Atormac
Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 987  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Search
 
  
 Resource Links
  »  Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
  »  Article in PDF (3,324 KB)
  »  Citation Manager
  »  Access Statistics
  »  Reader Comments
  »  Email Alert *
  »  Add to My List *
* Registration required (free)  

 
  In this Article
 »  Abstract
 » Introduction
 »  Materials and Me...
 » Results
 » Discussion
 » Conclusions
 »  References
 »  Article Figures
 »  Article Tables

 Article Access Statistics
    Viewed3018    
    Printed46    
    Emailed0    
    PDF Downloaded158    
    Comments [Add]    
    Cited by others 2    

Recommend this journal

 


 
Table of Contents    
ORIGINAL ARTICLE
Year : 2016  |  Volume : 64  |  Issue : 6  |  Page : 1220-1232

Craniovertebral junction anomalies: When is resurgery required?


Department of Neurosurgery, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication11-Nov-2016

Correspondence Address:
Dr. Kuntal Kanti Das
Department of Neurosurgery, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.193781

Rights and Permissions

 » Abstract 

Background: Craniovertebral junction (CVJ) abnormalities, such as atlantoaxial dislocation (AAD) with or without basilar invagination (BI), with or without associated Chiari malformation (CM), may cause a high cervical myelopathy. Occasionally, mechanical factors such as inadequate canal decompression, torticollis, and/or scoliosis may lead to lack of improvement following the primary surgery. Furthermore, implant-related factors, requiring implant revision/removal, or the presence of surgical site infections may cause the patient to undergo resurgery.
Aims: This study was aimed at highlighting the underlying etiopathogenesis of resurgery following the primary surgery undertaken in CVJ abnormalities.
Setting and Design: This was a retrospective study from a tertiary care referral institute focusing on 414 operated cases of CVJ anomalies.
Materials and Methods: The data of 55 patients who underwent resurgery included their clinicoradiological assessment and operative records. The inclusion criteria included failed primary procedure, repeat procedure for construct failure, infection at the surgical site, or wound dehiscence. Pure CM patients without bony anomalies were excluded from the study.
Results: A total of 137 procedures were performed in 55/414 (13%) patients. Causes of resurgery could be divided into ventral [redo or denovo transoral decompression (TOD) or wound-related complications, n = 33, 40.2%] and dorsal causes (implant-related factors/wound infections, n = 49, 59.8%). De novo TOD was done in persisting myelopathy following posterior fusion (PF) with C1-2 distraction (n = 15,18.3%,). Redo TOD was done for residual anterior bony compression [n = 8, 9.6%, OR 0.61; [CI = 0.20-1.86]. Causes for oral wound reexplorations (n = 10, 12.2%) included velopharyngeal insufficiency, wound resuturing, oral bleeding, and cerebrospinal fluid (CSF) leak. Dorsal causes included: (A) Implant factors (n = 27, 32.7%) and (B) neck wound reexplorations (n = 22, 26.8%). Presence of subaxial spine scoliosis, torticollis, and asymmetric joints increased the incidence of reexploration. Occipitocervical fusion rather than C1-2 fusion was more prone towards construct loosening.
Conclusions: Patients undergoing distraction with PF may require transoral surgery due to persisting myelopathy, especially in the presence of torticollis, scoliosis, and symmetrical joints. Single stage TOD+PF increases the chances of implant infection due to tissue contamination, bacteremia, or transfacetal migration of microbes. Chronic/recurrent sinus is usually a harbinger of deeper infection and can be cured with implant removal.


Keywords: Complication; craniovertebral junction anomalies; implant failure; posterior fusion; resurgery; transoral decompression


How to cite this article:
Sindgikar P, Das KK, Sardhara J, Bhaisora KS, Srivastava AK, Mehrotra A, Jaiswal AK, Sahu RN, Behari S. Craniovertebral junction anomalies: When is resurgery required?. Neurol India 2016;64:1220-32

How to cite this URL:
Sindgikar P, Das KK, Sardhara J, Bhaisora KS, Srivastava AK, Mehrotra A, Jaiswal AK, Sahu RN, Behari S. Craniovertebral junction anomalies: When is resurgery required?. Neurol India [serial online] 2016 [cited 2019 May 21];64:1220-32. Available from: http://www.neurologyindia.com/text.asp?2016/64/6/1220/193781



 » Introduction Top


Craniovertebral junction (CVJ) anomalies are well-recognized causes of myelopathy in the Indian subcontinent. Several studies from the region have focused on both the clincoradiological presentations and surgical nuances of the four commonly encountered CVJ anomalies, namely, reducible (RAAD) and irreducible atlantoaxial dislocation (IrAAD), basilar invagination (BI), and Chiari I malformation (CM).[1],[2],[3],[4],[5],[6],[7],[8],[9],[10],[11] Despite the significant improvement or stabilization of neurological status following surgical intervention in patients with AAD, a significant proportion of patients continue to have persistent myelopathy despite successful thecal sac decompression at the foramen magnum. The complex bony anatomical configuration of the region may lead to lack of attainment or sustenance of complete reduction of AAD.[6],[10] The debilitated condition of the patients, who often have severe myelopathy for prolonged periods of time, short and webbed neck, and compromised respiratory function may result in construct failure, pseudoarthrosis, wound related complications, and prolonged ventilatory support. Thus, the incidence of resurgery either due lack of improvement following the primary surgery, or because of complications occurring in the postoperative period is considerably higher than is generally believed, and there are no documented studies addressing this important issue.[12],[13],[14],[15] The aim of this study was to determine the incidence and the underlying reasons for resurgery following the primary surgery in symptomatic CVJ anomalies. Various factors that might have led to the failure of the first surgery were also determined.


 » Materials and Methods Top


This retrospective analysis, performed between January 2008 and December 2015, focused on 414 operated patients of CVJ anomalies who were managed at our centre. The patients who were focused on included both the categories, namely, those either primarily operated by us or those operated elsewhere and referred to us for further management. The patients included those with congenital RAAD or IrAAD, with or without associated BI or CM, and who underwent a repeat surgery directed at the CVJ. AAD was defined as an increase in the atlantodental interval (ADI) of more than 3.0 mm in adults and 4.5 mm in children (below 12 years).[6],[8],[11] The reducibility of AAD was determined preoperatively using dynamic lateral radiographs and/or 3–5 days of increasing Crutchfield's skull traction (starting with 7% of body weight increasing to a maximum of 7 kg).[16],[17] Patients who achieved C1-2 reducibility, either spontaneously or after institution of Crutchfield's cervical traction, were considered to be having a RAAD; those in whom the C1-2 dislocation failed to reduce were defined to be having an IrAAD. Patients with fracture of the odontoid, as well as those with tuberculous or rheumatoid AAD were excluded from the study. Patients with pure CM without a demonstrable AAD/BI, as well those having an additional spinal dysraphism, were also excluded from the study. The revision surgery was only considered for inclusion in the study if it had been directed primarily for AAD/BI. Thus, an additional tracheostomy, lumbar drain placement, and/or a feeding gastrostomy as a part of the postoperative management of the patients (without a repeat procedure addressed at the CVJ) were not considered be a second surgery that would merit inclusion of the patient in the study.

