Approach to Acute Or Subacute Myelopathy

Approach to acute or subacute myelopathy

mproved understanding of the differential diagnosis and improved investigative tech- Iniques, particularly neuroimaging and serologic testing, have facilitated the diagnosis of patients with acute and subacute myelopathy and reduced the proportion of patients who are labeled as having “idiopathic transverse myelitis.” Addi- tionally, these advances have identified subgroups of patients in whom progression of deficit or future relapses are anticipated, allowing intervention and prophylaxis as appropriate. However, early management remains empiric and consists of high- dose corticosteroids for most patients. In the event of an inadequate response to corticosteroids or a subsequent atypical course, further investigations to detect diagnoses other than “transverse myelitis” should be considered and additional treatments, such as plasmapheresis, may be appropriate. Indi- vidualized diagnosis and treatment is more feasible now than in the past.

IS IT AN ACUTE MYELOPATHY? Localizing an acute neurologic process to the spinal cord is often, but not always, straightforward (table 1). The as- cending sensory symptoms of acute inflammatory demyelinating polyradiculoneuropathy (AIDP) may confuse the diagnosis, as this complaint is also

Illustration by Amy P. Collins highly associated with acute myelopathy. Un- equivocal upper motor neuron signs exclude William F. Schmalstieg, AIDP, but are often not apparent in the early MD stages of a spinal cord insult. Although not invariably present, an unequivocal sensory level on the torso, Brian G. Weinshenker, sensory loss indicating involvement of spinal tracts (e.g., spinothalamic modality impairment contralateral to MD motor findings), or urinary retention localize to the spinal cord. Myopathy or neuromuscular junction disorders may be mistaken for myelopathy, particularly if the lower limbs are predominantly affected, but the absence of any sensory abnormality should suggest the correct localization. Bilateral mesial frontal lobe lesions Address correspondence and (e.g., bilateral anterior cerebral artery distribution infarcts) could mimic a myelopathy, although abulia or reprint requests to Dr. Brian G. other signs of frontal lobe dysfunction typically coexist. Autoimmune or paraneoplastic muscle stiffness syn- Weinshenker, Department of Neurology, Mayo Clinic College dromes, such as stiff-person syndrome associated with glutamic acid decarboxylase or amphiphysin autoanti- of Medicine, 200 1st Street SW, bodies, may be confused with spasticity and erroneously lead one to suspect myelopathy. Rochester, MN 55905 [email protected] Occasionally patients with chronic myelopathy may present a history that mistakenly suggests an acute process. For example, patients with primary progressive multiple sclerosis (MS) may experience acute, transient Neurology® Clinical Practice worsening (pseudoexacerbation) in the setting of an underlying infection or heat exposure. In such cases, 2010;75(Suppl 1):S2–S8 careful history will uncover symptoms that have been insidiously progressive over a longer interval than first

From the Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN. Disclosure: Author disclosures are provided at the end of the article.

S2 Copyright © 2010 by AAN Enterprises, Inc. systemic inflammatory disorders (e.g., Sjo¨gren syn- Table 1 Distinguishing acute myelopathy 1 from mimics drome and lupus). Transverse myelitis is the default diagnosis for an Signs strongly indicating myelopathy unexplained myelopathy evolving over the course of Sensory level on torso days to 3 weeks with subsequent stabilization or im- Spinal tract crossed findings (e.g., unilateral pyramidal signs provement. In practice, there are no satisfactory ways with contralateral spinothalamic findings) to distinguish among idiopathic transverse myelitis, Spinal tract-specific sensory findings (e.g., selective spinothalamic findings with preserved dorsal column parainfectious myelitis, and postvaccinial myelitis. findings; suspended band of spinothalamic sensory loss) When a viral illness occurs in close temporal associa- Urinary retention tion, parainfectious myelitis is often diagnosed, but Signs consistent with but not diagnostic of myelopathy the causal role of the associated infection is difficult Glove-and-stocking sensory loss (consider peripheral to determine for an individual patient. One can con- neuropathy) fidently link the two only when myelitis occurs con- Hyporeflexia/hypotonia (consider peripheral neuropathy) currently or within days of an infection known to be Unilateral or bilateral upper motor neuron signs (consider associated with myelitis (e.g., zoster) or when investi- brain or brainstem disorders) gation such as CSF PCR demonstrates unequivocal Signs suggesting alternative diagnosis evidence of CNS infection. Spasms, rather than spasticity (consider stiff-person syndrome) Nevertheless, serologic evidence of recent infection

