Abstract
Background Predicting which patients undergoing posterior cervical decompression and fusion (PCDF) will develop C5 palsy remains a significant challenge. We sought to determine whether a specific cervical laminectomy width in PCDF is associated with a reduced risk of postoperative C5 palsy.
Methods We reviewed the medical records of patients who underwent PCDF from 2016 to 2021. Our primary outcome was the presence of C5 palsy, defined as loss of at least 1 manual muscle test grade of the deltoid and/or biceps on hospital discharge from baseline. Laminectomy width was measured on postoperative cervical computed tomography images, and groups were stratified based on decompressions <18 mm, 18 to 22 mm, and >22 mm. Preoperative C3 to C5 cord signal change, ossification of the posterior longitudinal ligament, C4 to C5 neuroforaminal stenosis, and the C2 to C7 Cobb angles were also assessed.
Results Of the 111 patients included, 46 patients (41%) achieved laminectomy width <18 mm, 20 patients (18%) a width of 18 to 22 mm, and 45 patients (41%) a width of >22 mm. Eighteen patients (16.2%) developed C5 palsy. Multivariable analysis showed that a cervical laminectomy width >22 mm was significantly associated with increased odds of C5 palsy (OR = 13.1, 95% CI [2.43–70.41], P = 0.003). Subgroup analysis of individual risk factors further identified a significantly higher risk of C5 palsy in patients with C3 to C5 cord signal change, greater C2 to C7 Cobb angles, and existing C4 to C5 neuroforaminal stenosis.
Conclusions Narrow laminectomy (<22 mm) was associated with a significantly lower incidence of C5 palsy compared with wider laminectomy (>22 mm). Preoperative C3 to C5 cord signal change, C4 to C5 foraminal stenosis, and greater C2 to C7 Cobb angles were also independently linked to significantly increased odds of developing postoperative C5 palsy.
Clinical Relevance Developing C5 palsy is a significant cause of morbidity in patients undergoing PCDF. Performing a narrow laminectomy may help mitigate this risk and reduce patient morbidity.
Level of Evidence 3.
- C5 palsy
- deltoid palsy
- cervical laminectomy
- posterior cervical fusion
- cervical myelopathy
- cervical stenosis
Introduction
Posterior cervical laminectomy is an established treatment option for patients with cervical spondylosis with or without myelopathy or radiculopathy and is often combined with posterior instrumentation to enhance stability and correct sagittal alignment.1,2 A common and debilitating complication following posterior cervical decompression and fusion (PCDF) is C5 palsy, with incidence rates reported to be as high as 30%.3–9 It is often characterized as a decrease in deltoid muscle strength of at least 1 or 2 grades on the manual muscle test (MMT), with or without bicep involvement.10 Miller et al reported that C5 palsy adversely affected quality of life by reducing the capacity for self-care.11 Additionally, the costs of physical and occupational therapy for patients with C5 palsy were significantly higher, with an average difference of $2078 compared with those without the condition.11
The exact etiology of C5 palsy remains unclear but is likely multifactorial, involving factors such as iatrogenic nerve injury during surgery, posterior spinal cord drift, spinal cord ischemia with reperfusion injury, and C4 to C5 foraminal stenosis.12–14 Radcliff et al demonstrated that patients with C5 palsy had significantly greater mean postoperative spinal cord drift and that a wider laminectomy at C5 (mean width 17.9 ± 2.5 mm) increased the risk of this complication.15 Additionally, C4 to C5 neuroforaminal stenosis has been identified as a likely contributing factor to the incidence of C5 palsy.16 Various mitigation strategies, such as narrow laminectomy, laminoplasty, and foraminotomy, have shown promise in reducing C5 palsy rates. Despite these advances, predicting which patients will develop C5 palsy and determining the optimal surgical strategy remain significant challenges.
