MRI Features of Idiopathic Transverse Myelitis

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Idiopathic Transverse Myelitis: MR Characteristics

Kyu Ho Choi, Kwang Soo Lee, Sun Ok Chung, Jung Mee Park, Young Joo Kim, Hyun Sook Kim, and

Kyung S ub Shinn

PURPOSE: To describe the MR characteristics that can distinguish idiopathic transverse myelitis

from other intramedullary lesions. METHODS: A total of 3 2 initial a nd follow-up MR studies in 17

pa tients with clinica lly proved transve rse m yelitis were reviewed retrospe ctively. The loca tion, size,

pattern, and segm ental length of areas of hyperintensity were estimated on T2-weighted a xial and

sagittal images. In 15 of the patients, whose neurologic abnormalities were limited to the spinal

cord, the location and pattern of intramedullary contrast enhancement were evaluated on sagittal

and axial T1-weighted images. Follow-up MR studies were available for 10 patients. The statistical

significance of cord enha ncement bet ween t he groups wit h a nd wit hout cord expansi on was

calculated. RESULTS: Common MR findings of idiopathic transverse myelitis included a centrally

locat ed hyperint ensit y occupyi ng m ore t han t wo t hirds of t he cross-sectional area of t he cord

(88%); a lengt h of 3 t o 4 vert ebral segm ent s (53%), wit h variable presence of cord expansi on

(47%); a sm all central area of intensity, isointense with norma l cord, in the core of hyperintensity

(47%); focal, peripheral cord enhancement (53%), particularly in patients with cord expansion; and

a slow regression of T2 hyperintensity with an enhancing nodule. Although no linear correspon-

dence was observed between MR findings and neurologic signs and symptoms, all but 4 patients

improved clinically as MR findings improved or remained stable. CONCLUSIONS: MR findings are

helpful in detecting transverse myelitis and in differentiating this entity from multiple sclerosis and

cord tumors, but clinical assessment and observation of MR changes over time are essential in

making the diagnosis.

I ndex ter ms: Myelitis; Spinal cord, ma gnetic resona nce

A JN R A m J Ne u rorad iol 17: 11511160, June 1996

The spinal cord is the site of infectious andnoninfectious inflam ma tory processes. Trans-verse m yelit is , or m yelopathy, is diagnosedwhen both halves of the cord are involved withan inflammatory process (1, 2). The syndromehas m ultiple causes; it interrupts both m otorand sensory tracts at one level, commonly thethoracic; and it is known to be assoc iated withvarious viral infec tions, vacc inations, autoim-mune diseases , and carcinoma s, although mostcases are idiopathic (3).

Reports of the magnetic resonance (MR) im-

aging findings in patients with transverse myeli-t is , specifically in the acute stage, have de-s c rib e d lo c a l e n la rg e m e nt o f th e c o rd a n dincreased signal intensity on long repetitiontim e / e c h o tim e ( TR/ T E) s e q ue n ce s ( 1 , 2 ) .However, these findings are not sufficient to dif-ferentiate this condition from other similar le-sions, such as intramedullary tumors, compres-sive spinal cord disease, m ultiple sclerosis,hematoma, and vascular ischemia. In particu-lar, there is a paucity of published material on

the prevalence a nd pattern of contrast enhanc e-me nt in patients with transverse myelitis. Tohelp differentiate transverse myelitis from otherintrame dullary abn orma lities, we sought find-ings on unenhanced and enhanced MR imagesthat were characteristic of transverse myelitis.

Materials and Methods

The initial MR s tudies of 17 patients with clinically

proved transverse myelitis were reviewed retrospectively.

Received August 25, 1995; accepted after revision January 29, 1996.

From the Departments of Radiology (K.H.C., S.O.C., J .M.P., Y.J.K.,

H.S.K., K.S.S.) and Neurology (K.S.L.), Kangna m St Marys Hospital, Cath-

olic University Medical College, Seoul, Korea.

Address reprint reques ts to Kyu Ho Choi, MD, Departm ent of Radiology,

Kangnam St Marys Hospital, Catholic University Medical College, 505

Banpo-Dong, Seocho-Ku, Seoul, Korea.

