CME
JOURNAL OF MAGNETIC RESONANCE IMAGING 00:00–00 (2014)
Review Article
MRI in Transverse Myelitis
Christine Goh, MBBS, FRANZCR,* Patricia M. Desmond, MSc, MD, FRANZCR,
and Pramit M. Phal, MBBS, FRANZCR
Transverse myelitis is an acute inflammatory disease of
the spinal cord, characterized by rapid onset of bilateral
neurological symptoms. Weakness, sensory disturbance,
and autonomic dysfunction evolve over hours or days,
most progressing to maximal clinical severity within 10
days of onset. At maximal clinical severity, half will have
a paraparesis, and almost all patients have sensory dis-
turbance and bladder dysfunction. Residual disability is
divided equally between severe, moderate and minimal or
none. The causes of transverse myelitis are diverse; etiolo-
gies implicated include demyelinating conditions, collagen
vascular disease, and parainfectious causes, however,
despite extensive diagnostic work-up many cases are con-
sidered idiopathic. Due to heterogeneity in pathogenesis,
and the similarity of its clinical presentation with those of
various noninflammatory myelopathies, transverse myeli-
tis has frequently been viewed as a diagnostic dilemma.
However, as targeted therapies to optimize patient out-
come develop, timely identification of the underlying etiol-
ogy is becoming increasingly important. In this review, we
describe the imaging and clinical features of idiopathic
and disease-associated transverse myelitis and its major
differentials, with discussion of how MR imaging features
assist in the identification of various sub-types of trans-
verse myelitis. We will also discuss the potential for
advanced MR techniques to contribute to diagnosis and
prognostication.
Key Words: transverse myelitis; MRI; spinal cord; mye-
lopathy; parainfectious myelitis; neuromyelitis optica
J. Magn. Reson. Imaging 2014;00:000–000.
C 2014 Wiley Periodicals, Inc.
V transverse myelitis. An active inflammatory process
The diagnostic work-up of acute transverse myelopa-
thy first requires emergent MRI cord to exclude acute
cord compression. Further investigation will then
entail contrast enhanced MRI of cord and brain,
serum and CSF analysis (autoimmune markers, auto-
antibodies, microbial serology and PCR), and special-
Department of Radiology, Royal Melbourne Hospital, Parkville,
Melbourne, Australia.
*Address reprint requests to: C.G., Department of Radiology, Royal
Melbourne Hospital, Grattan Street, Parkville, Melbourne, Australia
3050. E-mail: christinegoh79@gmail.com
Received September 8, 2013; Accepted December 19, 2013.
DOI 10.1002/jmri.24563
View this article online at wileyonlinelibrary.com.
C 2014 Wiley Periodicals, Inc.
V 1
ised investigations such as visual evoked response
testing.
The critical initial treatment is often based upon a
presumptive diagnosis made with reference only to
the clinical features, MRI findings and basic CSF
analysis. Specialised investigations such as autoanti-
body testing may have greater specificity, but unfortu-
nately results are not usually available until well after
treatment has been instituted. This underscores the
importance of the careful assessment of MR imaging
appearances in narrowing the differential diagnosis
sufficiently to allow the early institution of the appro-
priate therapy.
Due to the diversity of aetiologies in transverse mye-
lopathy, a thorough understanding the clinical as well
as the imaging features of these conditions assists the
radiologist in their assessment.
GENERAL CONCEPTS
Diagnostic Criteria
The diagnostic criteria proposed by the Transverse
Myelitis Consortium Working Group (1) is outlined in
Table 1. The first requirement is an appropriate clini-
cal picture of bilateral symptoms referable to the spi-
nal cord, evolving to maximal clinical severity between
4 h and 21 days. The lower limit of 4 h onset is
designed to prevent cases of cord infarction, typically
of abrupt onset, from being erroneously diagnosed as
must be confirmed by the presence of a cellular infil-
trate and/or elevated protein on CSF analysis, or by
contrast enhancement on MRI of the spinal cord.
Further criteria divide transverse myelitis into two
main groups. Idiopathic transverse myelitis is a
diagnosis of exclusion, while those cases which are
attributable to underlying processes including demye-
lination (multiple sclerosis, MS; neuromyelitis optica,
NMO), a systemic autoimmune condition such as sys-
temic lupus erythematosus (SLE) and Sjogren’s syn-
drome, or an infectious/parainfectious etiology, are
referred to as disease-associated transverse myelitis.
Longitudinally Extensive Versus Acute Partial
Transverse Myelitis
Although no reference is made by the diagnostic crite-
ria to the length of the cord lesion, distinguishing
between longitudinally extensive transverse myelitis
2 Goh et al.

