) of the posterior compartment of thethigh, innervated by the tibial nerve, and of the musclesof the anterolateral compartment of the leg, innervated bythe peroneal nerve


with persistent symptoms after carpal tunnelrelease.

Typical MR findings in CTS are represented byenlargement of the median nerve within the prox-imal carpal tunnel, at the level of the pisiform.More distally over the carpal tunnel, at the level ofthe hamate, the nerve becomes flattened withbowing of the flexor retinaculum, and a hyper-intense signal of the nerve on T2 STIR images isoften observed, together with hypertrophy of fas-cicles, perineurial and epineurial edema, resultingin the damage of the axons and nerve sheaths. Theaverage cross-sectional area of the median nerveis reported to be 10–11 mm2 on MR imaging. TheMR features of carpal tunnel syndrome have been

well described, and axial views are the most usefulimages to demonstrate carpal tunnel syndromechanges (Fig. 12).

DTI tractography has gained increasing inter-est in CTS, and a correlation between mediannerve DTI metrics in the carpal tunnel andelectrophysiology has been recently reportedsuggesting a potential role of DTI as an in vivotool to assess axon and myelin sheath integrity.

FA has been demonstrated to be significantlyreduced in CTS patients with an overall 82.8%sensitivity and 77.8% specificity of the FA-baseddiagnosis (Wang et al. 2016). AD has been dem-onstrated to correlate with compound muscleaction potential (CMAP), apparently reflecting

Fig. 10 Right peronealnerve palsy in a 24-year-oldmale with knee distortion ina road accident. (a and c)Axial 2D MRN, (b) 3DMRN. Peroneal nerveenlargement andhyperintensity (arrow in a),with nerve continuity wellshown in the sagittaloblique reformat obtainedfrom the 3D MRN dataset(arrow in b). Denervationedema with increased signalintensity of the tibialisanterior, extensordigitorum, peroneus longus,and brevis muscles in theanterolateral compartmentof the leg (arrow in c). Thecombination of nerveenlargement,hyperintensity, and muscledenervation indicates aprobable axonotmesis


axon integrity, while RD and FA seem to correlatewith sensory nerve conduction velocity (sNCV),reflecting myelin sheath integrity.

However, despite the encouraging preliminaryresults, DTI of median nerve at the carpal tunnelshould be considered experimental at this stage,due to the relatively small datasets and the vari-ability of DTI thresholds used across differentstudies.

Ulnar Neuropathy at the Elbow

Ulnar nerve entrapment at the cubital tunnel is thesecond most common entrapment neuropathy,manifesting with sensory abnormalities of the

lateral hand and weakness of the flexor carpiulnaris, flexor digitorum, and intrinsic musclesof the 4th and 5th fingers. The dynamic US eval-uation during flexion/extension of the elbow iscrucial for showing subluxation/luxation of theulnar nerve and modification of the relationshipswith the surrounding structures. Ulnar nerveswelling can be detected proximally to the entrap-ment site at the elbow. US sensitivity in diagnos-ing ulnar nerve entrapment has been reportedhigher than nerve conduction studies (NCS).

High-resolution (HR) 3 T MRN is also able todiscriminate between symptomatic ulnar nerveentrapment at the elbow and asymptomatic con-trols with high diagnostic accuracy. Due to thehigh signal intensity variability of the normal

Fig. 11 A 50-year-old male with development of leftfemoral nerve palsy after surgical removal of a lipoma ofthe left iliac fossa. (a) 3DMRN (3 T), coronal oblique MIPview, (b) axial 2D MRN. Fusiform enlargement of the left

femoral nerve (arrow in a) with pseudocystic fascicularhypertrophy (arrow in b), indicating a neuroma incontinuity

Table 8 Common nerve entrapment syndromes

Involved nerve Site of entrapment

Carpal tunnelsyndrome

Median nerve Carpal tunnel, at the level of hamate (proximal alterations at thelevel of pisiform)

Ulnar neuropathy Ulnar nerve Cubital tunnel

Peroneal nerveentrapment

Peroneal nerve At fibular head or deep to the origin of peroneus longus muscle

Tibial nerveentrapment

Tibial nerve Tarsal tunnel

Piriformis syndrome Sciatic nerve Sciatic notch

Meralgiaparesthetica

Femoral lateralcutaneous nerve

Anterior superior iliac spine


ulnar nerve at the elbow, a combined quantitativeevaluation of the magnitude and longitudinalextension of the signal intensity abnormality ofthe ulnar nerve is preferentially used to identifythe development of intraneural edema (Baumeret al. 2011). In patients with electrophysiologi-cally and clinically evident ulnar nerve entrap-ment, DTI may show regional FA decrease at thecubital tunnel, correlating with the severity ofsymptoms (Fig. 13).

Other Entrapments

The radial and median nerve entrapment syn-dromes can be accurately evaluated by meansof US, especially when involving their mainbranches, the posterior interosseous nerves (PIN)and anterior interosseous nerves (AIN) at theforearm.

The superior contrast resolution of MRN com-pared to US may have relevant clinical implica-tions in the assessment the fascicular structure ofthe involved nerves at the site of entrapment.

PIN compression occurs secondary to trauma,space-occupying lesions, or fibrous bands at thelevel of the arcade of Frohse, which is the tendi-nous continuation of the proximal superficialhead of the supinator muscle. Motor neuropathy,characterized by deficit of digital extension andradial wrist deviation, is the hallmark feature ofthis syndrome. HR MRN can show PIN hyper-intensity with or without enlargement of thenerve, associated with denervation edema in theextensor compartment muscles of the forearm.

