espacio de neurorradiologÍa · 2018. 8. 20. · espacio de magnetic resonance neurography:...

37ARTÍCULO DE PUESTA AL DÍA / MD, Cecilia Rollán, Hernán Chaves MD, María Isabel Llovet MD, Claudia Cejas MD.

NEURORRADIOLOGÍAESPACIO DE

MAGNETIC RESONANCE NEUROGRAPHY:ASSESSMENT OF EXTRASPINAL LESIONS

MD, Cecilia Rollán, Hernán Chaves MD, María Isabel Llovet MD, Claudia Cejas MD.

Dpto. de Diagnóstico por Imágenes. Fundación par la Lucha de Enfermedades Neurológicas de la Infancia (FLENI).Montañeses 2325, C1428AQKBuenos Aires, Argentina.Corresponding author: Claudia Cejas Mail: [email protected]

AbSTRACT

The diagnosis of peripheral neuropathies was originally based on interrogatory, physical examination and electrophy-siological studies. Spinal magnetic re-sonancia imaging (MRI) may sometimes help solving the diagnosis, but in many other cases it´s insufficient. The latter development of high-resolution neuro-graphic sequences with wide field of view (FOV), helped improve the evalutation of extra-spinal pathology. The purpose of this iconographic review is to go over peripheral nerve anatomy and describe the most frequent neuropathies showing the utility of MRI neurography in the diagnosys of extra-spinal pathology.

Key words: Peripheral Nerves, Neuro-pahties, Magnetic Resonance Neuro-graphy.

RESUmEn

Históricamente el diagnóstico de las neuropatías se basó en el interrogatorio, el examen clínico y los estudios electrofisológicos. El estudio de resonancia magnética (RM) de columna muchas veces es el complemento que ayuda a resolver el diagnóstico de estos pacientes. En muchos casos, el resultado de este estudio es insuficiente para arribar al diagnóstico. El desarrollo de secuencias neurográficas de alta reso-lucion, con campo de visión amplio, para visualizar mas allá de los elementos de la columna, permite una aproximación al diagnóstico más adecuada de la patología extraespinal. En esta revisión haremos enfásis en la utilidad de la Neurografia por RM en el diagnóstico de la patología extraespinal, repasando la anatomía del nervio periférico y describiendo las causas más frecuentes de lesiones extraespinales con correlato iconográfico.

Palabras clave: Nervios periféricos, Neuropatías, Neurografía por Resonancia Magnética.

InTRODUCTIOn

Peripheral neuropathies were recognized more than 200 years ago and have been a topic of interest ever since. More than 150 years ago the correlation between clinical disease and autopsy findings was established. Although knowledge about the peripheral nervous system (PNS) kept increasing, new facts about the central nervous sys-tem appeared in far greater number. The fifties marked the start of electrophysiological studies and the renewal of interest about the PNS in the neurological community worldwide (1).For many years the diagnosis of neuropathies rested upon three pillars: anamnesis, physical examination and electro-physiological studies. The latter were considered the gold standard in this field (2). However, electrophysiological

studies may detect the deficiency only after 7 to 10 days, or even be negative (3, 4). A new era for the diagnosis of neuropathies began in the last 10 years, when Magnetic Resonance Neurography (MRN) was implemented (5-8). MRN enables the structural study of the peripheral ner-ves, the brachial and lumbosacral plexuses (BP, LSP), the perineural soft tissues and the muscles supplied by those nerves. If high-field equipment is used, 3 Tesla scanners in particular, and in combination with phased coils focusing on the region to be studied and tridimensional sequences, it is also possible to study the internal structure of the nerve (9-11).Classically neuropathies are classically grouped into two categories: mononeuropathies and polyneuropathies. The specialist confronted with a patient with clinical evidence of either usually demands as basic study a MR scan of the

Rev. Imagenol. 2da Ep. Jul./Dec. 2017 XXI (1):38

spine (cervical, dorsal or lumbar according to the presenta-tion) in order to rule out lesions of the spinal cord and/or the emergent nerve roots. In many cases the results of this study suffice to reach a diagnosis. However, the MR scan of the spine occasionally shows only degenerative changes due to age or sports activity, and no findings relating to the patient’s symptoms. The use of conventional sequences and a reduced field of view in the MR of the spine limit the study to this region. Once spinal lesions have been ruled out as causes for the patient’s clinical picture, how does one study the extraspinal lesions? The objective of this paper is to make an anatomical review of nerves and plexuses in the MR scan, to analyze imaging technique and to discuss nerve pathology in high-resolution MR neurography.