Out of the 414 patients who were admitted within the time frame of the study, 55 (13%) patients underwent additional surgeries directed at the CVJ after having undergone the primary surgery [either transoral decompression followed by posterior fusion (TOD+PF) or posterior fusion (PF) alone]. In total, 137 surgeries were performed in these 55 patients (the number of additional repeat surgeries being 82). TOD and PF were performed in a single stage in our study.

In these 55 patients, who underwent repeat surgery directed at the CVJ, the clinical and radiological records were evaluated. The repeat plain lateral radiographs, magnetic resonance imaging (MRI) scan of the CVJ, and the dynamic plain or intrathecal contrast computed tomographic (CT) scans with three-dimensional (3D) reconstruction images, performed prior to the repeat surgical intervention, were compared with the corresponding preoperative images, as well as with the ones undertaken immediately after the first procedure. The bony and soft tissue structures at the CVJ, the residual/recurrent spinal canal compromise, and the persisting cord intensity changes, CM, or syringomyelia were assessed in them. Non-reduction of AAD/BI and persistent odontoid impingement on the cord were noted. Facet joint asymmetry in the coronal plane of the CT and MRI scans (also termed as coronal asymmetry) was considered to be significant if the difference in the angulation of the C1-2 joints on either side exceeded an angle of 10°. In patients who required TOD as a second surgery after the initial PF, the facet joint morphology, coronal and sagittal inclination, and the presence of torticollis were analyzed. The direction and position of the construct prior to resurgery was compared with the preoperative imaging as well as with that obtained in the immediate postoperative period after the first surgery. Depending on the cause of the persistent problem, appropriate procedures were undertaken during resurgery.

The following terminology was used in the computation of results. Patients who continued to have progressive or non-improving myelopathy or oral wound complications following ventral decompression, and those in whom a ventral decompression was required following either a previous TOD with PF or following a primary PF were assigned to the category of ventral causes of resurgery. Patients who required reexploration of their PF wound or revision of their PF were assigned to the category of dorsal causes of resurgery. The term “de novo TOD” was used to describe the procedure of an additional TOD in patients who had a persistent ventral compression following posterior distraction and fusion (these patients had only undergone posterior stabilization with or without posterior distraction and not the transoral procedure). On the other hand, the term “redo TOD” referred to the additional TOD carried out for persisting ventral compression in patients who failed to improve following a primary TOD+PF (i.e., TOD was repeated during the reoperative procedure). “Implant factors” referred to implant failure (construct loosening, breakage of wire or rod, etc.) or infected implant removal. “Neck wound complications” refers to superficial or deep wound complications following PF that did not require implant removal.

Statistical analysis

Continuous variable normality was tested using Kolmogorov–Smirnov test. Independent samples Kruskal–Wallis H test was used to test the significance among non-normal continuous data. Categorical data were presented as frequency and percentages. Pearson chi-square test/Fisher exact test was used to compare the proportions at a significance level. Binary logistic regression model was used to calculate the odds ratio (OR). A P value of <0.05 was considered to be statistically significant. Statistical Package for Social Sciences version 22 (SPSS-22, IBM, Chicago, USA) was used for data analysis.


 » Results Top


Demographic characteristics

Fifty-five patients underwent 137 procedures. There were 44 male and 11 female patients in our study [male:female = 4:1, OR = 1.68, 95% confidence interval (CI) = 0.39–7.22; P = 0.73]. Their age ranged from 4 to 60 years, with a median age of 26 years, while the ages in the first and third quartiles were 18 and 39 years, respectively. There were 45 adults and 10 children (less than 16 years) in our study (OR = 1.21, 95% CI = 0.29–4.92, P = 0.79). Neither gender nor age at presentation were significantly associated with the incidence of reexploration. The time from the primary surgery to the first resurgery was variable and ranged from the day of primary surgery to as late as 19 years. Majority of the patients presented within the first year of primary surgery (n = 45, 81.5%), out of which 38 (69.1%) patients reported within the first 6 months. In this study, patients presenting for resurgery could be divided into two subgroups depending upon the time of presentation. The first subgroup consisted of patients presenting within the first year wherein implant failure was rare. The second subgroup, consisting of patients presenting for resurgery after 1 year of the primary surgery, had implant failure as a major cause of resurgery in a time duration ranging from the first year of surgery to as late as 19 years.

Primary diagnosis and initial procedures performed

The primary diagnosis of these patients and the number of resurgeries performed are enlisted in [Table 1]. A larger proportion of the patients with IrAAD underwent reexploration compared to the patients with RAAD (45 vs 10, OR = 2.67, 95% = CI 0.51–14.03; P = 0.23). Among the group with IrAAD, those with associated BI had a higher likelihood of undergoing resurgeries (OR = 2.27, 95% CI = 0.54–9.47; P = 0.25).
Table 1: A summary of the causes of resurgery in patients with CVJ anomalies

Click here to view


Transoral decompression (TOD) of the odontoid was performed in 30 patients. TOD+PF was done in 29 patients.[18],[19],[20],[21],[22] TOD as the sole procedure was carried out in 1 patient who had a posterior C1-2 bony ankylosis. Only posterior distraction and fusion was performed in 25 patients.[23],[24] Among these patients undergoing primary posterior C1-2 joint distraction with posterior stabilization (n = 25), 15 had an IrAAD whereas 10 patients had an RAAD, with or without BI [Table 2]. The various posterior stabilization procedures performed in the study included C1-2 (Brooks' technique)[25],[26],[27] or occipitocervical (O-C2) sublaminar wiring (Jain's technique)[28] (n = 4, and n = 16, respectively), contour rod stabilization (n = 11, Ransford's technique)[29] and Goel's C1-2 facet distraction and C1 lateral mass-C2 pars fusion technique (n = 23).[30]
Table 2: The causes of resurgery following various types of posterior fusion procedures performed

Click here to view


Different resurgeries performed

We categorized the different resurgeries performed in our series into ventral (n = 33, 40.2%) and dorsal resurgeries (n = 49, 59.8%). [Table 1] shows the breakup of the different resurgeries performed.