AJ NR 1 7 :1 1 5 1 1 1 6 0 , J u n 1 9 9 6 0 1 9 5 - 6 1 0 8 /9 6 /1 7 0 6 1 1 5 1

American Society of Neuroradiology

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Follow-up MR examinations, available for 1 0 of these pa-

tients, were also reviewed. The study group consisted of 16

men and 1 woman whose ages ranged from 28 to 56 years

(mean age, 41 years). Strict exclusion criteria included a

his tory of s pinal traum a, com pres s ive m yelopathy, car-

diac dis eas e, aortic aneurys m , a s pace-occupying les ion

in the spinal cord or sp ine, system ic ma lignancy, syringo-

myelia, multiple sc lerosis, collagen -vascular disease , a nd

respiratory infection or common cold within a few months

of the onse t of the neu rologic m anifesta tion of mye litis. No

patient had received a vaccination in recent years.

Routine laboratory studies included complete blood cell

count, fluorescent antinuclear antibodies test, rheum atoid

factor, VDRL test, tests for vitamin B12

, folate, and cere-

brospinal fluid tha t included white blood c ell with d ifferen-

tiation, protein, sugar, gram stain, acid-fast bacillus, India

ink, enzym e-linked im m unos orbent as s ay for paras ites ,

electrophoresis, myelin basic protein, human T-cell leuke-

mia/lymphotropic virus-1, and viral titer. If one of these

laboratory s tudies, except for lymphocytic-pleocytosis (9

to 130/ L) and/or elevated protein (0.050 to 0.139 g/dL)

in cerebrospinal fluid, was positive, the patient was ex-

cluded from the s tudy. A ll patients had a radiographic

s eries of the thoracic and/or cervicothoracic s pine, de-

pen ding on the level of neurologic de ficit. No po sitive p lain

radiographic finding was found in any patient who was

included in the study. Inclusion in the study required the

presence of an area of high signal intensity in the cord on

axial and sagittal T2-weighted MR ima ges.

Neurologists obtained the patients histories and per-

forme d the neu rologic e xam inations. All initial MR ima ges

were obtained immediately after the patients first visit to

the hospital for neurologic disorders and before the start of

steroid therapy. A follow-up MR study was considered

necessary when the patient did not improve with steroid

therapy after approximately 4 weeks or when the clinical

ma nifestations worsened during the observation period.

Patients who did not have a follow-up MR examination

either reco vered sufficiently to re fuse further stu dy o r failed

to visit the clinic.

MR studies of the brain were obtained in two patients

who had nonspecific symptoms, such as headache or diz-

ziness, in order to exclude p ossible intracranial lesions.

Brain MR imaging was not performed in the other 15 pa-

tients because their neurologic manifestations were limited

to the sp inal cord. MR ima ging of the s pine was done on a

1.5-T unit. T1-weighted (350 550/1117/2) (TR/TE/ex-

citations) and double-echo proton densityweighted andT 2 -we ig h te d ( 1 8 0 0 2 2 0 0 / 3 0 , 9 0 / 2 ) s p in - e c ho im a g e s

were obtained with a 3-mm section thickness, 1-mm in-

tersection gap, 256 192 matrix size, 32-cm field of view

for the sagittal plane, and 20-cm field of view for the axial

plane. In addition, in 15 patients , a xial a nd s agittal T1-

w eighted s pin-echo im ages w ere obtained im m e diately

after intravenous infusion of 0.1 mmol/kg gadopentetate

dimeglumine.

The interval between the onset o f neurologic symp toms

and signs and the initial MR exam ination varied from 3

days to 4 m onths . O ur cas es w ere arbitrarily clas s ified

according to the tim e between ons et of the neurologic

deficit and the initial MR study: less than 4 weeks, acute

( fiv e p a t ie n ts ) ; b e t we e n 4 a n d 8 we e k s , s u b a c u t e ( s ix

patients); and more than 8 weeks, chronic (six patients).

The vertebral s egm ental length of the high s ignal w as

estimated on the ba sis of findings on sagittal T2-weighted

images. Cross-sectional location, size, and pattern of the

high signal in the cord were determined by findings on the

axial T2-weighted images. Evaluation o f the a bnormal sig-

nal intens ity of the cord, s egm ental extent, and contras t

enhan cem ent was base d on the initial MR examination; for

the follow-up studies, these features were com pared with

the initial findings. The central linear high signal intensity

that was, in som e ca ses, see n above and be low the diffuse

high-intensity area on T2-weighted images was not con-

sidered in determining the extent of the abnormality. Cord

expansion was evaluated with respect to adjacent normal

cord on T1-weighted sagittal images.