PERIPHERAL nERVE AnATOmY

Structural knowledge of the peripheral nerve is essential to understand classifications of nerve lesions, because the basis of such classifications is the way the different nerve substructures are affected by the disease.Peripheral nerves consist of nerve components surroun-ded and shaped by three protective layers of connective tissue. Starting at the innermost layer, they are: endoneu-rium, perineurium and epineurium. The endoneurium surrounds each nerve fiber, which consists of an axon associated with a Schwann cell. Nerve fibers form groups called fascicles. Each fascicle is surrounded by the peri-neurium, which acts as a blood-neural barrier (12). Finally, a group of fascicles form a nerve, which is surrounded by the thickest of all three layers, the epineurium (Fig. 1) (13). The proximal epineurium is continuous with the dura mater and it tapers towards the periphery until it

merges with the perineurium. The epineurium consists of two sublayers, internal and external. Internal epineurium includes vascular structures as well as a variable quantity of interfascicular fatty tissue (14).Nutrient vessels penetrate peripheral nerves at frequent intervals in the whole of their length, providing irrigation to perineural vessels that course the length of the nerves (15).The minimal functioning unit of the peripheral nerve is the axon. The number of axons ranges from 1-3 for a distal peripheral nerve, to 200 for the sciatic nerve, the latter being the nerve with the greatest diameter in the body. Axons may be myelinated or not. In myelinated fibers, Schwann cells curl around each axon, forming a multilaminated myelin layer. All along its course, whose length ranges from 0.5 to 100mm, an axon is sheathed in multiple Schwann cells, separated by non-myelinated gaps called nodes of Ranvier (16).

Fibers and nerve fascicles form groups, connect with each other and branch out towards the extremities in the shape of plexuses. The most important of these plexuses are the brachial and the lumbosacral plexuses, for the innervation of the upper and the lower limbs, respectively. The an-terior rami of spinal nerves C5 to T1 constitute the roots of the brachial plexus (Fig. 2), which in turn subdivide as they progress distally into trunks, divisions, cords and finally peripheral nerves. The lumbosacral plexus consists of two separate plexuses, lumbar and sacral. The lumbar plexus consists of the anterior rami of spinal nerves T2 to L4 (Fig. 3). These anterior rami, or roots, branch out into anterior and posterior divisions which combine into further anterior and posterior rami, respectively. As regards the sacral plexus, it is formed by anterior rami L4 to S4, which also branch out into divisions and rami, anterior and posterior (Fig. 4).

Figure 1: Histological section of a sural nerve. a) Axial cut of nerve, Luxol fast blue stain. b) Axial cut of nerve, hematoxylin and eosin stain. c) Axial cut of nerve, hematoxylin and eosin stain. d) Longitudinal cut of nerve, Luxol fast blue stain. EN: endoneurium, PE: perineurium, EP: epineurium, FI: fiber, FA: fascicle, SC: Schwann cell, VA: epineural vessel, *epineural fatty tissue. Magnification on the bottom right-hand corner of each picture. Courtesy of Dr Naomi Arakaki, Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia Dr. Raúl Carrea (FLENI).

1a 1b

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TECHnICAL COnSIDERATIOnS

Ideally magnetic resonance neurography (MRN) is done with high-field, 3T scanners, because they provide a high signal-to-noise ratio, shorter acquisition times, greater contrast and a better imaging resolution (17).The scan consists of anatomical sequences and diffu-sion-weighted (functional) sequences. Conventional fast-spin-echo anatomical sequences have been replaced by 2D and 3D isotropic high-resolution sequences, which provide milimetric slices and consequently a better as-sessment of anatomical structures, regarding both their morphology and their signal. Due to the fatty content in perineural tissue, it is necessary to achieve homogeneous fat suppression. That is why the sequences of choice are Dixon method sequences, which are called IDEAL by GE Healthcare, Dixon TSE by Siemens Healthcare and mDixon by Philips Healthcare; they enable the use of T1- and T2-weighted imaging with four combinations of saturation pulses: water suppression, fat suppression, and two kinds of combined fat-water suppression, in-phase and out-of-phase (18).

