Showa Univ. J. Med. Sci. 3(2), 181189, December 1991

Case Report

Efficacy of MRI in Diagnosis of Acute Spinal Epidural

and Subdural Abscess

Report of Two Cases and Comparative Study with

Typical Neuroradiological Methods

Toshiya FUKUI, Hiroo ICHIKAWA, Nobuyuki KAWATE,

Taneyoshi NozAWA and Koujiro SUGITA

Abstract: One case each of a spinal epidural and a subdural abscess is presented

and utility of MRI as a diagnostic measure in these paraspinal suppurative

diseases is discussed. MRI examination of a 21-year-old male with back pain,

fever and quadriparesis revealed a linear lesion in the cervical epidural space. Lumbar tap yielded purulent fluid containing Staphylococcus aureus, thus diag-

nosed as spinal epidural abscess. Along with improvements with successful

antibiotic therapy, the lesion was observed to disappear on MRI. Upon exami-

nation of an 82-year-old female with a fever and paraplegia, lumbar tap yielded

pus with Escherichia coli and myelo-CT and MRI detected subdural masses in the low thoracic to the lumbar region, thus diagnosed as spinal subdural abscess.

The rostral-caudal extension of the lesion was more precisely depicted by MRI.

Concomitant spinal cord infarction at T-12 and L-1 escaped detection by MRI

but was most relevant to the neurological signs. In this study MRI seemed to

be a more suitable diagnostic tool than myelography or myelo-CT because MRI

is non-invasive and repeatable, does not require potentially hazardous contrast

medium and sagittal scanning of spinal cord is available which gives more precise

information on the longitudinal extent of lesions.

Key words: spinal epidural abscess, spinal subdural abscess, myelo-CT, MRI,

spinal cord infarction

Introduction

Acute spinal epidural and subdural abscess are rarely encountered in neurological practice and often escape a correct diagnosis, resulting in permanent neurological deficits. Both initially present with back pain, high fever and nerve root pain followed by rapidly progres-sive para- or tetraparesis and sphincter disturbances in the more advanced stage, and possible deaths1-5) . As is often the case, clinicians face the difficulty in differentiating the two similar but different diseases just by the clinical signs4,5). Although the early utilization of MRI is advocated for correct diagnosis6,7), there has been little comparative study on MRI with other radiological methods in these two paraspinal infectious states. The purpose of this report is

to present cases of a spinal epidural and a subdural abscess and to discuss the usefulness and limitations of MRI as a diagnostic tool.

Department of Neurology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142, Japan.

182 Toshiya FUKUI, et al.

Case Report

Patient 1; A 21-year-old male, with a previous history of cellulitis in the left leg six months

prior, suddenly developed progressively worsening low back pain and a fever on Oct 4, 1990, and subsequently was admitted to a local hospital. An epidural block was successful in con-

trolling the back pain, but on the following morning, the patient noticed severe nuchal pain

that limited neck movements, and numbness of ankles and feet. As lumbar puncture pro-

duced grayish yellow pus from which Staphylococcus aureus was isolated, a tentative diagnosis

of suppurative myelitis was established. Although intravenous ampicillin sodium was started

immediately, the patient continued to have a high fever, rapidly developed quardriparesis,

numbness below the sensory level C-5 dermatome and urinary retention. At this point he

was transferred to our hospital for further investigation and treatment.

Physical examination on admission revealed an acutely ill obese male with a body tempera-

ture of 37.9•Ž and severe spontaneous pain at spinous processes of C-6 and 7 with marked

tenderness. There was no evidence of any concurrent dermal, dental or rhino-ophthalmologic

infection. Neurological examination revealed that the patient was alert and oriented. The

cranial nerves were unremarkable. He showed flaccid tetraparesis, more prominent in the

lower as well as the left extremities, total areflexia with positive bilateral Babinski signs,

hypesthesia of all modalities at C-5 level extending caudally, and bowel and bladder

disturbances.

Acute inflammatory reactions such as leukocytosis (13,400/mm3), increased erythrocyte sedimentation rate (ESR) (120 mm/hr) and strongly positive C-reactive protein (CRP) (25.5

mg/dl) were noted on admission. Lumbar tap at L-4/5 again produced purulent fluid with countless numbers of polymorphonuclear leukocytes, protein 4,058 mg/dl and glucose 7 mg/dl, with the culture of the yield growing Staphylococcus aureus.

The roentgenograms and non-enhanced CT of the cervical spinal column were unremark-

able and there was no sign of osteomyelitis. Myelography or myelo-CT was not performed

because it was considered to be inappropriate when the presence of an acute paraspinal infec-

tion was highly suspected.