A total of 32 MR studies were obta ined, including fol-

low-up studies (6 patients had 1 follow-up, 3 had 2 follow-

ups, a nd 1 had 3 follow-ups). The time from initial exam -

ination to first follow-up ranged from 20 days to 7 months;

from initial examination to last follow-up, the time ranged

from 3 to 13 m onths . The location and extent of the in-

tram edullary contras t enhancem e nt were confirm ed on

contrast-enhanc ed a xial and s agittal T1-weighted ima ges.

Usual treatme nt for the pa tients consisted of me thylpred-

nisolone 1 g p er day for 3 to 5 da ys followed b y prednisone

1 m g/kg for 1 to 2 m onths , depending on the patients

clinical response.

To determine the differences in MR findings between

transverse m yelitis a nd c ord tumors, we evaluated the MR

findings of 13 patients w ith proved cord tum or. Thes e

included 6 cas es of ependym om a , 6 cas es of as trocytom a,

and 1 case of intramedullary metastasis from lung carci-

n o m a i n 9 m e n a n d 4 w o m e n w ho h a d a m e a n a g e o f 3 6

years. The cervical cord was involved in 6 patients and the

t ho ra c ic c o rd in 7 p a t ie n ts ( 2 c e r vic a l a n d 4 t h or a c ic

ependym om as , 4 cervical and 2 thoracic as trocytom as ,

and 1 thoracic m etas tas is ) . F or better com paris on, w e

selected the patients in whom MR studies were performed

on a 1.5-T unit with the sam e pa rameters a s those used for

our pa tients with transverse myelitis. S agittal a nd axial

T1-weighted images were obtained immediately after in-

travenous infus ion of 0. 1 m m ol/kg gadopentetate dim e-

glumine in all patients. The MR studies were examined for

cord expansion on T1-weighted sagittal images; for seg-

m ental body length of the high s ignal on T2-weighted

sagittal image s; for cross-sectional location, size, and pat-

tern of the high signal on T2-weighted ima ges; a nd for the

location, extent, and pattern of contras t enhancem e nt on

T1-weighted axial and sagittal ima ges.

Results

Th e h ig h s ig na l in te n sity o n a xia l T2 -weighted im ages was centrally located in allpatients and was well m arginated in all but 5

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pa tients; it occup ied m ore tha n two thirds of thecross-sectional area of the cord in 1 5 of the 1 7patients (less than half the c ross-sectional areain the other 2). In 8 of the 15 patients who ha da large area of central hyperintensity, a smalldot, isointense with the cord, was prese nt in the

core of the hyperintensity (central dot sign, Fig1).On the first follow-up MR studies (10 pa-

tients), the extent of the area of high T2 signalintensity in the cord either im proved or re-m ained unchanged. Of the 4 patients who hadno interval im provem ent, 2 patients had thesame extent for 4 and 6 months, respectively,and the other 2 pa tients had eventual imp rove-ment on later follow-up studies.

Expa nsion of the s pinal cord was de fined bet-

ter on sagittal than on axial T1-weighted im-ages. Cord expansion was observed in eightpatients, tapered smoothly to the normal cord,and was of lesser extent than the high T2 signalabn orma lity (Fig 2). The differenc e in degree ofcord expansion am ong the eight patients was

minim al, with the cereb rospinal fluid intensityaround the cord clearly visible on the axial im-ages in all cases.

Am o n g t he 1 5 p a t ie n ts wh o h a d c o n tra s t -enhanced studies with the initial MR examina-tion, 8 patients had a clear contrast-enhancingarea on both axial and sagittal T1-weighted im-a g e s. Th e e n ha n c em e n t wa s n od ula r ( 6 p a -tients) or diffuse (2 patients), occupying a por-tion of the segm ental cord, eccentric on oneside, and did not bulge outside the contour of

Fig 1. Case 4: 48-year-old man with a 6-month history of sensory dysesthesia below the T-10 level and newly developed motor

impairment of the left lower extremity.

A , Sa gittal T2-weighted ima ge of the thoracic spine sho ws long se gme ntal intrame dullary high s ignal intensity ( arrow s).

B, On axial T2-weighted image , hyperintensity is located centrally an d occ upies m ore than two thirds of the c ross-sectional area of

the cord, and a central dot sign ( arrow ) i s seen.

C, On sagittal T1-weighted image, no segmental enlargement is evident.

D, Postcont rast sagi tt al T1-weight ed i mage reveal s a poorly marginat ed area of cont rast enhancement in t he c ord ( arrow s). The

dorsally located enhancement along the posterior surface of the cord below the cord lesion ( arrow heads) most likely represent s a

prominent p osterior med ullary vein.