Other special volumetric acquisitions with high spatial resolution like T2 CUBE (GE Healthcare), SPACE (Siemens

Healthcare) or VISTA (Philips Healthcare) provide a com-plement to the neurography scan.T1-weighted sequences are optimal for the assessment of nerve anatomy, to define the limits of perineural fat tissue, to identify post-contrast enhancement and to eva-luate adjacent structures. T2-weighted sequences, on the other hand, are particularly suited to assess modifications of thickness or signal at nerve level. The acquisition of post-contrast images is reserved for cases where infection, inflammation, diffuse lesion of peripheral nerves or tumors are suspected (19).Volumetric sequences are processed into a variety of reconstructions: multiplanar (MPR), curved planar (CPR) and maximal intensity projection (MIP). It is therefore possible to display and track the peripheral nerves along their whole length.

DWI-based MR neurography, which remains investiga-tional, has the potential to overcome the limitations of anatomical MR on account of its ability to take tissue microstructures into consideration. DWI sequences with different b-values are useful for the assessment of periphe-ral nerves; they enable extensive MIP reconstructions with

1c 1d

Figure 2: Diagram of brachial plexus.

Figure 3: Diagram of lumbar plexus Figure 4: Diagram of sacral plexus

mAGnETIC RESOnAnCE nEUROGRAPHY:ASSESSmEnT OF EXTRASPInAL LESIOnS

ARTÍCULO DE PUESTA AL DÍA / MD, Cecilia Rollán, Hernán Chaves MD, María Isabel Llovet MD, Claudia Cejas MD.


blood suppression that achieve excellent imaging contrast. By means of water diffusivity they become excellent tools for the detection of highly cellular tumors and their diffe-rentiation from scar lesions.Diffusion tensor imaging (DTI) is useful for the detection of nerve sheath tumors; it also permits to calibrate neuronal integrity and to demonstrate early signs of nerve regene-ration in proximal nerve segments. This is done on the basis of quantitative parameters like fractional anisotropy, apparent diffusion coefficient and diffusivity (mean, axial and radial) in order to estimate the course and outcome of the lesions. The application of high b-values, approxi-mately 1000-1200s/mm2 is essential for this sequence (20, 21). The basic scan protocol in use in our department is itemized in Table 1.

DP FS

STIR

3D IDEAL T1

3D IDEAL T2

Axial

Coronal

Coronal

Coronal

3-0,3

4-0

1,2-0

1,2-0

TAbLE 1

Sequence Plane of slice Thickness of slice (mm)

eDWI:b0-200

3D IDEAL T1w/contrast

Axial

Coronal

4-0

1,2-0

3D CUbE T2 Sagital

Protocol for mR neurography scan

*All sequences are performed with a high-resolution, 256x320 matrix.*FOV is adjusted according to the area to be explored.

PATHOLOGY OF PLEXUSES AnD PERIPHE-RAL nERVES

The pathology of peripheral nerves consists of two disease groups: mononeuropathies and polyneuropathies. The for-mer may derive from trauma, entrapment or tumors; they may also be due to a segmental inflammatory process. In the last few years MRN has played an increasingly impor-tant role. The precise diagnosis it provides has produced fundamental changes in the therapeutic management of these patients (22).

Polyneuropathies may be hereditary or acquired; the latter are more frequent. In the first place, the use of MRN in the study of polyneuropathies makes it possible to redirect the diagnostic algorithm in those patients in whom a mo-noneuropathy was suspected on clinical grounds. In the second place, in patients clinically diagnosed for polyneu-ropathies, it helps to define the extent of the disease and to perform follow-up long enough to determine whether the disease is progressing or regressing.

mOnOnEUROPATHIES

Traumatic mononeuropathiesA traumatic lesion in a peripheral nerve may arise from traction, contusion or penetrating injury. Those entities may be concurrent and it may be difficult to differentiate them due to overlapping imaging characteristics (24).The nerves most likely to be injured are those exposed to high-energy traction, like those of the brachial plexus; nerves coursing through distal regions, like the peroneal nerve at the knee; or those near bony structures, like the sciatic nerve next to the ischium (25).

