1991. The British Journal of Radiology, 64, 386-402

Magnetic resonance imaging of spinal trauma By R. W. Kerslake, MRCP, FRCR, *T. Jaspan, MRCP, FRCR and B. S. Worthington, BSc, FRCR Sub-Department of Academic Radiology, and 'Department of Neuroradiology, University Hospital, Queen's Medical Centre, Nottingham NG7 2UH, UK

{Received September 1990 and in revised form December 1990) Keywords: MR imaging, Spine, Injuries, Spinal cord injuries, Syringomyelia

Abstract. A retrospective series of 118 magnetic resonance examinations of 110 patients who had sustained previous spinal trauma is reported. Examinations performed within 3 weeks of trauma showed extraspinal soft tissue (including ligamentous) injury in 48% and intraspinal lesions in 61% (mostly consisting of extradural haematoma and spinal cord contusion). In examinations performed more than 3 weeks after injury intraspinal abnormalities were shown in 51% and these represented spinal cord compression, atrophy, myelomalacia and syringohydromyelia. Magnetic resonance imaging has the unique capability of displaying non-invasively the late sequelae of spinal trauma permitting simultaneous evaluation of the extra-spinal soft tissues, vertebral column and spinal cord. It is therefore recommended as the technique of choice in the investigation of patients who have sustained previous spinal injury, particularly those with neurological deficit. In the acute phase potentially remediable causes of neurological impairment such as disc herniation or extradural haematoma can be identified. Signal changes in the cord may allow the prognosis for neurological recovery to be established. In the later stages sequelae such as cord atrophy, myelomalacia and syringohydromyelia are accurately identified and surgical therapy may be guided, where appropriate.

Magnetic resonance imaging (MRI) has the unique capability of displaying non-invasively the late sequelae of spinal trauma permitting simultaneous evaluation of the extra-spinal soft tissues, vertebral column and spinal cord. Materials and methods

A retrospective series of 118 MR imaging examinations of 110 patients who had sustained previous spinal trauma was analysed. The study population included all patients with a history of previous spinal trauma referred for spinal MR imaging between late 1985 and early 1990. Magnetic resonance imaging was performed to evaluate suspected vertebral column fractures or ligamentous injuries, spinal injuries with suspected cord damage or progressive neurological deficit or, in a minority of cases, the intervertebral disc status following spinal trauma. The interval from trauma to MR imaging was less than 3 weeks in 44 examinations (Group 1) and from 3 weeks to 40 years in 74 examinations (Group 2). The age range of the patients was 4 days to 80 years, mean 40 years. There were 75 males and 35 females. The male: female ratio was 3:1 in Group 1 and 2:1 in Group 2. The level of injuries is shown in Table I. Magnetic resonance imaging was carried out at 0.15 Tesla using a dedicated surface coil appropriate to the region in all but two cases (who were examined using the body coil). Short repetition time (TR)/short echo time (TE) spin-echo (TR, 500/TE, 40) sequences (^-weighted spin-echo, 7JAVSE) were routinely employed in the sagittal and axial planes, supplemented Address correspondence to: Dr R. W. Kerslake, MRI Unit, Queen's Medical Centre, Nottingham NG7 2UH. 386

Table I. Level of injuries Level

Group 1 (n = 44)

Group 2 (n = 74)

Cervical Upper thoracic (T1-T6) Lower thoracic (T7-T10) Thoracolumbar (Tl 1-L2) Lower lumbar (L3-L5) Two or more levels

23 6 5 6

33 7 6 21 4 4

2 4

by sagittal plane long TR/long TE (TR, 1600/TE, 80) (^-weighted spin-echo, 7JWSE) or short time to inversion recovery (STIR) sequences in most instances. Medically unstable patients were not imaged. Patients with potentially unstable injuries or those requiring traction were carefully transferred to the scanning table under medical supervision. Traction halos were left in place for two examinations. Each examination was assessed with respect to the extraspinal soft tissues, the vertebral column (including intervertebral discs) and the intraspinal contents. Image quality was also graded subjectively. A consensus report for each set of images was produced by two radiologists experienced in MR imaging. The MR images were reported without knowledge of the findings of either clinical examination or other imaging methods. Results

The proportion of scans showing abnormalities in the extraspinal soft tissues, the vertebral column and the intraspinal contents is shown in Table II. The detailed results for Groups 1 and 2 will be described separately. The British Journal of Radiology, May 1991

MRI of spinal trauma Table II. Proportion of examinations showing abnormalities in region Region

Group 1 (n = 44)

Group 2 (n = 74)

Extraspinal Vertebral column Intraspinal Normal

21 27 28 7

2 59 38 11

(48%) (61%) (63%) (16%)

(3%) (79%) (51%) (15%)

Group 1

Of the 44 examinations, 10 were obtained within 24 hours of injury and 34 within the first week. Image quality was judged to be good or excellent in 68%, fair or poor in 30% and non-diagnostic in 2%. No abnormality was present in seven examinations (16%). Extraspinal soft tissue abnormalities were shown in 21 scans (48%) and comprised prevertebral soft tissue

thickening and/or posterior Hgamentous complex abnormalities. These were not seen later than 6 weeks after injury in any case. Prevertebral soft tissue thickening was shown in 7 cases (16%) and in each case was accompanied by a vertebral body fracture or fracture dislocation. The soft tissue thickening was visible on 7JAVSE but was more conspicuous when STIR sequences were used where it was invariably of intense high signal intensity. Pathological confirmation of the nature of this material was not obtained in any case, but it probably represents haemorrhage and oedema. Posterior Hgamentous complex changes were seen in 19 cases (43%). These could often be appreciated on TjAVSE or T^WSE images, when areas of high signal intensity corresponding to the location of the interspinous and intertransverse ligaments were shown, but were optimally demonstrated using a STIR sequence when the signal from intermuscular fat planes was suppressed (Fig. 1). Abnormal signal intensities in the posterior Hgamentous complexes were accompanied by either vertebral column or intraspinal lesions in every

