1.2.1

New case reports

Here, we report on two clinical cases of Charcot spine in spinal cord injured patients. We provide a detailed description of the occurrence of the condition, the disease history, the clinical presentation, radiological aspects and treatment outcomes.

1.2.2

A detailed literature review

An exhaustive literature review was performed after searching the PubMed and Pascal databases with the following keywords.

“Charcot spine”, “Charcot spinal arthropathy” and “neuropathic arthropathy of the spine”. Only sufficiently detailed studies published between 1978 and 2008 were selected for review. The observations had to include at least the patient’s age, the cause of the neurological impairment and the spinal site affected. Updated studies lacking new case reports were not included in our analysis.

Quantitative variables are described by the mean and standard deviation, whereas qualitative parameters are described by the percentage frequency.

1.3.1

Case report 1

Our 61-year-old male patient had been suffering from complete ischaemic D10 sensorimotor paraplegia as a result of complications of emergency surgical treatment (at the age of 42) of a ruptured thoracic aorta aneurysm. The ASIA motor score was 50 out of 100, the ASIA light touch sensory score was 69 out of 112 and the ASIA pin-prick sensory score was 68 out of 112 (Frankel A).

At the age of 55, the patient started to complain of increasingly invalidating, chronic pain during movement of the lower lumbar region. This pain was progressively accompanied by major thoracolumbar kyphosis in the sitting position. Clinically, there was no change in neurological parameters or spasticity and no audible cracking sound during movement. We merely noted moderate pain on palpation of the area around the deformation. The patient’s body mass index was about 22. There was no evidence of infection and the laboratory results did not suggest the presence of an inflammatory syndrome.

In view of this radiological evidence, the possibility of a chronic infection or a cancerous process was nevertheless envisaged and prompted us to perform a vertebral needle biopsy. Cultures of central/disc liquid samples were negative. Histological examination revealed the presence of fibrous tissue with sequestered bone but no signs of malignancy. Screening for the HLA B27 gene was negative.

Finally, we arrived at a diagnosis of Charcot spine. Plain X-rays revealed the characteristic aspect of the disease around the L1-L2 joint, with a combination of disc and vertebral destruction, erosion of the L1 and L2 vertebral facets and the presence of paravertebral hypertrophic ossification with a pseudotumoral appearance ( Fig. 2 ). Dynamic X-ray imaging revealed the extent of the spinal instability ( Fig. 3 ) and a three-dimensional computed tomography (CT) scan highlighted the severity of the intervertebral dislocation in the lying position ( Fig. 4 ). The patient was not examined with magnetic resonance imaging (MRI) because he presented a contra-indication (a pacemaker).

Charcot spine in a paraplegic patient (case report 1), as revealed by a AP X-ray of the lumbar spine centred on the L1-L2 level. The disc and vertebral damage has resulted in formation of a “ball-and-socket”-type neo-joint.

Charcot spine in a paraplegic patient (case report 1), as revealed by a lateral X-ray of the lumbar spine in the lying position (3A) and sitting position (3B). The latter image reveals major instability of the spinal lesion, with 50° of kyphosis in the sitting position (versus 16° in the lying position).

Charcot spine in a paraplegic patient (case report 1), as revealed by 3D reconstructed computed tomography. The image shows the extent of the bone formation phenomenon, with ensheathing hyperostosis (complete ossification of the anterior longitudinal ligament).

In terms of therapeutic options, surgery was ruled out by the patient’s history of cardiovascular disease. Moreover, the extensive spinal ankylosis and widespread para-osteo-arthropathy around both hips ( Fig. 5 ) meant that stabilisation surgery would probably have had a poor functional outcome. External support with a bi-valve body jacket moulded for the sitting position was suggested to the patient but was refused. Hence, we were only able to implement regular clinical and radiological monitoring.

Bilateral ectopic hypertrophic ossification of the pelvis in a paraplegic patient (case report 1) presenting Charcot spine, as revealed by a AP X-ray of the pelvis. The X-ray also reveals pelvic imbalance in the frontal plane, with leftward tilt.

1.3.2

Case report 2

Our second case report concerns a 74-year-old male patient who developed incomplete T10 sensorimotor paraparesis (with leg mobility generally rated at between two and three out of five on the American Academy of Orthopaedic Surgeons motor scale) at the age of 65 following myelopathy due to thoracic canal stenosis and then partial surgical correction. A year previously, the patient had also undergone L2-L5 lumbar laminectomy for the associated degenerative, lumbar stenosis.