We sought to identify objective parameters related to posterior cervical decompressive surgery and their association with the development of postoperative C5 palsy. Our primary goal was to assess variations in laminectomy width to determine whether a precise, objective cutoff correlates with a higher incidence of C5 palsy. Our secondary objectives examined the impact of C4 to C5 foraminal stenosis, C2 to C7 Cobb angle, preoperative cord signal changes, and ossification of the posterior longitudinal ligament (OPLL) on the risk of C5 palsy.
Methods
Study Design
Institutional review board approval and waiver of consent were obtained prior to study onset (IRB: 17700–64). The study was completed at an academically affiliated tertiary center between January 2016 and January 2021 and included consecutive adult patients (aged 18 years or older) who underwent multilevel PCDF, including C4 to C5, for symptomatic adult degenerative cervical myelopathy, with or without radiculopathy.
Postoperative C5 palsy was defined as a decrease of at least 1 grade in MMT strength of the deltoid and/or biceps compared with the preoperative examination after excluding alternative causes such as postoperative cervical hematoma or pain-limited examination, as determined by the attending neurosurgeon. Patients were excluded if they underwent surgery for traumatic, neoplastic, or infectious conditions, had previous surgery at C4 to C5, lacked preoperative cervical spine magnetic resonance imaging (MRI) or both preoperative and postoperative cervical spine computed tomography (CT) images, had a preoperative MMT score below 4/5 in the C5 distribution, did not receive decompression at C4 to C5, or had documented intraoperative iatrogenic nerve root or spinal cord injury.
All participants remained hospitalized for at least 48 hours postoperatively. Patients without C5 palsy attended a minimum 1-month follow-up appointment, while those diagnosed with C5 palsy were followed for at least 6 months, with evaluations at 1-, 3-, and 6-month intervals to monitor improvement and resolution. Postoperative cervical spine CT scans were routinely obtained within 6 months of surgery. Postoperative C5 palsy was assessed by neurosurgical residents and attendings using standardized MMT during daily neurological examinations until discharge, with findings documented in the patient’s electronic medical record.
Radiographic Measurements
Measurement of laminectomy width was defined as the distance at the inferior margin of C4 between the lateral aspects of the residual laminae or lateral masses, depending on the extent of decompression (Figure 1). Measurements were made by 2 authors (A.A. and D.T.) who were blinded to the outcome of the study at the time of measurement. Additional effect modifiers were assessed using Merge PACS version 3 (Merge Healthcare Inc., Chicago, Illinois). C4 to C5 intervertebral neuroforaminal diameter was evaluated on axial T2/GRE MRI using the Kim criteria: 0 (none to mild), 1 (moderate), and 2 (severe; Figure 2).17 OPLL was assessed on CT or MRI based on the Japanese Ministry of Health and Welfare Investigation Committee OPLL Grading system.18 The C2 to C7 Cobb angle was measured pre- and postoperatively using lateral radiographs with Surgimap software (Nemaris Inc., New York, New York; Figure 3). Spinal cord signal change was evaluated on preoperative T2 axial and T2/short tau inversion recovery sagittal MRI. The Strengthening the Reporting of Observational Studies in Epidemiology Statement checklist was used to prepare this manuscript.19
Measuring laminectomy width. (A) A laminectomy measuring 14 mm from both ends at the lower C4 level. (B) A laminectomy measuring 26 mm from both ends at the lower C4 level.
Measuring the neuroforaminal diameter using Kim’s criteria.17 Schematic diagrams of the grading system for cervical neural foraminal stenosis in axial scans at the intervertebral disc level in the cervical spine. (A and B) Grade 0, normal-absence of neural foraminal stenosis with the narrowest width of neural foramen (arrowheads) more than extraforaminal nerve root (black arrows). Panel A shows no narrowing of the neural foramen, and panel B shows mild narrowing. (C) Grade 1, nonsevere cervical neural foraminal stenosis, including the narrowest width of neural foramen (arrowheads), same or less than (but more than 50% of) extraforaminal nerve root width. (D) Grade 2, severe cervical neural foraminal stenosis, including the narrowest width of neural foramen (arrowheads), same or less than 50% of extraforaminal nerve root width. Source: Figure is reproduced from the Korean Journal of Radiology, doi:10.3348/kjr.2015.16.6.1294, with permission from the copyright owner and Dr. Joon Woo Lee, MD, for noncommercial use.
