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clinical practice

Transverse Myelitis
Elliot M. Frohman, M.D., Ph.D., and Dean M. Wingerchuk, M.D.

This Journal feature begins with a case vignette highlighting a common clinical problem.
Evidence supporting various strategies is then presented, followed by a review of formal guidelines,
when they exist. The article ends with the author’s clinical recommendations.

An otherwise healthy 28-year-old woman presents to the emergency department

with progressive weakness that began 3 days earlier. She reports difficulty walking,
numbness in the body below her breasts, and urinary urgency, and she notes that
neck flexion triggers an electrical sensation that radiates to the coccyx. Physical ex-
amination reveals moderate paraparesis with hyperreflexia, a left extensor plantar
response, impairment of vibratory and proprioceptive sensation, and a sensory level
at T6. Magnetic resonance imaging (MRI) reveals a lower cervical cord lesion that
enhances after gadolinium administration, a finding that is consistent with trans-
verse myelitis. How should she be further evaluated and treated?

The Cl inic a l Probl em

From the Departments of Neurology and The term “transverse myelitis” describes a heterogeneous group of inflammatory
Ophthalmology, University of Texas South­ disorders that are characterized by acute or subacute motor, sensory, and auto-
western Medical Center at Dallas, Dallas
(E.M.F.); and the Department of Neurol­ nomic (bladder, bowel, and sexual) spinal cord dysfunction (Table 1).1 The clinical
ogy, Mayo Clinic, Scottsdale, AZ (D.M.W.). signs are caused by an interruption in ascending and descending neuroanatomical
Address reprint requests to Dr. Frohman pathways in the transverse plane of the spinal cord, and a resulting sensory level is
at the Department of Neurology, Uni­
versity of Texas Southwestern Medical characteristic of the syndrome. The transverse myelitis syndrome may arise from
Center at Dallas, 5323 Harry Hines Blvd., various causes, but it most often occurs as an autoimmune phenomenon after an
Dallas, TX 75235, or at elliot.frohman@ infection or vaccination (accounting for 60% of the cases in children) or as a result
utsouthwestern.edu.
of a direct infection, an underlying systemic autoimmune disease, or an acquired
N Engl J Med 2010;363:564-72. demyelinating disease such as multiple sclerosis or the spectrum of disorders re-
Copyright © 2010 Massachusetts Medical Society. lated to neuromyelitis optica (Devic’s disease, a demyelinating disease that is de-
fined by transverse myelitis and optic neuritis).2-7 However, after detailed evalua-
tion, 15 to 30% of the cases of transverse myelitis are ultimately categorized as
idiopathic.5,8
Estimates of the annual incidence of idiopathic or postinfectious transverse
myelitis range from 1.3 to 8 cases per million. Although the disorder can develop
An audio version
at any age, there is a bimodal peak in the incidence at 10 to 19 years of age and
of this article
is available at at 30 to 39 years.9,10 The incidence increases to 24.6 cases per million annually if
NEJM.org acquired demyelinating causes, especially multiple sclerosis, are included.11 There
is no clear pattern among cases of idiopathic transverse myelitis with respect to
sex, geographic distribution, or familial susceptibility.
The pathological hallmark of transverse myelitis is the presence of focal collec-
tions of lymphocytes and monocytes, with varying degrees of demyelination, axonal
injury, and astroglial and microglial activation, within the spinal cord.2 Neuro-
myelitis optica lesions contain deposits of immunoglobulin and complement
around small blood vessels, and necrosis can be observed in severe cases.7 The
observation that systemic infection or immunization precedes many cases of trans-