At the age of 68 (that is to say around three years after the onset of the neurological impairment), the patient’s condition was marked by significant spinal pain during movement. This worsened progressively over the months, as did the motor impairment. The patient also developed urinary disorders (dysuria and hyperactive bladder).

A clinical examination, in 2001, evidenced aggravation of the impairment with a leg motor scale score of 1 to 2 out of 5, compared with score of 2 to 3 initially. The ASIA motor score was 64 out of 100, the ASIA light touch score was 90 out of 112 and the ASIA pin-prick score was 80 out of 112 (Frankel C). Standing position was not possible. Examination of the legs revealed very low joint amplitudes. The patient’s body mass index of 32 corresponded to moderate obesity.

A diagnosis of Charcot spine was initially suggested by the progression of the radiological damage ( Fig. 6 ). In 2007, plain X-rays showed the characteristic appearance of the disease at the L1-L2 joint, with a combination of disc degeneration, vertebral erosion and massive osteophytosis. This damage had developed at the upper extremity of the laminectomized zone. Hence, the time interval between the onset of the paraparesis and the diagnosis of Charcot spine was about 5 years.

Change over time in the radiological appearance of Charcot spine in a paraplegic patient (case report 1), as revealed by AP X-rays of the lumbar spine centred on the L2-L3 region. Images were acquired in 1998 (6A), 2001 (6B) and 2007 (6C).

A CT scan confirmed the various aspects observed on plain X-rays and provided more detailed information on the paravertebral soft tissue calcification ( Fig. 7 ). The three-dimensional reconstructed images clearly revealed the association of bone destruction and construction phenomena. Furthermore, we noted moderate aggravation of the damage over a 4-year period (between 2001 and 2005) – essentially due to worsening of the L2-L3 retrolisthesis. The patient had not been examined with MRI.

Charcot spine in a paraplegic patient (case report 2), as revealed by computed tomography imaging in the axial (7A), frontal (7B) and sagittal (7C) planes. The images show the association of erosive lesions and hypertrophic ossification in the L2-L3 area.

In terms of therapy, the patient continues to refuse any kind of surgery treatment. The combined use of a thoracolumbar body jacket and symptomatic analgesics has helped relieve the patient’s spinal pain (presently three out of 10 on a visual analogue scale).

1.3.3

Literature data

Out of an initial list of 86 articles referenced in the PubMed and Pascal databases, 14 had been published before 1978, 11 described damage to a peripheral joint and seven dealt with Charcot-Marie-Tooth disease. In all, 36 publications were finally selected for review and featured a total of 111 cases of Charcot spine, including our two new case reports ( Table 1 ). Most of the publications reported on only one case ( n = 21 out of 36, i.e. 58,3%) and only four studies reported six or more cases.

1.3.3.4

Vertebra affected by Charcot spine ( n = 163)

The joints affected by Charcot spine are represented in Fig. 8 . We noted a total of 163 affected joints in 111 patients because several patients had damage to more than one joint. The most affected area was L2-L3. We noted the predominance of thoracolumbar and lumbosacral joint damage. The thoracic spine was very rarely affected. In all, 94.5% of the cases of damage were situated below T10 (corresponding to the start of the mobile spine).

Damaged vertebrae in Charcot spine ( n = 163 in 111 patients).

Damage concerned just one spinal joint in most patients ( n = 76 out of 111, i.e. 68.5%), two joints (adjacent or distant) in 25.5% of cases ( n = 28 out of 111) and more than two joints ( n = 7 out of 111) in only 6.3% of cases.

1.3.3.7

Radiographic aspects ( n = 61)

Only 61 cases were detailed enough to be included in our analysis. The frequencies of the various features are given in Fig. 9 .

Frequency of the main radiological features described in 61 patients. The total exceeds 100, since a given patient may present several radiographical signs.

Disc and vertebral damage was always present. Spinal deformity (usually kyphosis) was present in more than 50% of cases and intervertebral dislocation was seen in about 41% of cases. More than a third of the patients (36%) had undergone a biopsy at some point in their medical history; this was usually performed in order to eliminate another cause (either infectious or tumoral) and thus confirm the diagnosis of Charcot spine.

1.4.1

The different physiopathological hypotheses

The main disease mechanism in Charcot spine is impairment of joint innervation with loss of proprioception and sensitivity to pain/temperature ( Fig. 10 ). Furthermore, several cases have been described in patients with congenital insensitivity to pain and temperature – an autosomal disease characterized by the absence of small unmyelinated fibres .