(a) (b) Figure 1. Sagittal SE 500/40 (a) and STIR (b) images obtained 3 hours after injury (flexion-compression fracture of T4 with cord compression). Posterior Hgamentous disruption (curved arrow) and acute extradural haematoma Tl and T7 (arrow) are best appreciated on STIR images. Vol. 64, No. 761


R. W. Kerslake, T. Jaspan and B. S. Worthington

Figure 2. Sagittal SE 1600/80 (a) and STIR (b) images at 24 hours of a "Chance" type fracture at T8/9. High signal intensity changes extend from the prevertebral tissues into the widened disc space, anteriorly within the canal and involve the posterior ligamentous complex. Changes consistent with cord contusion are seen on the Z|WSE (arrow).

case, and may be considered a marker of more severe injuries. However, intraspinal abnormalities were present in seven cases where no extraspinal soft tissue changes were seen. In five of these, a STIR sequence was not used whilst in the remaining two cases, where a STIR sequence had been used, the additional findings were of traumatic disc protrusions causing cord displacement or compression. In four scans, high signal intensity changes were shown running between the prevertebral soft tissues, through the disc at the level of injury and into the posterior ligamentous complex, possibly representing the tissues which had sustained the greatest stresses at the time of injury. These were seen in one "Chance" fracture (Fig. 2), one fracture dislocation and two burst fractures. The anterior longitudinal ligament (ALL) appeared disrupted in five cases (four burst fractures of LI, one horizontal shearing type injury in the lower thoracic 388

region). Disruption of the posterior longitudinal ligament (PLL) was not seen in any case, probably because of the lack of contrast between the low signal intensity PLL, the low signal intensity cerebro-spinal fluid (CSF) and the low signal intensity posterior cortical bone on Tj'WSE; gradient echo techniques which highlight the CSF pool would clearly be helpful in this context. Vertebral column abnormalities were present in 27 examinations, of whom only two showed no overt lesion in the extraspinal soft tissues or intraspinal contents. Vertebral body fractures, shown by loss of normal vertebral body contour or alteration of signal intensity (Fig. 3), were the commonest finding (18 cases) while fractures of the posterior neural arch were diagnosed in two cases. Alteration of vertebral body signal intensity was shown in nine cases (increased signal on ZJWSE or STIR in eight, reduced in one). Focal canal stenosis was present in 17 cases and, in seven of these, The British Journal of Radiology, May 1991

MRI of spinal trauma

(a) (b) Figure 3. Sagittal SE 500/40 (a) and SE 1660/80 (b) images at 3 days after injury (burst fracture of LI with moderate canal stenosis but no spinal cord injury). Note the loss of marrow signal anteriorly in LI body on 7JWSE (a) and high signal posteriorly on 7JWSE. There is preservation of disc morphology and signal intensity. The PLL is elevated but intact (arrow).

disc protrusions contributed to focal canal narrowing. These cases are detailed in Table III. Disc protrusion was documented in seven out of 23 patients (30%) with recent cervical trauma. Spinal cord changes (contusion or compression) were present in all but one of these cases, though the degree of cord compression did not warrant decompressive surgery in any. Most of these patients were of ages such that coincidental disc protrusions or spondylotic changes would be uncommon. More severe disc injuries, such as

complete disruption, shown by loss of continuity of the superior or inferior disc margins were seen in only three cases. In each of these, reduced signal intensity of central disc material was shown on either ZJWSE or STIR sequences along with clear loss of margination of the affected disc. Two were thoracolumbar and one a cervical injury. Intraspinal abnormalities were present in 28 scans (64%), some showing more than one abnormality. These included extradural haematoma in 17, cord

Table III. Acute traumatic disc protrusions: level and intraspinal changes Case Age, years Level Cord compression Cord contusion Extradural Haematoma

1 22 C3/4 —


2 26 C2/3

3 39 C3/4

+ +

+ —

4 55 C6/7 —

+ —

5 35 C3/4 — —

6 42 C2/3

7 50 C4/5

+ —

+ —


Key: + feature present, — feature absent.

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R. W. Kerslake, T. Jaspan and B. S. Worthington

Figure 4. Sagittal SE 500/40 (a) and SE 1600/80 (b) images obtained 24 hours after axial loading injury. The cord morphology is normal (a), but there is high signal intensity anteriorly within the cord at C5 (b). Note the anterior compression of the body of C5 and high signal changes posteriorly in the interspinous ligaments (arrow).

compression or displacement in 15 and cord contusion in 11. Acute extradural haematomas were of intermediate to high signal intensity on all pulse sequences, but were most obvious when a STIR sequence was used. This was particularly true for examinations in the thoracic region where the presence of variable amounts of posteriorly situated extradural fat could cause diagnostic confusion (see Fig. 1). In two of the more recent cases, the presence of extradural haematoma was confirmed surgically; both of these were patients with incomplete neurological deficits examined within a few hours of injury. Magnetic resonance imaging allowed diagnosis and localization of an extradural haematoma, demonstrated the extent of cord compression and guided the surgical approach. In the remaining cases, pathological confirmation was not obtained; in one, a follow-up examination 10 days later showed resolution of the haematoma. In 12 examinations, the haematomas were localized around the injury site, involving one or two spinal segments, and in five cases were diffuse, involving three to seven, (mean five) segments. Vertebral column injuries were present in all but three of these cases, one of which was associated with an obstetric epidural anaesthetic. Extradural haematoma was responsible for cord compression or displacement in four cases and contributed to cord compression in a further six cases. Cord compression due to bone fragments was present in seven examinations and due to disc protrusion in four. In each case, the relationships of the spinal cord and theca to the cause of compression could be readily ascertained. 390

