The Diagnosis and Management of Traumatic Atlanto-occipital Dislocation Injuries
Theodore, Nicholas MD*; Aarabi, Bizhan MD, FRCSC‡; Dhall, Sanjay S. MD§; Gelb, Daniel E. MD¶; Hurlbert, R. John MD, PhD, FRCSC‖; Rozzelle, Curtis J. MD#; Ryken, Timothy C. MD, MS**; Walters, Beverly C. MD, MSc,FRCSC‡‡,§§; Hadley, Mark N. MD§§
*Division of Neurological Surgery, Barrow Neurological Institute, Phoenix, Arizona
‡Department of Neurosurgery, and
¶Department of Orthopaedics, University of Maryland, Baltimore, Maryland
§Department of Neurosurgery, Emory University, Atlanta, Georgia
‖Department of Clinical Neurosciences, University of Calgary Spine Program, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada
#Division of Neurological Surgery, and
§§Division of Neurological Surgery, Children’s Hospital of Alabama, University of Alabama at Birmingham, Birmingham, Alabama
**Iowa Spine & Brain Institute, University of Iowa, Waterloo/Iowa City, Iowa
‡‡Department of Neurosciences, Inova Health System, Falls Church, Virginia
Correspondence: Mark N. Hadley, MD, FACS, UAB Division of Neurological Surgery, 510 – 20th Street South, FOT 1030, Birmingham, AL 35294-3410. E-mail: firstname.lastname@example.org
ABBREVIATIONS: AOD, atlanto-occipital dislocation
BAI-BDI, basion-axial interval-basion dental interval
CCI, condyle-C1 interval
STS, soft tissue swelling
TBI, traumatic brain injury
* Computed tomography (CT) imaging to determine the CCI (condyle-C1 interval) in pediatric patients with potential atlanto-occipital dislocation (AOD) is recommended.
* If there is clinical or radiographic suspicion of AOD, CT of the craniocervical junction is recommended. The CCI determined on CT has the highest diagnostic sensitivity and specificity for AOD among all radiodiagnostic indicators in pediatric patients. The utility of CCI in adult patients has not been reported.
* A lateral cervical radiograph is recommended for the diagnosis of AOD. If a radiological method for measurement is used to determine AOD on the lateral radiograph, the basion-axial interval-basion dental interval (BAI-BDI) method is recommended. The presence of upper cervical prevertebral soft tissue swelling (STS) on an otherwise non-diagnostic plain cervical radiograph should prompt CT imaging to rule out AOD.
* Treatment with internal fixation and fusion using one of a variety of methods is recommended.
* Traction is not recommended in the management of patients with AOD, and is associated with a 10% risk of neurological deterioration.
Although traumatic atlanto-occipital dislocation (AOD) was perceived to be an uncommon injury resulting in frequent death, improvements in the emergency management of the patient in the field, rapid transport, and better recognition have resulted in more survivors of AOD in the past 2 decades. Infrequent observation of patients with AOD and missed diagnoses may impair outcomes of patients with this unusual injury.1 An assimilation of the reported experiences of clinicians evaluating and managing AOD in our scientific literature may facilitate development of diagnostic and treatment options for this traumatic disorder. The guidelines author group of the Section on Disorders of the Spine and Peripheral Nerves of the American Association of Neurological Surgeons (AANS) and Congress of Neurological Surgeons (CNS) produced a medical evidence-based guideline on this topic in 2002.2 The purpose of the current review is to update the medical evidence on the diagnosis and treatment of AOD since that early publication. Specific questions that were investigated include the sensitivity of plain radiographs, CT, and MRI in the diagnosis of AOD, as well as the safety and efficacy of various treatment modalities for AOD, including no treatment, traction, external immobilization, and internal fixation with fusion.
A National Library of Medicine computerized literature search of publications from 1966 to 2011 was performed using the following headings: “atlanto-occipital joint” and “dislocation.” The search was limited to the English language and human studies. An exploded search of these headings led to 522 and 11 257 citations, respectively. A subset of 178 citations contained both headings. The references of the identified articles were reviewed to identify additional case reports. The articles were reviewed using the following criteria for inclusion in diagnosis: human survivors, type of traumatic atlanto-occipital dislocation, and plain radiographic findings. The articles were also reviewed using the following criteria for inclusion in treatment: human survivors, type of traumatic AOD, management, and outcome. The observations from the published reports were combined because the usual methods for analysis were precluded by the infrequent observation of this injury. The type of dislocation was classified according to Traynelis et al3 into Type I (anterior), Type II (longitudinal), and Type III (posterior) dislocations. Lateral, rotational, and multi-directional dislocations that could not be classified into 1 of these 3 types were considered separately and are notated as “other Type.” The duration of follow-up ranged from none reported to 4 years. Of the articles meeting the diagnostic selection criteria reported, 68 articles with 105 patients provided data on 38 Type I, 45 Type II, 4 Type III, and 18 other Types of AOD. Two of these articles1,4 included 1 patient each from 2 previously published individual case reports.5,6 Of the articles meeting the treatment selection criteria, 56 articles with 84 patients provided data on 31 Type I, 33 Type II, 4 Type III, and 16 other types of AOD. Two of these articles1,4 included 1 patient each from 2 previously published individual case reports.5,6 The information provided by these reports was compiled and scrutinized and make up the basis for this guideline. Summaries of these reports are provided in Evidentiary Table format (Tables 1-2).
