Elsevier

World Neurosurgery

Volume 132, December 2019, Pages e193-e201
World Neurosurgery

Original Article
Posterior Screw-Rod Fixation and Selective Axial Loosening for the Treatment of Atlantoaxial Instability or Dislocation Caused by Os Odontoideum: A Case Series for a Single Posterior Approach

https://doi.org/10.1016/j.wneu.2019.08.208Get rights and content

Objective

To evaluate the effect of screw-rod fixation and selective axial loosening in the treatment of atlantoaxial instability or dislocation (including reducible and irreducible) caused by os odontoideum (OO) via a single posterior approach.

Methods

A consecutive series of patients with OO surgically treated in our hospital were retrospectively analyzed. For atlantoaxial instability and reducible atlantoaxial dislocation, C1-C2 screw-rod fixation and fusion were performed. OO combined with irreducible atlantoaxial dislocation was reduced after posterior axial loosening, followed by screw-rod fixation and fusion. The general information, clinical data, and radiographic data were compared between the 2 different procedures.

Results

There were 41 patients with an average age of 40.6 ± 21.7 years. All the patients underwent posterior reduction and C1-2 screw rod fixation, 6 with axial loosening and 35 without axial loosening. The clinical manifestations and radiographic data significantly improved after the operation with a low rate of complications. Except for clivus-canal angle and visual analogue score of cervical pain, there were no differences in clinical and radiographic data between the 2 procedures.

Conclusions

Posterior screws-rod fixation and selective axial loosening is appropriate for treating OO complicated with atlantoaxial instability or dislocation (including reducible and irreducible) without the need for anterior decompression.

Introduction

An os odontoideum (OO) appears as an isolated and smooth ossicle replacing the normal odontoid process, with smooth edges discontinuous with the base of the odontoid process or axis.1 OO was first reported by Giacomini in 1886. Its etiology has been controversially explained with 2 different theories: congenital or posttraumatic lesion.2 Each theory has their convincing evidence3, 4, 5, 6, 7, 8, 9; however, neither affect the choice of treatment.1

The clinical manifestation of OO ranges from no symptoms or only neck pain to severe myelopathy, disappearance of spontaneous breathing, and even sudden death.10, 11, 12

OO complicated with symptoms and signs of myelopathy or C1–2 instability requires C1–2 fixation. Clinical and radiologic surveillance or aggressive posterior C1–2 fixation and fusion can be selected for OO without myelopathy or instability.1 OO complicated with irreducible atlantoaxial dislocation (AAD) is a candidate for occipitocervical fixation and fusion with selective C1 laminectomy or ventral decompression followed by posterior atlantoaxial fixation.10, 13 Transoral decompression surgery risks more serious complications,14 whereas occipitocervical fixation restricts the motion of the atlanto-occipital joint and has a greater impact on function in patients.15

We found that OO combined with irreducible AAD could be partially reduced by heavy-weight skull traction under general anesthesia. Therefore, we performed posterior screw-rod fixation in patients with atlantoaxial instability, and heavy-weight skull traction-assisted loosening of the lateral atlantoaxial joints (we named “axial loosening”) in patients with OO complicated with irreducible AAD during a posterior procedure, followed by C1–2 screw-rod fixation for the purpose of treating OO via a single posterior approach.

Section snippets

General Information

We retrospectively analyzed a consecutive series of patients diagnosed with OO and treated surgically in our hospital from January 2012 to March 2017. The inclusion criteria were patients diagnosed with OO with atlantoaxial instability or dislocation who underwent surgical treatment. The diagnosis of OO relied on x-ray and/or computed tomography (CT) scans to detect ossicles with smooth cortical margin separated from the axis, with hypertrophy of the atlas anterior arch16 and a positive jigsaw

Clinical Data

There were 41 patients (15 men and 26 women) with an average age of 40.6 ± 21.7 years. The follow-up period ranged from 24–65 months, with an average of 40.7 ± 21.7 months. Nineteen patients (46.3%) had a certain history of trauma, 5 with remote trauma, 4 with no remote trauma, 32 with an unclear history, 15 (36.6%) with recent trauma, and 1 with a history of both remote and recent trauma.

Localized neck pain was found in 33 patients (80.5%), transient myelopathy in 13 (31.7%), progressive

Etiology of OO

It has been elucidated that patients with OO have higher rates of congenital lesions such as Down syndrome, Klippel-Feil syndrome, epiphyseal dysplasia, and other bone dysplasia than the general population.23 Kirlew et al.8 studied female twins without trauma and found that there were partial fusions of C2–3, hypertrophy of the C1 anterior arch, and depression of the C2 spinous process. Straus et al.24 studied identical twins with OO, patients with OO who were not twins, and 4 people without

Conclusions

Most AAD caused by OO are characterized as atlantoaxial instability or reducible AAD. Posterior screw-rod fixation and selective axial loosening are appropriate for treating OO complicated with atlantoaxial instability or dislocation (including reducible and irreducible variants) without the need for anterior decompression.

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    Conflict of interest statement: This work is supported by Overseas Research Project for Health Care and Family Planning Talents of Henan Province (grant number 2018090).

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