Paratonic rigidity (consider frontal lobe disorder) with pathogens known to be associated with myelopa-

Cognitive impairment (consider frontal lobe or diffuse brain thy (e.g., enteroviruses, Chlamydia, Mycoplasma) may disorder) limit the need for further diagnostic investigations in an Dysarthria and dysphagia (consider brainstem disorder, such otherwise unexplained myelopathy. Features suggesting as motor neuron disease) an infectious etiology include fever, rash (zoster, entero- virus, Lyme disease), meningismus, a history of recent travel (tuberculosis, parasitic infections such as schisto- suspected. Patients with myelopathy who have no somiasis with travel to endemic regions), suspected ra- clear lesion on spinal MRI or multiple chronic- bies exposure, or immunosuppression (herpes zoster, appearing lesions should be questioned to uncover cytomegalovirus). It is particularly important to con- subtle previous symptoms of chronic myelopathy sider treatable infections such as syphilis, HIV, tubercu- and examined to detect cognitive or bulbar impair- losis, Lyme disease, and herpesviruses. ment localizing elsewhere in the nervous system. Occasionally patients with WHEN IT IS AN ACUTE MYELOPATHY, WHAT CAUSES SHOULD BE CONSIDERED? In pa- chronic myelopathy may tients with recent onset symptoms, particularly ones present a history that that evolve rapidly, the initial priority is to exclude a surgical emergency such as epidural metastasis or ab- mistakenly suggests an acute scess. When the index of suspicion for an acute com- process pressive lesion is high, immediate imaging is required, ideally with MRI of the entire spine. If im- Other diagnoses that may be made confidently in aging demonstrates spinal cord compression due to most instances include cord compression, vascular an acute lesion such as epidural metastasis, definitive disorders, toxic/metabolic syndromes, neoplasm, management (i.e., surgery) should be pursued with- paraneoplastic syndromes, and sarcoidosis. Although out delay to prevent rapid and irreversible worsening. compression is often obvious as the cause of myelop- Often the cause of an acute or subacute myelopa- athy on MRI, spinal stenosis may cause impressive thy is inapparent after an initial evaluation. In a re- and occasionally longitudinally extensive T2 signal cent French series of patients presenting with acute abnormalities (Ն3 vertebral segments) on spinal noncompressive myelopathy, 101/170 (59.4%) were MRI that may lead one to suspect an inflammatory of uncertain cause initially, although 55/101 myelopathy. Circumscribed gadolinium enhance- (54.4%) patients were ultimately diagnosed with a ment at the point of maximal stenosis and a history demyelinating or inflammatory disorder. After aver- of progressive symptoms over many weeks to months age follow-up of 73.2 months, 49/170 (28.8%) had a are consistent findings in such cases (figure 1, A and final diagnosis of myelopathy of uncertain etiology. B).2 Vascular myelopathies include those due to in- The most commonly identified causes were demyeli- farction resulting from arterial embolism or hypo- nating disorders (MS and neuromyelitis optica), spi- perfusion, hemorrhage, or vascular malformations nal cord infarction, parainfectious myelitis, and associated with venous hypertension. Dural arterio-

Neurology: Clinical Practice 75(Suppl 1) November 2, 2010 S3 Figure 1 MRI of representative cases of acute and subacute myelopathies

(A, B) Sagittal T2 and gadolinium-enhanced T1 MRI showing longitudinally extensive cord signal change (A) and focal signet ring gadolinium enhancement (B) due to severe spinal stenosis. (C) Sagittal T2 and axial gadolinium-enhanced T1 (inset) MRI demonstrating longitudinally extensive, tract-specific lateral column enhancement due to paraneoplastic disorder in a patient with renal cell carcinoma. (D) Sagittal gadolinium-enhanced T1 and axial T2 (inset) MRI demonstrating focal enhancement and T2 signal change in the periphery of the cord in a patient with partial transverse myelitis due to multiple sclerosis. (E) Sagittal T2 and axial gadolinium-enhanced T1 (inset) MRI showing longitudinally extensive transverse myelitis extending rostrally into the me- dulla and central cord enhancement due to neuromyelitis optica–associated myelitis. (F) Sagittal and axial T2 (inset) MRI showing anterior cord signal change due to anterior spinal artery infarct. (G) Sagittal and axial T2 (inset) MRI, longitudinally extensive signal change extending to the conus and flow voids (eccentric to the left side of the cord) characteristic of dural arteriovenous fistula. (H) Sagittal and axial gadolinium-enhanced T1 (inset) MRI demonstrating nodular and subpial enhancement due to sarcoidosis.