TABLE 1-b Evidentiar...Image Tools
TABLE 1-c Evidentiar...Image Tools
TABLE 1-d Evidentiar...Image Tools
TABLE 2-b Evidentiar...Image Tools
TABLE 2-c Evidentiar...Image Tools
A variety of radiographic and descriptive features have been proposed for the diagnosis of AOD (Table 1). Initially, the descriptive measurements were all based on lateral cervical radiographs.7-12,70 A displacement of more than 10 mm between the basion and dens is considered abnormal by Wholey et al.7 A ratio of the basion-posterior atlas arch distance divided by the opisthion-anterior atlas arch distance greater than one is considered abnormal by Powers et al.8 A distance of more than 13 mm between the posterior mandible and anterior atlas, or 20 mm between the posterior mandible and dens are considered abnormal by Dublin et al.9 Failure of a line from the basion to the axis spinolaminar junction to intersect C2, or a line from the opisthion to the posterior inferior corner of the body of the axis to intersect C1, are considered abnormal by Lee et al.10 Finally, a displacement of more than 12 mm, or less than minus 4 mm between the basion and posterior C2 line, or a displacement of more than 12 mm from the basion to the dens (2 mm more than the Wholey recommendation) is considered abnormal by Harris et al.11,12 A comparative study by Lee calculated the sensitivity for the Wholey method of 50%, a 33% sensitivity for the Power's ratio, and a 25% sensitivity for the Dublin method. The authors determined that their X-line method had a sensitivity of 75%,10 although neither the Power's ratio nor X-line method could be applied in nearly half their patients. A comparative study reported by Harris et al found that the Power's ratio had a sensitivity of 60%, the Lee method a sensitivity of 20%, and the BAI-BDI method a sensitivity of 100% among those patients with AOD on whom the required landmarks could be identified on lateral cervical spine films.12 Przybylski et al1 reported failure to diagnose AOD in 2 of 5 patients with the Power's ratio, in 1 of 5 patients with the X-line method, and in 2 of 5 with the BAI-BDI method. No radiographic method reviewed has complete sensitivity. The BAI-BDI method proposed by Harris et al (which incorporates the basion-dens distance described by Wholey) is at present the most reliable means to diagnose AOD on a lateral cervical spine radiograph.7
Pang et al proposed the CCI as a sensitive diagnostic measurement of atlantooccipital dislocation as determined on CT imaging. They analyzed and compared CCI from sagittal and coronal reformatted CT images of the craniovertebral junction of 89 children without AOD and 16 children with AOD. They found the CCI to have sensitivity and specificity of 100% compared to “standard” tests on plain films that had sensitivity between 25% and 50% and specificity between 10% and 60%. They concluded that the CCI criterion has the highest diagnostic sensitivity and specificity for AOD among all radiographic methods. Their work provided Class I medical evidence for the diagnosis of AOD among pediatric patients.13,14
Horn et al attempted to determine whether magnetic resonance imaging (MRI) findings on short TI inversion recovery (STIR) sequences following acute trauma are predictive of cervical spinal instability. Abnormal soft-tissue (pre-vertebral or para-spinal) findings on MRI were correlated with those identified on CT and plain and dynamic cervical spine x-rays in an attempt to determine cervical stability in 314 trauma patients. They found that MRI is sensitive to soft-tissue injuries of the cervical spine. However, they concluded that when CT and cervical radiographs, including dynamic X-rays, detect no fractures or signs of instability, MRI does not assist in determining cervical stability. In this circumstance they reported that MRI findings may lead to unnecessary testing when not otherwise indicated.15
Many of the case reports and case series in the literature do not describe the radiographic/imaging method(s) used to diagnose AOD. Since the most sensitive method to identify AOD on a lateral cervical spine radiograph (the BAI-BDI) was proposed by Harris et al in 1994,12 this method was not likely used for many of the determinations. When the BAI-BDI was applied retrospectively, a diagnosis was possible on the first lateral radiograph in 53 of 105 patients, (sensitivity = 0.505). Of the 53 patients with AOD in whom the diagnosis was made on the first lateral radiograph, 4 were not stratified by type. Of the 49 remaining patients, there were 24 Type I, 23 Type II and 2 Type III dislocations. A second, late and consecutive lateral radiograph (11 cases), tomography (1 case), fluoroscopy (2 cases), CT (11 cases), CT in addition to lateral radiographs (3 cases), and MRI (6 cases) were required to establish the diagnosis of AOD in 34 of the 105 patients. Since these data were obtained from case reports and small case series, a determination of the accuracy of plain radiographs to identify AOD compared to patients without AOD could not be performed. As a result, specificity, positive/negative predictive values, and likelihood ratios cannot be discerned from the available literature.