Table 1
Diagnostic Criteria for Transverse Myelitis*
Inclusion criteria for diagnosis of transverse myelitis (idiopathic or disease associated)
Development of sensory, motor or autonomic dysfunction attributable to the spinal cord
Bilateral symptoms
Clearly defined sensory level
Exclusion of compressive aetiology by MRI or CT myelography
Spinal cord inflammation demonstrated by CSF pleocytosis or elevated IgG or gadolinium enhancement
Progression to clinical nadir between 4 hours and 21 days from onset of symptoms
Exclusion criteria for diagnosis of transverse myelitis (idiopathic or disease associated)
History of radiation to the spine within 10 years
Clear arterial distribution clinical defect consistent with anterior spinal artery occlusion
Abnormal flow voids on the surface of the cord consistent with AVM
Exclusion criteria for idiopathic transverse myelitis
Serologic or clinical evidence of connective tissue disease (sarcoidosis, Behcet’s disease, Sjogren’s syndrome, SLE, mixed connective
tissue disorder)
CNS manifestations of syphilis, Lyme disease, HIV, HTLV-1, Mycoplasma, other viral infection.
Brain abnormalities suggestive of MS
History of clinically apparent optic neuritis

*Transverse Myelitis Consortium Working Group, 2002.

(LETM), which extends over more than three segments
and involves all or most of the cross-section of the
cord, and acute partial transverse myelitis (APTM),
which has less than two segments of eccentric or
asymmetric cord involvement, is a helpful concept in
the search for an underlying etiology and may assist
in prognosis (2,3).
In combination with a normal initial MRI brain,
APTM has 10% risk of progression to clinically definite
multiple sclerosis (MS) over 61 months follow-up (4);
in a longer term study this increases to 21% risk of
progression at 20 years follow up (5). When nonspe-
cific white matter lesions are present in the brain,
there is a higher risk of progression to clinically defi-
nite MS, with rates of up to 88% reported (5).
LETM is associated with a very low rate of conversion
to MS (<2%), but up to 60% will be diagnosed with
NMO. Presence of autoantibodies to aquaporin 4 fur-
ther stratifies risk, with 83% of positive versus 25% of
negative patients going on to a diagnosis of NMO (6).
There is some evidence that the distinction between
LETM and APTM is less useful in the pediatric popula-
tion. Two studies of children with transverse myelitis
found that in children with LETM a higher proportion
(10%) went on to a confirmed diagnosis of MS (7,8).
due to advancements in our understanding of the
pathogenesis of disease associated transverse myelitis,
and as increasingly sensitive and specific microbial
assays and autoimmune markers are developed, idio-
pathic transverse myelitis may in future represent a
lesser proportion of myelopathy presentations (10).
The typical MRI appearance in transverse myelitis is
a central T2 hyperintense spinal cord lesion extending
over more than two segments, involving more than two-
thirds of the cross sectional area of the cord (11–14).
Although any cord level can be affected, the classic
description includes a preference for the thoracic
cord (14).
In half, the involved cord segment is expanded, and
enhancement is present in 37–74% of cases.
Enhancement patterns of lesions are variable: diffuse
enhancement, heterogeneous enhancement, and
peripheral enhancement have all been described.
When diagnostic criteria have not been met due to
lack of enhancement and normal CSF parameters,
follow-up imaging can be helpful, as enhancement
has been reported to be more frequent in the suba-
cute stage than at initial acute presentation (9,11,12).
Multiple Sclerosis

Transverse myelitis remains an uncommon initial pre-

CLINICAL AND IMAGING FEATURES OF
IDIOPATHIC AND DISEASE ASSOCIATED
TRANSVERSE MYELITIS
Idiopathic Transverse Myelitis
Essentially a diagnosis of exclusion, it is not yet clear
that there exists a distinct pathogenetic entity of idio-
pathic transverse myelitis. Idiopathic transverse myeli-
tis comprised 16.5% of acute myelopathy presentations
in one large series (9). However, heterogeneity of patient
demographics, treatment response, and outcome sug-
gests that this diagnosis incorporates several underly-
ing entities. As pointed out in a 2006 editorial in
Neurology entitled “Is the idiopathic form vanishing?”
sentation of MS, an inflammatory demyelinating dis-
order affecting brain, cord, and optic nerves. The
McDonald criteria for diagnosis requires clinical and
MRI evidence of characteristic lesions which are disse-
minated in time and space.
In contrast to transverse myelitis, classic spinal cord
lesions in MS are small, involve less than two seg-
ments, and often dorsolateral in location (Fig. 1) (15).
Active lesions are T2 hyperintense, with contrast
enhancement. Enhancement and cord swelling
decreases in subacute phase, and chronic lesions may
be associated with focal cord thinning. The relapsing
nature of MS helps differentiate MS from transverse
myelitis on imaging follow-up. In the rare cases where
Transverse Myelitis 3

Figure 1. The longitudinally extensive transverse myelitis typical of neuromyelitis optica (B) involves more than three seg-
ments and more than two thirds of the cross-sectional area of the cord, compared with multiple short segment eccentrically
positioned lesions usually seen in multiple sclerosis (A). In some cases, characteristic brain lesions such as hypothalamic
involvement (C, arrows) may assist in the diagnosis of neuromyelitis optica.