The anterior interosseous nerve (AIN) syn-drome is a rare entrapment neuropathy of themotor branch of the median nerve, for a longtime considered as a result of mechanical com-pression caused by fibrous bands from the deep orsuperficial head of the pronator teres to thebrachialis fascia. 3 T MRN can demonstrateselective fascicular abnormalities well above theentrapment site, suggesting a multifocal immune-mediated mononeuropathy rather than a result ofmechanical compression (Pham et al. 2011).

The contribution of MR in the evaluation ofsciatic nerve entrapment is clinically relevant

Fig. 12 Median nerveentrapment at the carpaltunnel. (a) Axial T2 STIRand (b) axial T1 at the levelof the pisiform, (c) axial T2STIR at the level of thehamate. Median nerveenlargement andhyperintensity at the level ofthe pisiform (18 m2 CSA,arrow in a and b). Mediannerve flattening moredistally, at the level of thehamate (arrow in c)


along its course, from the sciatic notch to the ankle.

Fig. 14 Peroneal nerve intraneural ganglion cyst in a63-year-old male with right peroneal nerve palsy. (a–b)2D MRN, axial sections at the tibiofibular joint. Enlarge-ment of the right peroneal nerve proximal to the peronealtunnel, characterized by thickened epineurium (arrow in

a). An irregular hyperintense cystic lesion (arrow in b) isidentifiable between the lateral outline of the fibular headand peroneal muscles, corresponding to an intraneuralganglion. Denervation edema and atrophy of the tibialisanterior and extensor digitorum muscles (asterisk in b)

Fig. 13 Ulnar nerve entrapment at the cubital tunnel in a48-year-old male with acute onset of right forearm pain andparesthesia on awakening. (a–c) 2D MRN axial sectionsat the right elbow (a), distal arm (b), and forearm (c).Moderately hyperintense and hypertrophic ulnar nerve at

the elbow (arrow in a, CSA 12 mm2). Proximally to theentrapment site the ulnar nerve is enlarged and markedlyhyperintense with fascicular hypertrophy (arrow in b, CSA21 mm2). Denervation edema of the flexor carpi ulnaris isrecognizable at proximal forearm (arrow in c)


The most frequent entrapment neuropathy atthe lower limbs involves the common peronealnerve and occurs at the level of the fibular heador as the nerve travels deep to the origin of theperoneus longus muscle. Among the differentcauses of extrinsic compression including crushinjury, osteochondroma, and aberrant muscles, 3DMRN is particularly suitable for the identificationof intraneural ganglia that can extend from theproximal tibiofibular joint into the articular branchof the common peroneal nerve and frequentlyunderlying nerve damage (Fig. 14).

An excellent agreement between high-resolution 3 T MRN and intraoperative findingshas been recently reported for tibial nerve entrap-ment at the soleal sling, where NCS is difficult toperform, due to the deep location of the nerve.

Posterior tibial nerve entrapment at the tarsaltunnel, caused by ganglion cysts, tenosynovitis,accessory or hypertrophic muscles, and foot

deformities, can be reliably diagnosedusing MRN.

Conversely, the diagnostic role of US in tarsaltunnel syndrome is less clear, because it cannotidentify unequivocal nerve abnormalities in themajority of cases, likely due to predominant axo-nal involvement.

The diagnosis of piriformis syndrome based onimaging findings is controversial, and the possi-bility of identifying abnormalities of the sciaticnerve at the sciatic notch is limited.

HR MRN may be useful in identifying pre-disposing factors such as anatomical variants ofthe piriformis muscles and abnormal course of thesciatic nerve within the muscle fibers. Asymmetryof the piriformis muscle associated with sciaticnerve hyperintensity at the sciatic notch has beenreported to have 93% specificity and 64% sensi-tivity in identifying patients with typical symp-toms compared to normal controls (Fig. 15).

Fig. 15 Piriformis syndrome in a 55-year-old female withchronic right gluteal pain and weakness of the right lowerlimb. T1 coronal section (a) and 3D MRN coronal MIPview (b) at the sciatic notch, 2DMRN (c), and axial T1 (d)at the gluteal region. Mild hyperintensity of the right sciatic

nerve (arrows in b and c) compared with the contralateral(arrowhead). Mild asymmetry of piriformis muscles(right<left) (arrows in d). The patient responded to theCT-guided injection of lidocaine and steroid into the rightpiriformis muscle


Demonstration of sciatic nerve entrapment atthe sciatic notch, caused by extrapelvic endome-triosis, is more consistent. Patients usually have along history of catamenial sciatic pain andunremarkable lumbar spine MRI findings. MRNmay reveal severe sciatic nerve neuropathy char-acterized by nerve enlargement and increasedsignal intensity, fascicular hypertrophy, andepineurial and intraneural contrast enhancement,due to either nerve entrapment by inflammatory-fibrotic tissue or perineurial and intraneural inva-sion by endometrial glands and stroma (Fig. 16).Hemosiderin deposits around or within the sciaticnerve may be better identified on T2*-weightedimages. Muscle denervation can be observed indistant target muscles of the sciatic nerve. Pro-gressive improvement after hormonal therapy ofcyclic sciatic pain has been reported.

Meralgia paresthetica is a common entrap-ment syndrome involving a branch of the femoralnerve, the lateral femoral cutaneous nerve

(LFCN), characterized by burning pain and par-esthesia along the proximal lateral aspect of thethigh. Predisposing factors include obesity, preg-nancy, tight clothing, or anatomical variations ofthe course of the nerve. Compression of the LCFNunder the attachment of the inguinal ligament tothe anterior superior iliac spine is considered themost common cause, which is responsible fordevelopment of perineurial edema and fibrosis.

Abnormalities of the LFCN are difficult tovisualize at MR imaging owing to the small sizeof the nerve, although HR MRN at 3 T has beenrecently demonstrated to be able to identify signalintensity changes which are consistent with theclinical symptoms (Fig. 17).