Ventral causes of resurgeries

Ventral causes of resurgeries could be subdivided into (A) TOD (n = 23, 28%) and (B) oral wound complications (n = 10, 12.2%). Patients requiring TOD could be further categorized into two subgroups. The first subgroup of patients, those belonging to the category of de novo TOD, included those who failed to show neurological improvement after only posterior distraction and fusion and continued to have residual AAD/BI causing thecal compression (n = 15, 18.3%, [Figure 1]) [Table 1]. The second subgroup of patients, those belonging to the group redo TOD, underwent a repeat TOD for residual ventral compression following an initial TOD that had been performed during the first setting (n = 8, 9.6%) [Figure 2], [Figure 3], [Figure 4], [Figure 5].[21],[22]
Figure 1: A 15-year-old boy presented with progressive high cervical myelopathy of 2-year duration. (a) His sagittal reconstructed CT images showed AAD, BI, occipitalized  Atlas More Details and C2-3 fusion. (b) Postoperative lateral radiograph of the cervical spine shows an O-C2 fixation, but the patient failed to improve and had persistent posterior angulation of the odontoid. (c) Postoperative sagittal reconstructed CT scan following TOD showing an adequate spinal decompression at the C1-2 level

Click here to view
Figure 2: A 4-year-old girl child suspected of Larsen syndrome, presented with progressive myelopathy and regression of motor milestones; (a) T2-weighted sagittal MRI was suggestive of compression of cervicomedullary junction with intensity changes with retroodontoid connective deposition. (b) Extension and (c) flexion sagittal CT images showing a reducible AAD. (d) Postoperative radiology showing reduction of AAD with C1-2 rod and screw fixation. In the postoperative period, the child had worsening myelopathy with difficulty in being weaned from ventilator. The child underwent a successful transoral decompression of connective tissue. (e) Intraoperative image showing a fibrocollagenous tissue compressing the thecal sac; (f) The exposed dura after removal of fibrocollagenous tissue; histopathology revealed a dense fibrocollagenous tissue with no evidence of granuloma/tumor/metastasis

Click here to view
Figure 3: A 40-year-old male patient presenting with progressive myelopathy of 5-month duration; (a) T2-weighted sagittal MRI suggesting an AAD with BI with cervicomedullary compression with cord intensity changes; (b) Sagittal reconstructed CT images showing the AAD with a high BI, occipitalized atlas and C2/3 blocked vertebra; (c) Coronal three-dimensional CT reconstruction showing the asymmetrical C1-2 vertical joints. (d) Following application of Crutchfield's cervical traction, the patient underwent sublaminar C1-2 sof'wire wire fusion by the posterior approach. (e) In the postoperative period, the patient had no improvement in myelopathy and therefore, TOD was performed; (e and f) Postoperative sagittal and (g) axial images showing an inadequate lateral decompression during the TOD. (h and i) Coronal and (j) three-dimensional sagittal images after redo transoral surgery showing the successful TOD including lateral decompression

Click here to view
Figure 4: A 32-year-old female patient presented with neck pain and progressive spastic quadriparesis of 15-year duration. The patient underwent an occipito-C2-C3 fixation with rod and screw followed by TOD at a later date. However, myelopathy failed to improve with TOD. (a) Sagittal CT scan showing the AAD causing canal compromise. (b-d) Postoperative parasagittal, axial, and coronal CT showing persistent ventral thecal sac compression on the lateral aspect despite an adequate ventral decompression

Click here to view
Figure 5: A 49-year-male presented 5 years after undergoing TOD with PF with worsening myelopathy. (a and b) Sagittal reconstructed images of CT scan showing the inadequate transoral surgery with bone graft of posterior fusion. (c and d) Coronal images showing the residual lateral bony pillar adjacent to the gutter created by the TOD and new subcapsular bone formation within the TOD cavity. Patient underwent a redo TOD which resulted in an improvement during the postoperative period

Click here to view


The group where surgery for oral wound complications (n = 10, 12.2%) was performed included those patients who underwent a palatoplasty for velopharyngeal insufficiency (n = 5), in whom resuturing was performed in cases with pharyngeal wound dehiscence (n = 3), in whom hemostasis of a pharyngeal bleeding vessel (n = 1) was required, and in whom repair of the cerebrospinal fluid (CSF) leak from the oral wound (n = 1) was performed.

We would like to further describe in greater details the characteristics of the subset of 15 patients with IrAAD in whom only the posterior approach was employed as the first procedure, all of whom required a TOD subsequently, either for persisting or progressive myelopathy, following the posterior distraction-fusion.[23],[24],[30] Of these, 2 patients were lost to follow-up. Hence, the clinical charts, imaging, and follow-up data of 13 of these patients were available for analysis. Of these 13 patients, 11 were adults [average age 35 years, (OR = 1.29, 95% CI = 1.10–1.52, P = 0.08) while there were 2 children in this subgroup. There was a male predominance similar to the overall analysis (male:female = 2.25:1, OR = 2.22, 95% CI = 0.53–9.29, P = 0.27).

On analysis of the CT scan of the CVJ, the average ADI of these patients was 9 mm (8–12 mm). Eleven (85%) out of the 13 patients had coronal asymmetry (mean asymmetry: 18.55°); in comparison to the other subgroups, this high incidence of coronal asymmetry was statistically significant (P = 0.01). Eleven out of these 13 patients also had an associated BI (P = 0.02), and 4 of them had platybasia. Twelve of these patients, therefore, had clinically manifest torticollis (P = 0.002). In 11 patients, the C1 arch was occipitalized and 10 patients had a C2/3 block vertebra. One patient also had CM with syringomyelia. Retroodontoid soft tissue causing persistent compression following seemingly successful reduction on the CT images was found in two patients; the histopathology of the excised tissue revealed the retroodontoid deposition to be composed of a dense fibrocollagenous tissue [Figure 2].[31],[32]

Dorsal resurgeries

Dorsal resurgeries could be attributed to (A) implant related factors (n = 27, 32.7%), and (B) neck wound complications (n = 19, 23.2%). The implant factors that resulted in resurgery were further divisible into two subgroups, namely, the biomechanical failure group (n = 14, 17.1%) and the infected implant group (n = 13, 15.6%).

