Tag: atlantoaxial fixation

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New Posterior Atlantoaxial Restricted Non-Fusion Fixation for Atlantoaxial Instability

New Posterior Atlantoaxial Restricted Non-Fusion Fixation for Atlantoaxial Instability

Neurosurgery 78:735–741, 2016

Loss of axial rotation and lateral bending after atlantoaxial fusion reduces a patient’s quality of life. Therefore, effective, nonfusion fixation alternatives are needed for atlantoaxial instability.

OBJECTIVE: To evaluate the initial stability and function of posterior atlantoaxial restricted nonfusion fixation (PAARNF), a new protocol, using cadaveric cervical spines compared with the intact state, destabilization, and posterior C1-C2 rod fixation.

METHODS: Cervical areas C0 through C3 were used from 6 cadaveric spines to test flexion-extension, lateral bending, and axial rotation range of motion (ROM). With the use of a machine, 1.5-Nm torque at a rate of 0.1 Nm/s was used and held for 10 seconds. The specimens were loaded 3 times, and data were collected in the third cycle and tested in the following sequence: (1) intact, (2) destabilization (using a type II odontoid fracture model), (3) destabilization with PAARNF (PAARNF group), and (4) rod implantation (rod group). The order of tests for the PAARNF and rod groups was randomly assigned.

RESULTS: The average flexion-extension ROM in the PAARNF group was 7.44 6 2.05, which was significantly less than in the intact (P = .00) and destabilization (P = .00) groups but not significantly different from that of the rod group (P = .07). The average lateral bending ROM (10.59 6 2.33; P = .00) and axial rotation ROM (38.79 6 13.41; P = .00) of the PAARNF group were significantly greater than in the rod group. However, the values of the PAARNF group showed no significant differences compared with those of the intact group.

CONCLUSION: PAARNF restricted atlantoaxial flexion-extension but preserved axial rotation and lateral bending at the atlantoaxial joint in a type II odontoid fracture model. However, it should not be used clinically until further studies have been performed to test the long-term effects of this procedure.

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Is atlantoaxial instability the cause of Chiari malformation? Outcome analysis of 65 patients treated by atlantoaxial fixation

Is atlantoaxial instability the cause of Chiari malformation?

J Neurosurg Spine 22:116–127, 2015

Understanding that atlantoaxial instability is the cause of Chiari malformation (CM), the author treated 65 patients using atlantoaxial stabilization. The results are analyzed.

Methods Cases of CM treated using atlantoaxial fixation during the period from January 2010 to November 2013 were reviewed and analyzed. Surgery was aimed at segmental arthrodesis.

Results The author treated 65 patients with CM in the defined study period. Fifty-five patients had associated syringomyelia. Forty-six patients had associated basilar invagination. Thirty-seven patients had both basilar invagination and syringomyelia. Three patients had been treated earlier using foramen magnum decompression and duraplasty. According to the extent of their functional capabilities, patients were divided into 5 clinical grades. On the basis of the type of facetal alignment and atlantoaxial instability, the patients were divided into 3 groups. Type I dislocation (17 patients) was anterior atlantoaxial instability wherein the facet of the atlas was dislocated anterior to the facet of the axis. Type II dislocation (31 patients) was posterior atlantoaxial instability wherein the facet of the atlas was dislocated posterior to the facet of the axis. Type III dislocation (17 patients) was the absence of demonstrable facetal malalignment and was labeled as “central” atlantoaxial dislocation. In 18 patients, dynamic images showed vertical, mobile and at-least partially reducible atlantoaxial dislocation. All patients were treated with atlantoaxial plate and screw fixation using techniques described in 1994 and 2004. Foramen magnum decompression or syrinx manipulation was not performed in any patient. Occipital bone and subaxial spinal elements were not included in the fixation construct. One patient died, and death occurred in the immediate postoperative phase and was related to a vertebral artery injury incurred during the operation. One patient had persistent symptoms. In the rest of the patients there was gratifying clinical improvement. More remarkably, in 7 patients, the symptoms of lower cranial nerve paresis improved. No patient worsened in their neurological function after surgery. Reductions in the size of the syrinx and regression of the CM were observed in 6 of 11 cases in which postoperative MRI was possible. During the follow-up period, there was no delayed worsening of neurological function or symptoms in any patient. Sixty-three patients improved after surgery, and the improvement was sustained during the average follow-up period of 18 months.

Conclusions On the basis of outcomes in this study, it appears that the pathogenesis of CM with or without associated basilar invagination and/or syringomyelia is primarily related to atlantoaxial instability. The data suggest that the surgical treatment in these cases should be directed toward atlantoaxial stabilization and segmental arthrodesis. Except in cases in which there is assimilation of the atlas, inclusion of the occipital bone is neither indicated nor provides optimum stability. Foramen magnum decompression is not necessary and may be counter-effective in the long run.

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