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AJR:193, December 2009 W505

diskovertebral unit or acet joints). Percutaneous

needle biopsy or bacteriologic and pathologic

studies was perormed when inection was sus-

pected. Whenever possible, we evaluated the clin-

ical and radiologic outcomes ater treatment.

Results

We identied 10 patients with spinal neu-

roarthropathy (Table 1). The underlying di-

agnosis was traumatic paraplegia in seven

patients, Guillain-Barr syndrome in one pa-

tient, transverse myelitis in one patient, and

Friedreichs ataxia in one patient. Presenting

symptoms consisted o lumbar pain in six

patients, worsening o the neurologic decit

in three, and kyphosis or instability in three.

One patient had a ever related to inection o

an intervertebral collection.

The patient with Friedreichs ataxia lost the

ability to walk at 41 years old and experienced

the rst symptoms o spinal neuroarthropa-

thy at 47 years old. In the other patients, the

symptoms developed several years ater the

injury (mean, 19 years; range, 540 years).The initial CT and MRI studies showed

infammatory changes o the vertebral end-

plates in three patients (patients 1, 2, and

6). On MRI, the aected endplates gener-

ated high signal on the T2-weighted and

STIR sequences as well as on the gadolin-

ium-enhanced T1-weighted sequence. Bone

erosions were also visible in these three pa-

tients. In the other seven patients, destruc-

tion and sclerosis o the diskovertebral unit

CT and MRI of SpinalNeuroarthropathy

Alexis Lacout1

Caroline Lebreton

Dominique Mompoint

Samia Mokhtari

Christian A. Valle

Robert Y. Carlier

Lacout A, Lebreton C, Mompoint D, Mokhtari S,Valle CA, Carlier RY

1All authors: Department o Radiology, Hpital Raymond

Poincar, Assistance Publique-Hpitaux de Paris,

Universit Paris Ile-de-France Ouest, 10 4 Blvd.

Raymond Poincar, 92380 Garches, France. Address

correspondence to A. Lacout.

Musculoskeletal Imaging Pictorial Essay

CME

This article is available or CME credit.

See www.arrs.org or more inormation.

WEB

This is a Web exclusive article.

AJR2009; 193:W505W514

0361803X/09/1936W505

American Roentgen Ray Society

Spinal neuroarthropathy, also

known as Charcot spine, is a de-

structive process that occurs

when neurologic damage causes

loss o the protective proprioceptive refexes.

In this article, we describe the dierent stag-

es o spinal neuroarthropathy as assessed by

CT and MRI, and we discuss the contribu-

tion o these imaging techniques to the man-

agement o aected patients.

Materials and Methods

Over a 4-year period, approximately 220 pa-

tients with severe neurologic impairments due to

spinal cord injury were admitted to our unit or

initial rehabilitation. During the same period, 800

patients were reerred to our unit or evaluation

and treatment o impairments rom older spinal

cord lesions. Among these patients, we identied

10 who had spinal neuroarthropathy and included

them in a retrospective study. Our institutional re-

view board approved the study.

We reviewed the medical records, including the

imaging studies, o the patients with spinal neu-roarthropathy. In all these patients, clinical and

radiologic examinations were perormed at symp-

tom onset and, when possible, later in the course

o the disease. Most patients underwent radiogra-

phy as well as CT and MRI o the lumbar spine.

When reviewing the imaging studies, we direct-

ed special attention to the detection o destructive

lesions, sclerosis, new bone ormation, vacuum

phenomena within disks, and intervertebral col-

lections. We recorded the site o each lesion (e.g.,

Keywords: Charcot spine, CT, MRI, spinal cord lesions,

spinal neuroarthropathy

DOI:10.2214/AJR.09.2268

Received December 18, 20 08; accepted ater revision

June 18, 200 9.

OBJECTIVE. The objective o this article is to describe the dierent stages o spinal neu-

roarthropathy as assessed by CT and MRI and to discuss their contribution to the manage-

ment o aected patients.

CONCLUSION. Early-stage ndings consisted o infammatory changes involving ad-

jacent vertebral endplates and mimicking degenerative disk disease with infammation. Sub-

sequently, progression o the lesions led to complete destruction o the intervertebral joint.

Knowledge o the initial eatures o spinal neuroarthropathy may allow earlier treatment,which may improve outcomes.