Sagittal cervical MRI (Toshiba MRT-50A, 0.5 tesla) revealed a sharply delineated mass of increased signal intensity with gadopentetate dimeglumine (Gd-DTPA) injection on Ti-weighted image, located around and mainly dorsal to the spinal cord. The lesion was situated in the epidural space between C-1 and C-7 without invasion into the intracranium. Thoracic

and lumbar MRI records were too poor due to motion artifacts for the lower end of the abscess to be determined. The epidural fat tissue, which would appear as a high-intensity band in epidural space, could not be isolated from the abscess in the lower cervical region

(Fig. 1A). T2-weighted scans were not available. Based on the clinical and laboratory manifestations, he was diagnosed as having an acute spinal epidural abscess.

The patient was soon responding to intensive intravenous antibiotic therapy with pipera-

cillin sodium while waiting for surgical intervention, which turned out to be unnecessary once

quick and promising recovery commenced. The abscess had disappeared on follow-up MRI one month after the onset of the symptoms (Fig. 1B), when the patient did not have a fever,

nuchal pain or paresis of the upper extremities, and was capable of ambulating with assistance

albeit he had remaining spastic paraparesis and moderate sensory deficits in the legs.

Patient 2; An 82-year old female, without a previous medical history of diabetes mellitus

MRI Study in Paraspinal Infections 183

Fig. 1. (patient 1) With T1-weighted (spin-echo technique, TR 300 ms, TE 14 ms) sagittal MRI with Gd-DTPA injection, the abscess is depicted as a sharply demarcated linear lesion of high signal intensity (arrows in A). The lesion is not seen after a successful antibiotic treatment (B). The high-intensity area anterior to the spinal cord suggests the presence of pus (A).

or any suppurative diseases, noticed vague low back pain while cleaning her house on Dec.

31, 1989. The next morning, her back pain was also accompanied by weakness of the legs

and a fever of 38.0•Ž. The paraparesis of the lower extremities rapidly worsened, followed

by mild consciousness clouding, total loss of all sensations in the lower extremities and loss

of bladder and rectal control within days. She was admitted to a hospital with a suspicion of

acute meningomyelitis. Myelography performed there showed a partial block of the spinal

column between T-9 and L-1 by an extramedullary lesion which was either intra- or extra-

dural (Fig. 2). On myelo-CT, the spinal cord appeared to be compressed anteriorly by

localized masses which projected into the enhanced subdural space in the same segment as

shown on myelography (Fig. 3). She was then on ampicillin sodium for a few days, which

did not bring about any amelioration of the symptoms.

When transferred to our hospital on the ninth day, she was febrile (38.6•Ž) and slightly

disorientated, complaining of nausea and headache with meningeal irritation signs, but was

devoid of spinal percussion tenderness or any other noticeable skin infection. Neurological

examination revealed that the patient had total paraplegia in the legs, all modal sensory

disturbances of a partial degree at L-1 to L-3 and a total sensory loss below L-3, brisker

but equal tendon reflexes in the upper extremities, areflexia in the legs with positive bilateral

Babinski signs and sphincter disturbances. However, she did not show any cranial nerve

palsy, weakness or cerebellar ataxia of the upper extremities.

Acute inflammatory signs such as leukocytosis (20,400/mm3), increased ESR (30 mm/hr)

and positive CRP (1.3 mg/dl) were remarkable among the laboratory findings on admission.

Urine culture grew Candida species under use of ampicillin sodium. A lumbar tap yielded

purulent fluid which contained more than 170,000 cells/mm3, 97 percent of which was poly-morphonuclear leukocytes, 5,000 mg/dl of protein, 44 mg/dl of glucose and culture of the

184 Toshiya Fuxui, et al.

Fig. 2. (Figs. 2 to 5 in patient 2) Lumbar myelography shows a partial block of the subarachnoid space at T-9 and L-1 due to an extramedullary lesion. It is inconclusive

whether the lesion is located intradurally or not.

Fig. 3. Myelo-CT at L-1 shows a few extramedullary masses in the subdural space. An

outer band of low density corresponding to the epidural fat tissue is clearly recognized.

fluid isolated Escherichia coli.

The roentgenograms of the vertebral column showed no sign of osteomyelitis. T1-weighted

sagittal MRI with Gd-DTPA of the thoracic region disclosed an ill defined mass of the

same or slightly higher signal intensity as the spinal cord, displacing it anteriorly from the

MRI Study in Paraspinal Infections

Fig. 4. A TI-weighted (spin-echo technique, TR 300 ms, TE 14 ms) sagittal MRI (A) and a transaxial image at T-10 (B) with Gd-DTPA. The lesion (arrows in A) is located dorsal to the spinal cord and anterior to the epidural fat from T-9 through L-1 but the lesion seems to extend further rostrally and caudally. A mass lesion of low signal intensity which is surrounded by a high-intensity band (black arrow in B), is present behind the spinal cord (asterisk in B). Epidural fat tissue (white arrow in B) can be recognized clearly separate from the mass lesion. The band of low signal intensity between them represents the dura mater.