Implant-related factors

Implant-related factors were one of the major reasons for revision surgery in our experience. Fourteen patients (17.1%) underwent implant revision. These factors included breakage of sublaminar wiring (n = 3) with recurring symptoms [Figure 6]; the presence of os odontoideum with reducible AAD that led to the hypermobility of atlas over axis causing thecal compression both in flexion and extension, and the PF had to be repeated in neutral position of the neck [Figure 7]a and [Figure 7]b; or postoperative hardware associated stenosis secondary to sublaminar wire placement [Figure 7]c and [Figure 7]d (n = 2) or redo implant (that is, a third surgery) after prior removal of the implant for control of infection (n = 3); vertebral artery injury (n = 2; an intraoperative injury requiring abandoning of the posterior fusion that was subsequently carried out after therapeutic embolization of the injured VA [Figure 8]; postoperative oral wound bleeding from an intraoperatively undetected VA injury that required therapeutic embolization of the parent VA);[33],[34],[35],[36] displacement of the ini (screw head used during final screw tightening; n = 1); revision of the rod and screw implant (n = 2) as the screws of previous implant loosened and there was failure to maintain alignment and achieve bone fusion; and dislodgement of implant from the bone (n = 1) [Figure 9]. The most common cause of implant revision was sublaminar wire breakage. Sublaminar wiring was associated with nearly 1.5 times higher risk of implant revision. Occipitocervical fusion (n = 3) rather than C1-2 (n = 1) fusion was prone towards construct loosening perhaps due to asymmetric occipital squama, and long lever arm bony construct leading to mechanical failure; and, the contiguous involvement of the occipitoatlantoaxial joints in the former rather than a single joint (C1-2) in the latter procedure, and, especially in the presence of significant scoliosis of the cervical spine where lateral mass screw placement was difficult [Table 2] and [Figure 9], [Figure 10].[10],[14],[15],[21]
Figure 6: (a-c) A 19-year-old male patient presented with worsening myelopathy after an initial improvement. Implant revision with reinsertion of sublaminar wire was done. (a and b) Flexion and extension lateral cervical images showing breakage of the sublaminar wire; (c) postoperative radiology showing the intact sublaminar sof'wire wire. Remnant braided wires from the previous surgery that were closely approximated to the bone and could not be pulled out, were also seen. (d and e) A 36-year-old male patient presented 12 years after the occipito-C2-C3 fusion (by sublaminar wiring) with reappearance of high cervical myelopathy following a road traffic accident. (d) Sagittal CT image showing a mild AAD, BI with an occipitalised atlas with the broken occipitocervical sublaminar wire. (e) Postoperative radiology showing the implant revision to occipito-C2-C3-C4 rod and screw fixation. The wire from the previous surgery was closely adherent to the bony tissue and was left in situ

Click here to view
Figure 7: (a) Lateral radiograph in extension and (b) flexion of the neck in a patient with os odontoideum with reducible AAD where the hypermobility of atlas over axis led to thecal compression in both extension and flexion of the neck. Therefore, C1-2 fusion had to be performed in neutral position of the neck after alignment of os odonteum with rest of C2 body had been determined. (c) Lateral radiograph of CVJ showing AAD with occipitalized atlas in another patient. (d) The sublaminar wire loops into the spinal canal causing thecal compression

Click here to view
Figure 8: A 25-year-old male patient presented with progressive spastc quadriparesis of 2-year duration. The patient had significant torticollis and developed vertebral artery injury during lateral mass rod and screw fusion, for which an immediate endovascular occlusion of the parent internal carotid artery was done. Postoperatively, the patient had an increase in myelopathy.At the last follow up, the patient presented with discharging sinus near the occipital end of wound. (a) Sagittal T2-weighted MRI scan showing AAD with compression of the cervicomedullary junction; (b) sagittal reconstructed CT showing significant AAD without BI; (c) digital subtraction image, right vertebral artery (VA) showing extravasation of dye from the rent in the third segment of right VA; (d)Left VA injection, anteroposterior view showing a good flow through it into the basilar artery. Coil occlusion of lumen of the injured right VA is performed. (f) Postoperative imaging showing occipito-cervical fusion with intravacular coils in situ. (g) Clinical photograph of the discharging sinus near the occipital end of the posterior incision. (h) Close up image of sinus with serosanguinous discharge with all probability of implant infection. Patient has been placed on antibiotics and regular dressing, and follow-up status is awaited

Click here to view
Figure 9: a) Anteroposterior view and (b) lateral view of the cervical spine radiograph showing implant failure in form of dislodgement of the occipital plate in a 24-year-old male patient. He underwent an implant revision to a C1-2 rod and screw fixation

Click here to view
Figure 10: (a) Sagittal, (b) axial, (c) three-dimensional coronal, (d) coronal CT scan of the CVJ and upper cervical spine showing significant scoliosis associated with C1-2 facet asymmetry and vertical facet joints. There is an ever-present danger of C1-lateral mass, C2 pars, and C3-6 lateral mass screws being directed laterally endangering the VA traversing through the foramen transversarium on either side

Click here to view


Implant removal, because of infection involving the hardware, was required in 13 (23.6%) cases. Eleven patients, who underwent TOD+PF required implant removal, and two patients, who initially underwent only PF, required implant removal due to the development of a deep-seated infection. Eight patients had an O-C2-3 fixation, 3 an O-C2 fusion, 1 patient each had an O-C2-4 fusion and an O-C2-3-4 fusion, respectively. Hence, 12 out of the 13 patients who eventually needed the implant to be removed due to infection had occiput included in the fusion. When the incidence of implant removal for infection was assessed amongst the different techniques used for performing the PF, a positive association with a higher incidence of construct removal was seen in the rod and screw fixation group (n = 6, OR = 1.89, P = 0.35) while the sublaminar wiring (n = 4, OR = 0.72, P = 0.75) and contoured rod fixation groups showed a negative association (n = 3, OR = 0.67, P = 1). Inclusion of the occiput in the construct was associated with 1.23 times risk of implant infection. TOD preceding PF was significantly associated with deep surgical site infection that eventually led to implant removal (OR = 6.31, 95% CI = 1.23–32.34, P = 0.02) [Figure 8].

Neck wound complications (n = 19, 23.2%)

Surgical site infections constituted 23.2% of the total resurgeries. These included stitch abscess or wound infection requiring superficial debridement without construct removal and a single case in whom a tense hematoma was drained.


 » Discussion Top


High rate of re-surgery and the consequences of variable duration of procedure related morbidity

Various case reports and original articles have referred to the morbidity and complications that occur following surgery for AAD, with or without BI or CM.[1],[2],[3],[4],[5],[6],[7] However, there is only one review that specifically focuses on the complications and failed craniocervical surgeries. In this study, 22 reports from 2274 procedures were analyzed for complications. The most commonly encountered perioperative complications were related to instrumentation failure after nonunion (7% during occipitocervical fusion and 6.7% during atlantoaxial fusion). Injury to the vertebral artery (1.3–4.1%) during placement of C1-C2 transarticular screws, most commonly occurred in the case of high-riding vertebral artery.[15] Thus, reporting of complications, which are an inevitable part of any surgical procedure, constitute an often neglected aspect.