transverse myelitis is the first presentation of MS, later
examinations may demonstrate new lesions in cord
and brain. Presence of oligoclonal bands in CSF,
found in more than 80% of patients, supports the diag-
nosis (16).
Neuromyelitis Optica
Compared with MS, this severe relapsing demyelinat-
ing condition is diagnosed at an older age (mean age,
39 years compared with 29 years at diagnosis), has a
greater female predominance and a higher incidence
in the non-white population (17,18). The spinal cord
and optic nerves are the main sites of involvement,
although classic brain lesions have now also been
described. Like MS, NMO is a relapsing disorder, but
attacks are often more severe and result in greater
residual disability. Oligoclonal bands are present in
only 15–30% of NMO cases compared with 85%
of MS cases, and CSF neutrophilia is often
present (17).
Although previously considered to be related to MS,
more recent work on the immunopathogenesis of
NMO has identified an autoantibody to the CNS water
channel protein aquaporin 4, highly specific (91%)
and sensitive (73%) to NMO and correlating with dis-
ease severity (19,20). In 2006, the diagnostic criteria
for NMO were revised to incorporate this new marker
for the disease. In patients with acute myelitis and
optic neuritis, the diagnostic combination of two of
three criteria: NMO IgG positivity, longitudinally
extensive cord lesion, or onset MRI brain nondiagnos-
tic for MS, provides 99% sensitivity and 90% specific-
ity for NMO (21).
In the presence of the NMO autoantibody, patients
with isolated LETM or optic neuritis can be consid-
ered part of a spectrum of NMO disorders, analogous
to the clinically isolated syndrome of MS. In LETM,
patients positive for the NMO autoantibody have a
greater relapse rate and level of disability. A total of
83.3% convert to NMO (60% in the first 2 years from
onset) compared with 25% in those negative for the
autoantibody (6).
On MRI the typical finding is long segment cord
involvement, more commonly unifocal than multifocal
(see Fig. 1). T1 hypointensity within the acute cord
lesion favors NMO over MS, thought to reflect the
greater tissue destruction in NMO. Enhancement and
cord expansion is common in acute lesions (18).
Although myelitis can extend cranially to involve the
brainstem, in the past MRI evidence of noncontiguous
brain involvement at presentation was excluded by
definition. However, it is now recognized that up to
60% will develop nonspecific white matter lesions,
and 10% will have lesions meeting McDonald criteria
for MS (22).
Characteristic T2 hyperintense brain lesions of
NMO occur at sites of high expression of aquaporin 4,
involving hypothalamus and periependymal regions,
typically periaqueductal and about the third and
fourth ventricles (Fig. 1) (23).
Ten to 40% of NMO patients have a coexistent auto-
immune disorder, most commonly SLE, antiphospho-
lipid disorder, and Sjogren’s syndrome, but also
4 Goh et al.
including autoimmune thyroid disease, rheumatoid
arthritis, and myasthenia gravis (24,25).
Systemic Autoimmune Conditions
Transverse myelitis attributed to a systemic autoim-
mune conditions has been most frequently reported in
SLE and antiphospholipid syndrome, but has also
been described in Sjogren’s syndrome, mixed connec-
tive tissue disease, sarcoidosis, Behcet’s disease,
rheumatoid arthritis, and ankylosing spondylitis.
Although an uncommon complication, incidence in
those with connective tissue diseases far exceeds that
of the general population. In one study of acute mye-
lopathy presentations, 16.5% were attributed to a sys-
temic autoimmune condition, and in almost half of
these cases transverse myelitis was the presenting
condition leading to that diagnosis (26).
Historically, pathogenesis of transverse myelitis in
systemic autoimmune conditions has been attributed
to vasculitis and arterial thrombi related to autoim-
munologic phenomena causing ischemic necrosis
within the cord. Autopsy studies in SLE patients have
described perivascular inflammation, and ischemic
necrosis, infarction or myelomalacia of the cord (27).
The more recent understanding of NMO as an auto-
immune disorder and the recognition of that up to
half of NMO patients also meet criteria for systemic
autoimmune conditions have given rise to an alterna-
tive theory: that in many cases transverse myelitis
previously attributed to conditions such as SLE or
Sjogren’s syndrome are due to unrecognized NMO
spectrum disorder (24,28,29).
However, two studies investigating SLE and Sjog-
ren’s patients, respectively, describe divergent clinical
pictures of myelopathy which suggest that, while
coexistent NMO is an important cause of myelopathy
in the setting of systemic autoimmune diseases, there
is also a separate entity of transverse myelitis related
to the underlying vasculitic process (30).
In the largest such cohort studied, Birnbaum et al
(30) found that 22 patients with SLE and myelitis
could be divided on clinical and outcome measures
into two groups. One had a rapid onset (<6 h in
72.7%) of flaccid paralysis, hyporeflexia, and urinary
retention, leading a poor outcome with persistent par-
aplegia, occurring on a background of a febrile pro-
drome, clinical and ESR evidence of active SLE, and
CSF profile of neutrophilia and elevated protein. The
other group had a more subacute onset of spasticity,
hyperreflexia, and mild to moderate weakness over
1 to 30 days, followed by a relapsing course. Rates of
optic neuritis (0% group 1 and 54.5% group 2) and
NMO IgG positivity (12.5% group 1 and 57.1% group
2) were significantly different between the two groups.
Williams and Butler (31), in their review of 17 previ-
ously reported cases of Sjogren’s syndrome and myeli-
tis, were able to distinguish between two distinct
clinical patterns. The first was rapid onset of severe
sensory and motor deficit with neck and interscapular
pain, with high mortality. The second had a subacute
onset of gait, sensory and urinary disturbance pro-
gressing to eventual paraplegia, associated with optic
neuritis in four out of five cases.
Systemic Lupus Erythematosis
CNS manifestations in SLE occur in more than half of
patients, most commonly aseptic meningitis and cere-
brovascular disease. While myelopathy is relatively
uncommon, occurring in less than 3%, it is the initial
presentation in up to half of cases (27,29,32).
Variability in descriptions of the clinical prodrome,
correlation with markers of lupus activity, clinical out-
comes, and imaging features in published cases of mye-
litis in SLE patients may potentially be accounted for by
the differences between SLE-associated myelitis and
NMO. The clinical presentation of SLE-associated myeli-
tis has been described as acute in onset, accompanied
by a short prodrome of fever, headache, and malaise.
CSF protein levels are elevated, without oligoclonal
bands (27,32). Co-existent optic neuritis, described in
21–48%, probably reflects the previously unrecognized
subset of patients with co-existent SLE and NMO.
MRI findings also vary in the literature; as most
reports were published before recent advances in
understanding of NMO, it is unsurprising that most
reports describe long segment central T2 hyperinten-
sity and expansion, with enhancement common but
variable (see Fig. 2). However, MRI of the spinal cord is
normal at presentation in 16–30% of patients with clin-
ical myelitis (32,33) and a few reports describe small
multifocal T2 hyperintense lesions (26,27,30,32).
Sjogren’s Syndrome
The hallmark of this chronic inflammatory exocrinop-
athy is the sicca complex of keratoconjunctivitis sicca,
xerostomia, and salivary gland inflammation, although
any organ system can be affected. Sjogren’s syndrome
can be associated with rheumatoid arthritis and less
commonly other autoimmune disorders such as SLE.
There is marked female predominance with onset usu-
ally in the 5th or 6th decade (34). CNS complications
are described in 25–30% of patient, but transverse
myelitis is rare, occurring in up to 1% of patients with
Sjogren’s syndrome (29,34).
In published cases that describe MRI findings, long
segment central T2 hyperintense cord lesion with
expansion and variable enhancement is the most
commonly described finding, but multifocal lesions
have also been described (26,31,35,36).
Behcet’s Disease
Rare in the Western world, this systemic inflammatory
disease is most prevalent in those of eastern Mediter-
ranean and Middle Eastern descent, with the highest
prevalence in Turkey. Onset is typically at 3rd to 5th
decade, with 2:1 male predominance (37,38).
The hallmark of Behcet’s disease is the triad of uvei-
tis with recurrent oral and genital ulcers. CNS manifes-
tations, reportedly twice as common in male patients,
occur in around 10% and may include meningoence-
phalitis (in 75%) and myelitis (in 10%) and venous
thrombosis (in 18%) (38).
Transverse Myelitis 5