level of T-7 at least to L-2. The lesion was recognized to have much more extensive rostral-

caudal distribution than was inferred from myelography and myeio-CT (Fig. 4A). The transaxial T1-weighted MRI scan at T-10 level showed more or less the same findings as myelo-CT, i.e., the spinal cord was anteriorly dislocated by a few blocks of mass lesions of the same intensity as the spinal cord, some of which appeared to be encapsulated by a membrane-like structure enhanced by Gd-DTPA, apparently inside a circular band of low intensity which would correspond to dura mater and attaching soft tisue. Epidural fat was

conspicuously depicted outside the dural sac and characterized by its strongly high signal intensity (Fig. 4B). Combined with lumbar tap results, those mass lesions were regarded as subdural pus. No abnormalities were detected in the spinal cord parenchyma on T1-weighted image with Gd-DTPA and T2-weighted scan was not available.

From these observations, the patient was diagnosed at having an acute spinal subdural

abscess caused by E. coli at the lower thoracic and upper lumbar region. The presence of

consciousness clouding suggested concomitant purulent meningitis as a result of extension of

inflammatory process into the intracranium as inferred from the MRI findings although

myelo-CT suggested otherwise. Candida in the urinary tract suggested prior infection by

suppurative bacteria including E. coli, which may have been adventitiously removed by anti-

biotic therapy. Because of her high age, severity of paraplegia and then a poor nutritional

state, she was rendered to be a poor candidate for surgical operation and was immediately

on piperacillin sodium and latamoxef sodium in place of ampicillin sodium. This regimen

was effective for her meningitis and back pain but no neurological improvement in myelo-

pathy was noted. She was on the same regimen without any neurological improvement and expired on the 21 st day because of concomitant cerebral hemorrhage and hemetemesis from

disseminated intravascular coagulopathy.

186 Toshiya FUKUI, et al.

Fig. 5. The gray matter and patchy areas of the white matter at T-12 (A) and an extensive

area of the ventral two thirds of the spinal cord at L-1 (B) are infarcted. These

areas may correspond to the territories irrigated by the anterior spinal artery.

Notice a large amount of abscess around the spinal cord and the absence of any

direct compression to the spinal cord. (Kltiver-Barrera stain, •~8)

At autopsy, no purulent exudate was encountered on the surface of the spinal dura mater,

but once it was opened, there was sticky purulent material covering the spinal cord from C-2

to cauda equina, the thickest pus being present at T-9 to L-3. There was no gross com-

pression or deformity of the spinal cord. Microscopically, the purulent material was con-firmed as an aggregation of polymorphonuclear cells confined to the subarachnoid space.

The spinal cord per se did not show any infiltration with acute inflammatory cells in its

parenchyma. Abscess masses had no encapsulating membrane against the inference from

MRI Study in Paraspinal Infections 187

MRI findings. The most striking pathological change was a spinal cord infarction most

prominently seen at T-12 and L-1 (Fig. 5). Whole of the gray matter and patchy areas of the white matter at T-12 (Fig. 5A) and the anterior two thirds of the spinal cord at L-1

(Fig. 5B) were completely infarcted and microscopically infiltrated by macrophages, whose

presence suggested that the infarction was in its subacute to early chronic stage. Mild ischemic change was also noted in anterior and lateral columns between T-10 and T-12.

The anterior spinal artery was patent and there was no engorgement of the spinal venous

plexus.

Discussion

As Heusnera8) and others4,5,9) described, the clinical features of both epidural and subdural

abscess follow similar courses and are characterized by back pain, radicular pain, limb paresis

and rapidly progressing quadriplegia. Therefore, these two entities are essentially indistin-

guishable from each other on clinical grounds. It is discussed that coexisting cerebral menin-

gitis, ventriculitis and spinal vascular lesions are more common in subdural abscess, and that spinal percussion tenderness is more common in epidural abscess4,10), but these are not

absolute distinctive differences11). Although some authors maintain that the distinction be-

tween the two is of little practical significance since surgical drainage and antibiotic treatment

are all-important in both situations12), it would be of neuroradiological interest as well as an adjunct help in selecting candidacy and timing for surgical treatment to know the exact

location and extent of a lesion.

Myelography is in some cases a successful method in distinguishing epidural from subdural

abscess13,4), but in others it does not suffice12,15,16). Some potential risk is also suggested

by implanting pathogenic organisms into the subarachnoid space from an epidural abscess via

spinal tapping16). Since patient 1 had an accelerated exacerbation of neurological symptoms

after epidural block to control the back pain, it is possible that an abscess originally localized

in the lumbar region might have been disseminated into the cervical area.