Fig. 16 Extrapelvic endometriosis in a 42-year-oldwoman with a long history of catamenial right sciaticpain. Coronal (a) and axial (b) 2D MRN, coronal (c) andaxial (d) post-gadolinium T1 fat-sat showing entrapmentof the right sciatic nerve by inflammatory-fibrotic tissue atthe sciatic notch. The nerve is enlarged and markedlyhyperintense, with thin linear hypointense bands

corresponding to intraneural hemosiderin deposits (arrowin a) and increased longitudinal fascicular patternextending to the proximal thigh (arrowhead in a).Epineurial thickening of the right sciatic nerve and edemaof the right gluteus maximus muscle (arrow in b).Epineurial and fascicular contrast enhancement of theright sciatic nerve due to inflammation (arrows in c and d)


Non-traumatic Brachial Plexopathies

MRN, due to its high contrast resolution andanatomic detail, can provide useful informationin the diagnostic work-up of brachial plexopathiesof different etiologies, although the evidence of its

clinical impact is mainly based on case reports andsmall series.

A recent single-center retrospective analysisof 121 MRN studies including inflammatory,traumatic, and neoplastic brachial plexopathiesreported modifications of the pre-imaging clinicalimpression in 75.2% subjects, with a substantialchange in 28% (Fisher et al. 2016).

In idiopathic neuralgic amyotrophy (INA), alsoknown as Parsonage- Turner syndrome, the acuteonset of severe pain usually precedes the devel-opment of brachial plexus palsy, and MRN can beused to confirm the clinical diagnosis whenperformed in the acute-subacute phase, showingswelling and increased signal intensity of theproximal brachial plexus, mostly involvingC5 and C6 nerve roots and the upper trunk, asso-ciated with denervation edema in supra- and

infraspinatus muscles (Fig. 18).The differential diagnosis between INA and

cervical spondilogenetic radiculopathy may bechallenging. In the acute phase, 3 T MRN is ableto detect enlargement and increased signal inten-sity of cervical nerve roots correlating with theforaminal stenosis and the distribution of muscleweakness.

Fig. 17 3 T MRN in a patient with meralgia paresthetica.The left lateral femoral cutaneous nerve (arrow) is enlargedand markedly hyperintense proximal to the inguinal liga-ment, at the level of the anterior superior iliac spine(asterisk)

Fig. 18 A 62-year-old male with acute idiopathic neural-gic amyotrophy. (a–b) 3D MRN of the brachial plexus,coronal MIP view (a) and paraxial oblique reformat (b)showing swelling and increased signal intensity of the left

C5 root, primary trunk, and posterior cord (arrows). (c)Axial 2D MRN showing denervation edema of the leftdeltoid (empty arrow) and infraspinatus (arrowhead)muscles


MR can reliably identify signal intensityabnormalities in the brachial plexus of patientsaffected by diabetic cervical radiculoplexus neu-ropathies, therefore providing a substantial con-tribution to the diagnostic work-up of thesyndrome.

In radiation plexopathy, which can developfrom few months to many years after radio-therapy, MRN shows diffuse hypertrophy andincreased signal intensity of the brachial plexusclosely correlating with the radiation field, with noor faint contrast enhancement, whereas neoplasticinfiltration of the brachial plexus is characterizedby focal or diffuse mass lesion with marked con-trast enhancement (Fig. 19).

The thoracic outlet syndrome (TOS) includesthree disorders involving the neurovascular bun-dle in its course through the interscalenic triangleand costoclavicular space: classic TOS, vascularTOS, and nonspecific TOS. Classic TOS or neu-rogenic TOS is the most frequent form affectingmiddle-aged adults especially women. Clinicallyit is characterized by chronic pain of the neck andsupraclavicular region irradiating to the arm,exacerbated by arm elevation and associatedwith paresthesia, numbness in C8 and T1 derma-tome, and progressive weakness and wasting ofthe thenar and hypothenar eminence and ulnarhand intrinsic muscles.

In the diagnosis of neurogenic TOS, electro-physiological and clinical provocative tests mayprovide nonspecific findings.

MR imaging has been successfully used fordemonstrating static or dynamic compression ofthe brachial plexus by structural abnormalitiessuch as cervical or anomalous first rib, longC7 transverse process, muscular anomalies, ornarrowed costoclavicular space (Aralasmaket al. 2012).

Non- traumatic LumbosacralPlexopathies

Lumbosacral radiculoplexus neuropathy is a raresubacute, mainly motor lower limb disorderaffecting multiple levels of lumbosacral plexus,nerve roots, and distal nerves, characterized bydebilitating pain, weakness, and atrophy of theproximal thigh muscles. This syndrome is usuallymonophasic and commonly occurs in diabeticpatients (DLRPN).

Fig. 19 Left radiation plexopathy in a 40-year-oldwoman, with laryngeal carcinoma treated with radiationand chemotherapy 15 years before. Coronal 2D MRN (a)

and T1 fat-sat post-gadolinium (b) show diffuse left bra-chial plexus swelling and hyperintensity (arrow), with mildfocal enhancement (arrowhead in b)


Conditions with similar clinical features,course, and distribution of symptoms have beenrecognized also in nondiabetic patients (non-diabetic lumbosacral radiculoplexus neuropathy,LRPN). Pathogenesis remains unknown, but animmune-mediated inflammatory microvasculiticmechanism, which causes secondary ischemia,has been proposed. Steroid treatment can improveclinical conditions.

The diagnosis of LRPN is primarily based onthe clinical and electrophysiological findings(Dyck et al. 1999).

MR neurography may support the clinicaldiagnosis by showing increased signal intensityand mild contrast enhancement asymmetricallyinvolving multiple nerve roots and terminalbranches of the lumbosacral plexus.

