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ABSTRACT: Magnetic resonance (MRN)is a relatively neurography new imaging technique that is highlysensitive detecting in lesionsin the peripheral nerves.We studiedsix cases of brachialplexopathies which MRN in played a pivotal role in making the correct diagnoses.All patientshad clinical, nerve conduction, and electromyographic findingsconsistent with brachial plexus lesions. Four patients had brachial plexitis and two had multifocal presenting brachialplexopathies. demyelinating neuropathy as MRN in all patientsshowed edema, thickening, and T2 hyperintensities localized the brachialplexusregion.We conclude to that MRN is a useful technique evaluating patients plexuslesions, in particularly with brachial in plexitis, casesof brachial whereconventional resonance magnetic imaging is generally normal. MuscleNerue 305-309.2004 30:

ROLE OF MAGNETIGRESONANCE NEUROGRAPHY IN BRACHIAL PLEXUS LESIONS

LAN ZHOU, MD, PhD,r DAVID M. YOUSEM, MD,z and VINAY CHAUDHRY, MD, FRCPI 1 Department of Neurology, Johns Hopkins University School of Medicine, 601 North Caroline Street,{HOC 5072-4, Baltimore, Maryland 21287-0876,USA z Department of Radiology, Johns Hopkins Hospital, Baltimore, Maryland, USA Accepted6 May 2001

Magnetic resonance neurography (MRN) is a relatively new technique that combines magnetic resonance imaging (MRI) with specially designed phased-array surface coils that allows for visualization of the peripheral nerves.1,6,8,e,11 surface coil The technology is combined with excellent fat-suppression highly T2-weighted magnetic resonance (MR) pulse sequences to best visualize the nerves amidst the other soft tissues. Compared to conventional MRI techniques, MRN has faster image acquisition and higher signal-to-noise ratio with resultant decreased motion artifact and higher resolution capable of showing fascicular organization of ner-vesto detect both extraneural and intraneural lesions. It lesions affecthas been used increasingly in assessing ing peripheral nerves, plexus, and spinal nerve roots.a,5,10,12,13 report six cases in which MRN We

played an important role in confirming the presence of lesions in the brachial plexus. CASE REPORTS Six patients, four with brachial plexitis (two postsurgical and two without precipitating factors) and two with multifocal demyelinating disorders affecting the brachial plexus, were studied with MRN. All patients underwent clinical evaluation, appropriate laboratory testing, nerve conduction studies (NCS), and electromyography (EMG). The study was approved by our Institutional Review Board. The imaging protocol utilized phased-array surface coils as well as body coil, and the MR protocol included axial and coronal Tl-weighted scans,axial and coronal inversion recovery fast spin echo T2weighted scans, and postcontrast axial and coronal images. Coronal scanswere obliqued parallel to the brachial plexus. Axial scans were performed from the C5 to T2 levels. case l. A 4Gyear-old woman developed pain over the left arm after abdominal surgery for pseudomlxoma peritonei. Three days later, the pain resolved, but she developed relatively acute onset of left thumb weakness with inability to flex the thumb. She was not evaluated for this problem until 5 months later, when she was referred to our neuro-

Abbreviations:AlN,anterior interosseous nerve; Cl\,/lAP, compound muscle EMG,electromyography; intravenous actionpotential; lVlg, infusion immuof noglobulin; magnetic MR, resonance; MRC,l\/ledical Fesearch Council; MRl, magnetic resonance imaging; resonance neurography; MBN,magnetic NCS, nerve conductionstudy; NF-1, type I neurofibromatosis; SNAP, sensory nerveaction potential plexitis; Key words: brachial demyelinating neuropathy; electromyography; nerveconductionstudy magneticresonanceneurography; [email protected] Correspondenceto: V. Chaudhry; e-mail: O 2004WileyPeriodicals, Inc. (www.interscience. Publishedonline21 July 2004 in Wiley Interscience D w i l e v . c o m ) . O I1 0 , 1 0 0 2 / m u s . 2 0 1 8