Figure 2. T2, T1, T1 postcontrast weighted sequences and ADC map (A) in a patient with known systemic lupus erythemato-
sis who presented with an acute paraparesis. A longitudinally extensive mid to lower thoracic cord lesion demonstrated lepto-
meningeal and patchy peripheral enhancement. Clinical markers of active SLE and absence of aquaporin 4 antibodies were
consistent with SLE myelitis rather than neuromyelitis optica. Low ADC values within parts of the lesion (arrowhead) are con-
sistent with the ischemic component thought to be part of the pathogenesis of SLE myelitis. Follow-up MRI cord (B) revealed
myelomalacia and gross cord atrophy.

Neuro-Behcet’s disease (NMD) in an acute trans-
verse myelitis presentation may be suspected based
on known history or the presence of uveitis and
ulcers, but is occasionally the presenting condition.
Typically patients have a CSF pleocytosis and elevated
ESR, which correlates with active disease (37).
On MRI of the spinal cord, the typical finding is T2
hyperintense lesions extending over more than two
segments, with preference for the posterolateral cord
(37–39). Myelitis is most often an isolated CNS mani-
festation. However, some cases of spinal involvement
have occurred in combination with meningoencephali-
tis, which typically manifests on MRI as unilateral T2
hyperintensity, edema, and enhancement in the
brainstem, thalamus, and basal ganglia (38).
body type 2 (PCA-2), PCA-1 (antiYo), anti-Ma, and
anti-Ta (40–42). The malignancy is often undiagnosed
at time of presentation and frequently remains occult,
but the combination of the pattern of clinical involve-
ment and autoantibody type can suggest the site of
underlying cancer (40).
In a review of 31 cases of clinically isolated para-
neoplastic myelopathy (41), neuronal autoantibody
was detected in 81%, and cancer was diagnosed after
the myelopathy symptom onset in 67%, with 12
months the median time to cancer detection. One
third of patients had a normal MRI spinal cord. In
48%, MRI showed symmetric T2 hyperintensity in a
tract/gray matter distribution that often showed sym-
metric enhancement.