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 clinical pr actice

verse myelitis suggests that mechanisms such

Table 1. Diagnostic Criteria for Transverse Myelitis.*
as molecular mimicry and the development of
autoantibodies may play roles in the pathogen- Bilateral (not necessarily symmetric) sensorimotor and autonomic spinal
esis of the syndrome.2,4 cord dysfunction
The prognosis after an attack of transverse Clearly defined sensory level
myelitis is highly variable among both adults and Progression to nadir of clinical deficits between 4 hours and 21 days after
children.8,11,12 Patients who have an attack of symptom onset
transverse myelitis associated with multiple scle- Demonstration of spinal cord inflammation: cerebrospinal fluid pleocytosis or
elevated IgG index,† or MRI revealing a gadolinium-enhancing cord lesion
rosis may have a substantial or even complete
recovery, but patients with transverse myelitis or Exclusion of compressive, postradiation, neoplastic, and vascular causes
neuromyelitis optica associated with other dis-
* Clinical events that are consistent with transverse myelitis but that are not as­
eases usually have clinically significant residual sociated with cerebrospinal fluid abnormalities or abnormalities detected on
neurologic deficits. Most of the recovery occurs MRI and that have no identifiable underlying cause are categorized as possi­
over the course of the first 3 months after the ble idiopathic transverse myelitis.
† The IgG index is a measure of intrathecal synthesis of immunoglobulin and is
event, although improvement may continue for a calculated with the use of the following formula: (CSF IgG ÷ serum IgG) ÷ (CSF
year or longer. In one study of idiopathic myelitis, albumin ÷ serum albumin), where CSF denotes cerebrospinal fluid.
more than one third of the patients had a rapidly
progressive course with a poor outcome (death
or inability to ambulate). The combination of radiate down the spine or limbs with neck flex-
severe weakness, hypotonia, and areflexia — ion) and paroxysmal tonic spasms (involuntary
“spinal shock” — was the only recognized pre- dystonic contractions of limb or trunk muscles).
dictor of a poor outcome.8 Urinary incontinence or retention, bowel inconti-
nence or constipation, and sexual dysfunction are
S t r ategie s a nd E v idence common but vary in severity among patients.
Once the clinical syndrome of myelopathy is
Diagnosis recognized, a knowledge of basic spinal cord
A history of motor weakness, sensory abnormal- anatomy and vascular supply helps to guide the
ities referable to the spinal cord, and bladder or differential diagnosis, which includes compres-
bowel dysfunction point to the diagnosis of my- sive, vascular, metabolic, neoplastic, and other
elopathy. Symptoms and signs of transverse my- causes (see Fig. 1 in the Supplementary Appen-
elitis typically evolve over the course of hours to dix, available with the full text of this article at
days and are usually bilateral; however, unilateral NEJM.org). Figure 1 provides a systematic ap-
or markedly asymmetric presentations can occur.1 proach to the evaluation of myelopathy.1-3 As a
Transverse myelitis is sometimes manifested as first step, MRI is warranted to rule out the pres-
rapid-onset, severe paraparesis or quadriparesis ence of structural lesions, especially those ame-
with areflexia, which may lead to diagnostic con- nable to urgent neurosurgical intervention. The
fusion with other causes of ascending weakness, entire spinal cord should be imaged so that false
such as the Guillain–Barré syndrome; otherwise, negative results that may be caused by mislead-
hyperreflexia and Babinski signs are present, con- ing localizing signs, such as a thoracic sensory
firming a central rather than a peripheral cause level caused by a cervical lesion, can be avoided.
of the muscle weakness. A well-defined truncal The finding of an intrinsic cord lesion (some-
sensory level, below which the sensation of pain times more than one) is characteristic of myelitis;
and temperature is altered or lost, distinguishes in the acute phase, such lesions usually enhance
myelopathy from cerebral lesions and peripheral with intravenous gadolinium administration. An
neuropathies. Neuropathic pain may occur in the assessment of the spinal cord syndrome at pre-
midline (an aching, deep pain) or in a dermato- sentation, together with an evaluation of the
mal distribution (radicular or lancinating pain or number, size, and shape of lesions detected on
a sensation of burning or itching), with the latter MRI, provides the basis for determining whether
pattern providing a clue to the anatomical level the lesion is consistent with myelitis. Lesions as-
of the lesion. Demyelination is responsible for the sociated with idiopathic transverse myelitis usu-
presence of Lhermitte’s sign (paresthesias that ally span at least two vertebral segments, as vi-

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 The n e w e ng l a n d j o u r na l of m e dic i n e

Clinical presentation: Acute myelopathy

MRI of entire spine with gadolinium

Compressive lesion?