This unique audit of the causes and factors that led to resurgeries in CVJ anomalies revealed a resurgery rate of 13% (performed in 55 out of 414 patients), which was a statistically significant figure. This high incidence could be attributed to the significant influence of extraneous factors such as the poor general condition, hygiene, and nutritional status of patients suffering from long standing myelopathy along with respiratory compromise, the often encountered inability to even carry out activities of daily living, as well as the inclusion of even superficial wound infections and stitch abscesses (where only a minor procedure under local anaesthesia was required) in the list of complications.[10],[11],[21],[22] However, there was no influence of the age of patients or their gender on the reoperation rate. Mazur et al., retrospectively reviewed their database of 127 children who underwent various occipitocervical procedures for an early complication and reoperation rate. They concluded, in findings similar to ours, that neither age nor gender had any impact on resurgery in this region.[37] However, in this era of growing elderly population, the study by Guppy et al., is important. Their database revealed that the mortality rate (27.7%) and resurgery rate (14.9%) was significantly higher in the elderly patients (>65 years) undergoing an occipitocervical posterior fixation.[38]

In our study, the time from the primary surgery to the first resurgery was extremely variable and ranged from the day of the primary surgery to as late as 19 years. It is also interesting to note that, during the first year after the primary surgery, wound-related issues took precedence for resurgery, while after the first year, implant failures were more likely to occur. It is also noteworthy that patients with IrAAD and BI were more likely to undergo resurgery than those with RAAD. In the former group, often two procedures (TOD+PF) were required rather than a single procedure (PF) in the latter group. Even if the technique of posterior distraction with PF was used in the former group, there was greater likelihood of incomplete C1-2 reduction and perisistent cervicomedullary compression.[6]

Both the high incidence of reoperations and the variable duration during which the procedure-related morbidity occurred led to the inevitable conclusion that a lifelong vigilance for the development of pseudoarthrosis or of graft-related complication,[39] as well as a high index of suspicion for the requirement of resurgery in some form, needs to be maintained in this extremely vulnerable patient population even after conducting an apparently successful primary procedure at the CVJ.

Ventral cause of reoperation

It is interesting to note that 15 (18.3%) patients in the category of de novo TOD failed to show neurological improvement after undergoing only posterior distraction and fusion and continued to have residual AAD/BI causing thecal compression [Figure 1]. This residual compression was particularly more pronounced in the presence of torticollis and grossly asymmetrical facet joints, including the presence of vertical joints.[40] Asymmetrical facet joints led to incomplete reduction during the distraction procedure; extensive drilling of facet joints as well as placement of the artificial joints has been suggested to circumvent this effect. The other factor that led to failure of only the posterior C1-2 distraction and fusion procedure included the presence of platybasia with a high BI associated with C2-3 fusion that led to insufficient distraction of the odontoid from the foramen magnum.

A redo TOD was required in 8 (9.6%) patients [Figure 2], [Figure 3], [Figure 4], [Figure 5]. The main reason was the coexisting torticollis that often led to a tendency towards asymmetrical odontoid drilling during the transoral procedure; and, therefore, the lateral part of the odontoid on one side was incompletely drilled in the presence of torticollis. Following an intrathecal contrast CT scan, a repeat TOD had to be performed. In the presence of torticollis, during redo TOD, it is imperative for the surgeon to become oriented with the distorted anatomy and to localize the midline by exposing both the C1-2 facet joints as well as the lateral edges of the vertebral body below. The presence of torticollis leads to asymmetrical bony drilling toward the dural sac and may cause bulging of the thecal sac on the side of lesser depth. This may lead to an erroneous estimation of the depth; the dural bulge may also hamper further drilling. Therefore, these factors may lead to persistent lateral compression. An angulation of the vertebral alignment may also, inadvertently, lead to an oblique drilling of the lateral vertebral pillar endangering the vertebral artery [Figure 8] and [Figure 10].[6],[11],[26],[41] A preoperative angiogram is imperative to assess the orientation of the vertebral artery, to ascertain the non-dominant side, to rule out an anomalous course, and to eliminate the possibility of vertebral artery injury either due to the vertebral artery not emerging through the atlantal foramen transversarium, the persistence of the first intersegmental artery or a low-lying posterior inferior cerebellar artery. The latter condition may result in the traversing of vertebral artery in close vicinity to the C1-2 joint, making it prone to injury. In case the vertebral artery is injured, an immediate therapeutic embolization or stent placement utilizing an interventional radiology procedure should be performed to prevent an exanguinating rebleed from the resultant pseudoaneurysm [Figure 8].[33],[36]

In two patients, a conglomeration of the transverse ligament, tectorial membrane, and additional dense fibrocollagenous tissue had formed a retroodontoid deposition that, being hypointense and nonenhancing, was not clearly distinguishable from the bony elements on the preoperative MRI. After adequate drilling of the odontoid, the repeat postoperative MRI revealed the lesion. A repeat TOD procedure was required for achieving an adequate decompression of the thecal sac [Figure 2].[31],[32]

The main oral wound reoperative procedure performed in 5 patients included a palatoplasty for velopharyngeal insufficiency that was causing troublesome rhinolalia and nasal regurgitation. Palatal wound splitting was performed in the initial TOD procedures, but was later discarded in favor of palatal retraction into the nasopharynx by utilizing intranasal Ryle's tubes inserted through both nostrils. After introducing palatal sparing TOD, this problem has not been encountered. However, one must be aware of its existence, in case a palatal split is required to access a high BI, especially in the presence of platybasia and subaxial Klippel Feil anomaly leading to a short neck. Oral wound dehiscence (n = 3) and retropharyngeal hematoma formation (n = 1) was prevented by a meticulous adherence to the protocol introduced in the surgical technique. This included not using cautery until the final stages of dissection of the soft tissue from the anterior surface of upper cervical vertebrae; strict adherence to the midline avascular pharyngeal raphe; visualizing the midline by inspecting the orientation of the longus coli muscles and the anterior longitudinal ligaments and, by palpating the lateral edges of the vertebral body; and by a two layer (muscular and mucosal–submucosal) closure of the oral wound using a polyglactin-based absorbable, braided suture. CSF leak occurring through the anterior dura may be closed primarily or using a patch graft. An additional lumbar drain may be instituted to induce a negative pressure at the site of leak. The practice of patch placement using fibrin glue is fraught with the danger of CSF releak once the adherence property of the glue wears off. There is an omnipresent danger of meningitis, precipitated by the CSF coming in contact with the potentially infected oral cavity, especially if the negative pressure created by the lumbar drain is also effective.[21],[22]