Of the 15 patients in whom the diagnosis was missed on the initial plain radiographs, the initial neurological condition of 3 patients was not described.16 Of the remaining 12 patients, 4 were neurologically normal (1 Type I, 1 Type III, 2 other type).17,18 Two of those 4 patients originally reported as normal developed a monoparesis (1 Type 1, 1 other type).19,20 Neither recovered completely. Eight of the remaining 12 patients had neurologic abnormalities from the outset, 5 of whom worsened. Four of the 5 transiently worsened, including 1 Type I injury patient with quadriparesis and Cranial Nerve IX, X, and XII palsies21 who improved but was spastic at last follow-up. One patient with a Type I injury developed a hemiparesis that recovered.22 One Type I injury patient who developed quadriparesis was hemiparetic at follow-up.23 One lateral AOD patient with paraparesis and toricollis reportedly recovered at last follow-up.24 One patient (Type I) with a monoparesis initially experienced permanent worsening and was quadriplegic at follow-up.25
The presence or absence of soft tissue swelling was described in half of the patients in whom plain spine films were obtained. The sensitivity of the presence of STS when AOD was confirmed by other radiographic means was determined to be 0.69 or 69% (43 of 62 cases). Although plain radiographs do not consistently and reliably identify AOD, the index of suspicion for the potential of AOD may be increased with the identification of prevertebral STS.
Acute craniocervical CT imaging was performed in 62 of the 105 patients with AOD. However, for 23 of the 62 patients studied by CT, the authors did not report whether AOD was diagnosed using this modality. The diagnosis of AOD was reportedly made by CT in 39 of 62 patients (sensitivity = 0.63). No CT abnormalities were reported in 15 of 62 patients. Twenty-eight patients with AOD studied with CT had hemorrhages (21 had craniocervical junction subarachnoid hemorrhage, 2 had paravertebral hemorrhage, 1 had a subdural hemorrhage, 2 had intraparenchymal cord hemorrhages, and 2 had spinal cord contusions). Craniocervical MRI was performed in 34 of 105 patients with AOD. The MRI findings were not reported for 4 of the 34 patients studied. The diagnosis of AOD could be made in 21 of 30 cases studied with MRI (sensitivity = 0.7, or 70%).
In summary, the diagnosis of AOD is often missed on spine plain radiographs, (sensitivity = 0.505), particularly in the circumstance of non-longitudinal AOD (non-Type II). Additional imaging of the craniovertebral junction with either CT or MRI is recommended in patients suspected of having AOD. Other imaging methods such as fluoroscopy, tomography, and myelography have been reported to confirm the diagnosis of AOD, particularly in the older literature, but accuracy data is not available nor can it be calculated. Neurological abnormalities including lower cranial nerve paresis (particularly cranial nerves VI, X, and XII), monoparesis, hemiparesis, quadriparesis, respiratory dysfunction including apnea, and complete high cervical cord motor deficits in the setting of normal plain spinal radiographs should prompt additional imaging with CT or MRI. The presence of prevertebral STS on plain radiographs and subarachnoid hemorrhage on CT at the craniovertebral junction should prompt consideration of the diagnosis of AOD. The CCI determined from CT images has the highest diagnostic specificity and sensitivity among imaging diagnostic criteria for AOD and should be employed when attempting to make a diagnosis of AOD.
Various treatment including rigid immobilization and internal surgical fixation and fusion have been described in the treatment of AOD (Table 2). Of 84 patients in whom treatment data are reported, 13 did not receive initial treatment for AOD.4,19,20,23-30,80 Six of 13 had Type I, 2 had Type II injuries and 5 had other type injuries. At last follow-up in this group of untreated patients, 2 died, 2 improved neurologically, 4 had unchanged deficits from presentation, and 5 worsened neurologically.4,19,20,25,26,31 There were 3 untreated AOD patients who presented with quadriplegia.26,31 One improved to quadriparesis at last follow-up; the 2 other remained quadriplegic. In summary, failure to treat AOD resulted in worsening in 7 of 13 patients (54%).
Of 21 patients with AOD initially treated with traction, 2 worsened transiently and developed worsening quadriparesis and CN VI deficits. Both had resolution of their CN VI deficits but had persistent quadriparesis at last follow-up. One patient had a Type II injury32 and 1 patient had a rotational other type dislocation.4 Four patients were initially normal and remained normal at follow-up.33-36 The remaining 15 patients with AOD treated initially with traction experienced improved neurological function compared to their initial findings at last follow-up. The improvement in neurological function in these patients could not be attributed to the initial period of traction. Ten had Type I injuries, 5 had Type II injuries, 2 had Type III injuries, and 2 had other type dislocations. In total, 1 of 6 patients with Type II injuries and 1 of 3 patients with other type, translational injuries experienced neurological worsening with the use of craniocervical traction. Because the frequency of neurological deterioration with traction in the treatment of AOD is approximately 10%, 10 times higher than that for subaxial injuries, the use of traction is not recommended in patients with AOD.