No Yes

Confirm myelitis Neurosurgical consultation

Intramedullary cord lesion?

No Yes

Reconsider myelopathy diagnosis Gadolinium-enhanced lesion on MRI?

Consider acute presentation of Pleocytosis on CSF examination?
metabolic or degenerative Increased IgG index on CSF exami-
myelopathy nation?
Consider repeat MRI in 2–7 days

No Yes

Consider noninflammatory
Determine cause of myelitis
myelopathies
Consider repeat MRI
in 2–7 days
Test for infection
Test for systemic inflam-
matory or autoimmune
disease
Test for cancer

Negative Positive

Further evaluate pattern Specific diagnosis

of myelitis and therapy

Partial TM Longitudinally extensive TM

Demyelination on brain MRI MRI of brain: neuromyelitis optica

Oligoclonal bands or increased spectrum disorder pattern, normal,
IgG index in CSF or not meeting MS criteria
Visual evoked potentials abnormal Positive for NMO-IgG (aquaporin-4
antibodies)

Yes All negative No Yes

High risk for MS Low risk for MS Reconsider history Neuromyelitis optica
spectrum disorder

Antecedent infection Antecedent vaccination

No Yes No Yes

Idiopathic TM Postinfectious TM Idiopathic TM Postvaccination TM

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 clinical pr actice

of multifocal cerebral involvement.4 Multiple scle-

Figure 1 (facing page). Diagnostic Algorithm for the
Evaluation of Acute Myelopathies and Myelitis. rosis is associated with short lesions (spanning
A systematic approach to the evaluation of acute mye­ fewer than two vertebral segments) that are lo-
lopathy syndromes allows for early identification of cases cated in the periphery of the cord, affecting
requiring emergency neurosurgical treatment and pro­ mainly white matter (“partial” transverse myeli-
vides the highest probability of establishing the specific tis) (Fig. 2), and there is usually concomitant
diagnosis of transverse myelitis, as well as determining
MRI evidence of demyelinating brain lesions.17
the cause of the syndrome. CSF denotes cerebrospinal
fluid, MRI magnetic resonance imaging, MS multiple Neuromyelitis optica is strongly associated with
sclerosis, NMO neuromyelitis optica, and TM trans­ longitudinally extensive transverse myelitis, de-
verse myelitis. fined by a lesion that spans three or more verte-
bral segments on MRI.6,7 Such lesions tend to be
sualized on MRI of the spinal cord (Fig. 2). symmetric and situated centrally within the cord
Normal MRI results should prompt a reconsid- (involving both gray and white matter) and may
eration of the diagnosis of myelopathy in favor extend into the brain stem, causing nausea, vom-
of other disorders of the central or peripheral iting, and hiccups (Fig. 2).18,19 Neuromyelitis
nervous system.2,3 optica is specifically associated with the serum
The transverse myelitis syndrome has an ex- autoantibody marker NMO-IgG, which targets
tensive differential diagnosis. The medical his- the astrocytic water channel, aquaporin-4.20,21
tory, medical review of systems, social and travel Identifying the cause of transverse myelitis
history, and general physical examination can facilitates the prediction of the future clinical
provide clues that point toward possible infec- course and informs the decision about whether
tious or paraneoplastic causes, as well as causes to provide prophylaxis against future neurologic
associated with systemic inflammatory or auto- events. The postinfectious, postvaccination, and
immune diseases such as systemic lupus ery- idiopathic forms of transverse myelitis are usu-
thematosus, Sjögren’s syndrome, and sarcoido- ally monophasic syndromes, whereas multiple