Paraneoplastic Myelopathy
Paraneoplastic neurological syndromes occur in per-
haps 0.1% of patients with cancer, either affecting an
isolated area or with multifocal involvement which
may include limbic encephalopathy, cerebellar dys-
function, necrotizing myelopathy, inflammatory mye-
lopathy, peripheral neuropathy, or retinopathy. Lung
and breast cancer are most commonly associated, but
hematological and gastrointestinal malignancies have
also been reported.
Many patients with paraneoplastic myelopathy have
identifiable autoantibodies in serum and CSF. Those
which have been associated with myelopathy, often in
association with encephalitis or cerebellar dysfunc-
tion, include amphiphysin antibody, antineuronal
nuclear autoantibody type 2 (ANNA-2 or anti-Ri),
ANNA-3, collapsing response-mediator protein 5,
ANNA-1 (anti-Hu), Purkinje-ell cytoplasmic autoanti-
Neurosarcoidosis
Sarcoidosis is a noncaseating granulomatous disease
whose pathogenesis is not well understood. There is
mild female predominance, with higher incidence and
younger age at onset in the African American than
Caucasian American population. In Europe, incidence
increases in the lower latitudes (43).
CNS involvement in sarcoidosis occurs in up to 10%
of patients, half as part of the presenting illness. Esti-
mated to occur in 6 to 8% of patients with neurosar-
coidosis, spinal sarcoid has been considered relatively
uncommon compared with intracranial manifestations
which may include basal meningitis, cranial neuropa-
thies, encephalopathy and parenchymal masses.
However, more recent studies incorporating MRI find-
ings frequently report spinal involvement (44). In one
study, spinal involvement (43%) was the most
6 Goh et al.
common manifestation in their cohort of 21 patients
with neurosarcoidosis (45).
The most common imaging abnormalities described
on MRI are long segment T2 hyperintense lesions with
patchy enhancement, although nonenhancing lesions
and multifocal short segment lesions have also been
described (Fig. 3). Associated leptomeningeal
enhancement is very common, and extradural mass
lesions and multiple cauda equina lesions have also
been described (45–51).
Parainfectious Transverse Myelitis
Parainfectious myelitis includes infectious myelitis,
where there is direct microbial infection within the
neuroaxis with tissue injury due either to the micro-
bial agent or to the host immune response to the
agent, and postinfectious myelitis which occurs due to
an immune mediated response in the convalescent
phase.
Parainfectious transverse myelitis can be diagnosed
when there is a history of an infectious prodrome
within 4 weeks of the clinical presentation of trans-
verse myelitis, accompanied by culture, serological or
PCR evidence of infection. Up to 40% of cases of pedi-
atric transverse myelitis are preceded by clinical signs
or serological evidence of a systemic infection, most
often viral (13,52). In studies of adult populations,
parainfectious etiology has been attributed to between
6 and 45% of presentations of acute transverse myeli-
tis (14,26,53).
Figure 3. A case of acute trans-
verse myelitis due to neurosarco-
dosis. T2-weighted images
demonstrate multifocal hyperin-
tensity of the cervical to mid tho-
racic cord. There are patchy
areas of enhancement within the
cord, while extensive enhancing
leptomeningeal thickening
extends proximally to involve
brainstem. Note the mediastinal
adenopathy appreciable on the
axial sequences through the tho-
racic cord (arrows).
Distinguishing between infectious and postinfec-
tious myelitis remains challenging. In some cases,
direct microbial infection of the CNS has been con-
firmed by CSF PCR positivity or by histopathological
evidence at biopsy or autopsy. In other cases the diag-
nosis relies on appropriate disease-specific clinical
features with rising serological titers. Implicated
pathogens are numerous, but as viral agents are more
commonly responsible than bacterial and fungal
agents the options for targeted antimicrobial treat-
ment are correspondingly limited.
Three main immune mediated mechanisms have
been described in the pathogenesis of postinfectious
myelitis. In the most common, damage to neuronal
structures is due to similarity between microbial anti-
gens and neuronal cell wall components, referred to
as molecular mimicry. In microbial superantigen medi-
ated infection, microbial peptides bind to a highly
conserved site on the T-cell receptor causing polyclo-
nal activation of T-cells. Humoral derangements may
also play a role, due to bystander activation, polyclo-
nal activation of B-cells, or by deposition of immuno-
complexes in the spinal cord.
These mechanisms are also involved in the pathoge-
nesis of postvaccination myelitis, which remains a
rare complication. Although up to 30% of children
with transverse myelitis have a history of recent vacci-
nation, this reflects high rates of immunization in
children rather than causation. One review found just
43 cases in the literature published between 1970
and 2009 (54), with vaccines for HBV, measles-
Transverse Myelitis
Figure 4. MRI of a patient with acute transverse myelitis fol-
lowing influenza vaccination, demonstrating extensive cen-
tral T2 hyperintensity throughout the thoracic cord with
patchier cervical cord involvement including a more focal
lesion at C4 level. Clinical deficit and MRI changes had
resolved at 3 months follow-up.
mumps-rubella or rubella, diphtheria-tetanus-
pertussis, or tetanus, rabies, oral poliovirus, influ-
enza, typhoid, and Japanese B encephalitis impli-
cated in descending order of frequency.
Findings on MRI of the cord in parainfectious and
postvaccination myelitis are often nonspecific, most
commonly long segment T2 hyperintensity, usually
with some degree of expansion, and often with
enhancement (Fig. 4). Associated leptomeningeal
and/or nerve root enhancement has been described
in many cases of infective myelitis with implicated
pathogens including HSV, EBV, VZV, mycobacterium
tuberculosis, Lyme disease, and parasitic agent.
Many of the infective organisms that have been asso-
ciated with myelitis are outlined in Table 2; when the
site and morphology of lesions or association with
nerve root enhancement may be helpful in suggesting
a causative organism based on imaging findings,
these features have been indicated.
Immunosuppression and Parainfectious Myelitis
In the setting of HIV/AIDS, bone marrow transplant
and immunosuppressive therapy post organ trans-
plant, there is increased risk of cord involvement by
opportunistic infections with CMV, VZV, HSV, toxo-
plasmosis, and tuberculosis (55,56).
Other considerations in HIV/AIDS are HIV myelitis
and vacuolar myelopathy. HIV myelitis often occurs in
7
association with HIV encephalitis and reflects direct
viral infection of the cord with a similar clinical and
imaging appearance to transverse myelitis (57). In
contrast, vacuolar myelopathy is a painless spastic
paraparesis which is slowly progressive and results in
nonenhancing symmetric dorsolateral T2 signal
hyperintensity of the mid to distal thoracic cord on
MRI (58,59).
OTHER CAUSES OF TRANSVERSE MYELOPATHY
Cord Ischemia
Diagnosis is uncomplicated when an abrupt onset of
symptoms is temporally related to an event such as
systemic hypotension, aortic dissection or thoracic
surgery. Severe atherosclerotic disease, vasculitis,
prothrombotic diseases, and endocarditis will increase
clinical suspicion of the diagnosis in the appropriate
clinical context. Embolism of a fibrocartilaginous disc
fragment is a rare cause.
Due to high metabolic demand of cell bodies, gray
matter is the site most sensitive to ischemia. With
increasing severity, ischemia involves the anterior col-
umns, central gray matter, or central cord with a rim
of spared peripheral white matter (60). If performed
immediately, MRI may be normal; T2 hyperintensity
and expansion evolve over hours, with enhancement
developing in the subacute setting (61,62). The mid to
lower thoracic cord is most vulnerable to occlusion of
the artery of Adamkiewicz (63,64), while watershed
ischemia typically involves the mid to upper thoracic
cord (62).
The diagnosis of cord ischemia can be difficult on
imaging grounds alone. In one study, only 45% of
cases had lesions evident on T2-weighted imaging.
When changes are present, the more suggestive
“snake eyes” appearance of bilateral anterior horn
infarction is not common, and a central T2 hyperin-
tense lesion is relatively nonspecific.
Diffusion-weighted imaging (DWI) of the spine
allows a more confident diagnosis of cord ischemia.
Apparent diffusion coefficient (ADC) reduction can be
appreciated as early as 3 h from onset of symptoms
and may last up to a week. Although only small stud-
ies on DWI for cord ischemia have been published,
results suggest confirm its usefulness in the timely
and accurate identification of infarction, with DWI
changes able to precede the evolution of T2 signal
change (65,66).
Spinal cord DWI has not yet been adopted as rou-
tine practice, due to the perceived technical difficul-
ties requiring optimization of specialized pulse
sequences. However, Andre et al demonstrated the
feasibility and clinical utility of DWI by adding to their
routine cord imaging a sagittal reduced field of view
DWI sequence (2 min, 30 s). Of 239 patients, only 16
were excluded due to patient motion or technical diffi-
culties. The DWI sequence increased diagnostic confi-
dence for 11 of 15 pathological subtypes, but was
most useful in evaluation of ischemia, demyelination,
infection, neoplasm, and intradural and epidural
infections (67). Multishot interleaved echoplanar
8 Goh et al.