With non-invasive plain CT, it is impossible to distinguish the soft tissues within the spinal canal, i.e., epidural fat, dura mater, arachnoid membrane, spinal cord and abscess if any. If an abscess is to be distinguished from the normal structures in the spinal canal, it would necessitate intrathecal injection of contract medium, therefore myelo-CT would carry the same risks as myelography6).

MRI is being recognized as a noninvasive, repeatable and potentially capable examination

tool for delineating the location and the extent of an epidural abscess2,3,6,7). MRI presen-tation of an epidural abscess in patient 1 may be characterized by a sharp margin, inability of an abscess to extend into the intracranium and disappearance of normally bright high intensity of epidural fatty tissue. The fact that cervical abscess has sharp boundaries and

that it does not extend into the intracranium even though it is closely adjacent to the foramen magnum would suggest that the abscess was located in the tight and closed epidural space which exists between the spinal dura mater proper and the periosteum of spinous

processes, both being joined to form one sheet of intracranial dura mater. Since the disap-pearance of epidural fat on CT is regarded as a pathognomonic feature in epidural abscess17) and whether abscess is located epi- or subdural space can be identified on myelo-CT with

ease, transaxial MRI seems to have no additional diagnostic advantage over myelo-CT except for its lowered risk due to absence of contrast medium. Sagittal MRI, however, would be

188 Toshiya FUKul, et al.

far more superior to myelo-CT in depicting the longitudinal extent of disease.

Subdural abscess, on the other hand, is a much rarer disease and there have been few

reports on MRI findings in subdural abscess. Recently Kurokawa et alY reported that the

subdural abscess was depicted •gintrathecally•h as an iso-intensity on T1-weighted and a

strongly high-signaled band on T2-weighted scan. MRI findings of the subdural abscess

in patient 2 are remarkable in that the demarcation of the abscess is more ill-defined, that

it is easy to identify epidural fat apart from an abscess and that the rostral-caudal extent of

abscess is more precisely correlated with autopsy findings than myelo-CT. As mentioned

above, transaxial myelo-CT may be as efficacious as MRI in defining size, configuration

and location of abscess in relation to dura mater, the superiority of MRI to myelo-CT in

diagnosis of spinal subdural abscess therefore may exist in its availability of diagnostically

valuable sagittal scans as well as its being noninvasive and easily repeatable. In this case,

enhancement by Gd-DTPA was not of much help in separating the lesion from the normal

structures and also careful interpretation of •gringed enhancement•h is needed because the

autopsy examination did not prove any capsular membrane around abscess masses. With-

out similar cases, it remains uncertain as to what it may represent.

Since paraplegia and sensory loss in the lower extremities observed in patient 2 were most likely to be ascribed to spinal infarction at T-12 and L-1 rather than to non-segmental and diffuse compression of the spinal cord by abscess. This may quite well coincide with

Freedman's estimation that spinal vascular lesion is more responsible for presentation of

neurological symptoms than the compression of spinal cord by abscess per se19). As the

lower thoracic to upper lumbar spinal cord is vulnerable to ischemia because this region corresponds to a border-zone between two adjacent radicular arteries20,21), it is possible that radicular arteries were compressed by abscess or arterial spasms were induced by the irrita-

tive nature of infection, resulting in spinal infarction at T-12 and L-1. Early detection of

spinal infarction which may consequently accompany subdural abscess would be of great

importance in determining a treatment strategy of conservative therapy in lieu of surgical intervention, since decompression and removal of abscess may not be effective or suitable in reducing neurological impairments of those afflicted with subdural abscess once accompanied

by spinal infarction.

According to the previous literature4,.5,11,12,19), the most common causative organism in both

spinal epidural and subdural abscess is Staphlococcus aureus. Patient 1 with epidural abscess

was not an exception, but patient 2 was one of the rare cases whose subdural abscess was

caused by an organism other than this common bacterium. Escherichia coli is regarded as

a rare cause of paraspinal infections and shares only two percent of all causative organisms

in a series of patients reviewed by Takenaka et al.11). In either case, it was impossible to

ascertain the exact route of entry of infectious organisms to the paraspinal regions, but it

was speculated that hematogenic dissemination from the respiratory or urinary tracts, for

instance, might be more probable than direct extension of infection from the nearby structures

to the spinal canal.

Acknowledgements

The authors would like to thank Dr. Nobutaka Arai, of the Department of Clinical Neuropathology,

Tokyo Metropolitan Institute for Neurosciences, for providing pathological findings of the spinal cord

and to Ms. Ramona Severson for syntactic revision of the manuscript.

MRI Study in Paraspinal Infections 189

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[Received October 25, 1991: Accepted November 5, 1991]