Trauma is the most frequent cause of brachial plexus palsy; it is generally due to road accidents, particularly if motor-cycles are involved. The lumbosacral plexus, on the other hand, is rarely directly affected by trauma because the axial skeleton protects it. But it can suffer indirect trauma in case of severe spinal trauma, hip fracture, hip luxation, pelvic fracture, surgical iatrogenesis and certain lesions of the psoas muscle, like hematomas and abscesses (26).Traumatic lesion of the peripheral nerves has been clas-sified by Seddon (27), according to severity, according to increasing compromise, into three groups: neurapraxia, axonotmesis and neurotmesis.

In neurapraxia there is axonal dysfunction, but neither axons nor nerve sheath suffer interruption. It is usually a transitory disorder that resolves completely. Axonotmesis implies axon discontinuity while the integrity all three layers of the connective sheath is preserved. In neurot-mesis, which represents the highest degree of injury, there is loss of continuity of both the axons and the perineural covers (26).

In neurapraxia and axonotmesis, MRN evidences an in-crease in size and T2-weighted signal of the altered nerve, as a manifestation of edema and wallerian degeneration (the latter is a feature of axonotmesis). The return to normal of these changes runs parallel to the functional recovery of the nerve. Muscle atrophy due to denervation is an indirect sign of nerve injury. Neurapraxia patients recover completely while in axonotmesis recovery may be complete, incomplete or nil.

In neurotmesis loss of continuity of the nerve may be identified in the acute stages, though it may be difficult due to concurrent inflammatory changes and perilesional hemorrhage. In the chronic stage the neuroma may be observed as round low-signal T2-weighted image in the uninterrupted nerve. It may be confused with a tumor of the nerve sheath, although neuroma does not enhance after contrast is delivered (28). Neurotmesis patients do not recover and their prognosis depends on prompt and appropriate surgery. In that case MRN is useful to map out the altered anatomic course of the nerve and to classify the lesion, all of which contributes to the clinical outcome (Fig. 5).

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Compressive mononeuropathiesCompressive or entrapment mononeuropathies are one of the most frequent chief complaints seen at the neurologist’s office. The diagnosis is usually clinical and electromyographic, especially for those compressive mo-noneuropathies with a classical presentation. In unclear cases resonance is a most useful study for diagnostic definition and subsequent therapeutic strategy in those patients (29).

Compressive neuropathy is produced by increasing cons-tant pressure on the nerve, which gradually compromises its blood supply. First the venous circulation is compro-mised, then the arterial; ischemic damage to the nerve ensues. In the course of time and under sufficient pressure, such damage may become irreversible (30).Peripheral nerves may be affected in any segment of their course, but some locations are more prone to entrapment on account of their anatomy, either because nerves run more closely to the surface, or because they go through a narrow passage (31). That is why it is essential to know the normal anatomy of the peripheral nerves and their usual compression sites, before planning and evaluating

the study of compressive mononeuropathies (Table 2).From the viewpoint of imaging, we usually find that both the compressed nerve and the muscles innervated by it are affected. Structures adjacent to the altered nerve may also be examined in order to identify the cause of com-pression. The compression site usually evidences a local enlargement with increased signal in T2- and DP-weighted sequences; these findings might relate to neural ischemia and edema. Other sites distal to the compression show nerve enlargement, normal nerve thickness or even de-creased thickness, along with increased signal in T2- and DWI- weighted scans (32). This aspect probably relates to wallerian degeneration in accordance with the duration of the process (32) (Fig. 6). Since small caliber structures are being evaluated, multiplanar and curved reconstructions are especially useful in order to study the whole course of the nerve. In this way it is possible to compare thickness and signal at the compression site with those of adjacent segments (33).

Signs of muscle denervation can often be the first findings to be observed in the magnetic resonance scan. Muscle edema is usually observed in both the acute and the

Figure 5Contiguity neuroma:

25-year old male with a past history of trauma to the knee.

a) IDEAL T2-weighted sequence with water, showing edema of

peroneal head (arrow) and adjacent soft tissues.

b) 3D FIESTA sequence with curved reconstruction, where the common

peroneal nerve (arrow) presents a pseudonodular thickening at the level of the peroneal head

(neuroma). c) 3D T2-weighted IDEAL sequence

after administration of contrast, showing enhancement of the

proximal peroneal nerve (dashed arrow) and mild peripheral

enhancement of neuroma (arrow) related to inflammatory changes.