Of 29 patients initially treated with external immobilization excluding traction, 17 were immobilized in anticipation of internal fixation and fusion and none worsened during the pre-surgical interval (5 Type I, 9 Type II, 3 other type).1,4,36-48 Of the remaining 12 patients treated with external immobilization alone excluding traction, 4 worsened transiently (3 Type I, 1 Type II).17,21,22,38,49 All 4 of these patients subsequently underwent craniocervical fixation and fusion. Of the remaining 8 patients managed with external immobilization alone, 3 were unstable after 6 to 22 weeks of immobilization (1 Type I, 2 Type II). Of these 3 patients with persistent instability despite external immobilization, 2 presented with quadriplegia and 1 was neurologically normal. All 3 underwent internal fixation and fusion without change in their neurological condition at last follow-up. Only 5 patients with AOD described in the literature were successfully treated with external immobilization alone (1 Type I, 2 Type II, 2 other type dislocations). Since 7 of 12 (58%) patients managed with external immobilization either deteriorated neurologically or failed to achieve craniocervical stability without surgical internal fixation and fusion, treatment of AOD with external immobilization alone should be considered with caution.
There is only initial neurological examination data reported on 79 of 83 patients in the surgical treatment group. Of those 79 patients in whom the neurological exam at admission could be discerned, 16 (20.3%) were reportedly normal (4 Type I, 3 Type II, 3 Type III, 6 other type), 6 (7.6%) had cranial nerves deficits only, 14 (17.7%) had a hemiparesis, 2 had a monoparesis (2.5%), 1 (1.25%) had paraparesis, 16 were reported as quadriparetic (20.2%), 3 (3.8%) had hemiplegia, 1 (1.25%) had hyperreflexia but no motor deficit, and 20 were quadriplegic (25.3%). Seventeen patients with an initial paresis were reported to have completely recovered at last follow-up. Six patients with plegia improved to paresis. Eight patients with paresis and 13 patients with plegia had stable neurologic examinations at the last reported follow-up (no worse and no better).
Cranial nerve deficits appear to be common with AOD. Thirty-eight patients (48.1%) were reported to have CN deficits at presentation, including CN III (3 patients), CN V (1 patient), CN VI (26 patients), CN VII (5 patients), CN IX (12 patients), CN X (15 patients), CN XI (6 patients), and CN XII (11 patients). Twenty-four patients in whom follow-up was reported had complete resolution of their CN deficits, 9 had partial resolution, 5 had no change in their CN deficits, and 3 patients developed new CN deficits at last follow-up.
Finally, 29 patients described in the literature were treated with planned early craniocervical fusion with internal fixation. Only 1 patient worsened neurologically following surgery. This patient with a Type II injury was normal initially and developed a CN X deficit which persisted at follow-up.1 All but 3 of the remaining 28 patients were reported to improve neurologically at last follow-up. Six had Type I, 17 had type II, 2 had Type III, and 4 had other type AOD injuries. None of the patients treated with craniocervical fusion and internal fixation were reported to have experienced late instability requiring reoperation or further treatment.
Recently, larger case series focusing on the diagnosis and treatment of AOD have been reported in the literature. Horn et al analyzed clinical and radiological factors that predict outcome and management in 33 patients treated at a single institution. Special attention was given to neurological injury at presentation and imaging factors that dictated/determined treatment. Screening cervical spine radiographs were initially obtained and thin-cut (2.5 mm) CT images were acquired thereafter. In addition, most patients underwent MRI imaging. Five patients with severe traumatic brain injury (TBI) received no treatment and died early in their hospital course. Of the remaining 28 patients, 23 underwent craniocervical fixation with fusion and 5 were treated nonoperatively with an external orthosis. Five other severely injured patients died, all of whom were treated surgically. Two died due to TBI, 3 others due to other multiple organ system injuries and medical co-morbidities. The 5 patients treated nonoperatively were managed in this fashion because they had no abnormalities identified on cervical CT images based on established criteria (Power's ratio, BDI, BAI-BDI, X-line methods), despite the presence of abnormal findings in the occipitoatlantal joints, tectorial membrane, alar ligaments, or cruciate ligaments on MRI. TBI at presentation correlated with a high mortality rate (7 of 33 patients). Five patients died from TBI without treatment. Two additional patients treated surgically died as a result of TBI. The authors concluded that the craniocervical junction in patients with CT-documented AOD is unstable and requires surgical fixation if they survive their initial injuries (particularly traumatic brain injuries) and resuscitation.50
Hosalkar et al described 16 pediatric patients with traumatic AOD. Eight of these 16 patients died on admission. Of the remaining 8, all were initially treated with halo immobilization. Three of the remaining 8 died due to severe TBI. Of the 5 surviving patients, 4 underwent craniocervical fixation with fusion and 1 was treated in a Minerva cast orthosis. At last follow-up, 1 patient was neurologically intact, 3 had mild hemi-paresis but were functional, and 1 patient was a ventilator-dependent quadriplegic. The authors concluded that early diagnosis, prompt intubation, and early immobilization of the neck and head with respect to the torso appeared to improve survival in young patients who survived their associated brain injuries.