Cobb angle was measured from the inferior endplates of C2 and C7.
Surgical Technique
Posterior cervical laminectomies were performed using standardized techniques by 6 separate fellowship-trained spine surgeons (2 orthopedic and 4 neurosurgeons). A standard midline posterior approach was utilized in all cases. Patients were in a prone position with slight neck flexion with either a Mayfield head holder (Integra LifeSciences, Plainsboro, NJ, USA) or Sugita head holder (Mizuho, Union City, CA, USA). The laminectomy width, however, varied according to each surgeon’s discretion. Lateral mass screws were inserted using the Roy-Camille technique, with intraoperative fluoroscopy employed to ensure accurate screw positioning. Pedicle screws were inserted if C2, T1, or T2 levels were included in the construct. The sequence of hardware placement and decompression varied between surgeons. The laminectomy was carried out with a 4 mm round-tip Midas Rex (Medtronic) drill. Decompression was carried out via trough-style drilling perpendicular to the lamina. Following decompression, the facet joints were decorticated, and autograft or allograft bone was packed into the joint space. Prior to rod insertion, each surgeon readjusted the head holder to slightly translate posteriorly and induce cervical lordosis under fluoroscopic guidance.
Statistical Analysis
Our dependent variable was the incidence of C5 palsy occurring within a minimum of 48 hours of hospitalization following PCDF. The primary predictor variable was laminectomy width (in mm), confirmed by postoperative CT. Potential confounders included patient demographics (age, body mass index, gender, smoking status, diabetes, and myelopathy) and operative characteristics (number of instrumented or decompressed levels).
Univariate analysis was conducted to compare demographic and preoperative characteristics between cohorts stratified by the presence of C5 palsy and by laminectomy width (<18 mm, 18–22 mm, >22 mm). Two-sample independent t tests were used for continuous variables, while χ 2 goodness-of-fit tests were applied to categorical variables. A subgroup analysis was performed on patients with existing C4 to C5 neuroforaminal stenosis and C3 to C5 cord signal change to assess potential effect modification. Multivariable logistic regression was used to determine whether laminectomy width was independently associated with the odds of developing C5 palsy, adjusting for relevant confounders. P values less than 0.05 were considered statistically significant. All analyses were performed using IBM SPSS Statistics for Windows, version 25.0 (IBM Corp., Armonk, NY).
Results
Participants and Descriptive Data
A total of 111 consecutive patients were included in the study. Laminectomy width in the entire cohort was 19.9 ± 4.4 mm (median 19.2, range 12.8–28.2). Of these, 46 patients (41%) had a laminectomy width <18 mm (range 12.8–17.2 mm), 20 patients (18%) had a width between 18 and 22 mm, and 45 patients (41%) had a width >22 mm (range >22.6–28.2 mm). There was a significant association between laminectomy width and sex. Patients with a laminectomy width >22 mm were more likely to be men (29 [64.4%] vs 16 [35.6%], P < 0.03), while those with a width <18 mm were more likely to be women (29 [63.0%] vs 17 [37.0%], P < 0.03). A significant difference in diabetes prevalence was also observed across laminectomy width categories. Patients in the >22 mm group had a higher rate of diabetes (21 [46.7%]) compared with those in the 18 to 22 mm (4 [20.0%]) and <18 mm (12 [26.1%]) groups (P < 0.04; Table 1).
Patient, operative, and radiographic characteristics by laminectomy width (N = 111).