Table 2
Infective Organisms Implicated in Infectious Transverse Myelitis*
Herpes viruses (91)
Herpes simplex virus 1, 2, 6, 7
Varicella zoster virus
Cytomegalovirus
Epstein Barr virus
Orthomyxoviruses (92)
Influenza A
Paramyxoviruses (93,94)
Measles virus
Mumps virus
Picornaviruses (95–98)
Enterovirus 71
Coxsackie virus A and B
Echovirus
Retroviruses (55,99,100)
HIV
Human T-cell lymphotropic virus
Bacterial (101–106)
Borrelia burgdorferi
Treponema pallidum
Mycoplasma pneumonia
Mycobacterium tuberculosis
Parasites (107–111)
Neurocysticercosis
Schistosomiasis
Gnathostomiasis
T2 signal changes and enhancement are most severe at dorsal root entry zone and posterior horn
of the affected dermatome
Thickening, clumping and enhancement of nerve roots and leptomeninges
Associated long segment cord "T2 signal favours conus
Nerve root and/or leptomeningeal enhancement may be present
Transverse myelitis with long segment "T2 is rare
The more common pattern is poliomyelitis-like syndrome with enhancement and "T2 in the anterior
horns
Consider vacuolar myelopathy rather than myelitis if subacute symptoms and dorsolateral column
involvement
Nerve root enhancement plus cord "T2 signal of adjacent segments. Leptomeningeal enhancement
may be present.
Long segment diffuse "T2 signal with patchy enhancement is relatively rare
Leptomeningeal enhancement may be present
May have areas of #T2 signal or cavitation
Diffuse, nodular or ring-like enhancement
Leptomeningeal and dural enhancement may be present
Intramedullary: cystic lesion that may develop irregular peripheral enhancement and oedema as it
degenerates
Extramedullary: clusters of cystic lesions, or thick irregular leptomeningeal enhancement
"T2 signal and mild to moderate expansion has preference for the distal cord and conus.
Nodular intramedullary or leptomeningeal enhancement and enhancing thickening of nerve roots
may be seen
Enhancement and haemorrhage are common
Scattered intracranial lesions may coexist