Changes consistent with spinal cord contusion were present in 11 cases. The spinal cord was of normal morphology in eight cases, focally enlarged in two cases and more diffusely swollen in one case. The cord was of normal signal intensity on 7JWSE, except in three cases, two of which demonstrated minimal hyperintensity and one focal hypointensity. Typically TjWSE showed hyperintensity, particularly anteriorly within the spinal cord (Fig. 4). The exceptions were a single case in which spinal cord hyperintensity was only shown on a STIR sequence and a further single case in which a central area of slightly reduced signal intensity was present on 7JWSE with surrounding hyperintensity (Fig. 5). The changes were confined to the level of injury in all except one case which showed abnormalities extending over three spinal segments (Fig. 6). Additional abnormalities such as extraspinal soft tissue injury, extradural haematoma or vertebral body fractures were present in the majority of instances (see Fig. 6). Group 2 Scan quality was judged to be good or excellent in 78%, fair or poor in 20% and non-diagnostic in 2%. Eleven (15%) of the scans were entirely normal. Changes in the extra-spinal soft tissues, with regions of high signal intensity in the posterior ligamentous complex were shown in two cases. Both examinations were obtained within 6 weeks of injury and these changes were best shown using the STIR sequence. The vertebral column was normal in 15 cases; of these, changes in the spinal cord were shown in five The British Journal of Radiology, May 1991

MRI of spinal trauma

(b) Figure 5. Sagittal SE 500/40 (a) and SE 1600/80 (b) images obtained 7 days after anterior decompression for herniated thoracic disc. Note the slight focal cord swelling and hypointensity in (a). In (b), central hypointensity and peripheral hyperintensity is shown, suggesting resolving haemorrhagic contusion.

cases (atrophy two, cystic myelomalacia two and a syrinx in one, the latter occurring following a stab wound). Abnormalities of the vertebral column or intervertebral discs were present in 59 (79%) of examinations. The changes shown included fractures of the vertebral body (49 scans), focal bony canal stenosis (21 scans), altered vertebral body signal intensity (six scans) and vertical vertebral body cleft (six scans). The development of a vertical vertebral body cleft over a 1-year period was documented in a single case in which MRI in the acute phase demonstrated endplate fractures and abnormal vertebral body signal intensity. Disc protrusions were present, either as an isolated feature or in association with bony changes, in 16 scans. These were associated with spinal cord abnormalities in 11 scans (compression, six; atrophy, two; syrinx, two; contusion, one). Abnormalities of disc height or signal intensity were shown in 25 cases. Two patterns were seen. The first was that of loss of disc height accompanied by loss of signal intesity on 7JWSE at the level of fracture-dislocations (usually cervico-thoracic). Secondly, the disc above the level of thoracolumbar Vol. 64, No. 761

burst fractures showed loss of height and signal intensity while the disc below the level of these fractures was usually normal (Fig. 7). Where a vertical vertebral body cleft had developed, disc material herniated into the vertebral body defect, mainly from the disc above, though without loss of signal intensity. Intraspinal abnormalities were shown in 38 (51%). Spinal cord compression or displacement was present in 17 cases, due to bony narrowing in 11 cases and disc protrusion in six (Fig. 8). Atrophy of the spinal cord was shown in 13 cases, not being seen earlier than 4 months following trauma. These changes were maximal at the site of injury and involved between three and 11 spinal segments, mean 5.7 segments (Fig. 9). High signal changes (^WSE) were seen within the cord on four of these scans. The features of myelomalacia (focal moderately well defined high signal intensity on T^WSE with or without small punctate regions of low signal intensity on TJAVSE) were present in eight cases. These changes were shown at the level of previous injury and were not seen earlier than 6 months post-trauma (Fig. 10). They were usually, but not invariably, accompanied by other 391

R. W. Kerslake, T. Jaspan and B. S. Worthington

Figure 6. Sagittal SE 500/40 (a) and SE 1600/80 (b) images obtained following an axial loading injury. There is diffuse cord swelling between C2 and C7, with hyperintensity anteriorly at C4/5 on 7JWSE (b). There is a traumatic protrusion of the C4/5 disc with craniad migration (straight arrow) and extensive anterior epidural haematoma (short arrows).

intraspinal abnormalities (cord compression or atrophy) and vertebral column abnormalities were present in all but two of these cases. In a single case, previous therapeutic transection of the cord was confirmed; the absence of residual syringohydromyelia was established b-y MW. SpmaA cord \eW\era\g, at \Y\e s\Ve o? VnjuT^ was shown in only one case, a cervical fracture-dislocation in which the cord was atrophic but surrounded by strands of intermediate signal intensity and intimately apposed to the posterior thecal sac. Tethering may have been present in other cases where the cord was apposed to the thecal sac but other factors such as the presence of canal stenosis or cord displacement by bone or disc did not permit positive identification of an abnormal cord position due to tethering. Syringohydromyelia was present in 10 patients, and was not seen earlier than 6 months following trauma. All were well defined regions of low signal intensity within the cord substance on Tj'WSE and involved between 3 and 20 spinal segments. In four of six cervical and upper thoracic injuries the size of the cavity above the level of injury was considerably greater than that below the level of injury (Fig. 11). Focal canal stenosis of 44-60% was present in these cases and the cord was noted to occupy the entire width of the spinal canal at the level of injury. Typically, the spinal cord was enlarged, the syrinx appeared distended and contained multiplefibroglialbands or septations above the level of injury, while below, it was smooth walled and the syrinx appeared partially collapsed with only minimal spinal 392

cord expansion (Fig. 12). A similar but less consistent pattern of abnormalities was seen with the thoracolumbar injuries in which a syrinx had developed. In one case, there was considerable expansion of the lumbar theca below the level of a previous LI burst fracture in which the conus, expanded by a distended syrinx, appeared to be causing a ball-valve type obstruction to cephalad CSF flow (Fig. 13). Discussion

