Chiari malformation I surgically treated with atlantoaxial fixation.

In this issue of the Journal of Neurosurgery: Spine, Professor Atul Goel submits a single-institution, singlesurgeon retrospective analysis of 65 adult and pediatric patients with “complex” Chiari malformations (CMs), that is, CM Type I associated with complex bony anomalies of the craniocervical junction and brainstem compression.4 Professor Goel is respected as a clinical pioneer and thought leader for disorders at the craniocervical junction. He asserts that the basic pathophysiological mechanism for CM with or without basilar invagination and with or without syringomyelia is C1–2 instability. This assertion challenges conventional theories. Bollo et al.1 recently thoroughly described this entity in the pediatric neurosurgical literature; the authors identified basilar invagination, CM 1.5, and a clivoaxial angle < 125° as patient risk factors necessitating reduction and occipitocervical fusion in addition to mandatory suboccipital decompression. In the present study Goel speculates that CM and syringomyelia are “Nature’s protective mechanism” of the body and compares CM to an “air bag.” This speculation, at best, is unsupported and unsubstantiated by evidence in the study and the literature and, at worst, sounds flowery and sophomoric. This literary metaphor seems out of place in a scientific journal. Professor Goel attempts to demonstrate in his series a new paradigm for treating symptomatic CM, that is, C1–2 posterior instrumented fusion alone using C-1 lateral mass screws and C-2 pars or pedicle screws—without any attempt at CM decompression and without occipitocervical fusion. Notably, in his series, there was one death (1.5%) from vertebral artery injury (out of 3 total vertebral artery injuries; approximately 5% rate of injury) while exposing entry points for the C-1 lateral mass screws. Professor Goel managed these patients with a C1–2 posterior instrumented fusion. As part of the preparation for placing the C-1 lateral mass screws, anomalous vertebral arteries needed to be “dissected” away from the C-1 facet process. Why? This seems completely unnecessary and adds significant risk to the procedure (vertebral artery injury or spasm). The C-1 arch is already fused to the occiput in more than a few examples provided as figures; therefore, fusing from the occiput (with occipital screws and plates) to C-2 would be a biomechanically equivalent construct, without the loss of additional range of motion at the craniocervical junction and without having to manipulate the vertebral arteries. Related to the above point, basilar invagination and/or platybasia are typically regarded as signs of craniocervical junction instability, and an occipitocervical construct is usually indicated. Moreover, in a subgroup of patients (Group A) in Professor Goel’s study, cervical traction was applied intraoperatively “to reduce basilar invagination and restore craniovertebral alignment.” How does a C1–2 fusion alone maintain this reduction? Again, occipitocervical fusion seems necessary to maintain this reduction. Mortality rates for CM decompression surgery with or without duraplasty range from 0% to 0.9% in large series.5,6 Vertebral artery injury rates range from 0% to 0.7% for posterior fossa decompression with and without duraplasty for the surgical treatment of CM.2 Professor Goel’s mortality rate and vertebral artery injury rate using this new surgical approach for CM seem alarmingly high, unjustified, and lie outside of published benchmarks for the surgical treatment of CM using suboccipital craniectomy plus or minus duraplasty. While the patient-reported outcomes seem very satisfactory (63 [97%] of 65) on health-related quality of life (HRQOL) outcome surveys (Japanese Orthopaedic Asso-