*On MRI of the spinal cord, long segment T2 hyperintensity with or without enhancement is the common imaging manifestation of infec-
tious transverse myelitis. Where the location of cord abnormality or associated findings may help to suggest a causative pathogen, these
features have been listed above.

imaging may have better signal to noise ratio (SNR) in identifying the level of the lesion and may facilitate
and reduced artifact compared with single shot EPI spinal digital subtraction angiography, which remains
and fast spin echo techniques (65,68). the gold standard (73).

Vascular Malformations Cobalamin and Copper Deficiency

Spinal vascular malformations may present with pro-
gressive myelopathy related to venous congestion or
arterial steal syndrome. Spinal dural arteriovenous
fistula makes up 70% of spinal vascular malforma-
tions, classically affecting middle aged males (69).
Cord expansion and T2 hyperintensity related to
venous congestion and ischemia may be associated
with diffuse enhancement. The diagnosis is suggested
by numerous vascular flow voids and enhancing ves-
sels (Fig. 5). Additional findings may be siderosis or
intramedullary T2 hypointense hemosiderin related to
previous hemorrhage (70–72). Contrast enhanced
MRA, including time resolved techniques, are useful
Subacute combined degeneration of the cord due to
vitamin B12 (cobalamin) deficiency, characterized by
loss of proprioception and vibration sense with sen-
sory disturbance, may occur in pernicious anemia,
ileal or gastric fundal resection, or due to severely
restricted diet. Subclinical deficiency can be
unmasked by nitrous oxide administration (74). Cop-
per deficiency can cause an indistinguishable clinical
and radiological appearance (75).
The characteristic MRI finding is long segment bilat-
eral T2 hyperintensity of the dorsal columns
described as an “inverted V” or “rabbit ear” appear-
ance (76–78). There are case reports of extension into
Transverse Myelitis
Figure 5. Long segment T2 hyperintensity of the thoracic cord in this case was due to a spinal dural AVF. Numerous intra-
thecal vessels can be appreciated on T2 and postcontrast T1-weighted images, with diagnosis confirmed by spinal
angiography.
the lateral columns, and cranially into brainstem and
cerebellum (79). Treatment related resolution of signal
abnormality precedes clinical improvement (76).
Radiation Myelopathy
As radiation myelopathy is a late complication, hav-
ing been reported beyond 10 years after radiother-
apy (26), and this clinical history may not be
available to this radiologist, the presence of fatty
marrow signal within vertebral bodies or associated
pulmonary fibrosis in a well demarcated margin cor-
responding to the radiation port may suggest the
diagnosis.
Cord edema and T2 hyperintensity often contains
patchy or ring-like areas of enhancement (80–82).
Over time, cord signal normalizes but severe atrophy
develops.
ADVANCED IMAGING TECHNIQUES
IN TRANSVERSE MYELITIS
Diffusion tensor imaging (DTI) in the spinal cord is
currently in its infancy, but techniques have been
described to overcome the technical challenges inher-
ent in imaging a relatively small structure in a site
prone to artifact (83).
Small voxel sizes are required to obtain good spatial
resolution within the cord, but causes a correspond-
ing reduction in SNR. Imaging at 3 Tesla (T) can maxi-
mize SNR and permit higher spatial resolution, with
distinction between anatomical regions such as corti-
cospinal tracts. However, higher field strength comes
9
at the cost of greater susceptibility-induced distortion
artifacts.
Local field inhomogeneity is a particular problem in
the spinal cord, as the change in magnetic susceptibility
at the bone tissue interface distorts images. Use of a
reduced field of view and techniques such as outer vol-
ume suppression have been used to obtain higher qual-
ity results.
CSF pulsation, breathing, and swallowing can also
cause artifacts in the spinal cord. Techniques to mini-
mize these artifacts aim to shorten the echo train
length and use parallel imaging techniques to shorten
the acquisition times.
The published literature exploring the clinical uses
of DTI in myelopathy is limited to small studies, how-
ever, results are encouraging. Both whole cord and
tract-based techniques have identified reduced frac-
tional anisotropy (FA) and increased mean diffusivity
(MD) as markers of abnormality in this setting.
Increases in radial diffusivity (perpendicular to axons)
and axial diffusivity (parallel to axons) have been
shown in animal spinal cord models with radiology-
histopathology correlation to correspond to demyelin-
ation and axonal injury, respectively.
While there is some evidence that DTI can identify
occult lesions and contribute to diagnostic confidence,
the most promising aspect may lie in the ability of
this technique to differentiate between more severe
and less severe pathology.
Transverse Myelopathy
A small study (84) comparing healthy subjects to 15
patients with inflammatory myelopathy of any cause
identified reduced FA within the lesions evident on
10
T2-weighted imaging. Moreover, additional lesions
occult on T2-weighted imaging were identified in 80%
of patients, which in 41.6% showed greater correla-
tion with the spinal level of clinical symptoms than
the T2-apparent lesion. A study comparing 10
patients with idiopathic transverse myelitis to healthy
subjects (85) found that a greater degree of FA reduc-
tion within the lesion and in normal appearing cord