Diffuse signal hyperintensity may be observedin the dependent muscles indicating denervationchanges, suggesting a recent onset of the disease(Fig. 20).

Inflammatory Neuropathies

Guillain-Barré Syndrome

Guillain-Barré syndrome (GBS) is an inflamma-tory disease of peripheral nerves, including thespinal and cranial nerves, with a reported inci-dence of 0.6–4/100.000, characterized by rapidlyprogressive bilateral and symmetric weakness ofthe limbs with loss of reflexes, with a monophasiccourse. The diagnosis is mainly clinical,supported by additional findings of elevatedprotein in the CSF with albuminocytologic disso-ciation and demyelinating and/or axonal involve-ment at electrophysiologic testing.

The most common form in western countriesis the acute inflammatory demyelinating poly-neuropathy (AIDP), whereas the axonal subtypes,acute motor axonal neuropathy (AMAN), andacute motor and sensory axonal neuropathy(AMSAN) are most frequent in Asia and Japan.

MRI studies are usually not necessary for diag-nosis, although a thorough medical assessment ofpatients may be needed to exclude “mimic disor-ders” (Vucic et al. 2009).

Nerve conduction studies (NCS) and CSFanalysis are important investigations that help

Fig. 20 Nondiabetic lumbosacral radiculoplexus neurop-athy (LRPN) in a 75-year-old woman with deficit of the hipflexion and proximal muscle atrophy, preceded by severepain at the right groin. (a–b) 2D MRN, coronal sections,(c–d) 2D MRN, axial sections. Enlargement and hyper-intensity of the right femoral nerve (yellow arrows in a and

c) and right obturator nerve (red arrow in b and c).Denervation edema and hypotrophy of the right iliopsoasmuscle (yellow asterisk in c), quadriceps femoris (yellowasterisk in d), adductor muscles (red asterisk in d), andright iliocostalis lumborum (white asterisk in c)


in confirming the clinical diagnosis of GBS,although NCS may be unrevealing when studyingpatients within days of symptom onset, and CSFmay be normal in the first week of the illness.

In the initial phase of GBS, breakdown of theblood-nerve barrier is the characteristic patho-logic change, which may lead to enhancement ofnerve roots in MRI studies (Table 9).

Although the enhancement of the intrathecalspinal nerve roots is not specific and can be seen inneoplasia and other inflammatory processes, theenhancement of only the anterior spinal nerveroots is strongly suggestive of GBS.

About 5% of patients initially diagnosed withGBS turn out to have chronic inflammatory

demyelinating polyradiculoneuropathy (CIDP)with acute onset (A-CIDP).

Differentiating A-CIDP from GBS prior torelapse is challenging at the onset of the diseaseand has implications for treatment as well as prog-nosis. Electrodiagnostic studies may distinguishpatients with A-CIDP from GBS; however thedemonstration of cauda equine enlargement atMR imaging may be useful for the differentialdiagnosis (Fig. 21).

Fig. 21 Guillain-Barré syndrome in a 56-year-old malewith rapidly progressive distal 4 limb motor deficit pre-ceded by sensory symptoms. (a–b) Sagittal and coronal T1fat-sat post-gadolinium of the lumbosacral spine, (c–d)

axial T1 fat-sat post-gadolinium at L3–L4 (c) and C5–C6(d). Contrast enhancement of cauda equina (arrows in a, b,c) and of ventral and dorsal nerve rootlets (arrows in d)

Table 9 MR imaging findings in inflammatory neuropathies

MR imaging findings Distribution

AIDP Enhancement of spinal nerve roots Bilateral andsymmetrical

CIDP Hypertrophy and T2 hyperintensity of nerve roots of brachial and lumbosacralplexus, with gradual normalization in distal nerves

Bilateral andsymmetrical

MADSAM Hypertrophy and T2 hyperintensity of peripheral nerve trunks Multifocal andasymmetrical

MMN Hypertrophy and T2 hyperintensityContrast enhancement of the brachial plexus

Asymmetrical


Chronic Inflammatory DemyelinatingPolyradiculoneuropathy

Chronic inflammatory demyelinating poly-radiculoneuropathy (CIDP) is an immune-mediated neuropathy characterized bysymmetrical proximal and distal weakness, withsensory loss, impaired balance, and areflexia.

CIDP include a broad spectrum of clinical phe-notypes, including atypical forms with pure motoror sensory impairment or distal, multifocal, orfocal distributions.

The diagnosis of CIDP is based on a combina-tion of clinical, electrodiagnostic, and laboratoryfindings, primarily directed at detecting signs ofdemyelination; however CIDP may be difficult todiagnose in clinical practice, especially in atypicalcases.

Despite the good overall sensitivity and speci-ficity of the current electrophysiological criteria,almost 20% of patients do not match these criteria.

The most frequent MRI finding in patientsaffected by CIDP is represented by bilateral and

symmetric hypertrophy of both brachial and lum-bosacral plexuses, which is invariably associatedwith increased signal intensity (Table 9), betterdisplayed by MRN (Fig. 22).

3D MRN has become a valuable tool for athorough assessment of the symmetry and longi-tudinal extent of the disease. Phenotypic featurescan be noninvasively characterized in patientswith atypical variants of CIDP using 3D MRNfor a detailed evaluation of brachial and lumbosa-cral plexus hypertrophy and signal intensityabnormalities, which typically involve longsegments with a different distribution, symmetricor asymmetric, diffuse or multifocal (Shibuyaet al. 2015).

Lewis-Sumner syndrome (LSS) or multifocalacquired demyelinating sensory and motorneuropathy (MADSAM) is characterized by asym-metry, presenting as a multifocal multiple mono-neuropathy most commonly in the upper limbs,accounting for 6–15% of CIDP patients.