Eighteen patients (16.2%) developed C5 palsy. Among those patients, 7 (39%) were women and 7 (39%) were diabetic. Laminectomy width was significantly larger in the C5 palsy group (26.0 ± 0.8 mm vs 18.8 ± 3.9 mm, P < 0.0001; Table 2). Analysis of known risk factors revealed significant associations with the development of C5 palsy. A higher proportion of patients who developed C5 palsy exhibited high-intensity cord signal change at the C3 to C5 region on preoperative MRI compared with those without C5 palsy (10 [55.6%] vs 26 [28.0%], P < 0.024; Table 2). Patients with C5 palsy also demonstrated significantly greater cervical lordosis, with a larger mean preoperative C2 to C7 Cobb angle (18.1° ± 7.7° vs 13.2° ± 7.9°, P < 0.017) and a significantly greater postoperative C2–C7 Cobb angle (21.5 ± 6.7 vs 14.6 ± 7.7, P < 0.001) compared with those without C5 palsy (Table 2). Additionally, all patients who developed C5 palsy had pre-existing severe neuroforaminal stenosis at C4 to C5 on MRI, compared with only 29.0% of those without C5 palsy (18 [100%] vs 27 [29.0%], P < 0.001; Table 2).
Risk factors of C5 palsy.
Outcome Data
All patients who developed C5 palsy had laminectomy width >22 mm (median 25.8, range 24.2–28.2). A laminectomy width of <18 mm or 18 to 22 mm was associated with a significantly lower risk of developing C5 palsy compared with widths >22 mm, with no cases observed in the narrower width groups (0 [0%] vs 0 [0%] vs 18 [40%], P = 0.001; Table 3).
C5 palsy by laminectomy width per patient (N = 111).
Follow-up was available for all patients who developed C5 palsy (median 10.5 months, range 1–36). At discharge, 11/18 (61.1%) patients had an MMT score of ≥3. Overall rate of complete recovery in patients who developed C5 palsy was 67.7% (12/18) at the longest available follow-up (Table 4). Of those, 4/12 (33.3%) had achieved full recovery by 3 months. Six of 18 patients (33.3%) with C5 palsy did not achieve full recovery at the longest available follow-up. Of these, 2 patients had 4/5 strength (1- and 12-month follow-up), 1 had 3/5 strength (11 months), 2 had 2/5 strength (both 1-month follow-up), and 1 had 0/5 strength (16 months). Fifteen patients who developed C5 palsy had follow-up for >6 months, and among those, 12/15 (80%) achieved full resolution (median 10.5 months, range 6–36; Table 5).
C5 palsy MMT grade and time to resolution (n = 18).
Characteristics of patients with C5 palsy.
Multivariable analysis revealed that laminectomy width >22 mm was independently associated with significantly increased odds of developing C5 palsy (OR = 13.1, 95% CI = [2.43–70.41], P = 0.003; Table 6). Other variables, including high-intensity cord signal change and pre- and postoperative C2 to C7 Cobb angles (data not shown), were not found to be statistically significant predictors of C5 palsy in the adjusted model.
Multivariable analysis of C5 palsy.
Other Analyses
Subgroup analysis was conducted to compare patients with and without C5 palsy by laminectomy width across different radiographic risk factors, including severe neuroforaminal stenosis at C4 to C5, high-intensity cord signal C3 to C5, and preoperative and postoperative Cobb angles. Among the 45 patients with severe neuroforaminal stenosis at C4 to C5 on preoperative MRI, those with a laminectomy width >22 mm had a significantly higher incidence of C5 palsy compared with those with more narrow decompressions (18 [100%] vs 3 [11.1%], P < 0.001; Table 6). Similarly, of the 36 patients exhibiting high-intensity cord signal change at C3 to C5, a significantly greater proportion with laminectomy width >22 mm developed C5 palsy compared with those with narrower decompressions (10 [100%] vs 6 [23.1%], P < 0.001; Table 6).