The physiopathology of Charcot spine.

Impaired innervation induces loss of the joint’s defence mechanisms which otherwise help avoid excessive distraction of the disc and ligaments and enable a more homogeneous distribution of the mechanical stresses. Normally, ligament over-extension induces reflex muscle contractions and thus stabilizes the joint .

At the synovial joint, the failure of this reflex process results in repeated microtrauma to the cartilage, leading to progressive destruction of the latter and the joint capsules . Next, one observes changes in the synovial membrane and capsule with hyperplasia and hypertrophy , respectively; this leads to chronic synovial effusion and then progressive sub-dislocation of the joint. The resulting instability triggers the formation of a large osteophyte around the joint. Histological examination reveals non-specific, chronic inflammation and the proliferation of fibroblasts (which replace the joint cartilage) . Destruction of the cartilage leads to osteosclerosis and hypertrophic osteophytosis. Bone necrosis is often observed in peroperative biopsies.

It has also been suggested that loss of sympathetic innervation is a trophic factor that promotes hyperaemia and osteoclast hyperactivity .

Trauma (either repeated microtrauma or a single, major event) appears to be an aggravating factor. In animal experiments performed at the beginning of the 20th century, Eloesser demonstrated the primordial role of trauma in the development of neuro-arthropathy, since loss of joint innervation alone was not a sufficient condition .

In terms of spinal neuro-arthropathy, mechanical factors appear to be critical. In paraplegic patients, spinal stress in the position sitting and during transfers (which repeatedly expose the mobile spine below the fused area to excessive stress) is significant. The risk of early occurrence of Charcot spine is greater in very active spinal cord injured patients . Thus, Charcot spine appears to affect inter-vertebral areas that are exposed to stress (i.e. the thoracolumbar and lumbosacral joints) and/or are fragile.

In previously operated patients, Charcot spine typically develops (in over 70% of cases) either within the operated area (e.g. a non-instrumented laminectomy) or below an extensively instrumented area . According to several authors, laminectomy appears to be an aggravating factor . The loss of posterior stabilizing elements (the interspinous ligaments, the spinous processes, the laminae, the ligamenta flava, the joint capsules) and potential paravertebral muscles damage following laminectomy or, in some cases, partial synovectomy increases the level of stress exerted on the remaining elements (the disc-vertebral body complex at the front and the facet joints at the rear). Six out of the seven laminectomized patients in Vialle’s series developed Charcot spine within the operated zone . Sobel reported similar observations in four out of five cases . In a non-traumatic paraplegic patient, Luke and Bridwell described a case of Charcot spine occurring only 6 months after a laminectomy and a series of rhizotomies performed to reduce spasticity . He thus recommended the performance of a graft and systematic instrumentation in laminectomized paraplegic patients.

1.4.2

Clinical aspects

The time lag between the onset of neurological impairment and a diagnosis of Charcot spine is usually long (17.3 years, on average). In Delvin’s series of 10 cases, the mean time interval was 19 years . The time lag between the first symptoms of Charcot spine and its diagnosis is also long in many cases, due to the relatively non-specific nature of the apparent symptoms.

In paraplegic patients with complete neurologic impairment, the most frequent symptoms are a feeling of instability in the sitting position and spinal deformity (usually with a thoracolumbar gibbosity and an audible cracking noise) . The deformity frequently leads to instability in the sitting position (in four out of 10 cases in Delvin’s series) . In fully paralyzed patients, the presence of spinal pain is frequent; it may be mechanical or inflammatory in nature and is sometimes difficult to differentiate from neuropathic pain. Changes in the neurological picture have also been described: accentuated spasticity in partial paraplegics, decreased spasticity in complete paraplegics and changes in bladder and bowel disorders .

In non-impaired patients or those with incomplete neurological impairment (particularly spinal cord injured patients), the appearance of Charcot spine usually aggravates the neurological status .

It should be noted that a totally unstable spine may be asymptomatic .

In tetraplegic or high paraplegic patients, Charcot spine (typically above T6) can sometimes be revealed by a dysautonomic syndrome that variously combines arterial hypertension, bradycardia, hyperhidrosis and headache . This syndrome can be triggered by certain trunk movements and/or adopting the sitting position . In the literature, surgical stabilization completely resolves the dysautonomic syndrome in such cases.