Lacout et al.CT and MRI o Spinal Neuroarthropathy

Musculoskeletal ImagingPictorial Essay

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CT and MRI of Spinal Neuroarthropathy

were seen (Figs. 18). Newly ormed bone

was visible in eight patients (Figs. 28). The

acet joints were consistently involved (Figs.

3 and 5). In seven patients, we ound an in-

tervertebral collection, which was inected

in one patient (Figs. 3, 4, 6, and 7). Vacuum

phenomena within a disk were noted in three

patients (Figs. 2 and 8). The lesions were lo-cated near the lumbosacral junction (L4L5

or L5S1) in seven patients and near the tho-

racolumbar junction (L1L2) in two patients.

Dynamic standard radiographs showed ver-

tebral mobility in one patient (Fig. 4).

Follow-up CT or MRI was perormed in

ve patients. There was no change in one pa-

tient ater 3 months. In three patients, the

mean interval between the two evaluations

was 19 months (range, 933 months) and

worsening o the destructive lesions was not-

ed. The remaining patient was treated with

arthrodesis, ater which spinal neuroarthrop-

athy lesions developed above and below the

xation (L1L2 and L5S1) (Fig. 7).

Discussion

Spinal neuroarthropathy, or Charcot spine,

is a process o progressive aseptic destruc-

tion o the spine that can complicate a variety

o neurologic disorders associated with loss

o proprioception and pain sensation, such as

tabes dorsalis [1, 2], traumatic brain or spi-

nal cord injury [3], diabetes mellitus [2], and

congenital insensitivity to pain [4]. The de-

structive process involves the disk, adjacent

vertebral bodies, and acet joints [5, 6].Pain and position sense play a key role in

joint protection by avoiding joint overuse as-

sociated with microtrauma [7]. When pro-

prioception and pain sensation are lost, repeat-

ed microtrauma to the joint occurs, leading to

joint damage. Thus, neuroarthropathy devel-

ops only in mobile joints [7]. The joint dam-

age caused by microtrauma urther increases

joint mobility, thus creating a vicious circle.

In most o our patients, the neuroarthropathic

lesions developed at spinal levels character-

ized by considerable mobilitythat is, near

the thoracolumbar or lumbosacral junction or

just above and below an orthopedic xation.Vacuum phenomena within the disk, present

in three o our patients, indicate mobility o

the aected spinal level.

In patients with neurologic impairment due

to spinal cord injury or disease, symptoms

that may prompt imaging studies o the spine

consist o increasing spasticity, autonomic hy-

perrefexivity, increasing pain during trans-

ers, and spinal instability. However, the clin-

ical diagnosis is dicult and oten delayed

because the classical symptoms are lacking.

The radiologist should careully examine

each diskovertebral unit or changes suggest-

ing spinal neuroarthropathy, especially at the

thoracolumbar and lumbosacral junctions.

We identied two stages in the develop-

ment o spinal neuroarthropathy (Fig. 9).Initially, nonspecic infammatory chang-

es were visible in two adjacent endplates.

These changes may mistakenly suggest disk

degeneration with infammation. However,

neuroarthropathy should be considered in

patients who have neurologic conditions as-

sociated with loss o proprioception and pain

sensation. Vacuum phenomena in the disk or

acet joints may be present. This nding may

indicate exaggerated local mobility as the

precipitating actor o the neuroarthropathy.

In patients with later-stage spinal neuroar-

thropathy, destruction o the diskovertebral

unit and acet joints was apparent. Concomi-

tant bone sclerosis and new bone ormation

were noted. These ndings were consistent

with earlier data [5, 6].

Neuroarthropathy may be dicult to dis-

tinguish rom inection [5]. Furthermore, in-

ection may complicate neuroarthropathy [8,

9], although the primary process is aseptic.

In a study comparing 19 patients with prov-

en disk space inection and 14 patients with

spinal neuroarthropathy investigated by CT

or MRI, the best discriminators were intra-

discal vacuum phenomena, osseous debris,

acet joint involvement, joint disorganiza-tion (spondylolisthesis and dislocations), and

signal patterns on T2-weighted and gadolin-

ium-enhanced T1-weighted MRI sequences

[5]. In neuroarthropathy, the vertebral bod-

ies usually generate high-intensity signal on

T2-weighted and gadolinium-enhanced T1-

weighted sequences, whereas the signal ab-

normalities are usually conned to the end-

plates in inection [5]. The disks usually

exhibit rim enhancement in neuroarthropa-

thy and diuse high signal in inection [5].