Bellabarba et al analyzed potentially correctable causes of delayed diagnosis of AOD and treatment options in a retrospective evaluation of 17 consecutive AOD patients who survived their injuries. In 13 of their 17 patients, (76%), the diagnosis of AOD was delayed by a mean of 2 days (range 1-15 days). Five (38%) of these 13 patients suffered profound neurological deterioration before AOD was clinically recognized. Surgical stabilization was undertaken in all 17 patients. Only 1 patient deteriorated following surgery. The authors concluded that a delay in the diagnosis of AOD was associated with an increased likelihood of neurological deterioration. Craniocervical instability due to AOD was frequently missed/misdiagnosed with the use of standard lateral radiographs.
AOD is an uncommon traumatic injury that can be difficult to diagnose and is frequently missed on initial lateral cervical spinal radiographs. AOD is often associated with severe traumatic brain injuries. Patients who survive AOD injuries often have neurological impairment including lower cranial nerve deficits, unilateral or bilateral weakness, or quadriplegia. Nearly 20% of patients with acute traumatic AOD will have a normal neurological examination on presentation. The lack of localizing physical/neurological examination findings and/or global neurological deficits from severe brain injury may impede/hinder the diagnosis of AOD in patients with normal-appearing initial cervical radiographs. A high index of suspicion must be maintained in order to diagnose AOD. Prevertebral soft tissue swelling on a lateral cervical radiograph or craniocervical subarachnoid hemorrhage on axial CT images have been associated with AOD and should prompt consideration of the diagnosis. Additional imaging including CT and MRI may be required to confirm the diagnosis of AOD if plain radiographs are inadequate. The Condyle-C1 interval as determined on CT imaging has the highest diagnostic sensitivity and sensitivity for AOD among all other radiodiagnostic indicators.
All patients with AOD should be treated. Without treatment, nearly all patients developed neurological worsening, many of whom never fully recover. Treatment of AOD with traction is not recommended. Treatment with external immobilization has been used successfully in selected patients but has a high failure rate. Craniocervical fixation and fusion is recommended for the treatment of patients with acute traumatic AOD.
KEY ISSUES FOR FUTURE INVESTIGATION
Although the use of external immobilization for AOD was often associated with late instability, several patients achieved stability without operative management. The complimentary usage of CT imaging (with 3-dimensional reconstruction images for more precise measurement of the magnitude of displacement) and MRI (for differentiation of partial and complete ligament tears from stretch injuries) may be useful in identifying a subgroup of patients in whom craniocervical stability might be achieved with external immobilization alone. Long-term follow-up of both surgically and non-surgically treated patients with AOD will aid our understanding of the ideal treatment strategy for this unusual and potentially lethal injury.
1. Przybylski GJ, Clyde BL, Fitz CR. Craniocervical junction subarachnoid hemorrhage associated with atlanto-occipital dislocation. Spine (Phila Pa 1976). 1996;21(15):1761–1768.
2. Diagnosis and management of traumatic atlanto-occipital dislocation injuries. In: Guidelines for the management of acute cervical spine and spinal cord injuries.Neurosurgery. 2002;50(3 suppl):S105–S113.
3. Traynelis VC, Marano GD, Dunker RO, Kaufman HH. Traumatic atlanto-occipital dislocation. Case report. J Neurosurg. 1986;65(6):863–870.
4. Dickman CA, Papadopoulos SM, Sonntag VK, Spetzler RF, Rekate HL, Drabier J. Traumatic occipitoatlantal dislocations. J Spinal Disord. 1993;6(4):300–313.
5. Pang D, Wilberger JE Jr. Traumatic atlanto-occipital dislocation with survival: case report and review. Neurosurgery. 1980;7(5):503–508.
6. Papadopoulos SM, Dickman CA, Sonntag VK, Rekate HL, Spetzler RF. Traumatic atlantooccipital dislocation with survival. Neurosurgery. 1991;28(4):574–579.
7. Wholey MH, Bruwer AJ, Baker HL Jr. The lateral roentgenogram of the neck; with comments on the atlanto-odontoid-basion relationship. Radiology. 1958;71(3):350–356.
8. Powers B, Miller MD, Kramer RS, Martinez S, Gehweiler JA Jr. Traumatic anterior atlanto-occipital dislocation. Neurosurgery. 1979;4(1):12–17.
9. Dublin AB, Marks WM, Weinstock D, Newton TH. Traumatic dislocation of the atlanto-occipital articulation (AOA) with short-term survival. With a radiographic method of measuring the AOA. J Neurosurg. 1980;52(4):541–546.
10. Lee C, Woodring JH, Goldstein SJ, Daniel TL, Young AB, Tibbs PA. Evaluation of traumatic atlantooccipital dislocations. AJNR Am J Neuroradiol. 1987;8(1):19–26.