S4 Neurology: Clinical Practice 75(Suppl 1) November 2, 2010 Figure 2 Differential diagnosis of acute myelopathy: Time course and MRI findings

*Relapses upon withdrawal of corticosteroids/immunosuppression. **MRI may be normal. ADEM ϭ acute disseminated encephalomyelitis; DAVF ϭ dural arteriovenous fistula; HTLV ϭ human T-lymphotropic virus; MS ϭ multiple sclerosis; NMO ϭ neuromyelitis optica; SCD ϭ subacute combined degeneration; SD ϭ systemic disease; TM ϭ transverse myelitis. venous fistula (DAVF)–associated myelopathies may tract-specific involvement. Sarcoidosis may present be distinguished by the distinctive history of stepwise as isolated myelopathy. Definitive diagnosis requires progression or transient worsening precipitated by biopsy evidence of noncaseating granulomatous inflam- walking or prolonged standing. This myelopathy can mation, either from the nervous system or other in- be successfully treated by obliteration of the fistula volved organs. A high serum angiotensin-converting and should not be missed. Toxic myelopathy due to enzyme level is suggestive but nonspecific. A diagnosis nitrous oxide abuse is a consideration in younger pa- of isolated CNS sarcoidosis should be suspected when tients and medical professionals; patients with under- subacute myelopathy is accompanied by patchy, asym- lying vitamin B12 deficiency are particularly metric, slowly evolving, and persistently enhancing gad- vulnerable. Vitamin and trace metal deficiencies usu- olinium cord lesions. A satisfactory therapeutic response ally cause chronic myelopathies, but as these etiolo- to empiric, long-term (months to years) corticosteroid gies are readily treatable, vitamin B12 and copper treatment provides a reasonable basis for a tentative but levels should be tested in unexplained steroid nonre- usually correct diagnosis. sponsive myelopathy. Spinal cord tumors may present subacutely or with apoplectic onset in the WHAT CLINICAL FEATURES SUGGEST A PAR- case of hemorrhage into tumor and are usually TICULAR DIAGNOSIS? The time course (figure readily identifiable on MRI, although rarely they 2), specific spinal cord syndrome, and symptoms may be mistaken radiologically for myelitis. Screen- other than those referable to the spinal cord may pro- ing for serum paraneoplastic autoantibodies includ- vide useful clues as to the diagnosis. Apoplectic onset ing collapsin response mediator protein-5 (CRMP-5) suggests a cord infarct or spinal hemorrhage, both of antibody3 should be considered in patients with which may worsen over hours to days. Parainfectious known cancer, constitutional symptoms, smoking or idiopathic myelitis, myelitis related to inflamma- history, or suggestive neuroradiology with isolated, tory demyelinating diseases, and some paraneoplastic

Neurology: Clinical Practice 75(Suppl 1) November 2, 2010 S5 aging signs of central cord involvement than does Table 2 Utility of diagnostic tests in evaluation of myelopathy MS-associated myelitis, which more commonly af- Test used to evaluate for: Sensitivitya Specificitya fects the periphery of the cord. Highly selective tract

Imaging studies involvement (e.g., pure corticospinal tract involve-

Spinal MRI Rule out compression, ؉؉؉ ؉؉ ment), especially when confirmed by MRI evidence define etiology of highly localized enhancing tractopathy, is charac- .(Brain MRI MS ؉؉ ؉ teristic of a paraneoplastic disorder (figure 1C -CT myelogram Cord compression ؉؉؉ ؉ Neurologic or constitutional symptoms not refer

-Spinal angiogram DAVF ؉؉ ؉؉؉ able to the spinal cord focus the differential diagno

CSF studies sis, but may be irrelevant and distract one from the true

-Oligoclonal bands MS ؉؉ ؉؉ diagnosis. Optic neuritis or a prior diagnosis of inter mediate uveitis may suggest MS. Severe optic neuri- IgG index MS ؉؉ ؉؉ tis and an episode of unexplained intractable nausea PCR for herpesviruses CNS herpesvirus infection ؉؉ ؉؉؉ or hiccoughs are characteristic of NMO.5 Coexist- ؉ ؉؉؉ Cytology Intramedullary neoplasm ing peripheral neuropathy can occur in sarcoid, Serologic and other blood tests Sjo¨gren syndrome, lupus, metabolic disorders (e.g., subacute combined degeneration), and para- NMO IgG NMO ؉؉ ؉؉؉ neoplastic syndromes. Antinuclear, SS, Systemic inflammatory ؉؉ anticardiolipin antibodies disease, NMO