Spinal trauma is a common and devastating event with important long term sequelae for both the individual and society. Neurological deficits may be transient, incomplete or complete. Patients with an incomplete deficit may benefit from aggressive therapy aimed at limiting secondary deterioration due to spinal cord ischaemia and compression consequent upon treatable causes such as disc herniation or extradural haematoma. Management is best provided in dedicated spinal injury units (Johnston, 1989). It is in patients with incomplete neurological deficits that MR imaging in the acute phase offers the most potential practical benefit. Particular advantages of MRI are the ability to monitor changes non-invasively within the spinal cord in both the short and longer term in an attempt to identify predictors of outcome and better understand the natural history of post-traumatic spinal cord syndromes. Classification of spinal trauma into acute and chronic categories is somewhat arbitrary. During the first week of spinal cord injury, most of the metabolic derangeThe British Journal of Radiology, May 1991

MRI of spinal trauma

(a) Figure 7. Images of a burst fracture of LI, 3 years after injury. There is moderate canal stenosis and the conus is displaced posteriorly (a: SE 500/40). Note the loss of height and signal intensity of T12/L1 disc on STIR images (b).

ments, vascular changes and oedema will have already occurred. The subacute and chronic changes subsequently evolve, but there are no clinical or radiological markers that permit their separation. Injury to the bony spine can be considered acute if it has occurred within 3 weeks, as during this period most fractures behave like fresh fractures and may be reduced by conventional distraction devices (Quencer, 1988). Magnetic resonance imaging in patients who have sustained spinal trauma allows direct visualization of the extraspinal soft tissues, the vertebral column and the intraspinal contents in a manner that has not previously been possible. While conventional radiography remains of paramount importance, MR imaging is capable of providing information of critical importance in determining patient management strategies in both acute (Goldberg et al, 1988; Mirvis et al, 1988a; Quencer, 1988) and chronic (Quencer et al, 1986; MacDonald et al, 1988; Quencer, 1988) spinal injuries. Technical considerations Magnetic resonance imaging in medically unstable patients remains difficult, though not impossible, partiVol. 64, No. 761

cularly at low field strengths. Cervical traction devices using metal weights and tongs may be temporarily removed in some cases (cervical dislocation without fracture or posterior element fracture only) or replaced by an MRI-compatible system using water bags (McArdle et al, 1986) in cases where traction should be maintained (vertebral body fractures with retropulsed bone fragments which have been reduced by traction) (Quencer, 1988). Traction devices may cause difficulties with surface coil placement and induction of eddy currents causing either local artefacts or heating effects, especially at high field (Kanal et al, 1990). Use of titanium rather than stainless steel wire for internal fixation may be of advantage in reducing local image degradation (Mirvis et al, 1988b). We experienced one case in which a Cl/2 fracture-dislocation could not be imaged owing to artefacts from a halo traction device (though a second clinically unsuspected high thoracic injury was revealed). In a single case, the presence of Luque rods resulted in a non-diagnostic examination. Truncation artefacts, which may mimic the appearances of syringohydromyelia, cause artefactual central low signal intensity within the cord (Czervionke et al, 393

R. W. Kerslake, T. Jaspan and B. S. Worthington

1988) or overestimation of cord atrophy (Yousem et al, 1990). These may be minimized by reduction of pixel size by either decreasing the field of view or increasing matrix size to 256 x 256 or greater (Czervionke et al, 1988). In our experience, the use of both sagittal and axial imaging planes is also crucial to the accurate assessment of cord morphology and signal characteristics, and helps to differentiate artefact from pathological cord changes. Operation at low field (0.15T) has advantages in limiting some artefacts, but at the cost of relatively poor spatial resolution, signal to noise ratio and minimum slice thickness. Use of phase-sensitive techniques would be an advantage in evaluating spinal cord tethering and CSF dynamics. With current spatial resolution, computed tomography (CT) myelography is still required for the assessment of post-traumatic radiculopathy and brachial plexus injuries.

Figure 8. Sagittal SE 500/40 image of fracture-dislocation of C5, 4 years after injury. There is severe focal canal stenosis and malalignment in the mid-cervical region. The spinal cord remains compressed and markedly atrophic.

Vertebral column Plain radiographs remain the mainstay of initial assessment of skeletal injury. In comparison with conventional radiographs, CT has been shown to be more sensitive in the detection of neural arch fractures and more accurate in assessing spinal canal and lateral recess narrowing (Lynch et al, 1986). The ability to diagnose stable fractures positively which may be treated by early mobilization or conversely to show indirect evidence of ligamentous disruption requiring open surgery are two further advantages of CT over

Figure 9. Sagittal (a) and axial (b) SE 500/40 images of an old C5/6 fracture with reversal of cervical lordosis and mild canal stenosis. The cord is not compressed but is severely atrophic.


The British Journal of Radiology, May 1991

MRI of spinal trauma

Figure 10. Sagittal SE 500/40 (a), SE 1600/80 (b) and axial SE 500/40 (c) images of cystic myelomalacia, 6 months after injury. Hyperintensity within cord on 7JWSE (b) and poorly defined hypointense foci on 7^WSE (arrows).




conventional radiography. However, assessment of longitudinally orientated structures such as the odontoid peg remains limited, even if reformatted images are obtained and evaluation of long segments of the spine is time-consuming and involves a significant radiation dose. Magnetic resonance imaging offers profound

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5 6 7 8 9 10 CASE Figure 11. Post-traumatic syringohydromyelia. The vertical extent and maximum transverse diameter of post-traumatic syringes are represented by proportionately-sized ovoids; those with internal septations or fibroglial bands are hatched whilst those with smooth walls are shaded. The level of injury is shown ( # ) and the percentage canal stenosis is also recorded.