However, no sign is entirely specic or neu-

roarthropathy [5]. Percutaneous biopsy with

bacteriologic examination, which was per-ormed in one o our patients, may be re-

quired. Another important dierential di-

agnosis is primary or metastatic vertebral

tumor [6]. The clinical picture oten suggests

a malignancy, and histologic examination o

a percutaneous biopsy specimen can estab-

lish the diagnosis.

The treatment o spinal neuroarthropathy

relies on immobilization o the aected spi-

nal levels. Surgery typically consists o re-

duction o the deormities, posterolateral spi-

nal usion with hooks and pedicular screws,

and posterior lumbar interbody usion [10,

11]. The resulting shit in mechanical load-

ing to other levels, together with mobility

just above or below the internal xation, may

lead to the development o neuroarthropathyat other spinal sites [12]. This complication

occurred in one o our patients.

An early diagnosis may help to improve the

management o spinal neuroarthropathy be-

cause early treatment at the stage o isolated

infammation might prevent the development

o destructive lesions. We suggest that MRI

may be the most sensitive investigation or de-

tecting early-stage spinal neuroarthropathy.

In conclusion, the early stages o spinal

neuroarthropathy may mimic infammato-

ry disk degeneration. Thus, MRI shows high

signal rom the vertebral endplates on T2-

weighted, STIR, and gadolinium-enhanced

T1-weighted sequences, as well as bone ero-

sions. CT and MRI may allow an earlier di-

agnosis, thereby improving treatment eca-

cy. Radiologists should be amiliar with the

imaging ndings, particularly those present

at the early stage.

References

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bylski GJ, Parker L. Can imaging ndings help

dierentiate spinal neuropathic arthropathy rom

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gy 2000; 214:693699

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aging ndings in spinal neuroarthropathy. Spine

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roarthropathy ater traumatic paraplegia. AJNR

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Inected Charcot spine. Spinal Cord 2005; 43:

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10. Suda Y, Shioda M, Kohno H, Machida M, Yam-

agishi M. Surgical treatment o Charcot spine. J

Spinal Disord Tech 2007; 20:8588

11. Arnold PM, Baek PN, Stillerman CB, Rice SG,

Mueller WM. Surgical management o lumbar

neuropathic spinal arthropathy (Charcot joint) a-

ter traumatic thoracic paraplegia: report o two

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A B

C D

Fig. 140-year-old man in whom L5S1 spinalneuroarthropathy developed 11 years ater traumaticparaplegia (thoracic cord 9, American Spinal InjuryAssociation impairment classication A [T9 ASIA A]).A and B, Sagittal at-saturated ast spin-echo T1-weighted image ater gadolinium injection (A) andCT scan with coronal reormation (B) show diskspace narrowing, erosions, and slight endplateenhancement. These ndings mimic degenerative

disk disease with infammatory changes(arrowheads).C and D, Sagittal at-saturated ast spin-echoT2-weighted image (C) and CT scan with sagittalreormation (D) obtained 9 months ater A andB show progression to complete destruction odiskovertebral unit with bone ragmentation andsclerosis (arrows).

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A B

C D

Fig. 234-year-old man in whom L2L 3 spinalneuroarthropathy developed 7 years ater traumaticparaplegia (thoracic cord 6, American Spinal InjuryAssociation impairment classication A [T6 ASIA A]).A and B, CT scan with sagittal reormation (A) and

sagittal at-saturated ast spin-echo T1-weightedimage ater gadolinium injection (B) show erosions,sclerosis, and slight endplate enhancement (arrows).These ndings mimic degenerative disk disease withinfammatory changes.C and D, CT scan with sagittal reormation (C) andcoronal STIR image (D) obtained 15 months ater Aand B show destruction o diskovertebral unit (thinarrows) with vacuum phenomenon within disk andnew bone ormation (thick arrows, D).

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Lacout et al.

A

Fig. 365-year-old woman with L3L4 spinal neuroarthropathy 20 years ater traumatic paraplegia (thoracic cord 10, American Spinal Injury Association impairment

classication A [T10 ASIA A]).A and B, CT scans with coronal (A) and axial (B) reormations show complete destruction o diskovertebral unit and zygapophyseal joints, with abundant osseous debrisextending beyond vertebral body (arrows) and intervertebral collection (arrowheads).C, CT scan with volumetric reormation shows complete destruction o L3 and L4 with osseous ragmentation (arrow).