The distribution of hypertrophy in typicalCIDP is symmetric and predominant in the nerve

Fig. 22 Chronicinflammatorydemyelinatingpolyradiculoneuropathy(CIDP). 3D MRN of thebrachial (a) andlumbosacral plexus (b), 2DMRN of the right (c) andleft mid-thigh (d). Diffusesymmetric hyperintensityand enlargement of thebrachial and lumbosacralplexus, predominant in thenerve roots, with gradualnormalization toward theproximal limb segmentsdistally. Axial sections ofright (c) and left (d) sciaticnerves (arrows) at themid-thigh, showingmoderately hyperintenseand enlarged sciatic nerves(arrows)


roots, with gradual normalization toward theproximal arm segments distally, whereas inMADSAM nerve hypertrophy is usually asym-metric and multifocal in the peripheral nervetrunks (Table 9).

Sensory predominant CIDP occurs in 5–35%of patients, often starting with lower limb numb-ness. The diagnosis is typically made on the basisof demyelinating electrodiagnostic features inmotor nerves, which may occur without motorsigns, although patients may develop weaknessat a later date.

This entity may be underdiagnosed at the onsetof symptoms which manifest at a young age, and3D MRN may represent a useful diagnostic toolwhen demonstrating symmetric hypertrophy ofthe brachial and lumbosacral plexus, which iscomparable to the typical form of CIDP(Gasparotti et al. 2015).

Like in other peripheral nerve diseases, DTI isincreasingly used to detect microstructural abnor-malities of nerves in CIDP patients. FA can besignificantly reduced in tibial nerves of patientswith variable disease duration, correlating withthe amplitude of compound motor action poten-tials, thus with the axonal damage, whereas

RD may represent a specific biomarker of demy-elinating neuropathy, inversely correlated withnerve conduction velocities (NCV) (Kronlageet al. 2017).

DTI may reveal low FA in sciatic nerves thatare correlated with clinical impairment in CIDPpatients treated with subcutaneous immuno-globulin, in whom MRN is unable to identifyabnormalities.

These preliminary results suggest a role of DTIas a research tool for identifying quantitative mea-sure of microstructural abnormalities, althoughfurther testing is needed to validate the method.

Multifocal Motor Neuropathy

Multifocal motor neuropathy (MMN) is a chronic,slowly progressive immune-mediated neuropa-thy, characterized by progressive, predominantlydistal, asymmetric limb weakness, mostly affect-ing upper limbs, minimal or no sensory impair-ment, and the presence of multifocal persistentpartial conduction blocks (CB) on motor nerves.Increased levels of serum IgM antibodies to the

Fig. 23 Multifocal motor neuropathy (MMN) in a54-year-old male with progressive asymmetrical limbweakness without sensory deficits. (a) 3D MRN, coronalMIP view of the brachial plexus, (b) 2DMRN at the pelvicgirdle, (c) 2D MRN at proximal thigh. Asymmetric hyper-trophy and hyperintensity of left C5 and C6 nerve roots and

superior and middle primary trunks (arrows in a). Bilateraland symmetric hypertrophy and hyperintensity of femoralnerves (arrows in b), left obturator nerve (arrowhead in b),mild hyperintensity and hypertrophy of sciatic nerves(arrows in c). Bilateral denervation and atrophy of quadri-ceps femoris (asterisks)


ganglioside GM1 is another typical feature of thedisease.

A recent revision of the European Federationof Neurological Societies/Peripheral Nerve Soci-ety on multifocal motor neuropathies (MMN) alsoincluded MRI as a supportive criterion for thedifferential diagnosis with other neuropathiessuch as CIDP or multifocal acquired demyelinat-ing sensory and motor (MADSAM) neuropathy(Lewis-Sumner syndrome) and motor neuron dis-ease (MND).

About 40–50% of the patients with MMNshow asymmetric hypertrophy and signal inten-sity abnormalities or contrast enhancement onMR of the brachial plexus (Table 9), and thepattern of signal alterations closely correlateswith the distribution of muscle weakness (VanAsseldonk et al. 2003) (Fig. 23).

Diffuse nerve swelling and hyperintensity ofthe affected nerves on T2-weighted images areusually found in areas outside the expected con-fines of entrapment neuropathy and reflect demy-elination and proximal conduction blocks.

The clinical presentation of MMN may mimicmotor neuron disease (MND), particularly inpatients with predominant lower motor neuronimpairment, and the differential diagnosis isimportant, as the prognosis and treatment ofthese diseases are different.

MRI can be used to help differentiate betweenMMN and MND, with brachial plexus MRI beingnormal in the latter.

Axonal multifocal motor neuropathy is a rareentity, which was first described in 2002, and ischaracterized by a slowly progressive multifocalmotor phenotype with neither conduction blocksnor other features of demyelination.

MR neurography may be helpful in the diag-nostic work-up of the axonal form of MMN,showing mildly increased signal intensity andsize of the involved nerves at the arm (Brianiet al. 2013).

Inherited Neuropathies

Charcot-Marie-Tooth disease (CMT) is the mostcommon inherited neuromuscular disorder, affect-ing 1/2,500 individuals, characterized by patho-logically and genetically heterogeneous motorand sensory neuropathy, presenting with slow,progressive muscle weakness and sensory impair-ment, primarily in distal leg muscles.

Autosomal dominant CMT is subdividedinto CMT1 or CMT2 depending on whetherthe primary pathological process affects the mye-lin sheath or the axon. The most frequent formsof CMTare demyelinating, and CMT1A accountsfor about 70% of cases of CMT1, causedby a duplication of chromosome 17p11.2–p12containing the peripheral myelin protein22 (PMP22) gene. CMT2A caused by mitofusin2 (MFN2) mutations is the most frequent formof CMT2.