11. Harris JH Jr, Carson GC, Wagner LK. Radiologic diagnosis of traumatic occipitovertebral dissociation: 1. Normal occipitovertebral relationships on lateral radiographs of supine subjects. AJR Am J Roentgenol. 1994;162(4):881–886.
12. Harris JH Jr, Carson GC, Wagner LK, Kerr N. Radiologic diagnosis of traumatic occipitovertebral dissociation: 2. Comparison of three methods of detecting occipitovertebral relationships on lateral radiographs of supine subjects. AJR Am J Roentgenol. 1994;162(4):887–892.
13. Pang D, Nemzek WR, Zovickian J. Atlanto-occipital dislocation—part 2: the clinical use of (occipital) condyle-C1 interval, comparison with other diagnostic methods, and the manifestation, management, and outcome of atlanto-occipital dislocation in children. Neurosurgery. 2007;61(5):995–1015; discussion 1015.
14. Pang D, Nemzek WR, Zovickian J. Atlanto-occipital dislocation: part 1—normal occipital condyle-C1 interval in 89 children. Neurosurgery. 2007;61(3):514–521; discussion 521.
15. Horn EM, Lekovic GP, Feiz-Erfan I, Sonntag VK, Theodore N. Cervical magnetic resonance imaging abnormalities not predictive of cervical spine instability in traumatically injured patients. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. J Neurosurg Spine. 2004;1(1):39–42.
16. Ahuja A, Glasauer FE, Alker GJ Jr, Klein DM. Radiology in survivors of traumatic atlanto-occipital dislocation. Surg Neurol. 1994;41(2):112–118.
17. Eismont FJ, Bohlman HH. Posterior atlanto-occipital dislocation with fractures of the atlas and odontoid process. J Bone Joint Surg Am. 1978;60(3):397–399.
18. Jevtich V. Traumatic lateral atlanto-occipital dislocation with spontaneous bony fusion. A case report. Spine (Phila Pa 1976). 1989;14(1):123–124.
19. Collalto PM, DeMuth WW, Schwentker EP, Boal DK. Traumatic atlanto-occipital dislocation. Case report. J Bone Joint Surg Am. 1986;68(2):1106–1109.
20. Sponseller PD, Cass JR. Atlanto-occipital fusion for dislocation in children with neurologic preservation. A case report. Spine (Phila Pa 1976). 1997;22(3):344–347.
21. DiBenedetto T, Lee CK. Traumatic atlanto-occipital instability. A case report with follow-up and a new diagnostic technique. Spine (Phila Pa 1976). 1990;15(6):595–597.
22. Hosono N, Yonenobu K, Kawagoe K, Hirayama N, Ono K. Traumatic anterior atlanto-occipital dislocation. A case report with survival. Spine (Phila Pa 1976). 1993;18(6):786–790.
23. Ramsay AH, Waxman BP, O'Brien JF. A case of traumatic atlanto-occipital dislocation with survival. Injury. 1986;17(6):412–413.
24. Watridge CB, Orrison WW, Arnold H, Woods GA. Lateral atlantooccipital dislocation: case report. Neurosurgery. 1985;17(2):345–347.
25. Woodring JH, Selke AC Jr, Duff DE. Traumatic atlantooccipital dislocation with survival. AJR Am J Roentgenol. 1981;137(1):21–24.
26. Bloom BM, Powell BP. Surviving atlanto-occipital dislocation. Emerg Med Australas. 2007;19(4):379–382.
27. Colnet G, Chabannes J, Commun C, Rigal MC, Alassaf M. Atlanto-occipital luxation and syringomyelia: 2 rare complications of cervical injury. Diagnostic and therapeutic effects. Apropos of a case [in French]. Neurochirurgie. 1989;35(1):58–63.
28. Georgopoulos G, Pizzutillo PD, Lee MS. Occipito-atlantal instability in children. A report of five cases and review of the literature. J Bone Joint Surg Am. 1987;69(3):429–436.
29. Labler L, Eid K, Platz A, Trentz O, Kossmann T. Atlanto-occipital dislocation: four case reports of survival in adults and review of the literature. Eur Spine J. 2004;13(2):172–180.
30. Roy-Camille R, Benazet JP, Saillant G, Henry P, Mamoudy P, Léonard P. [Traumatic atlanto-occipital luxation. Value of new radiologic signs (apropos of 2 cases)]. Rev Chir Orthop Reparatrice Appar Mot. 1986;72(4):303–309.
31. Zampella EJ, Duvall ER, Langford KH. Computed tomography and magnetic resonance imaging in traumatic locked-in syndrome. Neurosurgery. 1988;22(3):591–593.
32. Palmer MT, Turney SZ. Tracheal rupture and atlanto-occipital dislocation: case report. J Trauma. 1994;37(2):314–317.
33. Banna M, Stevenson GW, Tumiel A. Unilateral atlanto-occipital dislocation complicating an anomaly of the atlas. A case report. J Bone Joint Surg Am. 1983;65(5):685–687.