distal to the lesion predicted worse outcomes.
MS and NMO
Decrease in fractional anisotropy within MS plaques
has been attributed to loss of myelin, expansion of
the extracellular space fraction, and perilesional
inflammation (86). The finding in multiple studies
Goh et al.
Figure 6. Flow chart diagram
illustrates an imaging diag-
nostic approach to acute
myelopathy, incorporating
morphologic patterns of cord
involvement.
that average cord FA is lower in MS compared with
controls even in normal appearing white matter may
be accounted for by the presence of small T2 occult
lesions, and is consistent with imaging/pathologic
correlation study results finding that only 60–70% of
MS white matter lesions are appreciable on T2 or
FLAIR imaging. Average FA and MD values have been
shown to correlate with degree of disability (87).
A study of 16 patients with MS (88) assessed evolu-
tion of DTI findings between baseline and 3 months
follow-up in the setting of a cord relapse. MS patients
had lower FA both within lesion and in normal
appearing cord than normal subjects. Increased radial
diffusivity in acute lesions improved on follow-up
imaging. A lesser degree of FA reduction at baseline
predicted clinical recovery, while more marked FA
Transverse Myelitis
reduction at baseline was associated with residual
deficits.
Similar changes have been identified within the
cord lesions of NMO patients. Qian et al compared 10
NMO patients with healthy controls, finding that in
lateral and dorsal columns NMO patients had reduced
FA, increased MD and increased radial diffusivity
(RD). All parameters correlated to worse disability
score, with FA measurement the most sensitive to
mild severity NMO (89).
Although similar in kind, there is emerging evidence
that changes in DTI parameters may differ in degree
in NMO compared with MS. A small study comparing
spinal cord DTI findings in MS, NMO, and control
groups measured diffusion parameters in white mat-
ter tracts and gray matter separately (90). Although
mean diffusivity was increased in NMO and MS
groups compared with controls, measurements in
white matter were also able to differentiate between
NMO and MS. The greatest degree of abnormality was
within white matter tracts in T2 evident lesions, where
FA was reduced and radial diffusivity increased in
NMO and MS patients compared with controls. The
greater degree of alteration in NMO compared with
the MS group was believed to be consistent with
greater tissue damage and more marked loss of
myelin.
In contrast to MS, unaffected tracts in the NMO
group showed normal FA and RD values. Affected
tracts demonstrated a lesser but significant degree of
abnormality upstream and downstream from T2 evi-
dent lesions in the NMO and MS groups which was
thought to reflect Wallerian degeneration and retro-
grade axonal degeneration.
A DIAGNOSTIC APPROACH TO TRANSVERSE
MYELOPATHY
An approach to diagnosis in presentations of acute
myelopathy is outlined in (Fig. 6).
The first and most urgent investigation is spinal
cord MRI to exclude cord compression. If MRI is not
available or if there are MRI contraindications, CT
myelography is an acceptable alternative in the emer-
gent setting. Imaging assessment can then be com-
pleted with less urgency by performing contrast
enhanced MRI of cord and brain.
Features on the initial cord MRI may allow confident
diagnosis of a cause of myelopathy other than trans-
verse myelitis. This could include DWI evidence of
ischemia or cord abscess, flow voids related to a dural
AVF, or the classic dorsal column involvement in B12
or copper deficiency.
In transverse myelitis, recognition of the patterns of
cord involvement may assist by narrowing the imaging
differential diagnosis sufficiently to streamline clinical
questioning and direct the choice of specific investiga-
tions with which to minimize diagnostic delay.
In assessment of the morphology of otherwise non-
specific cord lesions, distinguishing between LETM
and APTM has the best evidence for diagnostic utility,
in identifying patients who would most benefit from
11
expedited aquaporin 4 antibody testing. A positive
test, present in 60% of cases in one study, will allow
diagnosis of NMO or an NMO spectrum disorder.
Symmetric tract involvement, particularly if associ-
ated with symmetric enhancement, may prompt a
search for an underlying malignancy and neuronal
autoantibodies. Leptomeningeal and/or nerve root
enhancement may point to sarcoidosis, or in the pres-
ence of an appropriate clinical prodrome may suggest
an infective cause such as viral pathogens or Lyme
disease.
When cord imaging is nonspecific, the brain MRI
should be interrogated for findings that support a
specific diagnosis. For example, classic lesions may
fulfill diagnostic criteria for MS, or be clustered
around sites of aquaporin 4 expression to suggest
NMO. Temporally similar brain lesions would support
a diagnosis of acute disseminated encephalomyelitis.
Unilateral brainstem involvement extending to thala-
mus may suggest Behcet’s disease, while bilateral
thalamic involvement might suggest a flavivirus. Even
in the absence of diagnostic lesions, presence or
absence of nonspecific white matter lesions will help
to stratify risk of eventual conversion of transverse
myelitis to clinically definite MS.
Clinical application of advanced techniques such as
diffusion tensor imaging remains in its infancy, but
has future potential in assessment of prognosis.
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