sis.1-3,13,14 Implication of a connective-tissue sclerosis and neuromyelitis optica–spectrum dis-
disease (e.g., systemic lupus erythematosus) as orders are relapsing diseases that are associated
the cause of transverse myelitis requires evidence with a high risk of future attacks of transverse
of systemic disease, and the diagnosis should myelitis and other neurologic events. The presence
not be based solely on the presence of serum on MRI of brain lesions that are characteristic of
autoantibodies (e.g., antinuclear antibody or ex- demyelination indicates a high risk of multiple
tractable nuclear antigen), because such antibod- sclerosis after a partial myelitis event (Fig. 2 in
ies may be present in patients with underlying the Supplementary Appendix). Seropositivity for
multiple sclerosis or neuromyelitis optica.15 Clini- NMO-IgG (and to a lesser extent, ssA autoanti-
cal features, laboratory tests, and diagnostic im- body) in a patient with longitudinally extensive
aging options that are helpful in making the transverse myelitis is highly predictive of relaps-
diagnosis are summarized in Table 2, as well as ing disease and, in the case of NMO-IgG, con-
in Table 1 in the Supplementary Appendix. The version to definite neuromyelitis optica, which
occurrence of transverse myelitis after infection can also be associated with abnormalities on
or vaccination does not preclude the need for MRI of the brain (Fig. 2 in the Supplementary
further evaluation, since infection or immuniza- Appendix).22,23 Factors suggesting that a person
tions may also trigger attacks of myelitis in the who has had a myelitis event is at high risk for
context of an underlying disease (especially mul- clinically definite multiple sclerosis or neuromy-
tiple sclerosis or neuromyelitis optica). elitis optica are summarized in Table 1 in the
Transverse myelitis is a common manifesta- Supplementary Appendix.
tion or presenting feature of acquired demyeli-
nating diseases of the central nervous system.16 Management
Among children, it is a frequent characteristic of Initial Immunotherapy
acute disseminated encephalomyelitis, which typ- The goals of therapy during the acute phase of
ically occurs after an infection or immunization myelitis (Table 2 in the Supplementary Appendix)
and is associated with clinical and MRI evidence are to halt the progression and initiate the reso-

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 The n e w e ng l a n d j o u r na l of m e dic i n e

A B C

D E F

Figure 2. Features of Common Myelitis Syndromes on Neuroimaging.

The findings on MRI are a key component of the diagnostic evaluation of transverse myelitis. Acute myelitis events
are associated with a focal lesion within the spinal cord. Panel A shows an example of a lesion associated with idio­
pathic myelitis (sagittal plane, T2 ­weighted sequence). Short­segment lesions, as shown in Panel B (sagittal plane,
T2 ­weighted sequence), and those that are asymmetric, as shown in Panel C (axial plane, T2 ­weighted sequence), are
characteristic of multiple sclerosis. Lesion enhancement after the administration of gadolinium, as shown in Panel D
(sagittal plane, T1­weighted sequence), suggests acute inflammation of the spinal cord. In contrast, a longitudinally
extensive lesion (i.e., one that spans several vertebral segments), as shown in Panel E (sagittal plane, T2 ­weighted
sequence), especially if it extends rostrally into the brain stem and is located centrally within the cord, as in Panel F
(axial plane, T2 ­weighted sequence), is typical of neuromyelitis optica.

