The thoracic anterior spinal cord adhesion syndrome

1T R TAYLOR, MRCP, FRCR, 1R DINEEN, MRCP, FRCR, 2B WHITE, FRCP, FRCS and 1T JASPAN, FRCP, FRCR

1Department of Imaging, Queens Medical Centre, Nottingham, UK, and 2Department of Neurosurgery, Queens Medical

Centre, Nottingham, UK

Objectives: This study included a series of middle-aged male and female patients whopresented with chronic anterior hemicord dysfunction progressing to paraplegia.Imaging of anterior thoracic cord displacement by either a dural adhesion or a duraldefect with associated cord herniation is presented.Methods: This is a retrospective review of cases referred to a tertiary neurosciencecentre over a 19-year period. Imaging series were classified by two experiencedneuroradiologists against several criteria and correlated with clinical examination and/or findings at surgery.Results: 16 cases were available for full review. Nine were considered to representadhesions (four confirmed surgically) and four to represent true herniation (threeconfirmed surgically). In the three remaining cases the diagnosis was radiologicallyuncertain.Conclusion: The authors propose ‘‘thoracic anterior spinal cord adhesion syndrome’’as a novel term to describe this patient cohort and suggest appropriateclinicoradiological features for diagnosis. Several possible aetiologies are alsosuggested, with disc rupture and inflammation followed by disc resorption and duralpocket formation being a possible mechanism predisposing to herniation at theextreme end of a clinicopathological spectrum.

Received 26 May 2010Revised 26 September2010Accepted 6 October 2010

DOI: 10.1259/bjr/81458631

’ 2012 The British Institute of

Radiology

Anterior spinal cord hernia is a rare and potentiallytreatable cause of progressive anterior spinal cordsyndrome. The cord prolapses through an anterior oranterolateral dural defect, resulting in a progressive,frequently asymmetrical, thoracic myelopathy. Patientstypically present in middle age with slowly progressiveneurological dysfunction relating to anterior hemicorddysfunction [1, 2]. The condition was described in 1973by Cobb et al [3], with the first idiopathic casesuggested by Wortzman et al [4] a year later; a numberof case reports and small series have been publishedsince. The exact causative mechanism has not been fullyelucidated. The radiological findings of true herniationare well described but not widely recognised as thenumber of cases in world literature remains relativelysmall.

In our clinical practice we have identified a number ofpatients who present with a clinical picture that isindistinguishable from patients with anterior spinal cordherniation and MRI demonstration of anterior corddeviation, but without imaging or surgical evidence of atrue cord hernia. Based on this observation, we suspectthat true hernia is positioned at the extreme end of apathological spectrum; other cases of anterior corddeviation and wasting—possibly caused by focal vulner-ability, deficiency of the anterior dura or anterior tetheringof the cord—appear to present with similar clinicalsymptoms. Evidence in support of this assertion is thecase reported by Ewald et al [5] demonstrating

progressive development of an anterolateral T6 cordherniation on successive MRI examinations, with asso-ciated progression in clinical symptoms over a 2-yearperiod prior to operative intervention. We propose thatthe association of thoracic myelopathic clinical symptomswith an anteriorly displaced and thinned thoracic cord,with or without radiological or surgical evidence of cordherniation, should be considered as a spectrum of thedisorder identified as thoracic anterior spinal cordadhesion syndrome (TASCAS).

In this single-centre series, we present the imagingresults of 16 patients presenting with clinical andradiological findings consistent with TASCAS, stressingboth the typical and less common imaging appearances.In addition, we review the possible patho-aetiology, andconsider how imaging appearances could suggest under-lying causative mechanisms. The increasing alertness ofradiologists to the imaging appearances, in conjunctionwith clinical awareness of the presenting features, willhelp the timely diagnosis of this potentially treatablecause of thoracic cord dysfunction. The radiologicaldiscrimination of anterior cord adhesion from corddisplacement by an arachnoid cyst or other lesion isabsolutely vital to the appropriate surgical planning andtreatment of these patients.