34. Bools JC, Rose BS. Traumatic atlantooccipital dislocation: two cases with survival. AJNR Am J Neuroradiol. 1986;7(5):901–904.
35. Farthing JW. Atlantocranial dislocation with survival; a case report. N C Med J. 1948;9(1):34–36.
36. Lee C, Woodring JH, Walsh JW. Carotid and vertebral artery injury in survivors of atlanto-occipital dislocation: case reports and literature review. J Trauma. 1991;31(3):401–407.
37. Bani A, Gilsbach JM. Atlantooccipital distraction: a diagnostic and therapeutic dilemma: report of two cases. Spine (Phila Pa 1976). 2003;28(5):E95–E97.
38. Donahue DJ, Muhlbauer MS, Kaufman RA, Warner WC, Sanford RA. Childhood survival of atlantooccipital dislocation: underdiagnosis, recognition, treatment, and review of the literature. Pediatr Neurosurg. 1994;21(1):105–111.
39. Gautschi OP, Woodland PR, Zellweger R. Complete medulla/cervical spinal cord transection after atlanto-occipital dislocation: an extraordinary case. Spinal Cord. 2007;45(5):387–393.
40. Gregg S, Kortbeek JB, du Plessis S. Atlanto-occipital dislocation: a case study of survival with partial recovery and review of the literature. J Trauma. 2005;58(1):168–171.
41. Hamai S, Harimaya K, Maeda T, Hosokawa A, Shida J, Iwamoto Y. Traumatic atlanto-occipital dislocation with atlantoaxial subluxation. Spine (Phila Pa 1976). 2006;31(13):E421–E424.
42. Kaufman RA, Dunbar JS, Botsford JA, McLaurin RL. Traumatic longitudinal atlanto-occipital distraction injuries in children. AJNR Am J Neuroradiol. 1982;3(4):415–419.
43. Kleweno CP, Zampini JM, White AP, Kasper EM, McGuire KJ. Survival after concurrent traumatic dislocation of the atlanto-occipital and atlanto-axial joints: a case report and review of the literature. Spine (Phila Pa 1976). 2008;33(18):E659–E662.
44. Nischal K, Chumas P, Sparrow O. Prolonged survival after atlanto-occipital dislocation: two case reports and review. Br J Neurosurg. 1993;7(6):677–682.
45. Payer M, Sottas CC. Traumatic atlanto-occipital dislocation: presentation of a new posterior occipitoatlantoaxial fixation technique in an adult survivor: technical case report. Neurosurgery. 2005;56(1 suppl):E203; discussion E203.
46. Salinsky JP, Scuderi GJ, Crawford AH. Occipito-atlanto-axial dissociation in a child with preservation of life: a case report and review of the literature. Pediatr Neurosurg. 2007;43(2):137–141.
47. Seibert PS, Stridh-Igo P, Whitmore TA, Dufty BM, Zimmerman CG. Cranio-cervical stabilization of traumatic atlanto-occipital dislocation with minimal resultant neurological deficit. Acta Neurochir (Wien). 2005;147(4):435–442; discussion 442.
48. van de Pol GJ, Hanlo PW, Oner FC, Castelein RM. Redislocation in a halo vest of an atlanto-occipital dislocation in a child: recommendations for treatment. Spine (Phila Pa 1976). 2005;30(14):E424–E428.
49. Govender S, Vlok GJ, Fisher-Jeffes N, Du Preez CP. Traumatic dislocation of the atlanto-occipital joint. J Bone Joint Surg Br. 2003;85(6):875–878.
50. Horn EM, Feiz-Erfan I, Lekovic GP, Dickman CA, Sonntag VK, Theodore N. Survivors of occipitoatlantal dislocation injuries: imaging and clinical correlates. J Neurosurg Spine. 2007;6(2):113–120.
51. Sweet J, Ammerman J, Deshmukh V, White J. Cruciate paralysis secondary to traumatic atlantooccipital dislocation. J Neurosurg Spine. 2010;12(1):19–21.
52. Vera M, Navarro R, Esteban E, Costa JM. Association of atlanto-occipital dislocation and retroclival haematoma in a child. Childs Nerv Syst. 2007;23(8):913–916.
53. McKenna DA, Roche CJ, Lee WK, Torreggiani WC, Duddalwar VA. Atlanto-occipital dislocation: case report and discussion. CJEM. 2006;8(1):50–53.
54. Saveika JA, Thorogood C. Airbag-mediated pediatric atlanto-occipital dislocation. Am J Phys Med Rehabil. 2006;85(12):1007–1010.
55. Feiz-Erfan I, Gonzalez LF, Dickman CA. Atlantooccipital transarticular screw fixation for the treatment of traumatic occipitoatlantal dislocation. Technical note. J Neurosurg Spine. 2005;2(3):381–385.
56. Gonzalez LF, Fiorella D, Crawford NR, et al.. Vertical atlantoaxial distraction injuries: radiological criteria and clinical implications. J Neurosurg Spine. 2004;1(3):273–280.
