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.
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.
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