Figure 6Entrapment of pudendal nerve

48-year old male with long-standing pudendal neuralgia. a) IDEAL T2-weighted sequence with

water, coronal plane. b) DWI sequence on the axial

plane, showing hypersignal and thickening of both the pudendal

nerve (P) in Alcock’s canal, and its rami: the inferior rectal nerve (RI),

the perineal nerve (Per) and the dorsal nerve of the penis (DP).

5a 5b 5c

6a 6b




subacute stages, while fatty replacement and atrophy characterize the chronic stage. It is important to know which myotomes correspond to each nerve in order to infer nerve involvement, even if we cannot identify the neural injury directly (34) (Table 2).

Supraescapular

Axillary

TAbLE 2

nerve Compression site

Compression sites of peripheral nerves and the involved muscles

median

Involved muscles

Angular incisure

Spinoglenoid notch

Humerotricipital quadrilateral space (space of Velpeau)

Elbow: more frequent in both bellies of pronator teres

Forearm: Anterior interosseous branch coursing through the membrane

Wrist: Carpal tunnel

Supraspinatus, infraspinatus

Infraspinatus

Teres minor, deltoid

Flexor pollicis longus, flexor di-gitorum profundus (radial belly), pronator quadratus

Thenar muscles

CubitalElbow: Cubital tunnel Flexor carpi ulnaris, flexor digitorum

superficialis, hypothenar muscles

Wrist: Guyon’s canal Thenar muscles

Arm: Spiral groove of the humerus

Elbow: Radial tunnel

Forearm: Posterior interosseous nerve

Triceps brachii, supinators and extensors of hand and wrist

Less significant motor involvement

Extensors of hand and wrist

Radial

Pudendal Alcock’s canal Less significant motor involvement

Sciatic Pelvis: Related to piriformis muscle Isquiotibial muscles, adductor major

Knee: Popliteal fossa

Ankle: Tarsal tunnel

Extensors of the foot, plantar flexor, intrinsic muscles of the foot

Plantar flexor, intrinsic muscles of the foot

Tibial

Common peroneal

Peroneal groove (head) Tibialis anterior, extensors and peroneal muscles

TumorsBenign tumors of the neural sheath are the most frequent tumors of the peripheral nerve. These tumors are divided into three groups: schwannoma (also called neurilemmo-ma and neurinoma), neurofibroma and perineurioma. Schwannomas and neurofibromas share some imaging characteristics: a well-defined fusiform shape and a dia-meter that rarely exceeds 5cm (35, 36). Schwannomas, however, are usually solitary, eccentric as regards the axis of the nerve and contained within the perineurium. If they are multiple, it is obligatory to rule out schwannomatosis.Neurofibroma can be either solitary or present as a plexiform neurofibroma. The latter form involves several nerves and is associated, as a rule, to neurofibromatosis

type I (NFI). The solitary form is the commonest one. It involves peripheral nerves more frequently than plexuses. The lesion is centrally located and non-encapsulated, and therefore difficult to separate from the nerve (Fig. 7).

Most benign tumors of the nerve sheath are isointense or mildly hyperintense in T2-weighted scans, if compared to muscle, and hyperintense in T1-weighted scans. The “target sign” (a more hyperintense halo around the tumor in T2 and STIR sequences) has been described in both schwannomas and neurofibromas. It is less frequent in schwannomas. It is due to the presence of myxoid tissue on the periphery and fibrosis in the center. Fascicular pa-ttern is another finding described in neurogenic tumors; it consists of “onion bulb” images, hyperintense T2-weighted images that show variable enhancement after gadolinium administration. In small tumors contrast uptake is usually homogeneous, while in large tumors enhancement may be central, peripheral or irregularly nodular (36, 37 and 38).Schwannomas of long standing usually undergo degene-

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ration phenomena and evidence a more heterogeneous pattern with calcifications, hemorrhagic areas and cystic degeneration that may simulate a sarcoma.Plexiform neurofibroma is almost pathognomonic of neurofibromatosis type I (NFI). It often begins to develop in childhood and antedates the appearance of cutaneous neurofibromas. Its malignization rate ranges from 8 to 12%. These tumors expand and distort extensive segments of one or several nerves and often present high-intensity sig-nal in T2-weighted sequences, showing a “bag of worms” aspect (Fig. 8). On account of their large size, these lesions extend beyond the epineurium into adjacent tissues (25, 37 and 39).