Postcontrast axial T1-weighted image s through the cord lesion a nd dorsally located e nhance me nt confirm intram edullary enha nce-

m e n t (arrow s in E) and posterior medullary vein (arrow in F).

G, Six months later, sa gittal T2-weighted image shows m arkedly improved segm ental intrame dullary hyperintensity ( arrow s).

H, The intramedullary contrast-enhancing area has resolved on this postcontrast sagittal T1-weighted image.

AJ NR: 1 7, J une 1 99 6 MYELITIS 11 5 3


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the cord (Fig 3 ). Enhancing lesions were lo-cated a t or nea r the m idpoint of the segm entalT2 hyperintensity. The frequency of p ositivecontrast enhancement was greater in patients inth e s u b a c ut e s t a g e ( 4 o f 6 p a t ie n ts ) t ha n inthose in the acute (1 of 4) and chronic (3 of 5)stage s. Among the 8 p atients who had follow-upcontrast-enhanced studies 1 to 7 months afterthe init ial study (4 patients had enhancem entand 4 had n o enha nce me nt at the initial study; 3patients had 2 or 3 follow-up MR examinations),3 patients with positive contrast enhancementhad interval improvement in the size of the en-hancem ent (3 m onths later in 1 patient and 7m onths later in 2 patients). O ne patient withp o sitive e n ha n c e m e nt h a d p ro gre s sio n 3m onths later a t the second follow-up; and 2months after that, the progression was further

im p r ove d ( F ig 4 ) . Am o n g t he 4 p a t ie n ts inwhom there was no init ial contrast enhance-m ent, abnorm al enhancem ent was absent in 3p a t i e n t s a n d t h e o t h e r p a t i e n t h a d a n e w e n -hancing nodule at the 1-month follow-up fol-lowed by improvement at the 2-month follow-u p . N o c o n ne c tio n c o u ld b e fo u nd b e twe e nprogression or new appea rance of an enha ncingarea and the time course of neurologic features.Despite temporary marked clinical progressionin 2 patients, the initial enhancing lesion was

im proved in 1 patient on the first follow-upstudy and showed persistent lack of enhance-me nt by the sec ond m onth in the other pa tient.

Six of the eight patients with cord expansionhad initial contrast-enhanced MR studies. En-hancem ent was seen in five of these patients,and no enhancem ent was present in the otherpatient. Of nine patients with no cord expan-s i o n , t h r e e h a d e n h a n c e m e n t a n d s i x h a d n oenhancement. The frequency of cord enhance-ment in the group with cord expansion was sig-nificantly greater than in the group without cordexpansion, but our analysis is base d on a sm allnumbe r of cases. The findings a re sum ma rizedin the Table.

MR findings of cord tum ors were significa ntlydifferent from those of transverse myelitis. In allpatients with cord tumors, the cord expansion

was present and accompanied a heterogeneoushigh T2 signal intensity that oc cup ied the e ntirecross-sectional area of the cord. The averages e g m e n ta l le n g th o f t h e h ig h s ig n a l o n T2 -weighted sagittal images was 4.5. Cavitary le-sions were associated in six c ases of ependy-moma and in two cases of astrocytoma. In twopa tients, a sm all ce ntral area of intensity, isoin-tense with the cord, was s ee n outside the a rea ofcontrast enhancem ent in the core of hyperin-tensity on axial T2-weighted ima ges. Intratu-

F ig 2 . C a s e 7 : 4 2 - ye a r -o ld

man wit h int olerance t o cold,

p ro g re s s iv e we a k n e s s o f b o th

lower extrem ities, and difficulty

urinating for 5 months.

A , Sagittal T2-weighted image

of t he t horaci c spi ne shows anarea of intramedullary high sig-

nal int ensit y at t he T8 9 level

(arrow s).

B, On axial T1-weight ed i m-

age, high signal intensity is s een

t o be associ ated wit h a fai nt ly

s e e n c e n tr a l is o in te n s it y (ar-

row ).

C, On sagittal T1-weighted imag e, the spinal cord is enlarged

at t he sam e l evel (arrow s).

After infusion of contrast material, a nodular enhancing area is

not ed i n t he c ord on sagi tt al (arrow , D) a n d a x i a l (arrow , E)

T1-weighted imag es.