lution of the inflammatory spinal cord lesion, or route of administration is lacking. Oral regi-
thereby speeding clinical recovery. Corticosteroids mens may be used in the case of patients with
are the standard first-line treatment; however, relatively mild episodes of myelitis who do not
because there have been no randomized, con- require hospitalization (e.g., in cases associated
trolled trials of corticosteroid therapy of patients with established multiple sclerosis).25,26 Potential
with transverse myelitis, supporting evidence for adverse effects of pulsed corticosteroid therapy
the use of corticosteroids as first-line therapy is include gastrointestinal symptoms, insomnia,
derived from case studies or extrapolation from headache, anxiety, mania, hypertension, hyper-
trials involving patients with multiple sclero- glycemia, and electrolyte disturbances.
sis.1-5,7,17,24,25 Approximately 50 to 70% of pa- Rescue therapy with plasma exchange may
tients have partial or complete recovery and are benefit patients who do not have a response to
ambulatory with or without aid.8,24 High-dose corticosteroids.27-29 In a randomized, crossover
intravenous regimens are typically used (e.g., trial involving 22 patients with idiopathic in-
1000 mg of methylprednisolone daily, generally flammatory demyelinating syndromes (7 of which
for 3 to 5 days),25 although evidence of the supe- were cases of myelitis) that did not respond to
riority of a particular corticosteroid drug, dose, corticosteroids, 42% of the patients had moder-

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 clinical pr actice

Table 2. Concise Differential Diagnosis and Diagnostic Testing for Transverse Myelitis.*

Possible Cause Diagnostic Tests

Infection Blood serologic studies; CSF culture, serologic studies, and PCR; chest radiography
and other imaging as indicated
Systemic autoimmune or inflammatory disease Clinical examination; serologic studies; chest and joint radiography; other tests or
imaging as indicated by history and examination
Paraneoplastic cause Chest radiography, computed tomography, or positron-emission tomography;
comprehensive serum and CSF paraneoplastic antibody panel
Acquired CNS demyelinating disease (multiple Brain MRI with gadolinium enhancement; CSF examination for cell count and differ­
sclerosis, neuromyelitis optica) ential count, oligoclonal bands, and IgG index; tests of visual evoked potentials;
serum NMO-IgG testing
Postinfectious or postvaccination cause History taking that reveals clear, recent history of infection or vaccination; serologic
confirmation of recent infection; exclusion of other causes

* CNS denotes central nervous system, CSF cerebrospinal fluid, NMO neuromyelitis optica, and PCR polymerase chain reaction.

ate to marked improvement during plasma ex- confirm the specific efficacy of therapeutic or
change, as compared with only 5.9% of patients prophylactic interventions in patients with trans-
undergoing a sham procedure.27 Hypotension, verse myelitis; therefore, recommendations are
electrolyte imbalance, coagulopathy, thrombocy- based on observational studies or clinical experi-
topenia, catheter-related thrombosis, and infec- ence with patients who have multiple sclerosis or
tion are recognized complications of plasma other neurologic diseases. Most patients with
exchange. new-onset myelitis are hospitalized for observa-
In an uncontrolled, retrospective study involv- tion and management of their condition.
ing 122 patients with transverse myelitis from
various causes, 56 patients with severe impair- Respiratory and Oropharyngeal Support
ment that did not respond to corticosteroid ther- Transverse myelitis can cause respiratory failure
apy were further treated with plasma exchange, by involving the upper cervical spinal cord and
cyclophosphamide, or both. Plasmapheresis was brain stem7; therefore, regular reassessment of
associated with an improvement among patients respiratory and oropharyngeal functions are re-
who had some remaining sensorimotor function quired during the evolution of myelitis. Dyspnea,
at the nadir of the attack, but patients who had the use of accessory muscles, or a weak cough
complete loss of sensorimotor function gener- requires further evaluation with the use of tests
ally appeared to have improvement only when of respiratory forces and pulmonary function. In-
they were treated with both cyclophosphamide tubation for mechanical ventilation is required
and plasmapheresis. Adjunctive short-term im- for some patients. Dysarthria, dysphagia, or re-
munosuppressive strategies deserve further inves- duced tongue function or gag reflex warrants a
tigation. formal investigation of the patient’s swallowing
Among patients with underlying demyelinat- function to assess the need for the temporary
ing disease, long-term immunomodulatory or placement of a feeding tube, through which ad-
immunosuppressive therapies have been shown equate nutrition can be provided while the risk of
to reduce the risk of future attacks.30,31 A discus- aspiration pneumonia is minimized.
sion of these therapies is beyond the scope of
this article. Motor Weakness and Complications of Immobilization
Administration of low-molecular-weight heparin
Treatment of Symptoms and Complications for prophylaxis against deep-vein thrombosis is
There are several important stabilizing and pre- warranted for all patients with immobility.32 Non-
ventive measures that can be taken to reduce the ambulatory patients benefit from frequent ad-
symptoms and complications of transverse my- justments of their position while they are sitting
elitis (Table 2 in the Supplementary Appendix). or in bed to promote comfort and maintain skin
No data from randomized trials are available to integrity. Collaboration with a physical medicine