At present, perineurioma is included among benign nerve sheath tumors. It was formerly considered a pseudotumor. It presents more frequently in peripheral nerves than in plexuses. It appears as a spindle-shaped image, isointense in comparison with the nerve in T1-weighted scans and hyperintense in T2-weighted scans; it shows intense homogeneous enhancement after contrast injection (40).

Malignant tumors of the nerve sheath may be primary or secondary. Malignant schwannoma, also called neurofi-brosarcoma or neurogenic sarcoma, accounts for 5-10%

of all soft-tissue malignancies. Mostly it presents de novo, i.e. it is not associated to a preexisting schwannoma, and it involves peripheral nerves. Around 25-50% of these tumors are associated with neurofibromatosis type I (NFI). The most frequent form of presentation is a spindle-shaped or eccentric mass in a nerve trunk, extending through the epineurium and the perineurium. It often metastasizes to lungs, liver, bone and subcutaneous tissue. The prognosis is poor due to a high relapse rate (36, 41 and 42).Malignant schwannomas resembles benign nerve sheath tumors in the MR scans, although they tend to have a larger size (more than 5cm) and their borders are imprecise and heterogeneous (Fig. 9).

Perineural infiltration has been described in other type of tumors, lymphoma for example, but it is extremely rare. It appears like a diffuse thickening of a neural segment with a high-intensity signal in T2 pulses, isointense in comparison with the muscle in T1-weighted scans, with mild post-contrast enhancement (42, 43).Finally, any pelvic tumor that invades the ischiorectal fossa may compromise a peripheral nerve or the LS plexus at some point of their course (11). The same happens if an apical thoracic tumor invades the inferior trunk and the divisions of the brachial plexus (10).

Figure 7Neurofibroma in a 33-year

old female patient. IDEAL T2-weighted neurographic

sequence. a) coronal plane

b) oblique reconstruction showing spindle-shaped

nodular thickening of the right lumbosacral trunk

(arrow). c) IDEAL T1-weighted

sequence with fat saturation and endovenous contrast.

Intense homogeneous enhancement of the lesion is

observed.7a 7b 7c

8a 8b 8c

Figure 8Plexiform neurofibroma

in a 20-year old male patient diagnosed with

neurofibromatosis type I. IDEAL neurographic sequences: Cluster-like nodular thickenings

are observed, involving roots of the lumbosacral plexus and

both sciatic nerves, with a) iso-hypotense signal in T1-weighted sequences, and b) hyperintense

signal in T2-weighted FAT SAT sequences. (c) Coronal STIR

sequence.




POLYnEUROPATHIES

The best-known hereditary polyneuropathy is Char-cot-Marie-Tooth disease, a genetically transmitted entity, which presents 5 genetically determined types. The most frequent type is the IA (CMT IA) type, which is produced by the deletion of PMP22 gene (44). In this form of the disease, MRN T2-weighted sequences show hypersignal of thickened peripheral nerves, resulting in fascicular hyper-trophy with no pattern distortion, and also hypertrophy of interfascicular fatty content. Involvement tends to be more distal than proximal (45).

The most salient acquired polyneuropathies are the immune-mediated and the vascular ones. Among the former, some are worth mentioning: chronic inflammatory demyelinating polyneuropathy (CIDP), Guillain-Barré sy-ndrome and amyotrophic neuralgia or Parsonage-Turner syndrome. The main entity in the vascular group is diabetic polyneuropathy, while the non-diabetic vasculitis group takes second place. Other polyneuropathies of lesser in-

cidence have been described; they include those linked to radiation, amyloidosis and sarcoidosis (46, 47).CIDP is an immune-mediated polyneuropathy charac-terized by the hypertrophy of nerves and plexuses. As opposed to CMT disease, CIDP tends to a proximal involvement, rather than a distal one (48). MRN findings are described as focal or diffuse hypertrophy assuming a spindle shape, with restructuring of the fascicular pattern in both nerves and plexuses; T2-weighted scans show hypersignal (49) (Fig. 10).