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moral T2 hypointense areas that suggest pres-ence of hem osiderin deposition, a result of oldbleeding, were noted in three cas es of ependy-m o m a a n d a s t r o c y t o m a . I n c a s e s o f c o r d t u -mors, the contrast enhance me nt was p resent inall patients; it was larger in size, occupying the

entire cross-sectional area of the cord on axialima ges except in one patient (in whom it stilloccupied m ore than half the cross-sectionalarea); a nd it showed a variable, heterogeneouspattern in all but two patients. Sharp superiorand inferior enha ncing m argins on T1-weighted

Fig 3. Case 15: 48-yea r-old m an with left leg pa resthesias for 3 m onths and right leg weakne ss for 3 days.

A , Sagittal T2-weighted image of the thoracic spine shows an area of intramedullary hyperintensity at the midthoracic level (arrow s).

A herniated disk is present three levels below the intramedullary abnormal signal compressing the cord.

B, On axial T2-weighted image, a small area of isointensity relative to the cord (arrow ) is seen in the center of the large intramedullary

hyperintensity.

C, Postcontrast sa gittal T1-weighted ima ge shows no definitive e nhancing a rea.

Sagittal (D) and axial (E) T2-weighted ima ges at 1 -month follow-up show a lmos t the s am e extent and size of high signal intensity in

the cord (arrow s).

Postcontrast axial (F) a nd sa git tal ( G) T1-weighted images show an eccentric contrast-enhancing area in the cord (arrow s).

Two a nd a half months later, the e xtent of high signal in the cord has reduced on a sagittal T2-weighted image (arrow s, H), and t he

significant c entral hype rintens ity is still presen t with be tter visibility of the cord along the periphery on axial T2-weighted ima ges (arrow s,I). The contrast-enhancing area has reduced on postcontrast axial (arrow s, J) and sagittal ( arrow , K) T1-weighted image s. The p atient

improved clinically as the contrast enhancement lessened.



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s a g itta l im a g e s we re s e e n in fo ur c a s e s o f ependym om a and in one case of astrocytom a.

Discussion

Trans verse m yelitis, or m yelopathy, is an un -com m on syndrom e characterized by bilateralmotor, sensory, a nd autonomic dysfunction re-sulting from the involvement of both halves of

the spinal cord in the absence of a preexistingneurologic or systemic disease (2, 4). The dis-ease commonly begins with back or radicularpain followed by the abrupt onset of bilateralparesthesias of the legs, an ascending sensorylevel, and a paraparesis that often progresses toparaplegia (5). Middle-aged adults are com -monly affected, and the thoracic sp inal cord isthe mo st frequ ent site of involvem ent. Althoughtransverse m yelitis ha s be en rec ognized for sev-e ra l d e c a d e s , it is a p o o rly u n de rs to o d s y n-

drome pa thologically an d etiologica lly. Thereare many etiologic associationssuch as withviral disea ses , vac cinations, dem yelinating pro-cesses such as multiple sclerosis, collagen-vas-cular disea ses s uch a s systemic lupus e rythem-atosus, vascular disorders, and paraneoplasticsyndrom esbut m ost cases are idiopathic (3,6). Polio virus, herpes zoster, and human im-munode ficiency viruses are known to involve

the spinal cord directly. Whenever possible, aprecise etiologic diagnosis should be estab-lished on the basis of clinical, laboratory, andradiologic findings. None of our 17 patients re-called a history of upper respiratory infection inthe 3 to 4 m onths preceding the onset of theneu rologic deficit.

Classification, as described by Adam s andVictor (7), into a cute, subac ute, or chronic va-rieties was not feasible with our p atients be-cause the t im e interval between the onset of

Fig 4 Case 16: 31-yea r-old ma n with a history of parapa resis and pa resthesias of both lower extrem ities for 5 months.

A , Sa gittal T2-weighted ima ge of the thoracic sp ine shows expa nsile high signal intensity in an enlarged cord (arrow s). In addition,

the central hyperintensity extends inferiorly to the midthoracic level ( arrow h eads ).

B, Axial T2-weighted imag e at the level of superiorly located expansile hyperintensity a gain shows a large central high signal

(arrow s).

C, An inferiorly loca ted c entral hype rintens ity is see n slightly anterior to the m idpoint of the c ord on a xial T2-weighted ima ge ( arrow ),

suggesting that this hyperintensity is unlikely to be the dilated central ca nal.

Postcontrast sagittal (D) and axial (E) T1-weighted images show a contrast-enhancing area in the cord (arrow s).