R. W. Kerslake, T. Jaspan and B. S. Worthington

Figure 12. Sagittal (a) and axial (b) SE 500/40 images 6 months after RTA. Shear type fracture dislocation of C4/5. There is an extensive syrinx (from Cl to Tl 1) which above the fracture is complex with fibroglial bands (b) while, below the fracture level, the syrinx is unilocular. There is marked focal canal stenosis and the enlarged spinal cord completely fills the canal at this level.

advantages compared with CT in being capable of surveying large regions of the spine, in producing direct sagittal images and showing direct evidence of ligament disruption or contusion. The ability to reveal injuries unsuspected clinically and on the basis of conventional radiography is of obvious benefit. Previous studies have documented the utility of MRI in acute spinal trauma (Kulkarni et al, 1987; Tarr et al, 1987; Beers et al, 1988; Goldberg etal, 1988; Mirvis etal, 1988a; Schaefer etal, 1989). Magnetic resonance imaging is well suited to evaluation of the discovertebral junction and intervertebral discs. In comparison with CT, MRI detects more traumatic disc herniations, epidural haematomas and spinal cord abnormality, though is less sensitive in the detection of posterior element fractures (Tarr et al, 1987). Traumatic cervical disc herniations are probably more common than previously recognized, occurring in 40-50% of cases in some series (Mirvis etal, 1988a; Schaeffer etal, 1989) and in 30% of our material. Acute central injury to the cord (with an intact vertebral column) is more common in the elderly population, in whom the cervical canal is already reduced in size by degenerative disease •(John396

ston, 1989). Disc herniations in the presence of spondylosis may give rise to an anterior spinal cord syndrome in the absence of vertebral column fractures or dislocations (Mirvis etal, 1988a; Johnston, 1989) and signal changes within the spinal cord may be shown by MRI in such cases (Yamashita et al, 1990). Vertebral body fractures are readily detected by MRI and CT in most, but not all, cases (Tarr etal, 1987; Mirvis et al, 1988a). In keeping with previous studies of spinal trauma, we found a preponderance of male patients with cervicothoracic and thoracolumbar injuries. In our series, both increased and decreased signal intensity was shown in fractured vertebral bodies, as has been previously reported (Beers etal, 1988). Fractures of the posterior elements were less readily shown (Tarr etal, 1987) but often attention was indirectly drawn to them by the presence of ligamentous abnormalities shown on the STIR sequence. Computed tomography remains valuable in the detection of neural arch fractures in the cervical region and also in demonstration of small bone fragments within the cervical canal which may remain undetected by MRI. In general, osseous lesions are better shown by conventional radiography The British Journal of Radiology, May 1991

MRI of spinal trauma

Figure 13. Sagittal SE 500/40 (a) and SE 1600/80 (b) images of a small septated syrinx in conus at level of previous burst fracture. There is moderate focal canal stenosis and the expanded distal cord completely fills the canal at this level. Note the distended distal thecal sac containing CSF of higher signal intensity (arrow) than that above level of block to CSF flow (curved arrow) on ZJWSE and peripheral hyperintensity to syrinx.

and CT, but vertebral alignment may be better appreciated by MRI in the cervicothoracic region (Goldberg et al, 1988). Magnetic resonance imaging is also of value in the diagnosis of multilevel injury and may reveal clinically unsuspected injuries, as was our experience in at least one case. An added advantage is the facility of MRI in demonstrating the cervicothoracic junction region, which, owing to artefacts, may be difficult to demonstrate by conventional radiographs of CT. There is poor correlation between radiographic appearances of burst fractures (including assessment of posterior element fracture, translocation and degree of canal narrowing) and neurological status, though lumbar burst fractures with more than 50% canal narrowing show an increased risk of instability and neural damage (Willen etal, 1989). The skeletal deformity is well shown by CT, but MRI has the advantage of demonstrating the precise relationships of the spinal cord to the vertebral column or retropulsed fragments at the level of injury (Kulkarni etal, 1987). Magnetic resonance imaging is useful in orientating fragments within the canal, though in severely comminuted burst fractures, CT is capable of showing larger numbers of displaced fragments (Tarr etal, 1987). Where subluxation is present, this is better assessed by MRI than CT; MRI also optimally distinguishes between impingement on the theca or cord by subluxed vertebrae or concurrent haematoma (Tarr et al, 1987). Vol. 64, No. 761

Coronal (vertical) body cJefts in adults are usually the result of either trauma or metabolic bone disease. In traumatic cases, remodelling may result in the late development of a complete vertical cleft into which the cranially and caudally related discs herniate and become apposed, in some cases without desiccation of the central component of the disc (Wilson etal, 1989). Magnetic resonance imaging permits the long term sequelae of disc trauma to be studied non-invasively and is of value in demonstrating which discs become dehydrated or protruded, information which may be of value when surgical fusion is planned. While ligamentous injuries may be indirectly inferred from conventional radiographic or CT examinations, MRI is uniquely capable of demonstrating ligamentous disruption (Kulkarni et al, 1987; Goldberg et al, 1988; Mirvis etal, 1988a; Beers etal, 1989). We identified disruption of the anterior longitudinal ligament (ALL) in five cases, four of which were thoracolumbar burst fractures. A diagnosis of posterior longitudinal ligament (PLL) rupture was not made in any case. This probably reflects the difficulties encountered in identifying the PLL given the technical limitations of our MRI scanner, rather than the lack of PLL injury. In an autopsy study, Willen et al (1989) found complete or partial rupture of the PLL in all of their patients dying acutely with thoracolumbar burst fractures; avulsion of the ALL from the injured vertebral body and the vertebral body 397