-Angiotensin converting Sarcoidosis ؉؉ ؉ WHAT INVESTIGATIONS SHOULD BE PER enzyme FORMED? MRI scan of the spinal cord with and Serologies for infectious Parainfectious or infectious ؉؉؉ agents myelopathy without gadolinium contrast is the initial investiga- tion of choice in the evaluation of acute myelopathy. Electrodiagnostic studies Contraindications are limited to MRI-incompatible EMG Myelopathy associated with ؉؉ ؉ peripheral neuropathy (e.g., ferromagnetic medical devices or foreign bodies and sarcoid, Sjögren, paraneoplastic) incompatibility with the scanner due to habitus. With careful coordination between cardiologists and ϭ ϭ ϭ Abbreviations: DAVF dural arteriovenous fistula; IgG immunoglobulin G; MS multiple radiologists, MRI can be performed in selected pa- sclerosis; NMO ϭ neuromyelitis optica; SS ϭ Sjögren syndrome. a The symbols ϩ, ϩϩ, and ϩϩϩ indicate low, intermediate, and high sensitivity/specificity, tients with cardiac pacemakers who are not entirely respectively. pacemaker-dependent. For patients unable to undergo MRI, CT myelography may be considered syndromes evolve over days to weeks, but generally when cord compression is suspected. CSF evaluation reach a nadir within 3 weeks, after which there is including cell count, glucose, protein, oligoclonal either improvement or stability.4 When a myelopa- bands, immunoglobulin G (IgG) index, and cytology thy develops insidiously or continues to progress af- is appropriate unless imaging, history, and examina- ter 3 weeks, transverse myelitis becomes unlikely and tion already suggest a clear diagnosis. The results of the differential diagnosis includes an intrinsic cord spinal MRI and clinical suspicion should guide the tumor, compressive lesion, DAVF, metabolic de- selection of additional investigations (table 2). rangement, sarcoidosis, or a degenerative process. For noncompressive myelopathy, the results of The clinical syndrome of spinal cord involvement MRI can be broadly subdivided into 3 categories: may suggest a particular etiology, although none are 1. Short T2 hyperintensity (Ͻ3 vertebral segments specific. Incomplete Brown-Se´quard syndrome (loss in length). of pain and temperature sensation contralateral to weakness) may be associated with either compression Focal, discrete lesions that do not occupy the en- or an intrinsic cord lesion such as demyelination. An tire cord in axial cross-section are highly sugges- anterior spinal cord syndrome with bilateral cortico- tive of MS (figure 1D), although remote, spinal and spinothalamic involvement sparing dorsal sometimes forgotten trauma can occasionally pro- column function is typical of anterior spinal artery duce such lesions. MRI scan of the brain may help distribution infarction, but may also occur in MS. A to clarify the cause; detection of 1 or more brain complete spinal cord syndrome with bilateral in- lesions typical of MS (discrete periventricular, volvement of all spinal tracts is rarely caused by an juxtacortical, or infratentorial T2 hyperintense MS relapse or infarct, but may occur in idiopathic or foci) correlates with at least an 85%–90% future neuromyelitis optica (NMO)–associated transverse risk of developing MS.6 Oligoclonal bands and myelitis or cord compression. NMO-associated my- elevated CSF IgG index help to confirm a sus- elitis more commonly presents with clinical and im- pected MS diagnosis, but CSF analysis may be

S6 Neurology: Clinical Practice 75(Suppl 1) November 2, 2010 superfluous if other clinical and radiographic fea- months) gadolinium enhancement or menin- tures are highly suggestive. geal and nerve root enhancement suggest sarcoidosis (figure 1H) or, rarely, lymphoma. 2. Longitudinally extensive T2 hyperintensity (Ն3 vertebral segments in length). 3. Normal MRI.