Hereditary neuropathy with liability to pres-sure palsies (HNPP) is an autosomal dominantdisorder also known as a “tomaculous neuropa-thy,” characterized by acute, painless, and recur-rent mononeuropathies that are secondary tominor trauma or compression, and is caused by adeletion in the same PMP22 gene as CMT1A.

Diagnosis of CMT and HNPP is based on thecombined information of clinical and family his-tory, physical examination, nerve conductionstudies, and genetic testing.

A negative family history is not uncommon,and patients may be repeatedly investigated withelectrophysiology, genetic testing, and at timesnerve biopsy.

Ultrasonography has been demonstrated to bea reliable tool for the differential diagnosisbetween CMT1A and HNPP. In CMT1A nervehypertrophy and enlargement of fascicles aremultifocal among multiple nerves, whereas inHNPP it is restricted to sites of entrapment.

In patients with demyelinating Charcot-Marie-Tooth disease (CMT), MRN has been used toreveal bilateral hypertrophy of the brachial andlumbosacral plexuses, as well as diffuse symmet-rical enlargement of peripheral nerves and/orcauda equina, which represent typical findings inthe demyelinating form CMT1A (Ellegala et al.


2005). Most peripheral nerves are uniformlyaffected, and characterized by diffuse fascicularhypertrophy and markedly increased MRN signalintensity, which is related to the long-standingprocess of demyelination-remyelination. The sci-atic nerve cross-sectional area (CSA), measured atthe mid-thigh with MRN, is significantly greaterin CMT than in CIDP and may be used to supportthe differential diagnosis (Sinclair et al. 2011)(Fig. 24).

In HNPP MRI has been reported to be able toidentify asymmetric swelling and hyperintensityof the individual fascicles of the ulnar nerve at thecubital tunnel and peroneal nerves along with anincrease of the nerve size.

Amyloid Neuropathy

Amyloid neuropathies occur in a context of hered-itary or acquired amyloidosis. They present usu-ally as severe and progressive polyneuropathyinvolving sensory, motor, and/or autonomic fibersand carry a poor prognosis.

Acquired amyloid neuropathy is almost exclu-sively represented by immunoglobulin light chainamyloidosis (AL) and is frequently associatedwith renal manifestations and monoclonal proteinin serum or urine. Peripheral neuropathy occurs inabout 35% of cases of AL but is a rare presentingsymptom.

On MR imaging, both focal amyloidoma anddiffuse enlargement of unilateral/bilateral nerveswith associated multifocal lesions have beenreported. These lesions most commonly involvesegments of the lumbosacral plexus or the sciatic

Fig. 24 Charcot-Marie-Tooth disease type 1A.(a–b) 3D MRN of brachial(a) and lumbosacral plexus(b), (c) 2D MRN at themid-thigh. Diffusesymmetric hypertrophy andhyperintensity of thebrachial plexus andintercostal nerves (a) andlumbosacral plexus (b).Bilateral hyperintensity andhypertrophy of sciaticnerves, with diffuselyenlarged fascicles (arrowsin c)


nerve and are characterized by variable contrastenhancement of the affected nerves.

Transthyretin familial amyloid polyneuropathy(TTR-FAP) is the most common form of inheritedamyloidosis. Endemic areas of TTR-FAP arePortugal, Japan, Sweden, and Brazil. Patientswith FAP may experience different patterns ofneuropathy including focal neuropathies, sensori-motor polyneuropathy, autonomic neuropathy, orcombinations of the three. The median nerve atthe wrist is a common and early site of involve-ment in FAP.

The diagnosis relies on a positive family his-tory and requires TTR gene analysis showing

Met30TTR mutation and positive labial salivarygland biopsy (LSGB) for amyloidosis.

Its early diagnosis is crucial to allow patientsstarting disease-modifying therapies.

HR 3 T MRN has been recently shown tobe able of identifying and quantifying the distri-bution of peripheral nerve abnormalities inTTR-FAP patients, involving the fascicles of thesciatic nerves from proximal to distal, even beforethe manifestation of symptomatic disease inasymptomatic gene carriers, in whom imagingdetection may precede clinical and electrophysio-logical manifestation (Kollmer et al. 2015)(Fig. 25).

Fig. 25 Transthyretin familial amyloid polyneuropathy(TTR-FAP). (a–b) Axial 2D MRN of sciatic nerves at thegluteal region, (c–e) axial 2D MRN of the intrapelvicfemoral nerves. Bilateral and symmetrical sciatic nerveT2 enlargement and hyperintensity (arrows in a), withcross-sectional area measurement (arrowheads in b,

right = 152 mm2, left = 158 mm2, reference values60 mm2). Bilateral and symmetrical enlargement andhyperintensity of femoral nerves behind psoas muscles(arrows in c), along the iliopsoas muscle (arrows in d)and at the inguinal ligament (arrows in e)


Diabetic Polyneuropathy

Diabetic peripheral neuropathy (DPN) is the mostcommon form of the diabetic neuropathies seen ineither type 1 or type 2 DM, with similar frequency.DPN is a common late complication of diabetesand has been recently defined as a symmetric,length-dependent sensorimotor polyneuropathyattributable to metabolic and microvascular alter-ations as a result of chronic hyperglycemia expo-sure and cardiovascular risk covariates.

Recently HR 3 T MRN has been applied to arelatively small group of diabetic patients with

distal symmetric polyneuropathy with the aim todetect intraneural signal intensity abnormalities insciatic nerves. Multifocal fascicular lesions withinthe proximal tibial and peroneal divisions of thesciatic nerves within proximal nerve trunks weredetected in patients with higher neuropathy deficitscore (NDS), demonstrating a possible role ofhigh-resolution in vivo MRN in the evaluationof diabetic nerve (Pham et al. 2011).