57. Brinkman W, Cohen W, Manning T. Posterior fossa subarachnoid hemorrhage due to an atlantooccipital dislocation. AJR Am J Roentgenol. 2003;180(5):1476.
58. Rose L, Muburak O, Saber AA, Plaisier B. Traumatic atlanto-occipital dislocation. Am J Surg. 2003;185(4):376–377.
59. Tomasini A, Berlot G, Randino A, Viviani M. Atlanto-occipital traumatic dislocation. Am J Emerg Med. 2002;20(2):133–135.
60. Grabb BC, Frye TA, Hedlund GL, Vaid YN, Grabb PA, Royal SA. MRI diagnosis of suspected atlanto-occipital dissociation in childhood. Pediatr Radiol. 1999;29(4):275–281.
61. Naso WB, Cure J, Cuddy BG. Retropharyngeal pseudomeningocele after atlanto-occipital dislocation: report of two cases. Neurosurgery. 1997;40(6):1288–1290; discussion 1290-1291.
62. Yamaguchi N, Ikeda K, Ishise J, Yamashita J. Traumatic atlanto-occipital dislocation with long-term survival. Neurol Med Chir (Tokyo). 1996;36(1):36–39.
63. Guigui P, Milaire M, Morvan G, Lassale B, Deburge A. Traumatic atlantooccipital dislocation with survival: case report and review of the literature. Eur Spine J. 1995;4(4):242–247.
64. Harmanli O, Koyfman Y. Traumatic atlanto-occipital dislocation with survival: a case report and review of the literature. Surg Neurol. 1993;39(4):324–330.
65. Matava MJ, Whitesides TE Jr, Davis PC. Traumatic atlanto-occipital dislocation with survival. Serial computerized tomography as an aid to diagnosis and reduction: a report of three cases. Spine (Phila Pa 1976). 1993;18(13):1897–1903.
66. Bundschuh CV, Alley JB, Ross M, Porter IS, Gudeman SK. Magnetic resonance imaging of suspected atlanto-occipital dislocation. Two case reports. Spine (Phila Pa 1976). 1992;17(2):245–248.
67. Farley FA, Graziano GP, Hensinger RN. Traumatic atlanto-occipital dislocation in a child. Spine (Phila Pa 1976). 1992;17(12):1539–1541.
68. Belzberg AJ, Tranmer BI. Stabilization of traumatic atlanto-occipital dislocation. Case report. J Neurosurg. 1991;75(3):478–482.
69. Hladky JP, Lejeune JP, Leclercq F, Dhellemmes P, Christiaens JL. Traumatic atlanto-occipital dislocation [in French]. Neurochirurgie. 1991;37(5):312–317.
70. Maves CK, Souza A, Prenger EC, Kirks DR. Traumatic atlanto-occipital disruption in children. Pediatr Radiol. 1991;21(2):504–507.
71. Montane I, Eismont FJ, Green BA. Traumatic occipitoatlantal dislocation. Spine (Phila Pa 1976). 1991;16(2):112–116.
72. Jones DN, Knox AM, Sage MR. Traumatic avulsion fracture of the occipital condyles and clivus with associated unilateral atlantooccipital distraction. AJNR Am J Neuroradiol. 1990;11(6):1181–1183.
73. Hummel A, Plaue R. Diagnosis and treatment of atlanto-occipital ruptures [in German]. Unfallchirurgie. 1988;14(6):311–319.
74. Putnam WE, Stratton FT, Rohr RJ, Stitzell W, Roat G. Traumatic atlanto-occipital dislocations: value of the Powers ratio in diagnosis. J Am Osteopath Assoc. 1986;86(12):798–804.
75. Zigler JE, Waters RL, Nelson RW, Capen DA, Perry J. Occipito-cervico-thoracic spine fusion in a patient with occipito-cervical dislocation and survival. Spine (Phila Pa 1976). 1986;11(6):645–646.
76. Rockswold GL, Seljeskog EL. Traumatic atlantocranial dislocation with survival. Minn Med. 1979;62(3):151–152, 154.
77. Fruin AH, Pirotte TP. Traumatic atlantooccipital dislocation. Case report. J Neurosurg. 1977;46(5):663–666.
78. Page CP, Story JL, Wissinger JP, Branch CL. Traumatic atlantooccipital dislocation. Case report. J Neurosurg. 1973;39(3):394–397.
79. Evarts CM. Traumatic occipito-atlantal dislocation. J Bone Joint Surg Am. 1970;52(8):1653–1660.
80. Gabrielsen TO, Maxwell JA. Traumatic atlanto-occipital dislocation; with case report of a patient who survived. Am J Roentgenol Radium Ther Nucl Med. 1966;97(3):624–629.
Atlanto-occipital dislocation; BAI-BDI method; Condyle-C1 interval; Cranio-cervical instability
Copyright © by the Congress of Neurological Surgeons
Highlight selected keywords in the article text.