Lastly (and very rarely), Charcot spine was revealed by a paravertebral, pseudotumoral mass in one case and thrombosis of the left common iliac vein (due to direct compression by an L5 prevertebral bone lesion) in another .

1.4.3

Radiological aspects

The radiological aspects reflect the disease mechanism and usually combine the following features :

• •
  

  significant disc degeneration;

  
  
• •
  

  destruction/erosion of the vertebral body that mirrors the disc space, associated with osteosclerosis or osteolysis and, occasionally, the presence of sequestra or debris resulting from fragmentation of the subchondral bone ;

  
  
• •
  

  hypertrophic osteophytosis within paravertebral soft tissue, with a markedly pseudotumoral appearance ;

  
  
• •
  

  early-onset damage to the facet joints ( Fig. 11 ).

  
  

  
  

  
  

  

  
  

  
  

  Schematic diagram of the radiological features of Charcot spine. The cardinal signs are disc destruction, bone erosion (sometimes with fragmentation and debris), disordered paravertebral bone formation and spinal deformity (sometimes leading to true intervertebral dislocation).

  
  

As the disease progresses, the damage may take on the radiographic appearance of hypertrophic pseudarthrosis, with the formation of a new intervertebral joint in some cases, so-called ball-and-socket aspect (clinical case 1).

Although the presence of hypertrophic osteophytosis with exostosis is strongly suggestive of Charcot spine, some authors distinguish between a hypertrophic form and an atrophic form in which these giant bone formations are absent and bone destruction phenomena predominate . Delvin found the hypertrophic form in only two of his 10 patients; the remainder had an intermediate form (two cases) or an atrophic form with predominant osteolysis (six cases), . The hypertrophic forms are more often observed around the spine and the proximal joints of the limbs .

Damage to all three columns can induce instability and sub-dislocation (or even full dislocation), leading to kyphotic, scoliotic or combined spinal deformity . Vialle et al. reported the presence of dislocation and/or kyphosis in 90% of cases . Dislocation is present in over 40% of the 111 case reports identified in the present review. This instability can be very significant, as seen in our second case report. Some authors have reported on patients in whom the flexion-extension angle difference is around 60° . In the series described by Morita et al. , the intervertebral mobility observed near the degenerative lesion when comparing the lying and sitting position was 43°, on average 24° to 72°. According to this same study, the severity of the radiological instability correlates with difficulty in maintaining the sitting position. These aspects underline the need to perform dynamic X-ray imaging as part of a patient’s radiological examination.

Furthermore, Morita et al. reported vertebral ankylosing hyperostosis phenomena in seven out of nine patients, with the notable presence of ossification of the anterior longitudinal ligament (as in our first case report).

A CT examination is useful for assessing the severity of vertebral body bone destruction and the extent of paravertebral bone formation. In MRI, one finds frequent peripheral contrast uptake (attesting to the chronic inflammation that accompanies the disc and vertebral damage) and more occasional paravertebral gadolinium uptake . Fluid build-up (seen as hypo-intense areas in T1-weighted images and hyper-intense areas on T2-weighted images) may be found around the paravertebral soft tissues or in the intervertebral space ; this aspect may then suggest spondylodiscitis. The presence of fluid build-up around the arthropathic lesion was seen in eight of Morita et al.’s nine Charcot spine patients (i.e. about 90% of cases) . Furthermore, the authors showed that the fluid volume correlated with extent of the instability seen on X-rays .

1.4.4

Differential diagnoses

The two main differential diagnoses are chronic infectious phenomena and tumoral process . There are no Charcot-spine-specific signs that enable these two diagnoses to be formally ruled out. The following signs are non-discriminant: bone erosion, osteophytosis, narrowing of the intervertebral space and a paravertebral mass . The presence of intervertebral space is strongly suggestive of a degenerative pathology. This explains the high frequency of disc/vertebra biopsies in these patients (36% of cases) with a view to ruling out these differential diagnoses and confirming the diagnosis of Charcot spine. The needle biopsy must be centred on the fluid collection, if the latter is present . The performance of a biopsy appears to be especially justified by the fact that the infection of pre-existing Charcot spine lesions has been reported (14% of the patients in the literature) . It can then be difficult distinguish between post-infected Charcot spine on one hand and primary spondylodiscitis that has induced Charcot-like degenerative lesions on the other. The risk of spinal infection is greater in patients who suffer from recurrent infections (particularly urinary infections). Cases of skin fistula have been reported ( Table 3 ).