DPN also include radiculoplexus neuropathieswhich affect roots, plexus, and individual nervesin the cervical, thoracic, or lumbosacral segments.

Fig. 26 Brachial plexus schwannoma. (a) Coronal T1, (b)coronal T1 fat-sat post-gadolinium, (c) axial T1, (d) axial2D MRN, (e) 3D MRN, MIP coronal view. Oval-shapedlesion, isointense in T1 (arrow in a and c), hyperintense atMRN (arrow in d), with intense and inhomogeneous

enhancement (arrow in b). 3D MRN can depict the originof the schwannoma from the right C6 nerve root and theanatomical relationships with the other roots of the brachialplexus (arrows in e)

Table 10 MR features of peripheral nerve tumors

Location MR findings Capsule Enhancement

Neurofibroma Not separated fromthe normal nerve

Target sign, split fat sign, fascicularsign

No Homogeneous or ringenhancement

Schwannoma Usually eccentric tonerve

Target sign, split fat sign, fascicularsign

Yes Homogeneous, ring,or heterogeneous

Perineurioma Not separated fromthe normal nerve

Uniform, homogeneous fascicularenlargement and hyperintensity

No Avid homogeneousenhancement

MPNST Irregular Irregular shape, rapid growing,perilesional edemaT1 heterogeneity intratumoral cysts,diffusion restriction

No Heterogeneous


Diabetic lumbosacral radiculoplexus neuropa-thy (DLRPN), which is characterized by debilitat-ing pain, weakness, atrophy of the proximal thighmuscles, and abnormal protein content in CSF, isthe best studied subtype.

The occurrence of a cervical diabeticradiculoplexus neuropathy (DCRPN) sharingmany of the clinical and pathological features ofDLRPN has also been recently demonstrated.

Peripheral Nerve Tumors

The high-contrast resolution and sensitivity toblood-nerve barrier disruption after contrast injec-tion make MRI the most useful imaging tool for

the diagnosis and characterization of peripheralnerve tumors.

Neurogenic tumors are typically identified asfusiform or round-shaped soft tissue lesions incontinuity with the nerve, creating the so-calledtail sign. They are characterized by high periph-eral signal and low-to-intermediate signal onT2-weighted sequences (“target sign”), reflectingthe distribution of myxoid material and fibroustissue and variable contrast enhancement.

Conventional MR imaging cannot reliably dif-ferentiate localized or solitary neurofibromasfrom schwannomas, although a hypointense cap-sule on T2-weighted images representing the epi-neurium may be more typical of schwannomasthan neurofibromas.

Fig. 27 Tibial nerve malignant peripheral nerve sheathtumor (MPNST) in a 62-year-old woman with rapid devel-opment of leg pain and weakness of the foot. (a–b) Sagittal2D MRN (a) and T1 fat-sat post-gadolinium (b), (c–e)axial 2D MRN (c), T1 (d), and T1 fat-sat post-gadolinium(e). Fusiform tibial nerve mass lesion, hyperintense atMRN (arrow in a and c), isointense in T1 (arrow in d),

with marked and inhomogeneous enhancement due tocystic intralesional components (arrow in b and e).Denervation edema of the muscles of the posterior com-partment of the leg innervated by the tibial nerve (asteriskin a). Perilesional edema into the muscles surrounding thetumor (arrow in c)


With the advent of 3DMRN, multiplanar nervereconstructions can accurately display the ana-tomical relationships with the schwannoma thattypically originate from the sheath of a singlefascicle, leaving the main trunk of the nerveattached to the tumor (Fig. 26).

Conversely, neurofibromas are not separatedfrom the normal nerve (Table 10).

MRN is particularly suitable for demonstratingthe diffuse involvement of the brachial or lumbo-sacral plexus in neurocutaneous syndromes,such as plexiform neurofibroma or plexiformschwannoma.

The distinction between benign and malignantperipheral nerve sheath tumors (MPNST) may bechallenging. MPNST have higher prevalence inpatients with neurofibromatosis type 1 (NF1) and

can develop as a long-term side effect of radiationtherapy. The combination ofMR imaging findings(e.g., rapid growing, peripheral enhancement,peritumoral edema, intralesional cysts) has beenreported to provide 61% sensitivity and 90% spec-ificity in detecting MPNST (Matsumine et al.2009) (Table 10).

F18 fluorodeoxyglucose positron emissiontomography (FDG-PET) can be a valid diagnostictool complementary to MRI, particularly for iden-tifying tumors with aggressive behavior (Broskiet al. 2016) (Fig. 27).

Whole-body MRN has been recently intro-duced in the clinical practice as useful to assessthe tumor burden in patients with NF1, NF2, andschwannomatosis. It allows a comprehensiveevaluation of brachial and lumbosacral plexuses

Fig. 28 Left tibial nerve perineurioma in a 30-year-oldwoman with progressive deficit of left plantar flexion.(a–b) Sagittal 2D MRN (a) and T1 fat-sat post-gadolinium(b) of the knee, (c) axial 2D MRN at distal thigh, (d) axialT1 of the left leg. Fusiform enlargement of the tibial

division of the left sciatic nerve (12 cm) (arrow in a andc), with fascicular hypertrophy and avid contrast enhance-ment (arrow in b). Chronic denervation with fatty atrophydegeneration of the muscles of the posterior compartmentof the leg (asterisks in d)


and nerve trunks of the limbs using multiple sur-face coils and the identification of the lesion type(e.g., focal or plexiform), number, distribution,and size (Plotkin et al. 2012).