Case review

A retrospective review of potential cases of thoracicanterior cord adhesion presenting to our centre wasperformed, spanning a period of 19 years and yielding 17cases. In one of these cases, imaging could not be

Address correspondence to: Dr Timothy Taylor, Department ofImaging, Queens Medical Centre, Derby Road, Nottingham NG72UH, UK. E-mail: timt@nhs.net

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retrieved for review; intra-operative ultrasound was theonly imaging modality available for evaluation. Clini-cal notes and imaging series were obtained for theremaining 16 cases. There were seven men and ninewomen, with a median age of 60 years (range 28–80 years).

In all cases for which reliable clinical examinationfindings were available, the presentation was one of aprogressive neurology attributable to a spinal cordlesion. At least half of the cases in their early stagesmanifested classical anterior hemicord features ofstiffness in one leg and pain/temperature sensorydisturbance in the other, but preserved proprioceptionin both, followed by progressive sensorimotor distur-bance progressing towards paraplegia over severalyears [6]. Several cases presented with less typicalconstellations of symptoms, including bilateral lowerlimb motor weakness, myoclonic episodes and focal

position-related radicular pain. This correlates withpreviously documented clinical manifestations of simi-lar cohorts [7].

7 of the 16 patients underwent surgery by a posteriorapproach. Of these seven, five cases were found to havesignificant oval defects of the anterior dura, with asym-metric herniation of the thoracic cord into the outpouch-ing. In two of these cases, an anterior dural defect could bedemonstrated on pre-operative imaging (Figure 1). In theremaining two operative cases no definite dural defectwas identified either at imaging or surgery (Figure 2);instead, the cord was displaced and tethered in ananterior position by adhesions arising from surroundingarachnoid and/or dentate ligaments. In all cases there wasevidence of focal arachnoid inflammation/thickening as aprobable consequence of the cord injury, which can beeasily mistaken for a displacing posterior arachnoid cyst if

(a) (b)

(c) (d)

Figure 1. (a) Sagittal three-dimen-sional (3D) T2 (constructive interfer-ence in the steady state) imagedemonstrates significant anterior dis-placement and thinning of the cord atT4/5. (b) Anterior displacement isconfirmed on T2 axial series. (c)Reconstructed 3D T2 demonstratesherniation through a visible duraldefect. (d) Post-surgical sagittal T2confirms thoracic cord release, butwith significant pre-existing atrophy.

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the radiological and clinical findings are not appreciated.Failure to appreciate or search for and repair the anteriorlesion would not address the underlying cause, withresultant continued progressive disability. In the remain-der of our case cohort, where a definite anterior tether/hernia was suspected, and after having been counselledthat although an operation may relieve radiologicalfeatures of cord tether or displacement and preventclinical progression they may not regain neurologicalfunction which had already been lost, some patientselected not to continue with a surgical approach and werefollowed up clinically.

All radiological series were reviewed independentlyby two experienced neuroradiologists (TJ, RD) blinded tothe original clinical findings or radiological reports. Thereviewing radiologists were asked to classify the visibleabnormalities based on the (1) vertebral level at whichthe abnormality occurred; (2) presence of cord thinning;(3) alterations in cord signal; (4) visibility of dural defect;(5) proximity of cord or dural abnormality to discalabnormality; and (6) nature of discal abnormality, ifpresent. The reviewers were also asked to classify thecord lesion as either ‘‘hernia’’, ‘‘adhesion’’, ‘‘uncertain’’between hernia or adhesion, or ‘‘other diagnosis’’.

Radiological findings

Table 1 summarises the clinicoradiological–surgicalfindings (Table 1).

A high level of agreement was present between thereviewing radiologists. All lesions were well demon-strated on standard 1.5 T MRI sagittal and axial T1 and T2

sequences without the need for contrast imaging ormyelography; visualisation was improved in caseswhere a high-resolution T2* technique such as construc-tive interference in the steady state (CISS) imaging wasemployed. The majority of lesions were demonstrated atmid-thoracic levels (T3 to T9/10), with 63% found at or

between T4/5 and T7/8. In all cases the spinal cord wasdisplaced anteriorly. Similarly, there was focal cordatrophy in 14–15 of 16 cases [1] (in 1 case there wasdisagreement about the presence of cord atrophy). T2

hyperintensity within the affected cord was a commonfeature, present in 10 of 16 cases. A demonstrableanterior dural defect was not a common imaging finding,being seen in only 3–4 of 16 cases (the numeratorvariation was due to disagreement between the 2reviewing radiologists). True herniation was felt to bepresent by both reviewing radiologists in four cases. In afurther two cases, one reviewer diagnosed a herniawhereas the other was uncertain or diagnosed adhesiononly. In all other cases, cord adhesion was felt to bepresent. Typically the cord is sharply kinked anteriorly atthe level of a hernia in distinction from the soft curve ofcord displacement by a posteriorly placed lesion.