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 The n e w e ng l a n d j o u r na l of m e dic i n e

team should be considered so that multidisci- placebo and amantadine for the treatment of fa-
plinary neurorehabilitation can be initiated early.33 tigue associated with multiple sclerosis,44 but larg-
Ambulation can be aided with the use of appro- er, controlled trials are required to corroborate this
priate devices. An oral sustained-release potassi- finding. Stimulants such as dextroamphetamine or
um-channel blocker, 4-aminopyridine, has been methylphenidate are occasionally used to treat se-
shown to improve walking speed in patients with vere, refractory fatigue that occurs after an epi-
multiple sclerosis, possibly by prolonging the du- sode of myelitis, but the usefulness of these agents
ration of the action potential, although this agent in treating patients with myelitis has not been
has not been studied specifically in patients with tested in randomized, controlled trials.
transverse myelitis.34
Genitourinary and Bowel Dysfunction
Abnormalities of Tone The placement of a urethral catheter is usually
Severe myelitis may be associated with hypotonia necessary during the acute phase of transverse
in the acute phase (during spinal shock), but this is myelitis, owing to retention of urine in the blad-
typically followed by the emergence of increased der. After the acute phase, detrusor hyperreflexia
resistance to movement (tonic spasticity), along typically develops and is characterized by urinary
with involuntary muscle spasms (phasic spastic- frequency, urgency, urge incontinence, and the
ity). Spasticity is an adaptive response that can perception of bladder spasms.45 These symptoms
facilitate ambulation, but when it is excessive, are usually reduced with the administration of
painful, or intrusive, it may require treatment anticholinergic agents (e.g., oxybutynin and tolt-
with physical therapy and medications. Data from erodine).30,46 Less frequently, there is inadequate
controlled trials support the benefits of baclofen, relaxation of bladder sphincters during detrusor
tizanidine, and benzodiazepines for the treat- contraction (detrusor–sphincter dyssynergia), re-
ment of patients with spasticity associated with sulting in retention of urine, with an increased
disorders of the brain and spinal cord.35 risk of vesicoureteral reflux, infection, and cal-
culus formation. Urinary symptoms are unreli-
Pain able in differentiating poor bladder compliance
Pain is common during and after an attack of (failure to store urine) from bladder retention.
myelitis and can be caused by direct neural injury Ultrasonographic assessment of residual urine
(neuropathic pain), orthopedic factors (e.g., pain volume in the bladder after voiding is useful to
due to postural derangements or bursitis), spas- rule out urinary retention, but urodynamic studies
ticity, or some combination of these factors. may be required to fully characterize the urinary
Neuropathic pain may respond to treatment with dysfunction.45 Drugs that inhibit α1-adrenergic re-
anticonvulsant agents, antidepressant medica- ceptors can promote urinary sphincter relaxation
tions (tricyclic antidepressants and reuptake in- and bladder emptying in patients with excess
hibitors of serotonin and norepinephrine), non- sphincter activity, but some patients require in-
steroidal analgesics, and narcotics.30,36-40 termittent catheterization to adequately empty
their bladder.47
Fatigue In the acute and chronic phases of transverse
Reduced mobility, medications, pain, and other fac- myelitis, bowel dysfunction is characterized by
tors can contribute to excessive fatigue after an epi- constipation and the risk of impaction, difficulty
sode of myelitis; systematic evaluation and man- with bowel evacuation from the rectal vault, and
agement of the causes of the fatigue are warranted in some cases incontinence, which is usually as-
(Table 2 in the Supplementary Appendix). Phar- sociated with an inadequate bowel program to
macotherapy is reserved for cases in which these reduce constipation and control the timing of
causes have been ruled out or treated.41 Data from defecation.30
randomized, controlled trials have shown the effi- Sexual dysfunction is a frequent consequence
cacy of amantadine for the treatment of fatigue as- of transverse myelitis and may be manifested as
sociated with multiple sclerosis, and in one study 42 reduced genital sensation, pain, reduced ability
— but not another 43 — modafinil was shown to be to achieve arousal, or anorgasmia.48 Therapeutic
beneficial. A randomized, blinded, crossover, pilot options are outlined in Table 2 in the Supple-
study showed that acetyl L-carnitine was superior to mentary Appendix.