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muscular clinic because the weakness had not improved. Examination showed weakness limited to the left flexor pollicis longus lgrade 0 on the Medical Research Council (MRC) scalel, pronator quadratus (4), and flexor digitorum profundus to digits 2 and 3 (4) . Sensory examination and deep tendon reflexes were normal. Median and ulnar sensory ner-ve action potential (SNAP) amplitudes and latency values were normal. Needle EMG examination showed abundant fibrillation potentials and positive sharp waves, and a few high-amplitude and longduration voluntary motor units only in the muscles supplied by the left anterior interosseous nerve (AIN), i.e., flexor pollicis longus, flexor digitorum profundus of the second and third digit, and pronator quadratus. MRN of the left forearm was normal. MRN of the left brachial plexus showed edema, with increased T2 signal of the plexrrs at the level of trunks and divisions, consistent with left brachial plexitis (Fig. 1). Evaluation for other etiologies. including for vasculitis, was negative. In particular, erythrocyte sedimentation rate, antinuclear antibody, and antineutrophil cytoplasmic antibody were normal. There were no risk factors for brachial plexus injury related to the surgery, such as use of shoulder braces, head-down position, or malposition of arms.3 Ten months after the onset, the patient reported significant improvement of her weakness. Gase2. A 17-year-old woman developed acute right upper-extremity weakness I day after spine fusion surgery for scoliosis. During the surgery, right median somatosensory evoked potentials were intact. Immediately after the surgery, she was able to move her right arm. She denied sensory syrnptoms although she was on narcotics for postoperative pain. Examination showed profound weakness (MRC

grade 0-1) of the right deltoid, biceps, triceps, wrist extensors, and wrist flexors, and moderateiy severe weakness (2-3) of the interossei and thumb abductor. Patchy sensory loss in the right upper arm was present. Deep tendon reflexes were absent in the right arm. NCS of the right upper extremity, 2 days after the onset of symptoms, showed severe motor conduction block across the Erb's point to axillary segments of the right median and ulnar newes and absent F-waves in these two nerves. Right median and ulnar SNAPswere normal. Needle EMG showed scattered fibrillation potentials and positive sharp waves,lack of recruitment of any motor units in the proximal muscles, and only a few motor units in the distal muscles of the right arm. Follow-up study 6 u'eeks after the onset of q.'rnptoms showed absent SNAPs and severely reduced compound muscle action potential (CMAP) amplitudes of the right median and ulnar nerves. Profuse abnormal spontaneous activity (fibrillation potentials and positive waves) was now present in the right deltoid, biceps, triceps, extensor digitorum communis, pronator teres, abductor pollicis brevis, and first dorsal interosseousmuscles.No motor units were recruited in the right deltoid and biceps, and motor unit recruitment was severely reduced in the other noted muscles. MRN, 2 days after the onset of right arm weakness, showed mild edema and thickening along the course of the fibers of the right brachial plexus, consistent with right brachial plexitis. At l-year follow-up, marked improvement to near-normal strength had occurred in the right arm. Case 3. A 23-year-oldwoman developed acute right shoulder pain lasting for 3 days followed by weakness that evolved over a period of 4 weeks. There was no antecedent infection, trauma, or surgery. Four months after the onset of syrnptoms,when there was no improvement, she was referred to our neuromuscular clinic. Examination showed right-sided scapular winging, mild weakness (MRC grade 4 or 4*) in the right rhomboid, supraspinatus, infraspinatus, deltoid, biceps, and brachioradialis, and moderately severeweaknessin the wrist extensors (1) and finger extensors (3). There was patchy sensory loss to pinprick in the lateral aspect of the right upper extremity. NCS showed reduced right radial and musculocutaneous SNAP amplitudes; the median and ulnar SNAPs were nonnal. Needle EMG showed some abnormal spontaneous activity (fibrillation potentials and positive waves) and high-amplitude long-duration voluntary motor units in the right biceps, brachioradialis, extensor digitorum comrnunis, extensor indicis, and serratus anterior muscles. MRN

FIGURE1. Left brachialplexitis: Coronalinversionrecovery, fast spin echo, T2-weightedscan shows higher signal in the left brachial plexus at the trunks and divisionslevel (arrowheads) than the right (arrows).