Intraneural perineurioma is a rare benign andslowly growing nerve tumor arising from the peri-neurial cells surrounding the peripheral nervefibers, most commonly occurring in teenagersand young adults without sex predilection andpresenting with progressive muscle weakness.

The clinical presentation can be very insidiousand the diagnosis is often delayed.

Perineuriomas are characterized by a typicalMR imaging pattern: enlargement of the nerveover a considerable length, fusiform shape, mildincrease in signal intensity on MRN sequences,isointense signal on T1-weighted images, andmoderate to severe contrast enhancement(Table 10). The fascicular architecture is usuallymaintained on axial and longitudinal MRNimages, and individual fascicles are uniformlyenlarged, with a “honeycomb” appearance, betterdisplayed by gadolinium-enhanced T1 fat-satsequences (Fig. 28).

In perineuriomas, only a segment of a singlenerve is usually involved by the tumor, and thisis relevant for the differential diagnosis withimmune-mediated inflammatory demyelinatingneuropathies, which are characterized by symmet-ric or asymmetric hypertrophy of multiple nerve

trunks. Multiple perineuriomas, although veryrare, have also been described.

As these tumors are static or slowly progres-sive, remain confined to their original distribution,and have low morbidity, they should not beresected routinely, taking also into considerationthat nerve reconstruction is unable to modify thenatural history of the disease.

When clinical and radiological criteria are sat-isfied, the need for targeted fascicular biopsy isobviated (Mauermann et al. 2009).

DTI tractography can provide relevanttopographical information on non-neurogenicsoft tissue tumors and adjacent nerves when con-ventional MR sequences are unable to depict thecourse of the involved nerves or distinguish pos-sible nerve infiltration (Kasprian et al. 2015).

Case 1

Patient history: Female, 15 years old, with weak-ness of right lower limb and progressive right footdrop; no history of trauma.

Clinical diagnosis: Motor neuropathy of theright peroneal nerve.

Imaging technique: MR scans of the lowerlimbs: axial T1 and T2 STIR, coronal T2 FSE,axial and coronal contrast-enhanced T1 fat-satsequences. All sequences acquired with 3.5 mmslice thickness (0.35 mm gap).


Contrast agent and dose: Single dose(0.1 mmol/Kg bw) macrocyclic gadoliniumagent (0.1 mmol/kg).

MR findings: Fusiform sciatic nerve enlarge-ment over a considerable length, T2 hyperintenseand T1 isointense, with marked contrast enhance-ment (arrows in A and B). Uniform enlargementof individual fascicles of the right sciatic nerve,giving a honeycomb appearance to the nerve(arrows in C and D). Chronic denervation of themuscles of the anterolateral compartment of theright leg innervated by the peroneal nerve, withfatty atrophy degeneration (empty arrow in E).

Interpretation: Intraneural perineurioma ofthe right sciatic nerve.

Comment: The selective involvement of theright sciatic nerve and the diffuse homogeneousenhancement allows to exclude a polyneuropathy,

e.g., demyelinating inflammatory poly-neuropathy, and to address the diagnosis to anerve tumor. The differential diagnosis is withother nerve sheath tumors like schwannomas,which are more hyperintense in T2-W images,are characterized by loss of fascicular architec-ture, and do not cause muscle denervation.Perineurioma is a benign nerve tumor that typi-cally presents in childhood and young adulthoodand leads to a progressive loss of nerve function.

Case 2

Patient history: Male, 48 years old, with chronicpain of the right knee, walking instability, anddeficit of plantar flexion of the right foot.


Clinical diagnosis: Tibial nerve palsy, con-firmed by electrophysiology.

Imaging technique: MR scans of the lowerlimbs: axial T1 and T2 STIR, 3DMRN with MIPreconstructions, 3D diffusion-weighted MRN,axial contrast-enhanced T1 fat-sat sequences.

Contrast agent and dose: Single dose(0.1 mmol/Kg bw) macrocyclic gadoliniumagent (0.1 mmol/kg).

MR Findings: Enlargement of the right tibialnerve at the popliteal fossa, which is markedlyhyperintense with a cyst-like appearance and T1hypointense (arrows in A and B). Contrastenhancement of some fascicles of the tibialnerve after gadolinium administration (arrow inC). Multilobulated cystic lesion, in connectionwith the superior tibio-peroneal joint, with fluidsignal intensity, infiltrating the right tibial nervein a retrograde fashion (arrow in E and F).Denervation edema into the right posterior tibialmuscle (asterisk in D).

Interpretation: Intraneural ganglion cyst ofthe right tibial nerve.

Comment: MR is the gold standard to excludeother mass lesions responsible of the tibial nerve

entrapment. After the MR study, the patientrecalled a previous trauma that could be thecause of the intraneural ganglion cyst formation.

Reporting Checklist

• MR findings suggesting peripheral nerveabnormalities– Signal T2 hyperintensity– Focal or global enlargement– Increased or decreased visualization of

fascicles– Contrast enhancement

• Traumatic lesions– Peripheral nerves

T2 hyperintensityNeuroma in continuity/end-bulb neuromaMuscle denervation

– Brachial/lumbosacral plexusPseudomeningoceleReduction/absence of rootletsRootlet swelling and T2 hyperintensityMuscle denervation

• Non-traumatic plexopathies


– Nerve root swelling and hyperintensity– Muscle denervation edema– +/� contrast enhancement

• Inflammatory neuropathies– Nerve root hypertrophy and T2

hyperintensity– Nerve root enhancement– Distribution

Symmetrical/asymmetricalBilateralMultifocal

• Peripheral nerve tumors– Fusiform or round-shaped soft tissue lesion

in continuity with the nerve (tail sign)– T2 hyperintensity of the lesion (target sign)– Contrast enhancement

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