In 14 of 16 cases, the cord abnormality occurredimmediately adjacent to the intervertebral disc, or withan intervertebral disc at the upper margin of the cordlesion. In 8 of 14 cases where the lesion was spatiallyrelated to an intervertebral disc, discal abnormality waspresent and most commonly was degenerative innature.

Discussion

We present a series of middle-aged patients of bothsexes presenting with a syndrome of chronic progressiveanterior cord dysfunction (which is frequently asymme-trical and may spare the dorsal columns), with imagingdemonstration of anterior thoracic cord displacementeither by a dural adhesion or a dural defect (withassociated cord herniation). Cord thinning was fre-quently found, but the presence of cord signal changewas not a consistent feature in our case series. A duraldefect was not commonly demonstrated on MRI,although absent visualisation did not exclude a defect

(a) (b)

Figure 2. (a) Sagittal and (b) axial T2thoracic spine series. There is focalanterior cord displacement with asso-ciated parenchymal thinning at T7/8,adjacent to an otherwise insignifi-cant mid-thoracic disc bulge. Nodural defect is identified. Surgicalfindings confirmed anterior tetherby arachnoid adhesion, withoutdural defect.

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Table 1. Clinical and radiological findings of 16 cases for which pre-operative MRI was available for review. A further case of thoracic hernia (confirmed at surgery) has not beenincluded as only pre-operative ultrasound was available. Surgical findings provided where available

SexAge(years) Clinical findings MRI level

Cordwasting?

Cord signalabnormality?

Duraldefect?

Proximity todisc

Adjacent disc/bonyabnormality Final diagnosisa Surgical findings

F 32 No historyavailable

T7/8 Yes T2 hyperintensity/normal

No At disc level None Adhesion Not operated

M 37 ProgressiveBrown–Sequardsyndrome

T8/9 No/yesb Normal No At disc level Degenerate disc Adhesion Dorsal laminectomy andexploration; no hernia found,cord tethered anteriorly bydentate ligaments anddistorted posteriorly by anteriordisc at T8/9. Cord released

F 42 C6/7radiculopathy

T4/5 Yes T2 hyperintensity No Disc atuppermargin oflesion

None Adhesion Not operated

M 46 Right radicularpain anddysaesthesiato mid-flank

T3/4 Yes T2 hyperintensitysuperiorly

No At level None Adhesion Not yet operated

F 59 Progressive rightsided weaknessand sensorydisturbance

T5/6 No Normal No At disc level Disc bulge Adhesion No arachnoid adhesions. 264 cmdural defect between T5/6roots. Neuropatch graft + bonechips to cover defect

M 61 Diffuse weakness.No focal motoror sensoryabnormality

T7/8 Yes Normal No Disc atuppermargin oflesion

None Adhesion Not operated

F 62 ProgressiveBrown–Sequardsyndrome

T6/7 Yes Normal /T2

hyperintensityNo At disc level None Adhesion Posterior arachnoid adhesions.

Long inviscerated anteriorspinal hernia, largest right side;possible areas of cordinfarction. Tight adherence todural edge. T6 root sacrificedand cord delivered. Bone chipsto obliterate defect, neuropatchgraft

M 65 Right back/flankpain, worse onrotation. Nomotor orsensory loss

T5 Yes Normal No Mid-vertebrallesion

None Adhesion Laminectomy. Thoracic cordcaught up in arachnoid scarringat T7/8

F 66 Bilateral legweakness andhyper-reflexia

T4/5 Yes T2 hyperintensitysuperiorly

No At disc level None Adhesion Not available

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SexAge(years) Clinical findings MRI level

Cordwasting?

Cord signalabnormality?

Duraldefect?