F, Two and a half months later, the expansile intramedullary hyperintensity ( arrow s) and inferiorly located central hype rintensity(arrow head s) appear more extensive and obvious on sagittal T2-weighted image.

G, Axial T2-weighted ima ge aga in shows the central expans ile hyperintensity (arrow s). (Figure continues.)

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neurologic deficit and the first visit to the hos-pital for medical attention varied greatly. Thetime at which the disease reached peak severitycould not be recalled by every pa tient, a nd thetime interval between sym ptom onse t and initialMR e xa m in a tio n ra n ge d fro m 3 d a ys to 4months.

In the literature, MR findings of transve rsemyelitis have been described for a small num-ber of patients (1, 2, 6, 8). The largest number(seven patients) was reported by Holtas et al(1). In their series, four pa tients had a focale n la r ge m e n t o f t h e c o rd , a n d a ll s h o we d a n

increased signal on long-TR/TE sequences. Inour cases, cord enlargem ent was better a ppre-ciated on sagittal than on axial T1-weightedima ges. Like others (1 , 2), we found se gme ntalhigh signal intensity (usually three to four ver-tebral se gm ents) on T2-weighted im ages re-gardless of cord expansion. Barakos et al (2)reported that in four of their five patients, thesignal abnorm a lity extended over a t least sixspinal segm ents as opposed to the m ore com -m o n t hre e t o fo u r s e g m e n t s in o u r p a t ie n ts .

Patients with cord expansion had no more ex-tensive segmental hyperintensity than did pa-tients without cord expansion. We believe that acentrally located hyperintensity that occupiesmore than two thirds of the cross-sectional areaof the cord on the long-TR/TE images found inmost of our patients is characteristic of trans-verse myelitis.

The central isointensity, or dot (Figs 1B, 3B,and 4K), is believed to represent simply centralgray m a tter squeezed by the uniform , evenlydistributed edematous changes of the cord. Itma y not be a spe cific s ign of trans verse m yelitis

or have any clinical significance. Reviewing ourc a s e s o f c o rd t um o r, o n ly t wo h a d a c e n tra lisointensity, and in both it was located outsidethe contrast-enhancing area of the tumor. Be-c a u s e o f i ts d e s tru c tive n a tu re a n d m a s s iv ee d em a , we th in k it is le s s c o m m o n in th etumors.

The ability to distinguish transverse myelitisfrom other intram edullary d isea ses , es pec iallycord neoplasm , is of param ount im portance,b e c a u s e it c a n m e a n t he d iffe re n c e b e twe e n

Fig 4, continued.

The enhancing nodule has also enlarged on postcontrast sagittal ( arrow s, H) and axial (arrow s, I) T1-weighted images.

After treatment with corticosteroids for 2 months, the extent of the intramedullary hyperintensity has significantly resolved on sagittal

T2-weighted image (J ), and the central isointensity becomes more apparent on axial T2-weighted image ( arrow , K).

Contrast-enhanced sagittal (L) and axial (M) T1-weighted images show markedly improved enhancement ( arrow s). Clinically, the

patient improved steadily, in a ccordanc e with ima ging findings.



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surgery, possible postsurgical com plications,and radiation, or not. The usefulness of gado-pentetate dim eglum ine has been described inthe detection of cord tumors as well as in thedelineation of their location and extent in rela-t ion to surrounding edem a . Pronounced con-trast enhancem ent is usually noted with cordtumors (9 12). A few published reports havedescribed patterns of contrast enhancement inpatients with transverse myelitis: a mode rateincrease in signal intensity of the cord after in-

jec tion of ga dop e nte ta te dim eglum ine in on e offive patients reported by Barakos et al (2); adiffuse abnormal contrast enhancement in the

anterior aspect of the cervical cord that laterb e c a m e p a t c hy in o n e p a t ie n t d e s c rib e d b ySanders et al (8); and an undefinable, fluffypattern of enhancement at the midthoracic levelin o n e p a t ie n t re p o rt e d b y Pa r da t s c he r e t a l(13). Contrast enhancem ent in our eight ca seswas focally nodular or diffuse at the peripherallocation with maintenance of the cord contour(Figs 2E, 3F, a nd 4E). The enhanc ing area wasmuch smaller as compared with the extensivehyperintensity on T2-weighted image s, and no

case was associated with syringomyelia, a find-ing that may be associated with cord tumors.