Pseudarthrotic fracture of an ankylosed spine is another differential diagnosis ; however, the clinical context and the radiological aspect of the over- and underlying spine enables one (in principle) to differentiate this condition from Charcot spine. Lastly, in patients with a history of spinal surgery, it is sometimes difficult to differentiate a true case of Charcot spine from pseudarthrosis of the original fracture zone or post-laminectomy instability.

Although some authors recommend bone scintigraphy, the technique lacks specificity.

1.4.5

Treatment

Although natural progression of the disease is slow, it is clearly related to aggravation of disc/vertebral lesions . It is also important to emphasize the risk of secondary neurological aggravation in incompletely paraplegic patients . The various therapeutic options consist of monitoring, immobilization with a body jacket and surgery.

Orthopaedic treatment has shown its limitations for medium- and long-term relief and can at best stabilize the disease . It is, however, sometimes the only option for a fragile patient and/or one who refuses any form of surgical intervention . Morita et al. have emphasized the systematic failure of non-surgical treatment alone in cases of infection .

The most radical treatment option is thus surgery , even though some authors consider that the latter is only indicated when orthopaedic treatment fails. Surgical outcomes appear to be better for the spine than for the limbs ; nevertheless, this is a complex surgery, which should only be performed by well-trained teams.

The aim of surgery is to stabilize the diseased spinal segment by obtaining high-quality fusion ( Table 4 ). Debridement of necrotic/inflamed tissue (above all sclerosed and hypovascularized bone) is usually preferable , in order to optimize conditions for bone fusion. The debridement is best performed via an anterior approach . All authors insist on the need to graft the anterior column (the intervertebral space) via either an anterior approach or a posterolateral route (50% of the cases in Vialle’s surgical series). The choice of the exact type of surgery appears above all to be a question of the surgeon’s training and personal preferences.

A single, anterior phase is not sufficient in terms of stabilization and runs the risk of mechanical complications . Arnold described the successful operation of two cases of post-trauma Charcot spine via the posterolateral route with decompression, an interbody bone graft and posterior instrumentation . The same was true of the case reported by Mohit et al. (with a T11-T12 interbody cage), . However, most authors recommend stabilization via a combined approach in one or two steps. In 1991, McBride reported the treatment of four cases of Charcot spine with anterior fusion and staged posterior fusion. Only one patient experienced mechanical complications and solid fusion had been obtained in all patients 30 months later . Vialle et al. reported on a series of nine operated patients, with a combined approach applied in eight of these . Fusion was achieved in all cases and resulted in improvements in pain, spasticity and function. In 2007, Suda et al. reported on a series of four cases treated surgically via a combined anterior and posterior approach, with excision of the necrotic and inflammatory tissue, an autologous bone graft and posterior stabilisation with osteosynthesis. The authors noted satisfactory results, with complication-free surgical outcomes, disappearance of the Charcot-related symptoms and successful bone fusion in all four patients.

In order to reduce kyphosis, some authors have suggested performing a posterior shortening osteotomy .

In cases in which bone destruction is limited, a single posterior phase with interbody fusion might be sufficient. Morita et al. notably recommend this strategy in complete sensorimotor paraplegic patients where the risk of neurological aggravation is absent; this approach facilitates surgery which can be awkward if an anterior approach is used . In Morita et al.’s series, bone fusion had occurred in all patients 6 months post-operative.

The boundaries of the instrumented zone (and particularly the lower boundary) are subject to much debate. After fusion, there is a risk of developing damage below the operated spinal segment and above it . In 1992, Brown et al. reported on a series of eight treated surgically cases; two patients experienced mechanical complications and two others developed fresh neuro-osteo-arthropathic damage below the operated zone . Some authors recommend the systematic extension of the operation to the pelvis, in order to eliminating the risk of seeing additional neuro-osteo-arthropathy develop below the instrumentation. However, disadvantages of this approach include:

• •
  

  the complexity of the surgery;

  
  
• •
  

  the functional impact in terms of residual mobility when performing transfers.

In a series of 10 cases (with a mean postsurgical follow-up period of 4 years), Delvin et al. obtained fusion in eight cases (80%) and insisted on the fact that no unfused segments should be left between new and old fusions . However, he suggested that extension to the sacrum is not always necessary, even though the risk of seeing a new Charcot spine zone developing between the instrumentation and the pelvis remains. He recommended using a combined anterior and posterior approach for cases of non-reducible, rigid deformity or multiple-level Charcot involvement. For other cases, he performed bone grafting of the anterior defect via a posterolateral approach.