Proximity todisc

Adjacent disc/bonyabnormality Final diagnosisa Surgical findings

F 28 Progressive backpain andsensorydisturbance

T7 Yes T2 hyperintensesegment

No At disc level Degeneratedisc, partialvertebralcollapse

Hernia 4 level laminectomy. Dural defectwith hernia. Hernia reduced,neuropatch graft to coverdefect

F 47 Progressivesensorydisturbance

T6/7 Yes T2 hyperintensity No At disc level Degenerate disc,vertebralhaemangioma

Hernia Not operated

F 60 ProgressiveBrown–Sequardsyndrome

T4/5 Yes normal Yes At disc level Bony barat disc level

Hernia 3 level laminectomy. Dural defectwith hernia anteriorly.Neuropatch graft to coverdefect

M 61 ProgressiveBrown–Sequardsyndrome

T6/7 Yes Normal Yes At disc level Disc bulge,focal bonedefect

Hernia Anterior dural hernia, left-sided.Some arachnoid adhesions.Cord prolapsed into vertebralbody cavity. Neuropatch graft +bone chips into defectNeuropatch cord sling

F 53 Previousdiscectomy

T9/10 Yes T2 hyperintensity Yes At disc level Vertebral fusion(post surgery)

Hernia/uncertainb Not operated

M 80 Large myocloniccontractions inboth legs and Larm. No powerloss. No sensoryabnormality

T3 Yes T2 hyperintensitysuperiorly

No Mid-vertebrallesion

None Hernia/adhesionb Not operated

M 79 Pain andparaesthesialeft leg following L3 laminect-omy 10 yearspreviously

T9/10 Yes T2 hyperintensityinferiorly? Syrinx

No At disc level Degenerate disc Uncertain/adhesionb

Not operated

F, female; M, male.aBased on surgical findings, or, if not available, on radiological consensus.bNo radiological consensus.

Table 1. Continued

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at surgery. Conversely, the series has demonstrated thatclinical features previously attributed to herniationthrough a dural defect can be present in patients inwhom no defect is found at surgery; instead, the cord canbe anteriorly tethered by arachnoid or dentate adhesions.

We propose TASCAS as a novel term to describepatients presenting in this way. Anterior cord herniationis now well described in the literature. However, anteriorcord tethering is less well described, and the similaritiesin clinical and imaging findings to patients with anteriorcord herniation have not, to our knowledge, beenpreviously studied. We believe that the term TASCASis conceptually useful as it unites two pathologies(anterior cord adhesion and anterior cord herniation)that are indistinguishable on clinical examination, cannotbe reliably distinguished on imaging and for which thedecision to operate is based on clinical severity andpatient choice, and not on positive pre-operative identi-fication of either herniation or adhesion per se. Groupingthese conditions under the term TASCAS also acknowl-edges the possible common aetiology, although thisremains to be confirmed.

A number of mechanisms leading to spinal cordherniation have been described by other authors,including congenital anterior dural defects or duplica-tion [8–11], and trauma is specifically implicated incertain cases [12–14], although the onset of symptoms isoften delayed with at least one reported case of onset ofclinical symptoms many years after the initial traumaticevent [15]. Several authors have also postulated thatthere may be a common underlying aetiology betweenarachnoid cyst and cord hernia, with examples ofcoexistent cyst and ventral deviation of the thoracic cord[16, 17]. Previous authors have suggested that in cases ofuncertainty, it may be appropriate to perform cerebrosp-inal fluid flow studies to delineate an underlyingarachnoid cyst [18]. However, they also acknowledgethat radiologically demonstrated arachnoid ‘‘cysts’’ maycorrespond to intramural diverticula at myelography orsurgery. At surgery there is almost always some poster-ior arachnoid scarring, which in the past may have beentreated without understanding that there is underlyingpathology at the anterior aspect of the cord. Unless theanterior aspect of the cord and dural surface isvisualised, anterior pathology can be easily missed;however, intra-operative mobilisation of the cord is notwithout risk. Therefore, identification of a possibleanterior pathology on pre-surgical imaging is an impor-tant part of the proper diagnosis, surgical approach andsafe treatment of these patients.

In their recent review, Darbar et al [19] reviewed 89reported cases of cord herniation through a dural defect(confirmed at surgery) in the published literature since1974. They found that the great majority of patientspresented with a complete or incomplete Brown–Sequard syndrome, and postulated that clinical symp-toms might relate not only to parenchymal damage fromanterior herniation, but also to ischaemia due toinvolvement of cord vasculature secondary to tethering.Similar work by Watters et al [20] attempted to classify asmaller literature series of 30 cases into post-traumatic(10%), iatrogenic (3%) and spontaneous (87%) cohorts.However, Watters did not attempt to identify thepresence of disc abnormalities associated with cord

herniation. Numbers in our series are too small forstatistical comparison; nonetheless, the majority of casesappear to be spontaneous, with one directly linked to aprior traumatic injury and one (in which there is someradiological uncertainty) related to a previous discec-tomy and post-operative bony defect.