R. W. Kerslake, T. Jaspan and B. S. Worthington

below was seen in 50% of cases and loosening of the ALL in the remainder, but in no case was the ALL completely ruptured. However, in cases treated surgically, an intact PLL is often preserved even though stretched (Webb, Personal communication). The PLL, adjacent cortical bone and CSF are all of low signal intensity on 7JAVSE; use of either 7JWSE or gradientecho techniques to produce high signal intensity CSF should reduce problems of PLL identification. We noted that the PLL was lifted from the underlying vertebral body by either haematoma (presumed) or disc protrusion in five cases; in these, because of the nature of the contained material, the PLL could be clearly identified (though was not ruptured). It is interesting that the PLL in each case appeared to be fixed at the cranial and caudal limits of its elevation at the level of the midvertebral body, often at the level of the basivertebral vessels. Abnormal signal intensity within the interspinous ligaments was often present on both Tj'-weighted and ^-weighted images, but was best appreciated using the STIR sequence, where the high signal intensity of intermuscular fat planes was suppressed. We were unable to differentiate between the changes due to soft tissue contusion, haemorrhage or ligamentous rupture as pathological confirmation was not present in this material. Identification of the true extent of ligamentous injury is important practically and may alert clinicians to the risk of instability and delayed spinal cord compression (Goldberg et al, 1988). Isolated rupture of the posterior ligamentous complex is insufficient to cause instability, though additional rupture of the PLL and posterior annulus fibrosus permits instability in flexion to occur. It was this latter observation which led to the proposal of a three-column spinal structure (Denis, 1984). In some cases, a line of high signal intensity extending from anteriorly to posteriorly through the injured level can be seen, possibly indicating the regions that have experienced maximal disruptive forces (Beers et al, 1988). This was seen in four of our cases. These findings can, perhaps, be considered as a visual extension of the concept of "fingerprints" of spinal trauma (Daffner et al, 1986), and promise to assist in understanding the mechanisms of vertebral trauma, particularly with regard to ligamentous damage which cannot be shown by other means. Spinal epidural haematoma may be of variable appearance on CT (Williams & Nelson, 1987) and is frequently difficult to detect in acute cervicothoracic injury as a result of beam hardening artefacts in the shoulder region. While the MRI appearances of epidural haematoma are relatively characteristic (Rothfus et al, 1987; Bernsen et al, 1988; Pan et al, 1988) there may also be contributions to epidural thickening from venous engorgement and oedema (Beers et al, 1988), all of which result in increased signal intensity on ^-weighted images. Use of the STIR sequence facilitates the diagnosis of thoracic region epidural haematoma, where suppression of the signal from normally situated 398

posterior epidural fat leads to greater conspicuity of epidural haematoma. In contrast to parenchymal haemorrhage, extraparenchymal blood appears of high signal intensity on short TE images and may be isointense on long TE images. In experimental animal models, this is probably because of the rapid formation of methaemoglobin where the wounds are exposed to atmospheric oxygen (Hackney et al, 1986). Traumatic spinal epidural haematoma has previously been considered to be uncommon (Pan et al, 1988), but in our material was shown in 4 1 % of examinations performed within 7 days. Two of our recent cases, imaged within a few hours of injury and with incomplete neurological deficits, were operated on following the MRI demonstration of extensive epidural haematoma causing cord compression. The MR images were of value in planning the surgical approach and extent of exploration, as has been suggested by other workers (Beers et al, 1988). The role of such early operative intervention has yet to be fully evaluated. Other workers have described extradural haematoma arising distant to the fracture site, but this was not seen in our material (Goldberg et al, 1988). Spinal cord Clinical evaluation of spinal trauma cannot reliably distinguish between cord transection, necrosis, haemorrhage or oedema, as shown by those patients who improve after initially complete clinical lesions. Electrophysiological testing is of limited prognostic value as only specific pathways are evaluated (Hackney et al, 1986). Assessment is further complicated by the fact that the clinical level of spinal cord abnormalities may be different from the site of injury. The late sequelae of spinal trauma include spinal cord atrophy, tethering, myelomalacia and syringohydromyelia. These may be localized at the injury site or extend extensively into non-traumatized regions of the cord. Abnormalities of the vertebral column and intervertebral discs may occur due to the original injury or as a result of mechanical instability subsequent to previous decompressive surgery and these may, in turn, contribute to further cord injury (MacDonald et al, 1988). Magnetic resonance imaging readily demonstrates the relationship of the thecal sac and spinal cord to the vertebral column and provides a non-invasive means of demonstrating spinal cord displacement or compression and the presence of cord atrophy, tethering, myelomalacia or syringohydromyelia. Computed tomography scanning and CT myelography are insensitive to spinal cord abnormalities following trauma (Quencer et al, 1986; Tarr et al, 1987; Beers et al, 1988; Goldberg et al, 1988). Magnetic resonance imaging provides a wealth of information, though pathological correlation has frequently not been obtained. In vitro micro-imaging studies in animal models have shown loss of the grey/white matter interface at the level of injury and low signal intensity regions representing haemorrhage (Lemaire et al, 1990). Other authors have described very low signal intensity lesions on long TE sequences with iso- or hypointensity The British Journal of Radiology, May 1991