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showed thickening with increased T2 signal throughout the course of the right brachial plexus, consistent with right brachial plexitis. The patient improved over the course of 2 years. Gase 4. A?7-year-old man developed acute pain in both shoulders, followed 3 days later by weaknessin both arms. There was no history of antecedent infection, trauma, or surgery. He was seen by us 3 months later. At that point, he had already noted spontaneous improvement of his weakness.Examination showed left scapular winging and weaknessin both deltoids (MRC grade 4) and infraspinati (4on the left and 4 on the right). Sensory examination was normal. NCS was normal and EMG showed only a few fibrillation potentials, positive waves,and large voluntary motor units in the C5-6 myotomes bilaterally, including deltoid, infraspinatus, and serratus anterior muscles. Cervical spine MRI was normal. MRN showed increased T2 signal in both brachial plexuses, especially the left, consistent with bilateral brachial plexitis. The patient had improved close to his normal state 4 months after the onset of slirnptoms. Gase 5. A 40-year-old man was evaluated for 2 years of progressive right hand weakness.He had noticed difficulty with his grip and was dropping objects. No sensory symptoms were present except for mild numbness in the right fourth and fifth digits. Examination showed weakness in the right rhomboid (MRC grade 4), spinati (4), deltoid (4), triceps (4-), wrist extensors (1), finger extensors (2), interossei (4-), and thumb abductor (4-) muscles. Sensory examination was normal. Deep tendon reflexes were absent at the right triceps and brachioradialis, and normal elsewhere. NCS showed normal distal CMAP amplitudes in median, ulnar, and radial nerves bilaterally. Normal CMAP amplitude of the extensor indicis despite severeweaknessof this muscle suggestedthe presence of a proximal conduction block in the radial nerve. Bilateral ulnar SNAP amplitudes were reduced and ulnar motor conduction velocities were also reduced across the elbow segments. Needle EMG showed fasciculation potentials and fast-firing units in the extensor indicis muscle. A few positive waves were present in the triceps and deltoid muscles, where a neurogenic recruitment pattern was seen. The cervical paraspinal muscles were normal. MRN showed marked enlargement of the upper and middle trunks of the right brachial plexus with increased T2 signal and no extrinsic mass lesions. Given the progressive nature of this plexopathy in the absence of a mass lesion and with

an indirect suggestion of a conduction block on NCS, multifocal motor neuropathy presenting as weakness confined to the right brachial plexus distribution was diagnosed. After intravenous infusion of immunoglobulin (I\4g), the patient had dramatic improvement in strength, most notably of the wrist and finger extensors (MRC grade 4). Gase 6. A 4O-year-old chef with a history of type 1 neurofibromatosis (NF-1) was seen with progressive right arm weaknessfor 3 years. Examination showed severeweaknessin the right upper trunk distribution involving the deltoid (MRC grade 3), biceps (3), brachioradialis (4), rhomboid (4-), spinati (3), and serratus anterior (4+) muscles. Sensation was slightly reduced in the radial aspect of the right hand and forearm. He was areflexic. Cewical spine MRI showed mild disc bulging at C6-7. Conventional MRI of the right brachial plexus showed an enlarged plexus suggestive of a neurofibroma or Schwannoma. Surgical intervention was considered. MRN showed diffuse enlargement of the upper and middle trunks and the lateral cord of the right brachial plexus measuring over 4-5 cm in length but without contrast enhancement (Fig. 2). NCS showed partial motor conduction block in the forearm segments of both median and the right ulnar nerves, with markedly prolonged F-wave latencies. Median and ulnar sensory conduction velocities were reduced and sural SNAP amplitudes were asyrnmetrically reduced. Needle EMG examination showed no abnormal spontaneous activity and decreased recruitment with a few high-amplitude and long-duration voluntary motor units in the above-named weak muscles. These findings were suggestiveof multifocal chronic inflammatory demyelinating polyneuropathy. A right sural nerve biopsy showed many thinly myelinated fibers confirming a demyelinating and remyelinating process. The patient received I\rIg with near-total recovery of the severe weakness. He continues to receive N{g every 2 months and has also been placed on mycophenolate mofetil with stabilization of his syrnptoms.