Longitudinally extensive transverse myelitis oc- Patients with suspected myelopathy and appar- curs in idiopathic transverse myelitis, NMO (fig- ently normal MRI should undergo careful review ure 1E), acute disseminated encephalomyelitis, of the images for subtle findings of cord signal cord infarction, and myelitis associated with sys- change, atrophy, or extrinsic compression by un- temic diseases such as systemic lupus erythemato- common causes (e.g., epidural lipomatosis). If ex- sus. Serum NMO IgG testing is indicated before amination demonstrates unequivocal evidence of assigning a diagnosis of idiopathic transverse my- a spinal cord process and the MRI is normal, con- elitis.7 Brain lesions on MRI eventually occur in sider and test for degenerative, infectious, and the majority of patients with NMO, but usually metabolic causes of myelopathy. EMG and nerve NMO does not lead to the discrete Dawson finger conduction studies occasionally help to identify a pattern of periventricular lesions characteristic of primary peripheral process (e.g., AIDP) or my- MS. However, confluent and linear lesions encir- elopathy associated with concomitant peripheral cling the ventricles may occur in NMO. CSF oligo- neuropathy as can be seen in sarcoidosis and sub- clonal bands are usually absent in NMO. acute combined degeneration. Certain patterns of signal abnormality on MRI predict a vascular disorder. Anterior and central HOW SHOULD AN ACUTE MYELOPATHY BE cord signal change and swelling with sparing of TREATED? Controlled studies of treatment of acute the posterior columns suggest infarct, particularly myelitis are lacking. In myelitis due to demyelinat- in patients with a suggestive history (figure 1F). ing, inflammatory, or undetermined cause, expert Posterior flow voids on spinal MRI representing consensus favors high-dose IV corticosteroids, typi- dilation of the epidural venous plexus are a fairly cally 1 gram of IV methylprednisolone daily for 5 specific but less sensitive indicator of DAVF, days. This treatment should not be withheld in the whereas longitudinally extensive gadolinium en- case of suspected recent viral infection; the role of ste- hancement and T2 hyperintensity often extend- roid treatment in patients with definitive evidence for ing to the conus are typical but nonspecific direct viral infection of the cord (e.g., myelitis occurring findings (figure 1G). Magnetic resonance angiog- simultaneously with or within days of a zoster eruption) raphy may help to visualize a DAVF, but spinal is unclear. Plasmapheresis should be considered in pa- angiography is required for definitive diagnosis tients who continue to have significant impairment af- and treatment. ter high-dose corticosteroids. In a sham-controlled trial If symptoms suggestive of recent infection or CSF of plasma exchange in patients with an acute relapse of pleocytosis (Ͼ50 leukocytes/␮L) are present, demyelinating disease unresponsive to corticosteroid CSF PCR testing for herpesviruses (e.g., herpes treatment, many of whom had acute myelitis, 8 of 19 simplex, cytomegalovirus, varicella zoster) and se- (42.1%) treated patients experienced moderate to rologic testing for HIV, syphilis, and Lyme dis- marked improvement vs 1 of 17 (5.9%) who received ease should be considered. Prominent CSF sham treatment.9 There are no established treatments pleocytosis and occasionally neutrophilic pleocy- for patients with cord infarction. tosis may occur in myelitis associated with NMO. Long-term treatment to reduce recurrent attacks or Symptoms and signs of systemic inflammatory progression of deficit is required for patients with disease such as polyarthritis should prompt auto- NMO, neurosarcoidosis, and systemic inflammatory immune serologic testing (i.e., antinuclear anti- disorders. Options to be considered for NMO include bodies, SS-A, SS-B antibodies). In the absence of azathioprine, mycophenolate mofetil, mitoxantrone, clinical indications of these diseases, positive sero- and rituximab. Sarcoidosis is usually treated with pro- logic tests may be unimportant, although they may longed high-dose oral corticosteroids (e.g., prednisone 1 indicate NMO; a quarter of NMO spectrum disor- mg/kg/day for 6–12 months). Oral steroids and der patients have nonspecific serologic evidence of steroid-sparing immunosuppressive agents are also typi- autoimmunity, usually in the absence of clinical cally prescribed when systemic inflammatory processes signs of other autoimmune disorders.8 Indiscrimi- involve the nervous system. Immunomodulatory treat- nate use of autoantibody testing in all patients ment should be considered in patients who are at high with myelitis is not recommended. MRI find- risk for developing relapsing-remitting MS by virtue of ings including nodular and persisting (Ͼ2 having additional lesions on MRI of the head.