MRI of spinal trauma

on short TE sequences corresponding to pathologically those with Type II pattern and if this was relieved, confirmed cord haemorrhage and the presence of deoxy- neurological outcome was improved in some cases. haemoglobin. More diffuse high signal intensity changes Patients with a central cord syndrome showed Type II in the cord seen on long SE sequences correspond to changes in two thirds of the cases, often without assooedema, but differentiation of necrosis from non- ciated vertebral column injury. Some of these necrotic oedema is not possible (Hackney et al, 1986). progressed to gliosis only, while others showed progresIn human studies, MRI has demonstrated various sive liquefactive necrosis. Type IV changes (atrophy) patterns of abnormality within the acutely injured spinal were only seen as a late phenomenon in their patients, cord. Although pathological material is sparse, reason- all of whom had a long history of post-traumatic myeloable correlation of MRI patterns with pathology has pathy or cord compression. We have observed atrophy been obtained (MacDonald et al, 1988). Spinal cord in patients examined as early as 4 months after injury, swelling is best shown on ^-weighted images (Beers although in the majority of cases atrophy was only seen et al, 1988). Focally increased signal intensity on 7JWSE in those scans obtained 2 years or more following probably represents oedema while focal hypointensity trauma. Patients developing Type III changes (low on long TE images is consistent with the presence of ^WSE, high Z;WSE) suggesting myelomalacia had a deoxyhaemoglobin (Beers et al, 1988). At high field poor neurological outcome, as did those with Patterns strength (1.5T), Kulkarni et al (1987) describe three IV and V (atrophy and syrinx). patterns of cord damage in acutely spine injured Clinico-pathological studies have resulted in the patients corresponding to (1) central haemorrhage concept of a spectrum of post-traumatic spinal cord which increased with time, (2) central petaechial pathology from arachnoiditis to microcystic degenerahaemorrhage resolving with time and (3) oedema and tion to syringohydromyelia (MacDonald etal, 1988; contusion only. Prognosis seems to relate to these cate- Stevens etal, 1988; Yamashita etal, 1990). Ascending gories, being worst in those with intraparenchymal and descending post-traumatic myelopathy is thought haemorrhage (Pattern 1) (Kulkarni et al, 1987; Schaefer to begin at the time of injury or soon after and may etal, 1989; Bondurant et al, 1990) while those with involve mechanisms such as the release of destructive oedema or petaechial haemorrhages exhibit the poten- enzymes, free radical products or other toxic agents tial for some neurological recovery (Kulkarni et al, (Stevens etal, 1988; Fox etal, 1988). Central or dorsi1987; Schaefer et al, 1989; Bondurant et al, 1990). Type central cores of necrotic tissue may extend for several 2 changes were the commonest (63%) and were usually segments from the level of injury and these could liquefy associated with clinical improvement (Kulkarni et al, and form a cavity. Conversion of this area of necrosis 1987). Patients in both Patterns 1 and 2 were seen into a true cyst may take months to years and this without neurological deficit. We observed the Type 2 probably accounts for the apparent continuum of nonpattern in all but one of our cases. Focal cord contu- cystic to cystic myelopathy to syrinx. The rate of sions encompassing only one spinal segment or less are progression in individual cases appears to be highly associated with less severe neurological deficits than variable. Our study included patients examined at 6 more extensive contusions (Schaefer et al, 1989). In the months after injury and in whom examples of myelocase of spinal cord haemorrhages, peripheral hyper- malacia, atrophy and syringohydromyelia were all seen. intensity around central hypointensity may be seen on We found no significant difference in the interval follow-up at 3-7 days in cases where initial scanning between trauma and MRI in those patients with myeloshowed just hypointensity (Kulkarni etal, 1987; malacia (mean, 9.5 years) compared with those with Quencer, 1988). This was the pattern seen in one of our atrophy (mean, 10.1 years). cases imaged at 7 days after injury (see Fig. 5). In our Delayed CT following water-soluble myelography experience, cord contusion was only rarely an isolated may show contrast accumulation within the spinal cord abnormality, evidence of skeletal injury frequently being in both cystic and non-cystic myelopathy (Stevens et al, present. Patients with a central cord syndrome typically 1988), but MRI appears to be more reliable in have no discernible skeletal injury (Johnston, 1989; predicting the presence of surgically-drainable Yamashita etal, 1990). syringohydromyelia (Quencer etal, 1986; Quencer, The changes seen on sequential MRI appear to be of 1988). However, microcystic degeneration may mimic prognostic significance. Five MRI patterns have been these appearances, particularly when lesions are small described in patients scanned sequentially following (MacDonald etal, 1988). Intra-operative ultrasound injury (Yamashita etal, 1990). Those patients showing should permit an accurate distinction to be made before Type I (normal signal intensity on both ^WSE and myelotomy is undertaken (MacDonald etal, 1988; 7^WSE) in the acute stage frequently snowed no Quencer, 1988). progression of MRI appearances and had a good neuroSyringohydromyelia may occur as a consequence of logical outcome. Of those with Type II changes (normal extramedullary compressive lesions, possibly owing to 7^WSE, high signal 7TWSE) in the acute stage, the ischaemia of the cord with secondary degeneration of subgroup showing resolution to Type I had an the grey matter or by filling of the central canal by improved neurological outcome while those with extrachoroidally produced CSF (Castillo etal, 1988). persisting Type II changes showed no improvement. Extrinsic compression may lead to neuroglial damage Persisting cord compression was observed in 83% of with enlargement of extracellular perivascular spaces; Vol. 64, No. 761