When surgery is used, it is important to evaluate the functional impact of arthrodesis. Morita et al. reported the case of a patient who could no longer perform self-catherization after surgery, due to post-arthrodesis spinal ankylosis. In this respect, the status of the coxofemoral joints must be carefully analyzed, since ankylosis of the hips leads to excessive strain on the lumbar spine; this can result in severe postoperative mechanical complications, such as instrumentation failure and/or pseudarthrosis . An operation to free up the hips can be considered on a case-by-case basis.

Lastly, it is important to take as many peroperative tissue samples as possible, in order to screen for any associated spondylodiscitis or (after histological examination) to rule out a tumour.

2.2.1

Cas cliniques

Nous rapportons deux cas cliniques de neuro-ostéo-arthropathie de Charcot avec atteinte rachidienne chez des patients blessés médullaires. Nous détaillons les circonstances de survenue, l’histoire de la maladie, la présentation clinique, les aspects radiologiques et la prise en charge thérapeutique.

2.2.2

Analyse détaillée de la littérature

Une revue exhaustive de la littérature a également été réalisée à partir des bases de données Pubmed et Pascal en utilisant les mots clés suivants : Charcot Spine , Charcot spinal arthropathy et neuropathic arthropathy of the spine . Seules les études suffisamment détaillées et publiées entre 1978 et 2008 ont été retenues. Les observations devaient comprendre au minimum l’âge du patient, la cause du déficit neurologique et le niveau du Charcot. Les études proposant une mise en point mais sans description de cas originaux n’ont pas été inclues dans l’analyse.

Les variables quantitatives sont décrites en termes de moyenne et écart-type alors que les paramètres qualitatifs sont présentés en termes de fréquence.

2.3.1

Cas clinique 1

Il s’agit d’un patient de 61 ans qui présente depuis l’age de 42 ans une paraplégie sensitivomotrice complète de niveau D10, d’origine ischémique, survenue dans les suites du traitement chirurgical en urgence d’une rupture d’un anévrisme de l’aorte thoracique. Le score ASIA moteur était à 50/100 et le score ASIA sensitif à 69/112 pour le tact et 68/112 pour la piqûre (Frankel A).

À partir de l’âge de 55 ans environ, le patient se plaignait de douleurs mécaniques chroniques, de plus en plus invalidantes, au niveau de la région lombaire basse. Ces douleurs s’accompagnaient progressivement d’une cyphose thoracolombaire majeure en position assise. Cliniquement, on ne notait aucune modification de l’examen neurologique, pas de modification de la spasticité, pas de craquement à la mobilisation. On retrouvait simplement une douleur modérée à la palpation en regard de la déformation. L’IMC a été évalué autour de 22. Il n’existait pas de tableau infectieux et le bilan biologique ne mettait pas en évidence de syndrome inflammatoire.

Devant les données du bilan radiographique, un processus infectieux chronique ou tumoral a néanmoins été évoqué et ont conduit à la réalisation d’une ponction-biopsie discovertébrale. Les cultures du liquide centrodiscal étaient stériles et l’examen anatomopathologique retrouva un tissu fibreux avec séquestres osseux sans signes de malignité. La recherche HLA B27 s’est avérée négative.

Finalement, le diagnostic de neuro-ostéo-arthropathie de Charcot était retenu. Les radiographies standards retrouvaient un aspect caractéristique de la maladie au niveau de l’articulation L1-L2 associant une destruction discovertébrale avec érosion corporéale des plateaux des vertèbres L1 et L2 et la présence d’ossifications exubérantes paravertébrales, réalisant un aspect pseudotumoral ( Fig. 2 ). Les clichés dynamiques révélaient l’importance de l’instabilité rachidienne ( Fig. 3 ) et le scanner 3D la sévérité de la dislocation intervertébrale en position couchée ( Fig. 4 ). Le patient n’a pas eu d’IRM puisqu’il présentait une contre-indication (patient porteur d’un pacemaker).

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

Effects of running retraining after knee anterior cruciate ligament reconstruction The relationship between muscle strength and physiological age: A cross-sectional study in boys aged from 11 to 15 Validity and reproducibility of the PPLP scoring scale in the follow-up of athletes after anterior cruciate ligament reconstruction Un an de version bilingue pour notre revue Treatment of genu recurvatum in hemiparetic adult patients: A systematic literature review Rehabilitation in Women with Breast Cancer

Stay updated, free articles. Join our Telegram channel

Join