Dtscus6tol{

MRN has been used to image the peripheral nervous system directly because of the improved signal-tonoise ratio from dedicated surface coils. which allows higher resolution scanning. The principle of this technique has been elucidated in great detail elsewhere.r'll The peripheral nerves are isointense on Tl-weighted spin echo and slightly hyperintense on fat-saturated T2-weighted fast spin echo due to the

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FIGURE2. Markedenlargement the brachialplexuswithoutenhancement: of The inversionrecovery, fast spin echo,T2-weighted scan shows very high signaland enlargement the right brachialplexusaffecting of the C6 root [(A) arrowhead], upper and middletrunks the plexuson the postcontrast There is no enhancement the rightbrachial and the lateralcord [(A) arrows]. of T1-weighted study[(B), arrows].

presence ofendoneurial fluid. Peripheral nerves can be easily distinguished from surrounding tissue because muscle is very hlpointense on T2-weighted scans, the inversion recovery technique suppresses signal from adipose tissue, and vessels usually contain signal void. Peripheral nerve disorders from various etiologies, including trauma, compression, and inflammation, usually result in increased T2 signal with increased ner-ve,/musclesignal intensiry ratio due to increased water content in the nerves.As with conventional MRI, the Tl-weighted sequence is useful for evaluating anatomy and the T2-weighted sequence for demonstrating pathology. MRN appears to be a highly sensitive new imaging technique to localize and delineate root, plexus, and peripheral nerve lesions. It has been shown to successfullydetect cer-vicaland lumbosacral radiculopathies, lumbar plexopathy, and sciatic and median mononeuropathies related to entrapment, nerve trauma, ischemia, neoplastic infiltration, sheath tumor, cyst, and granulomatous infiltration.5,8'10,12,13 useful in presurgical evaluation to It is guide operative inter-vention. In our study, MRN detected six brachial plexus disorders with inflammatory and demyelinating etiologies. Even though a previous study has shown that the sensitivityof conventional MRI in brachial plexus disorders is 637a,MRI has been utilized primarily for detecting neoplastic and traumatic lesions but not inflammatory brachial plexus lesions.zAs noted by our study, inflammatory brachial plexus lesions show abnormalities on MRN. MRN has higher sensitivity

than conventional MRI in the evaluation of inflammatory brachial plexus lesions. In addition, the presentation of brachial plexitis as predominantly an AIN disorder, although previously reported,7,14,16 has never been verified by imaging studies to be localized to the brachial plexus. Our study of case I provides confirmatory radiological evidence for this disease entity with MRN. Although MRN changes can be mild, side-to-side comparisons facilitate the detection of abnormalities. Case 6 is complicated because brachial plexopathy was present in a setting of NF-l and demyelinating changes on NCS. The management of these two causesdiffers, one requiring surgery and the other immunomodulation. MRN showed a nonenhancing plexus lesion consistent with demyelination but not neurofibroma, which resulted in effective treatment. Brachial plexus lesions shown on MRN can be more diffuse and proximal than suggestedby NCS/ EMG and clinical findings, as exemplified by our case1. Although clinical presentation and EMG findings suggested a pure anterior interosseous newe lesion, MRN showed signal changes at the level of trunks and divisions of the brachial plexus. There has been some debate as to why a brachial plexus lesion gives rise to a pattern of predominantly motor involvement of peripheral nerves. AJthough localization to the brachial plexus has been problematic in many cases, intraneural topography studies have shown that some nerye branches retain a significant localization for considerable distances above the sites of branching.15 Fiber bundles destined for the