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 clinical pr actice

Psychiatric Considerations ratory tests, and an MRI study of the brain, to-
Mood and anxiety disorders are among the most gether with an assessment of the characteristics
common long-term consequences of transverse of the spinal cord lesion, allow for a rapid assess-
myelitis and influence other symptoms, such as ment of the likelihood that the episode of trans-
pain and sexual function. Pharmacotherapy is verse myelitis is associated with an infection, an
commonly prescribed, either alone or in conjunc- underlying systemic disease, or a demyelinating
tion with psychological counseling. disease such as multiple sclerosis. Admission to
the hospital is warranted for observation of the
A r e a s of Uncer ta in t y evolution of the syndrome and for treatment of
the patient. Data from randomized trials to in-
Identifying the cause of transverse myelitis is of- form the treatment specifically for patients with
ten challenging, and in many circumstances the transverse myelitis are lacking; however, on the
cause remains unknown. The yield of several tests basis of clinical experience and trials involving
appears to be low, and there is no consensus re- patients with other demyelinating diseases, high-
garding the optimal evaluation in terms of cost- dose corticosteroids are considered to be the
effectiveness. Data from randomized trials to guide first-line therapy. Assessments by physical and
decisions regarding initial therapy, indications for occupational therapists and treatment of symp-
intensification of treatment, and the optimal toms such as pain and urinary dysfunction are
management of associated symptoms are scarce. indicated. Counseling about the natural history
of transverse myelitis and the prognosis must be
Guidel ine s given on an individual basis, depending on the
cause of the condition (if it is identified), and
Consensus criteria for the diagnosis of transverse patients and families should be offered support
myelitis have been developed.1 However, to our in managing this debilitating condition.
knowledge, there are no professional guidelines Dr. Frohman reports receiving speaking fees from Biogen
for the management of transverse myelitis. Idec, Teva Neuroscience, Bayer, and Novartis and consulting fees
from Biogen Idec, Teva Neuroscience, Abbott, and Genzyme;
and Dr. Wingerchuk, receiving research support from Alexion,
C onclusions a nd Genzyme, Genentech, Organon (now part of Merck), and the
R ec om mendat ions National Multiple Sclerosis Society and consulting fees from
Novartis, Teva Neuroscience, VLST, and the Guthy–Jackson
Charitable Foundation. No other potential conflict of interest
The patient described in the vignette presented relevant to this article was reported.
with classic clinical and neuroimaging manifes- Disclosure forms provided by the authors are available with
tations of acute transverse myelitis. Information the full text of this article at NEJM.org.
We thank Marvin Ruona, Mayo Clinic Media Support Ser-
obtained from the clinical history, an analysis of vices, for assistance with Figure 1 in the Supplementary Ap-
the cerebrospinal fluid, the results of other labo- pendix.

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entry points to clinical content. In each collection, articles are cited in reverse
chronologic order, with the most recent first.

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