Diffe re n t p a t te rn s o f e n h a nc e m e n t in in -trame dullary tum ors were found in our ana lysis.Common patterns included a large area of en-h a n c e m e n t o c c u p yin g t he e n tire c ro s s -s e c -tio na l a r e a o f th e c o rd o n a t le a s t o ne T1 -weighte d a xia l im age a nd va ria blyheterogeneous e nhance me nt frequently a ssoci-ated with a central or marginal cavity. Even withthese findings, it is not always possible to dif-ferentiate between these two conditions. Closelyspac ed follow-up MR studies ma y aid in thisendeavor. In two of our cases, interval progres-

sion of the enhancing lesions eventually im -proved 3 and 5 months, respectively, after theinitial s tudies. For cas es without contrast en-hancement, as in seven of our patients, exclu-sion of a cord tumor would be equ ally d ifficult.

Multiple sclerosis is freque ntly m entioned asa potential underlying condition when trans-verse myelitis is first diagnosed. Both multiplesclerosis and transverse myelitis commonly in-volve young adults. Although the prevalence ofmultiple sclerosis is lower in Asians than in

Seventeen patients with transverse myelitis

C ase

Level of

Sensory

Deficit

Initia l MR Im a ging F ollow-up MR Im a ging

Cord

Expansion

S eg m en tal

Extent of

T2 HSI

Contrast

E n h an cem en t

No. of Studies

(m o n th s s in ce

initial stu dy)

Significant Changes

1 T-4 T8-12 2 ( 3) No c on tra s t e nh a nc e m en t, im p ro ve d T2 HS I

2 L-1 T7-11

3 T-1 0 T9-11 1 (4 ) No c ha nge

4 T-1 0 T8-11 1 ( 6) Im p ro ve d c on tra st e nh an ce m en t a nd T2 HS I

5 T-7 T1-2

6 C-6 C5-6

7 None T8-9

8 None T7-10

9 T-5 T7 -9 . . . 2 (1 3 ) No c ontra s t enha nc e m ent

Resolved T2 HSI

1 0 T-5 T1 -2 . . . 1 (6 ) Are a of c ontra s t e nha nce m e nt on follow-up

No change in T2 HSI

1 1 T-9 T4-5

1 2 T-8 T2-6 1 ( 7) No c on tra s t e nh a nc e m en t, im p ro ve d T2 HS I

1 3 T-9 T2-6 1 ( 5.5 ) No c on tra s t e nh a nc e m en t, im p ro ve d T2 HS I

1 4 T-9 T7-10

1 5 T-1 1 T6-9 2 ( 2 .5 ) N ew c o nt ra s t e n ha n c em e n t a t 1 - m on th fo llo w- up

Improved T2 HSI

1 6 T-9 T2-5 3 ( 4.5 ) Pro gre s se d c on tra s t e nh an ce m e nt a t 2 .5 -m o nt h

follow-up

No contrast enhancement at 4.5-month follow-up

Improved T2 HSI

1 7 None T1-2 1 ( 2.5 ) Im p ro ve d c on tra st e nh an ce m en t

Improved T2 HSI

Note.HSI indicates high signal intensity in the cord; , p resen t; an d , ab sen t.

11 5 8 CHO I AJ NR: 1 7 , J une 19 9 6


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whites, multiple sclerosis causing transversemyelitis seems to be uncommon. Altrocchi (14)fo u nd th a t o n ly 4 o f 6 7 p a t ie n ts wit h a c u tetransverse myelopathy had multiple sclerosis.Lipton a nd Tea sda ll (15 ) found only 1 pa tient of

34 in whom the diagnosis of multiple sclerosiscould be m ade after 5 to 42 years of observa-tion. The frequency with which multiple sclero-sis was found to follow acute transverse myelitisin cases reported in the literature ranged from2% to 8% (me an, 5%) (4 ). In 4 c ases of multiplesclerosis in a series reported by Aichner et al(16), plaque s of the sp inal cord appe ared large,multiple, sharply demarcated, and sometimesconfluent (kissing plaques). Although the num-ber of patients they exam ined was sm all , theenhancing pattern of multiple sclerosis appearsdifferent from the transverse mye litis found in

our patients.The characteristic MR appearance of spinal

multiple sclerosis in 68 patients (124 plaque s)was doc um ented in an article by Tartaglino et a l(17). In their study, multiple sclerosis plaqueswere located peripherally, were less than 2 ver-tebral segm ents in length, and occupied lessthan h alf the c ross-se ctiona l area o f the co rd. Incomparison, the T2 hyperintense lesions in ourcases of transverse myelitis were centrally lo-cated, were 3 to 4 segments in length, and oc-cup ied m ore than two thirds of the c ords cross -sectional area. These significantly differentfindings will help distinguish the 2 conditions.