Neurology: Clinical Practice 75(Suppl 1) November 2, 2010 S7 Ongoing clinical observation is an important part Received July 14, 2010. Accepted in final form September 2, 2010. of the care of patients with an unexplained myelopathy. Subsequent appearance of new neurologic or REFERENCES systemic symptoms may reveal a demyelinating or 1. Debette S, de Seze J, Pruvo JP, et al. Long-term outcome systemic inflammatory disorder. Patients with relent- of acute and subacute myelopathies. J Neurol 2009;256: lessly progressive symptoms despite appropriate em- 980–988. piric treatment may require spinal cord biopsy for 2. Kelley BJ, Erickson BJ, Weinshenker BG. Compressive myelopathy mimicking transverse myelitis. Neurologist definitive diagnosis, particularly when follow-up im- 2010;16:120–122. aging demonstrates worsening. 3. Keegan BM, Pittock SJ, Lennon VA. Autoimmune myelopathy associated with collapsin response-mediator DISCUSSION Acute and subacute myelopathies re- protein-5 immunoglobulin G. Ann Neurol 2008;63:531– quire urgent medical evaluation. Imaging, preferably 534. by MRI, should be performed without delay to ex- 4. Proposed diagnostic criteria and nosology of acute trans- clude a compressive lesion. Subsequently, history and verse myelitis. Neurology 2002;59:499–505. physical examination should guide subsequent inves- 5. Takahashi T, Miyazawa I, Misu T, et al. Intractable hiccup tigations to reach a definitive diagnosis. As the etiol- and nausea in neuromyelitis optica with anti-aquaporin-4 antibody: a herald of acute exacerbations. J Neurol Neuro- ogy is often unclear at initial presentation, empiric surg Psychiatry 2008;79:1075–1078. treatment should be provided while conducting fur- 6. Brex PA, Ciccarelli O, O’Riordan JI, Sailer M, Thompson ther investigations to determine the etiology of my- AJ, Miller DH. A longitudinal study of abnormalities on elopathy. A thorough evaluation often reveals MRI and disability from multiple sclerosis. N Engl J Med evidence of a treatable disorder or one that may re- 2002;346:158–164. lapse without preventive treatment. 7. Weinshenker BG, Wingerchuk DM, Vukusic S, et al. Neuromyelitis optica IgG predicts relapse after longitudi- DISCLOSURE nally extensive transverse myelitis. Ann Neurol 2006;59: 566–569. Dr. Schmalstieg reports no disclosures. Dr. Weinshenker has served on 8. Pittock SJ, Lennon VA, de Seze J, et al. Neuromyelitis data safety monitoring boards for Novartis and Biogen Idec; serves on the optica and non organ-specific autoimmunity. Arch Neurol editorial boards of Multiple Sclerosis, the Canadian Journal of Neurological 2008;65:78–83. Sciences, and the Turkish Journal of Neurology; receives research support from the Guthy-Jackson Charitable Foundation; and receives license roy- 9. Weinshenker BG, O’Brien PC, Petterson TM, et al. alties from RSR Ltd. and may receive royalties from Mayo Medical Ven- A randomized trial of plasma exchange in acute central tures for a patent/intellectual property re: Aquaporin-4 associated nervous system inflammatory demyelinating disease. Ann antibodies for diagnosis of neuromyelitis optica. Neurol 1999;46:878–886.

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S8 Neurology: Clinical Practice 75(Suppl 1) November 2, 2010 Approach to acute or subacute myelopathy William F. Schmalstieg and Brian G. Weinshenker Neurology 2010;75;S2-S8 DOI 10.1212/WNL.0b013e3181fb3638

This information is current as of November 1, 2010

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References This article cites 9 articles, 2 of which you can access for free at: http://n.neurology.org/content/75/18_Supplement_1/S2.full#ref-list-1 Citations This article has been cited by 4 HighWire-hosted articles: http://n.neurology.org/content/75/18_Supplement_1/S2.full##otherartic les Subspecialty Collections This article, along with others on similar topics, appears in the following collection(s): All Demyelinating disease (CNS) http://n.neurology.org/cgi/collection/all_demyelinating_disease_cns All Spinal Cord http://n.neurology.org/cgi/collection/all_spinal_cord MRI http://n.neurology.org/cgi/collection/mri Transverse myelitis http://n.neurology.org/cgi/collection/transverse_myelitis Permissions & Licensing Information about reproducing this article in parts (figures,tables) or in its entirety can be found online at: http://www.neurology.org/about/about_the_journal#permissions Reprints Information about ordering reprints can be found online: http://n.neurology.org/subscribers/advertise

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