The frequency with which adjacent disc abnormality isseen in the present series and previous surgical casereports [21] supports the role of disc disease in theaetiology of TASCAS. Previous authors have suggestedan inflammatory aetiology [22]: one possible mecha-nism would involve inflammatory change, incited by adiseased disc, causing adhesions with the adjacent dura.The anterior cord surface becomes tethered by asso-ciated arachnoid and/or dentate ligament adhesions.Subsequent disc resorption could result in formation of adural retraction pocket predisposing to progressivepathological cord displacement and subsequent hernia-tion, as described by Barrenechea et al [23]. Other factorsmay also be contributory, such as the relatively anteriorposition of the cord in the mid-thoracic spine due to thenormal physiological thoracic kyphotic status, bringingthe spinal cord into close apposition with the discover-tebral complexes.

If disc disease is to be considered as an importantcontributory factor, and as thoracic disc disease iscommon, why do we not see more cases of TASCAS?One explanation is that the MRI appearances of ananteriorly tethered cord might be interpreted instead asbeing secondary to a dorsally positioned arachnoid cyst.It is also possible that in patients with low-graderadiculopathic symptoms, the subtle findings of anteriorcord displacement and parenchymal thinning may notbe appreciated if a ‘‘classic’’ discovertebral lesion isdemonstrated at another level. We have demonstratedseveral cases with progressive clinical symptoms of corddysfunction, where MRI shows focal anterior deviationof the cord with parenchymal thinning consistent with acord tether, but without a dural herniation. We suspectthat increasing knowledge of this condition amongradiologists combined with improvements in MRI andsequence design, and more frequent use of high-resolution T2* imaging, will lead to an increase in thedetection and reporting of TASCAS as a potential causeof clinical symptoms.

A potential drawback of this study is the lack ofinvasive myelographic imaging, used alone or as anadjunct to either CT or MRI. In a relevant recent reviewon imaging of this condition [7], MRI was consideredsufficient for the diagnosis of cord herniation in mostcases, with myelography and CT assessment for clar-ification in equivocal cases. In our local experience wehave found that the routine use of three-dimensionalvolume T2* sequences (such as CISS) in these casesprovide high-resolution images which aid the surgicaldecision-making process while limiting the need for aninvasive procedure. Even with these high-resolutionseries, the exact nature of the abnormality can onlyreally be defined at surgery. In any case, the decisionwhether to operate or not is ultimately made on clinicalrather than radiological grounds. In the patient withcharacteristic clinical symptoms and an angulated anddeviated thoracic cord, if a surgical approach is to becontemplated then we suggest that the anterior aspect of

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the cord should be visualised intra-operatively, regard-less of the degree of radiological certainty in the pre-operative differentiation between hernia or adhesion.

Conclusions

TASCAS characteristically presents in the middle-agedpatient of either sex, with chronic progressive anteriorcord syndrome, which is frequently asymmetrical anddorsal column sparing, and MRI demonstration ofanterior thoracic cord displacement. In conjunction withclinical features compatible with focal cord injury orabnormality, the radiological findings of anterior corddisplacement at a single spinal level, without evidenceof an arachnoid cyst or other dorsal mass on high-resolution T2* series, should suggest a diagnosis ofTASCAS, with radiological appearances of associatedcord thinning, signal change or visible cord herniationbeing less uniform features in the cohort we describe.The underlying patho-aetiology may represent eithercord adhesion or true herniation, and although these twopossibilities may not be reliably differentiated prior tosurgery, pragmatically this is often not an importantdistinction, as in both possibilities clinical severity willdictate the need for surgical intervention. The patho-aetiology of TASCAS remains unclear. We suggest thatinflammation related to adjacent disc disease may becontributory, with anterior cord tethering associatedwith disc abnormality, followed by disc resorption anddural pocket formation, being a possible mechanismpredisposing to herniation at the extreme end of theclinicopathological spectrum.

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