Although som e articles have been writ tenabout the role of contrast m edia in m ultiplesclerosis of the spinal cord, an analysis of thec o n tra s t -e n h a n c in g p a t te rn is la c k in g . In 4case s of contrast-enhanc ed multiple sclerosislesions in articles by Tartaglino et al (17) andLarsson et al (18) (2 cases each), the lesionsshowed enhanc em ent in the c entral zone of pe-ripherally located high signal intensity on T2-weighted images. A similar enhancing patternwas found in the brains of 12 pa tients d esc ribed

by Grossm an et al (19). All had enhanc em ent inthe sam e location of high-signal-intensity le-sions on T2-weighted images. In cases of trans-verse myelitis, on the other hand, e nhance me ntis in the periphery of a centrally located area ofhigh T2 signal intensity. Pathologically, cases ofidiopathic acute transverse m yelopathy m ayshow a nonspec ific necrosis that a ffects grayand white matter indiscriminately and destroysaxons and cell bodies as well as m yelin. Thelesions may be focally transverse or they may

diffusely involve a considerable length of thecord (1 4).

The role of corticosteroid treatment in trans-verse m yelitis is unc ertain; but beca use this d is-e a s e m a y s t e m f r o m a n a u t o i m m u n e m e c h a -

nism like multiple sclerosis, many neurologiststreat transverse myelitis with corticosteroids.Our patients were treated sporadically, mainlyduring the acute stage, so the treatments effecton the outcome could not be as sesse d. Beca useall initial MR exam ina tions were d one be fore th estart of steroid therapy, there could not havebeen any steroid effect on the degree of cordhyperintensity or on the p attern of contrast en-hance me nt; but in the follow-up studies, ste-roids may have helped restore the bloodspinalcord barrier and reduce edem a in view of thesteady improvement or stabilization of imaging

findings in all but two of our cases. In one ofthese patients, a new contrast-enhancing lesionwas evident on the first follow-up study (case15; Fig 3 C a nd G) and in the other patient, anenlarged enha ncing lesion was seen on the se c-ond follow-up examination (case 16; Fig 4D, E,H, and I). Both lesions were improved on sub-sequent follow-up studies (Figs 3K and 4L andM). Clinically, these two patients did not showgross worsening. In ge neral, although there wassome degree of relapsing-remitting neurologicm an ifes tations du ring the follow-up p eriod, slowimp rovem ent seem ed to be the rule. No pa tientdied during the follow-up period.

The clinical outcom es were variable in p a-tients with transverse myelitis studied by us andothers. Som e of our patients have recoveredwell enough to lead normal lives while othershave imp roved at a slower rate, with residualneurologic deficits. F ollow-up data on 67 pa-tients with acute transverse m yelopathy re-ported by Altrocchi et al (14 ) sho wed that ab outone third had a good recovery, one third a fairre c o ve ry , a n d o n e th ir d a p o o r r e c ov e ry a s

jud ged by th e crite ria of Pa ine a nd Bye rs for

classifying degrees of functional recovery (20)(55% of the patients were followed up for 2years, 22 patients for 6 or m ore years, and 10patients for more than 10 years).

In sum m ary, the characterist ic findings of transverse myelitis in our patients include nor-ma l size or segm ental enlargeme nt of the cord,m ost com m only thoracic; central hyperinten-s ity o c c u py in g m o r e t ha n t wo t hird s o f t h ecross-sectional area of the cord on long-TR/TEsequences that usually affected three to four



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vertebral levels; a central dot in the core of h yp e rin te n s it y; n o t u n c om m o n c o n tra s t e n -hance me nt; and, when present, a focal nodularor diffuse enha ncing area at the periphery of thecord that did not change the cord contour. The

prevalence of cord enhancem ent was signifi-cantly higher in patients with cord expansionthan in thos e with norm al cord s ize. These find-ings can be valuable in distinguishing trans-verse myelitis from multiple sclerosis, cordtumors, or other intram edullary lesions. Intra-me dullary hyperintensity and c ontrast enha nce -m ent did not correspond linearly to clinicalimprovement.

Acknowledgments

We thank Tae S ub Chung, Nam J une Lee, S un Yong

Kim, and Woo Suk Choi for a llowing us to review theircase s, and J une K. Lee for editorial assistance.

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MRI Features of Idiopathic Transverse Myelitis

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