DBT polyneuropathy is currently more frequent, due to increased survival of diabetic patients. Its pathologic foundation is vasculitis (50). MRN findings have been des-cribed: diffuse thickening of one or more nerves, with an unchanged fascicular pattern. Some denervation changes may occasionally be observed in muscles supplied by the involved nerves: edema and/or atrophy of paravertebral muscles may be observed as a sign of involvement of the posterior roots of the brachial and lumbosacral plexuses, for example (51).

Figure 9: Malignant schwannoma. 65-year old female patient. IDEAL neurographic sequences: at the location of the right obturator internus nerve a heterogeneous fusiform shape with irregular borders is observed (arrows); a) it evidences a hyperintense signal in T2-weighted FAT SAT scans, and b) irregular enhancement in T1-weighted FAT SAT scans with contrast; c) axial T2-weighted FAT SAT sequence.

Figure 10: Chronic inflammatory demyelinating polyneuropathy. 37-year old female patient clinically and electromyographically diagnosed for CIDP. IDEAL T2-weighted water neurographic sequence, where hypersignal and diffuse thickening of the roots, the primary and the secondary trunks of the brachial plexus are observed.

Figure 11: Parsonage-Turner syndrome in an 18-year old male. In this IDEAL T2-weighted water neurographic sequence, thickening and hypersignal of the trunks and divisions of the left brachial plexus are in evidence (arrows).

9a 9b

9c

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Parsonage-Turner syndrome is an immune-mediated plexitis of unknown etiology that affects middle-aged patients. Clinical features are pain and subsequent quick denervation of shoulder and upper limb muscles on the affected side (52). MRN shows diffuse hypertrophy and hypersignal of the branches of the brachial plexus in T2-weighted scans. It is worth pointing out that minor branches, like the long thoracic nerve, the suprascapular nerve and the subscapular nerve, may be affected. On the other hand, involvement may be bilateral in 30% of the cases, although clinical manifestations may remain one-si-ded. Neurography can make an important contribution, in pointing out the bilateral involvement which indicates the rehabilitation of both limbs although the patient perceives symptoms only on one side (53) (Fig. 11).

Guillain-Barré syndrome is the commonest post-infectious immune-mediated polyneuropathy and constitutes a neurologic emergency (54). MRN manifestations vary ac-

cording to the nerves involved. The most frequent finding is increased thickness and post-contrast enhancement of the cauda equina roots (55). Hypertrophy and post-con-trast enhancement may also be observed in plexuses, whose involvement is less common and even in cranial nerves, where it is rare. Neurography is also useful for the follow-up of diagnosed lesions (56) (Fig. 12).

Radiation neuropathy is observed with increasing frequen-cy due to its progressively widespread use in combination with chemotherapy in many neoplasms where it was not indicated formerly, and also on account of the longer survival of treated patients. The greatest challenge for the radiologist is to differentiate radiation neuropathy from perineural invasion in tumor relapse. Clinically, radiation neuropathy presents several years after treatment. MRN shows thickening of nerves and/or plexuses with an intact fascicular pattern; edema of adjacent tissues is associated but there is no mass pattern, which rules out a tumor (57, 58) (Fig. 13).

Figure 12Guillain-Barré syndrome in a 9-year old boy. IDEAL T2-weighted water sequence, showing thickened branches of the lumbar plexus, with diffuse hypersignal. a) Conventional FSE T1-weighted spine scans. b) Axial scan with contrast. c) Sagittal scan without contrast. d) Sagittal scan with contrast, showing thickening and enhancement of cauda equina roots.

12a 12b

12c 12d



Rev. Imagenol. 2da Ep. Jul./Dec. 2017 XXI (1):46 75 -82

COnCLUSIOn

Magnetic Resonance Neurography permits an exhaustive study of the characteristics of the peripheral nervous system. It is an alterna-tive test that is playing a progressively active role in the diagnosis of extraspinal pathology.

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Figure 13Radiation plexopathy.43-year old female patient, with a past history of partially removed and later irradiated malignant nerve sheath tumor. IDEAL T2-weighted water neurographic sequence: coronal scan showing diffuse thickening of left divisions of L4 and L5 (arrows). Notice image of tumor remnants in root of right L5 (asterisk).

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