CB

A B

C D

Fig. 458-year-old man in whom L4 L5 spinalneuroarthropathy developed 27 years ater traumaticparaplegia (thoracic cord 10, American Spinal InjuryAssociation impairment classication A [T10 ASIAA]).A and B, CT scans with sagittal (A) and axial (B)reormations show destruction (arrowheads),sclerosis (thin arrows), and new bone ormation (thickarrows, A).C, CT scan with sagittal reormation obtained 33months ater A and B shows increased destruction odiskovertebral unit and central vertebral collection(star).D, Lateral dynamic radiograph o lumbar spine showsposterior and inerior displacement o L5 (star)between S1 (thin arrow) and L4 (thick arrow).

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A B

C D

Fig. 558-year-old man in whom L1L2 spinalneuroarthropathy developed 40 years ater traumaticparaplegia(lumbosacral cord [L1]).A and B, Sagittal ast spin-echo T1-weighted (A)and coronal ast spin-echo T2-weighted (B) images

show complete destruction o diskovertebral unit,intervertebral collection (star), and ormation oabundant new bone (arrows, B).C and D, Lateral (C) and anteroposterior (D)radiographs o lumbar spine show anterior and lateralnew bone ormation in diskovertebral unit (thickarrows) and zygapophyseal joints (thin arrow, C).

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A

Fig. 657-year-old man with L3L4, L4L5, and L5S1 spinal neuroarthropathy 13 years ater aortic dissection responsible or paraplegia (thoracic cord 4, AmericanSpinal Injury Association impairment classication A [T4 ASIA A]).A and B, Coronal reormation (A) and sagittal STIR (B) CT scans show lesions o L3 L4, L4 L5, and L5S1 (thin arrows, B). At L3 L4, note intervertebral collection (star,B) and abundance o new bone (thick arrows, A). At L4L5 and L5S1, lesions are less severe and consist o disk space narrowing and endplate erosions ( arrowheads, A).C, Anteroposterior radiograph o lumbar spine shows lateral new bone ormation (arrows).

CB

A

Fig. 737-year-old man in whom L5S1 spinal neuroarthropathy developed 29 yearsater traumatic paraplegia (thoracic cord 4, American Spinal Injury Associationimpairment classication A [T4 ASIA A]).AC, Sagittal ast spin-echo T1-weighted (A) and sagittal (B) and coronal (C) ast spin-echo T2-weighted images show destruction o L5S1 diskovertebral unit (arrow, Aand B) and intervertebral collection (stars). Lesions developed just below orthopedic xation.

(Fig. 7 continues on next page)

CB

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D

Fig. 7 (continued)37-year-old man in whom L5S1 spinal neuroarthropathy developed 29 years ater traumatic paraplegia (thoracic cord 4, American Spinal InjuryAssociation impairment classication A [T4 ASIA A]).D and E, CT scans with sagittal (D) and axial (E) reormations show destruction, intervertebral collection (stars), and abundant osseous debris extending beyond vertebralbody (arrowheads) and into spinal canal. This patient underwent orthopedic xation 7 months later.F, CT scan with coronal reormation obtained 17 months ater surgery shows orthopedic xation at L5S1 ( arrow) and development o L1L2 lesions just aboveorthopedic xation (arrowhead).

FE

A

Fig. 852-year-old woman in whom L2L3 and L4 L5 spinal neuroarthropathy developed 5 years aterGuillain-Barr syndrome responsible or paraplegia(thoracic cord 4, American Spinal Injury Associationimpairment classication C [T4 ASIA C]).A and B, Coronal at-saturated ast spin-echo T1-weighted image ater gadolinium injection (A) and CTscan with coronal reormation (B) show destruction(thin white arrow, A), new bone ormation (thickarrows), sclerosis, vacuum phenomena in disk (blackarrows), and L2L 3 enhancement.

B

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Lacout et al.

Changes best depicted on MRI

Inflammatory

signal on MRI

Changes best depicted on CT

Stages

ofthed

isease

Vertebralcollection

Bony

erosions

Destruction,

fragmentation,

new bone

formation

Fig. 9Graphic shows stages o development o spinal neuroarthropathy.

F O R Y O U R I N F O R M A T I O N

This article is available for CME credit. See www.arrs.org for more information.

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