Implant-related factors

Fourteen patients (17.1%) underwent implant revision. The most common cause of implant revision was sublaminar wire breakage or cutting through of the metal wire through the C1 posterior arch [Figure 6]. An increased distance between the posterior arch of C1 and the lamina of C2 led to further looping of the sublaminar wiring into the spinal canal. This thecal compression by the sublaminar wire may be further exaggerated if the sublaminar fusion is attempted without determining the adequacy of C1-2 joint reduction [Figure 7]c and [Figure 7]d. The sublaminar wire also fails to prevent axial C1-2 movements and may, therefore, loosen during axial neck movements.[10],[13],[14],[37],[39],[41] Sublaminar C1-2 fusion was associated with nearly 1.5 times higher risk of implant revision. It is still very effective in young children, but is rarely used in the adult population. In patients with os odontoideum with a hypermobile atlas, in flexion of the neck, the odontoid process moved backwards to cause spinal canal compromise; in extension of the neck and during the PF, the atlas with os odontoideum moved backward to again cause thecal compression. Therefore, the fusion had to be revised with neck in neutral position and the os odontoideum in proper alignment [Figure 7]a and [Figure 7]b.[41]

The contoured rod fusion always fuses the occipitocervical joint.[29] The long segment stabilization often led to significant neck movement restriction. The construct failure often occurred due to telescoping of the contoured rod through loosened wires closely apposing the rod to the C2-3 laminae. It was also noticed in our study that an occipitocervical fusion (n = 3) rather than C1-2 (n = 1) fusion was prone towards construct loosening perhaps due to the asymmetric occipital squama; the long lever arm of the bony construct that led to mechanical failure; or, the contiguous involvement of the occipitoatlantoaxial joints in the former, rather than a single joint (C1-2) in the latter procedure [Figure 9]. Inclusion of occiput in the construct was associated with a 1.23 times risk of implant infection. This was usually due to either the dehiscence of the thin skin over the upper end of the incision or due to the development of a bed sore/collar sore at the level of external occipital protuberance. In the case of C1-2 screw and rod technique, the presence of torticollis and asymmetrical C1-2 lateral masses led to a disproportionate strain on one side of the construct, leading to loosening of the screw and its mechanical failure. The fact that an implant could fail even 19 years after its placement points towards the implication of pseudoarthrosis. This may either be due to failure to achieve an adequate bone decortication; failure to maintain sufficient bony contact between the autologous bone graft and the occipitocervical bone; inadequate neck immobilization; graft lysis; insufficient quantity of trabecular bone with inadequate osseous progenitor cells; or loosening of the metal construct due to improper bone purchase, osteoporosis, or subclinical infection.[11],[13],[14],[42],[43]

Infection

Superficial wound infections could often be resolved by incising the infected wound edges and removing the culprit infected subcutaneous sutures. One of the culpable factors was subcutaneous tissue pouting through the skin, the presence of a short and webbed neck, and maintenance of neck in an extended position. Thus, a meticulous subcutaneous and skin closure was required, especially in the intertriginous areas of the neck skin folds. Care had to be taken so that the upper part of the midline incision of the neck did not extend up to the external occipital protuberance. In the supine position, in a recumbent patient, who is unable to turn himself in bed, this area is most prone to developing bed sores and also infecting the surgical wound. Prolonged usage of a collar may also cause neck skin sores that has the potential to infect the wound [Figure 11] and [Figure 12]. If a persistent sinus through the main wound fails to heal (although there may be no superficial evidence of inflammation) despite local and systemic antibiotics and superficial wound debridement, then it indicates that the infection has involved the construct as well as the onlay bone graft and will only heal by removal of the implant [Figure 8]. The removed construct can again be successfully implanted in its primary position after 6 weeks of complete resolution of the sinus.[21]
Figure 11: The dorsal aspect of head, neck, and upper back with prominent landmarks labelled. Light colored area shows the area of posterior maximum bony protuberance in the occipital region. The conventional incisions start from the inion to the C4 spinous process. The C1-2 fixation can be performed with a lesser exposure that does not extend up to the inion

Click here to view
Figure 12: (a-c) Intraoperative photograph showing incision marked 4 cm below inion and the muscular layers exposed. Trapezius, splenius capitis, and semispinalis capitis are retracted by the self-retaining retractor. (d-f) Intraoperative photographs showing exposure of external occipital protuberance (EOP) with the thick layer of faciomuscular tissue covering it being dissected into a triangular flap. (d) This triangular flap is being retracted with ligatures. (e) At the conclusion of the procedure, the EOP is well covered with fascial tissue. (g-i) Intraoperative photographs showing a faulty exposure with dissection through the midline reaching the EOP. At the conclusion of procedure, it is difficult closure the fasciomuscle layer over the bony prominence of the EOP, which therefore lies just below the skin not covered by any soft tissue

Click here to view


In patients in whom a combined TOD+PF procedure was performed, two potential sources of construct infection could be determined. The first cause of infection in the initial couple of patients was the use of a couple of common instruments simultaneously in both the procedures when the two procedures were being performed in the same setting. Treating both these surgeries conducted in a single stage as completely different procedures (with the TOD being considered as being done through a potentially infected corridor), utilizing completely different sets of sterile sheets and the theatre apparel, and sterilizing the implant instruments twice prior to the procedure, circumvented this problem. The second cause was the drilling of the C1-2 facet joints both during the TOD and PF procedures, thus allowing spread of infection from the oral cavity to the construct through the C1-2 articular cavity. One has to be careful in not carrying out the C1-2 drilling simultaneously through both the corridors and in allowing the joint capsule to remain intact as a potential barrier during either of the approaches.[44] Thus, TOD preceding PF was significantly associated with deep surgical site infection that eventually led to implant removal (OR = 6.31, 95% CI = 1.23–32.34, P = 0.02).

Limitations of the study

Despite the prospective collected database, the retrospective nature of the study has its inherent drawbacks. The major one among them is that resurgery was required at follow up but the patient chose to undertake it at another centre. Some of the patients perhaps reconciled to their disability and chose not to undergo a secondary procedure. The frequency of resurgery was, therefore, not synonymous with the actual disability figures in the patient population, and the rates of disability may have been underestimated. The recruitment of participants for this study at one point in time may not have given the actual prevalence rates of the persistent morbidity. To quote an example, with time, velopharyngeal insufficiency may show a significant improvement and may cease to remain a cause of concern for the patient. This morbidity would, however, be counted as a cause of major morbidity requiring a surgical procedure when the patient is being considered prior to the improvement of the symptom. Inclusion amongst the resurgery procedures of even superficial wound infection, despite a significant improvement in the neurological status of a patient, may lead to the erroneous impression of an exaggerated morbidity associated with a particular procedure. A systematic clinicoradiological correlation with the causes of neurological deterioration in the patients included in the study would have been very illuminating.