R. W. Kerslake, T. Jaspan and B. S. Worthington

the formation of arachnoid adhesions may alter CSF dynamics so that abnormal entry of CSF into the cord via the enlarged Virchow-Robin spaces results in syringohydromyelia (Castillo et al, 1988) which enlarges and propagates due to a water-hammer effect (Sherman et al, 1986). We observed differing patterns of syrinx above and below the level of injury in all cases of cervicothoracic fracture dislocation, each associated with significant focal canal stenosis. In these cases, the spinal cord was noted to fill the narrowed spinal canal completely. If there is a high degree of subarachnoid block and focal compression of the syrinx by a fracture/ dislocation, locally altered CSF dynamics may result in turbulence of CSF within the syrinx above the block and stagnation below, resulting in a variable appearance of the syrinx in these two locations (Quencer, 1988). This was found in four out of six cervicothoracic and one of four thoracolumbar injuries where a syrinx had developed. The moderate to severe canal stenosis that we have observed and the associated differing patterns of syrinx above and below may also reflect the severity and mechanism of the original injury, possibly modified by abnormal spinal motility relating to the injury and/or subsequent surgical intervention. In some cases, trauma may result in the formation of rents in the spinal cord (perhaps due to laceration by bone fragments) which communicate directly with the spinal subarachnoid space and result in the formation of syringes which are clinically indistinguishable from those formed more conventionally. Fissures in the spinal cord communicating with the spinal subarachnoid space have also been shown in syringomyelia associated with Chiari malformations (Aubin et al, 1987). These fissures may enlarge as a result of a ball-valve effect due to adhesions and may be improved by shunting. Post myelographic CT may demonstrate immediate entry of contrast into the cord and high resolution MRI is also capable of demonstrating thesefissures(Post et al, 1987; Stevens etal, 1988), though none was identified in our material. Demonstration of the complex nature of syringohydromyelic cavities requires use of both sagittal and axial imaging planes (Aubin et al, 1987). Partial septations or fibroglial remnants are commonly observed, particularly above the level of injury, and their demonstration may be important if surgical drainage is contemplated, since they may indicate the need for multiple drains or syringotomies. When 7JWSE are used, the contents of some syringes (particularly when large) are of lower signal intensity than CSF, probably indicating the presence of pulsatile fluid shifts leading to reduced signal intensity due to both time of flight and phase shift phenomena (Sherman etal, 1986). This has been described in syringes of Chiari associated (Sherman etal, 1986; Aubin etal, 1987), tumour-associated (Sherman et al, 1987) and post-traumatic origin (Sherman etal, 1986; Quencer, 1988). Those cysts demonstrating low signal intensity on non-gated ^-weighted sequences may be undergoing active expansion and a stronger case for surgical shunting of these 400

syringes may be made (Quencer, 1988). In our series, 7JWSE images were obtained in only one case with a syrinx; this demonstrated a central flow void within the syrinx as well as peripheral hyperintensity around the syrinx. Areas of high signal intensity on 7^-weighted images surrounding syringes have been noted and are due to surrounding gliosis, oedema, microcystic change or demyelination (Sherman etal, 1986). Gliosis occurs in response to distending forces acting upon the syrinx walls and is therefore seen predominantly at the circumference of the syrinx and also at its cranial apex where it develops to withstand the upward pulsations of the syrinx fluid (Sherman etal, 1986). In patients with extrinsic cord compression due to spondylosis, Jinkins etal (1986) have described features consistent with central grey matter necrosis and cavitation occurring at the level of compression, possibly due to repeated trauma or ischaemic change. In some cases, thin central regions of necrosis or cavitation extending both cranially and caudally to the compressive level were observed. The factors responsible for the initial formation and later propagation of these abnormalities are probably different (Sherman etal, 1986; Stevens etal, 1988), but may be important where continuing spinal cord compression is present as a result of post-traumatic canal stenosis. Post-traumatic syringomyelia may be limited to a single spinal level at the site of injury or involve the entire cord (Aubin et al, 1987). Distinguishing between a small syrinx or an area of myelomalacia may be difficult using MRI; syringes usually demonstrate a sharp interface with the adjacent cord, contain no internal signals and may show a flow void. Myelomalacia usually involves only a short segment of the cord, is limited to the site of injury and has a less distinct interface with the surrounding cord and has no flow void (Quencer, 1988). This judgement is of only academic interest if the syrinx is very small (less than 1 cm) as this would not be surgically drained. Intra-operative ultrasound is capable of distinguishing between these two entities, but requires surgical exposure of the theca. Conclusion

The contribution of MRI to the overall management of acutely and chronically spinal injured patients has yet to be fully defined. In the acute phase, the greatest potential role is in the identification of remediable intraspinal problems in those patients with an incomplete neurological deficit. The soft-tissue components of spinal trauma are particularly well demonstrated with MRI and the incidence of disc herniation and epidural haematoma is far greater than previously suspected. The precise level of intramedullary abnormalities may be shown though differentiation between oedema, haemorrhage, gliosis or microcystic myelopathy remains suboptimal (Fox et al, 1988). The signal patterns appear to be of prognostic importance (Yamashita et al, 1990). In the more chronic stages, surgically treatable problems may be assessed non-invasively and without hazard The British Journal of Radiology, May 1991

MRI of spinal trauma Iopamidol CT-myelography. American Journal of to the patient. Syringomyelia is readily identified, Neuroradiology, 7, 693-701. although intra-operative ultrasound may be required to distinguish microcystic myelomalacia from smaller JOHNSTON, R. A., 1989. Management of old people with neck trauma (Editorial). British Medical Journal, 299, 633-634. syringes. Continuing cord compression is clearly shown KANAL, E., SHELLOCK, F. G. & TALAGALA, L., 1990. Safety and may be clearly distinguished from established cord considerations in MR imaging. Radiology, 176, 593-606. atrophy. KULKARNI, M. V., MCARDLE, C. B., KOPANICKY, D., MINER, Apart from conventional radiography, MRI is recomM., COTLER, H. B., LEE, K. F. & HARRIS, J. H., 1987. Acute mended as the investigation of choice in spinal injury, spinal cord injury: MR imaging at 1.5T. Radiology, 164, particularly when a neurological deficit is present or is 837-843. LEMAIRE, C , DUNCAN, E. G., SOLSBERG, M. D. & ARMSTRONG, progressing. Acknowledgments We are grateful to the Department of Health and the Medical Research Council for the continuing support of research work in the Nottingham MRI Unit. Dr R. W. Kerslake is supported by the DOH and MRC. References AUBIN, M. L., BALERIAUX, D., COSNARD, G., CROUZET, G., DOYON, D., HALIMI, P. & MANELFE, C , 1987. MRI in

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The British Journal of Radiology, May 1991

Magnetic resonance imaging of spinal trauma.

A retrospective series of 118 magnetic resonance examinations of 110 patients who had sustained previous spinal trauma is reported. Examinations perfo...
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