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AIN can be identified as high as the medial and lateral roots of the median nerve. Therefore, a selective AIN palsy can occur from a lesion within the brachial plexus.ra MRN is helpful in detecting this involvement. MRN is a useful imaging technique in diagnosing peripheral nerve and plexus disorders. It not only helps surgical decision-making, but also facilitates accurate diagnoses and thus appropriate therapy for nonsurgical cases.It is particularly useful to confirm the diagnosis of idiopathic brachial plexitis, which hitherto has largely been a diagnosis of exclusion.

This study was presented at the 50th annual meeting of the American Association of Electrodiagnostic Medicine, September 2003. San Francisco. Calilornia.

REFEREI{CES l. Aagaard BD, Maravilla KR, Kliot M. Magnetic resonance neurography: magnetic resonance imaging of peripheral nerves. Neuroimaging Clin N Am 2001;ll:13l-146. 2. BilbeyJH, Lamond RG, Mattrey RF. MR imaging of disorders of the brachial plexus.J Magn Reson Imaging 1994;4:13-18. 3. Cheney FW, Domino KB, Caplan RA, Posner KL. Nerve injury associated with anesthesia. Anesthesiology 1999;90: 1062-1069. 4. Dailey AT, Tsuruda JS, Filler AG, Maravilla KR, Goodkin R, Kliot M. Magnetic resonance neurography of peripheral newe degeneration and regeneration. Lancet 1997;350:12211222.

5. Dailey AT, Tsuruda JS, Goodkin R, Haynor DR, Filler AG, Hayes CE, Maravilla KR, Kliot M. Magnetic resonance neurography for cervical radiculopathy: a preliminary report. Neurosurgery I 996;38:488- 492. 6. Filler AG, Howe FA, Hayes CE, Kliot M, Winn HR, Bell BA, Griffiths JR, Tsuruda JS. Magnetic resonance neurography. -661. Lancet 1993;34:659 7. Gaitzsch G, Chamay A. Paralytic brachial neuritis or Parsonage-Turner syndrome anterior interosseous nerve involvement. Report of three cases.Ann Chir Main 1986;5:288-294. 8. Grant GA, Britz GW, Goodkin R,JarvikJc, Maravilla K Kliot M. The utility of magnetic resonance imaging in evaluating peripheral nerue disorders. Muscle Nerve 2002;25:314-331. 9. Howe FA, Filler AG, Bell BA" GriffithsJR. Magnetic resonance neurography. Magn Reson Med 1992;28:328-338. 10. Kuntz CT, Blake L, Britz G, Filler A, Hayes CE, Goodkin R, TsurudaJ, Maravilla K, Kliot M. Magnetic resonance neurography of peripheral nerve lesions in the lower extremity. -756. Neurosurgery 1996;39:750 11. Maravilla KR, Aagaard BD, Kliot M. MR neurography: MR imaging of peripheral newes. Magn Reson Imaging Clin N Am 1998;6:179-194. 12. Moore KR, Blumenthal DT, Smith AG, WardJH. Neurolymphomatosis of the lumbar plexus: high-resolution MR neurography fi ndings. Neurology 2OOl;57:740 -7 42. 13. Moore KR, TsurudaJS, Dailey AT. The value of MR neurography for evaluating extraspinal neuropathic leg pain: a pictorial essay.AJNR 2001 ;22:786 -7 94. 14. Rennels GD, OchoaJ. Neuralgic amyotrophy manifesting as anterior interosseous nerve palsy. Muscle Nerve 1980;3:160164. 15. StewartJD. Peripheral nerve fascicles: anatomy and clinical relevance. Muscle Nerve 20O3;28:525-541. 16. Wong L, Dellon AL. Brachial neuritis presenting as anterior for diagnosis interosseous nerve compression-implications and treatment: a casereport.J Hand Surg [Am] 1997;22:536539.

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