The variety of PF techniques used for a plethora of combinations of CVJ anomalies precluded the comparison of individual techniques, as well as the regulation of standards for the procedures being followed. Thus, an unequivocal message pertaining to complication avoidance utilizing each procedure was not forthcoming. While sincerely acknowledging the drawbacks inherent in this study, the authors wish to highlight the need for a meticulous long-term follow-up of these patients. It is imperative that the surgeon does not lose focus on the patient's developing need for surgery even years after the initial procedure.


 » Conclusions Top


The requirement for reoperation in patients with AAD, with or without BI or CM and the relatively long duration during which procedure-related morbidity may occur points towards the requirement of a lifelong clinicoradiological vigilance of these patients. Within the first year of the patient undergoing a primary CVJ surgery, implant failure was rare and the main cause of resurgery was infection. Patients presenting for resurgery after 1 year of the primary surgery, however, had implant failure as a major cause of resurgery. The presence of torticollis and grossly asymmetrical facet joints, including the presence of vertical joints, may occasionally lead to incomplete C1-2 reduction in the posterior distraction and fusion technique and may require a de novo transoral procedure. The same factors may lead to residual lateral thecal sac compression occasionally requiring a redo transoral surgery. A single stage transoral procedure followed by PF increases the chance of implant infection due to tissue contamination, bacteremia, or transfacetal migration of microbes. Chronic/recurrent sinus usually points towards the existence of a deep seated infection involving the implant and its recalcitrance indicates the need to remove the implant.

Acknowledgments

A part of this study was presented as an oral presentation by Dr. Pavaman Sindgikar at the Congress of Neurological Surgeons, San Diego, USA, 2016.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
 » References Top

1.
Wadia NH. Chronic progressive myelopathy complicating atlanto-axial dislocation due to congenital abnormality. Neurology 1960;8:81-94.  Back to cited text no. 1
    
2.
Bharucha EP, Dastur HM. Craniovertebral anomalies. Brain 1964;87:469-80.  Back to cited text no. 2
    
3.
Srinivasan K, Balasubramaniam V, Ramamurthi B. Craniovertebral anomalies. Neurol India 1967;15:42-5.  Back to cited text no. 3
    
4.
Sinh G. Congenital atlanto-axial dislocation. Neurosurg Rev 1983;6:211-20.  Back to cited text no. 4
    
5.
Shukla R, Kar AM, Nag D. Congenital atlantoaxial dislocation. Indian J Pediatr 1979;46:332-3.  Back to cited text no. 5
    
6.
Salunke P, Behari S, Kirankumar MV, Sharma MS, Jaiswal AK, Jain VK. Pediatric congenital atlantoaxial dislocation: Differences between the irreducible and reducible varieties. J Neurosurg 2006;104(2 Suppl):115-22.  Back to cited text no. 6
    
7.
Goel A, Achawal S. The surgical treatment of Chiari malformation association with atlantoaxial dislocation. Br J Neurosurg 1995;9:67-72.  Back to cited text no. 7
    
8.
Behari S, Kalra SK, Kiran Kumar MV, Salunke P, Jaiswal AK, Jain VK. Chiari malformation associated with atlanto-axial dislocation: Focusing on the anterior cervico-medullary compression. Acta Neurochir 2007;149:41-50.  Back to cited text no. 8
    
9.
Goel A, Bhatjiwale M, Desai K. Basilar invagination: A study based on 190 surgically treated cases. J Neurosurg 1998;88:962-8.  Back to cited text no. 9
    
10.
Kale SS, Ailawadhi P, Yerramneni VK, Chandra PS, Kumar R, Sharma BS, Mahapatra AK. Pediatric bony craniovertebral junction abnormalities: Institutional experience of 10 years. J Pediatr Neurosci 2011;6(Suppl 1):S91-5.  Back to cited text no. 10
    
11.
Sardhara J, Behari S, Jaiswal AK, Srivastava A, Sahu RN, Mehrotra A, et al. Syndromic versus nonsyndromic atlantoaxial dislocation: Do clinico-radiological differences have a bearing on management? Acta Neurochir 2013;155:1157-67.  Back to cited text no. 11
    
12.
Sindgikar PP, Das KK, Jaiswal AK, Sahu RN, Srivastava AK, Mehrotra A, et al. Resurgery in craniovertebral junction abnormalities. Neurosurgery 2016;63(Suppl 1):168.  Back to cited text no. 12
    
13.
Elliott RE, Tanweer O, Boah A, Morsi A, Ma T, Frempong-Boadu A, et al. Outcome comparison of atlantoaxial fusion with transarticular screws and screw-rod constructs: Meta-analysis and review of literature. J Spinal Disord Tech 2014;27:11-28.  Back to cited text no. 13
    
14.
Winegar CD, Lawrence JP, Friel BC, Fernandez C, Hong J, Maltenfort M, et al. A systematic review of occipital cervical fusion: Techniques and outcomes. J Neurosurg Spine 2010;13:5-16.  Back to cited text no. 14
    
15.
Lall R, Patel NJ, Resnick DK. A review of complications associated with craniocervical fusion surgery. Neurosurgery 2010;67:1396-402.  Back to cited text no. 15
    
16.
Jain VK. Atlantoaxial dislocation. Neurol India 2012;60:9-17.  Back to cited text no. 16
[PUBMED]  Medknow Journal  
17.
Jain VK, Mittal P, Banerji D, Behari S, Acharya R, Chhabra DK. Posterior occipitoaxial fusion for atlantoaxial dislocation associated with occipitalized atlas. J Neurosurg 1996;84:559-64.  Back to cited text no. 17
    
18.
Menezes AH, VanGilder JC, Graf CJ, McDonnell DE. Craniocervical abnormalities. A comprehensive surgical approach. J Neurosurg 1980;53:444-55.  Back to cited text no. 18
    
19.
Dlouhy BJ, Dahdaleh NS, Menezes AH. Evolution of transoral approaches, endoscopic endonasal approaches, and reduction strategies for treatment of craniovertebral junction pathology: A treatment algorithm update. Neurosurg Focus 2015;38:E8.  Back to cited text no. 19
    
20.
Srivastava SK, Aggarwal RA, Nemade PS, Bhosale SK. Single-stage anterior release and posterior instrumented fusion for irreducible atlantoaxial dislocation with basilar invagination. Spine J 2016;16:1-9.  Back to cited text no. 20
    
21.
Jain VK, Behari S. Management of congenital atlanto-axial dislocation: Some lessons learnt. Neurol India 2002;50:386-97.  Back to cited text no. 21
    
22.
Jain VK, Behari S, Banerji D, Bhargava V, Chhabra DK. Transoral decompression for craniovertebral osseous anomalies: Perioperative management dilemmas. Neurol India 1999;47:188-95.  Back to cited text no. 22
[PUBMED]  Medknow Journal  
23.
Goel A. Atlantoaxial facetal distraction spacers: Indications and techniques. J Craniovertebr Junction Spine 2016;7:127-8.  Back to cited text no. 23
    
24.
Goel A, Shah A. Atlantoaxial joint distraction as a treatment for basilar invagination: A report of an experience with 11 cases. Neurol India 2008;56:144-50.  Back to cited text no. 24
[PUBMED]  Medknow Journal  
25.
Grob D, Crisco JJ 3rd, Panjabi MM, Wang P, Dvorak J. Biomechanical evaluation of four different posterior atlantoaxial fixation techniques. Spine 1992;17:480-90.  Back to cited text no. 25
    
26.
Brooks AL, Jenkins EB. Atlanto-axial arthrodesis by the wedge compression method. J Bone Joint Surg Am 1978;60:279-84  Back to cited text no. 26
    
27.
Crockard A. Evaluation of spinal laminar fixation by a new, flexible stainless steel cable (Sof'wire): Early results. Neurosurgery 1994;35:892-8.  Back to cited text no. 27
    
28.
Jain VK, Takayasu M, Singh S, Chharbra DK, Sugita K. Occipital-axis posterior wiring and fusion for atlantoaxial dislocation associated with occipitalization of the atlas. Technical note. J Neurosurg. 1993;79:142-4.  Back to cited text no. 28
    
29.
Ransford AO, Crockard HA, Pozo JL, Thomas NP, Nelson IW. Craniocervical instability treated by contoured loop fixation. J Bone Joint Surg Br 1986;68:173-7.  Back to cited text no. 29
    
30.
Goel A, Laheri V. Plate and screw fixation for atlanto-axial subluxation. Acta Neurochir 1994;129:47-53.  Back to cited text no. 30
    
31.
Milhorat TH, Bolognese PA, Nishikawa M, McDonnell NB, Francomano CA. Syndrome of occipitoatlantoaxial hypermobility, cranial settling, and Chiari malformation type I in patients with hereditary disorders of connective tissue. J Neurosurg Spine 2007;7:601-9.  Back to cited text no. 31
    
32.
Goel A, Phalke U, Cacciola F, Muzumdar D. Atlantoaxial instability and retroodontoid mass-two case reports. Neurol Med Chir 2004;44:603-6.  Back to cited text no. 32
    
33.
Sardhara J, Behari S, Mohan BM, Jaiswal AK, Sahu RN, Srivastava A, et al. Risk stratification of vertebral artery vulnerability during surgery for congenital atlanto-axial dislocation with or without an occipitalized atlas. Neurol India 2015;63:382-91.  Back to cited text no. 33
[PUBMED]  Medknow Journal  
34.
Mehrotra A, Chunnilal JS, Das KK, Srivastava A, Kumar R. Atlanto-axial dislocation associated with anomalous single vertebral artery and agenesis of unilateral internal carotid artery. Asian J Neurosurg 2013;8:164.  Back to cited text no. 34
[PUBMED]  Medknow Journal  
35.
Sawlani V, Behari S, Salunke P, Jain VK, Phadke RV. “Stretched loop sign” of the vertebral artery: A predictor of vertebrobasilar insufficiency in atlantoaxial dislocation. Surg Neurol 2006;66:298-304.  Back to cited text no. 35
    
36.
Patra DP, Salunke PS, Sahoo SK, Ghuman MS. Redundant anomalous vertebral artery in a case of congenital irreducible atlantoaxial dislocation: Emphasizing on the differences from the first intersegemental artery and operative steps to prevent injury while performing C1-2 joint manipulation. Ann Neurosci 2015;22:245-7.  Back to cited text no. 36
    
37.
Mazur MD, Sivakumar W, Riva-Cambrin J, Jones J, Brockmeyer DL. Avoiding early complications and reoperation during occipitocervical fusion in pediatric patients. J Neurosurg Pediatr 2014;14:465-75.  Back to cited text no. 37
    
38.
Guppy KH, Brara HS, Bernbeck JA. Occipitocervical fusions in elderly patients: Mortality and reoperation rates from a national spine registry. World Neurosurg 2016;86:161-7.  Back to cited text no. 38
    
39.
Singh SK, Rickards L, Apfelbaum RI, Hurlbert RJ, Maiman D, Fehlings MG. Occipitocervical reconstruction with the Ohio Medical Instruments Loop: Results of a multicenter evaluation in 30 cases. J Neurosurg 2003;98(3 Suppl):239-46.  Back to cited text no. 39
    
40.
Salunke P, Sharma M, Sodhi HB, Mukherjee KK, Khandelwal NK. Congenital atlantoaxial dislocation: A dynamic process and role of facets in irreducibility. J Neurosurg Spine 2011;15:678-85.  Back to cited text no. 40
    
41.
Chandra PS, Prabhu M, Goyal N, Garg A, Chauhan A, Sharma BS. Distraction, compression, extension, and reduction combined with joint remodeling and extra-articular distraction: Description of 2 new modifications for its application in basilar invagination and atlantoaxial dislocation: Prospective study in 79 cases. Neurosurgery 2015;77:67-80.  Back to cited text no. 41
    
42.
Behari S, Jaiswal A, Srivastava A, Rajput D, Jain VK. Os odontoideum with “free-floating” atlantal arch causing C1-2 anterolisthesis and retrolisthesis with cervicomedullary compression. Indian J Orthop 2010;44:417-23.  Back to cited text no. 42
[PUBMED]  Medknow Journal  
43.
Kukreja S, Ambekar S, Sin AH, Nanda A. Occipitocervical fusion surgery: Review of operative techniques and results. J Neurol Surg B Skull Base 2015;76:331-9.  Back to cited text no. 43
    
44.
Behari S, Nayak SR, Bhargava V, Banerji D, Chhabra DK, Jain VK. Craniocervical tuberculosis: Protocol of surgical management. Neurosurgery 2003;52:72-81.  Back to cited text no. 44
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12]
 
 
    Tables

  [Table 1], [Table 2]

This article has been cited by
1 Management of a case of neglected atlantoaxial rotatory dislocation
Atul Goel,Sonal Jain,Abhidha Shah
Neurology India. 2017; 65(5): 1170
[Pubmed] | [DOI]
2 Evaluating Atlantoaxial Dislocation Based on Cartesian Coordinates: Proposing a New Definition and Its Impact on Assessment of Congenital Torticollis
Jayesh Sardhara,Sanjay Behari,Pavaman Sindgikar,Arun Kumar Srivastava,Anant Mehrotra,Kuntal Kanti Das,Kamlesh Singh Bhaisora,Rabi N. Sahu,Awadhesh K. Jaiswal
Neurosurgery. 2017;
[Pubmed] | [DOI]



 

Top
Print this article  Email this article
   
Online since 20th March '04
Published by Wolters Kluwer - Medknow