Discussion
Our results indicate that a laminectomy width of <22 mm is independently associated with significantly lower odds of developing postoperative C5 palsy. Furthermore, preoperative MRI findings of cord signal change at C3 to C5 and severe foraminal stenosis at C4 to C5 were independently linked to a significantly increased risk of postoperative C5 palsy, even after adjusting for known radiographic risk factors. Although patients in the >22 mm group had a higher rate of diabetes (46.7%) and male sex (64.4%), patients who developed C5 palsy were not disproportionately diabetic (38.8%) or men (61.2%). Overall, the incidence of C5 palsy observed in this study is comparable, though perhaps slightly higher, to the rates reported in recent literature.7
Previous studies have identified wider cervical laminectomy width as a key factor influencing the incidence of C5 palsy.15,16,20 Radcliff et al concluded that reducing laminectomy width minimizes spinal cord drift, thereby decreasing the risk of postoperative C5 palsy.21 Conversely, Klement et al found no association between laminectomy widths and C5 palsy development; however, their definition of a “narrow” laminectomy was 23 mm, which is considerably wider than the 19 mm width described by Radcliff et al.21,22 Our study supports the findings of Radcliff et al, with a significant reduction in C5 palsy incidence when the laminectomy width is kept under 22 mm.21
Severe C4 to C5 neuroforaminal stenosis may further increase the risk of C5 palsy by exacerbating traction on the C5 nerve root during posterior spinal cord drift following decompression.15,23 In this context, a narrower laminectomy may limit spinal cord migration and reduce nerve root traction, thereby potentially decreasing the likelihood of postoperative C5 palsy. Our findings supported this, as all patients who developed C5 palsy had severe neuroforaminal stenosis at the C4 to C5 level and had a wide laminectomy. Notably, all patients who developed C5 palsy in this study had laminectomy widths greater than 24 mm, which theoretically would allow for maximal spinal cord drift and potentiate traction on the C5 nerve root. Previous studies have observed that preventive foraminotomy at C4 to C5 performed during PCDF can significantly reduce the incidence of C5 palsy, likely by mitigating nerve root tethering and compression in those with pre-existing foraminal stenosis.16 Additional studies evaluating the incidence of C5 palsy following C4 to C5 foraminotomy performed in conjunction with a narrow laminectomy during PCDF may be a point of interest.24
Additionally, our findings revealed that high-intensity cord signal changes from C3 to C5 on preoperative MRI are associated with a higher incidence of C5 palsy. This may reflect greater spinal cord recoil after decompression.25 While subgroup analysis indicated that cord signal changes remain a significant risk factor with wider laminectomies, multivariable regression did not find it to be an independent predictor.
The final radiographic parameter we evaluated, which showed a stronger association with C5 palsy, was the pre- and postoperative C2 to C7 Cobb angle. Liu et al demonstrated that increased cervical lordosis correlates with greater spinal cord drift.26 They further reported a significant relationship between the cervical Cobb angle, spinal cord drift, and the incidence of C5 palsy.26 Our findings align with these results, as both increased pre- and postoperative Cobb angles emerged as risk factors for C5 palsy.
Previous studies have demonstrated associations between laminectomy width, existing C4 to C5 neuroforaminal stenosis, and greater C2 to C7 Cobb angles with C5 palsy.4,9,21,26 These studies, however, are limited by smaller sample sizes and retrospective designs. As such, our study supports existing published data while providing actionable guidance for surgical planning by suggesting quantitative thresholds for laminectomy width during PCDF.
Limitations
Our study is limited by its retrospective design, which allows for identification of associations but does not establish causation. The width of the decompression performed was left to each involved surgeon’s discretion, introducing variability. Given the retrospective nature of this study, we were unable to control for differences in surgical skill and technique among surgeons over time. The surgical decision-making and patient indications are also difficult to standardize. Moreover, including multiple surgeons may invariably impact operative characteristics and/or patient outcomes. Resident participation may also affect this. Further prospective studies would better control for surgical variability and should be investigated. Operative characteristics such as estimated blood loss and operative time have not previously been correlated with the development of C5 palsy; however, their reporting may have helped contextualize the findings of our study.9 With only 3 patients meeting criteria for OPLL included, we were unable to establish associations between OPLL and C5 palsy. Further analyses, with more appropriately powered cohorts demonstrating OPLL, are needed to clarify any potential relationship between OPLL and C5 palsy. Additionally, our study demonstrated a relatively small number of patients who developed C5 palsy (n = 18), which may limit the statistical power and generalizability of our findings. A multicenter study, with a larger patient cohort, would likely enhance external validity and provide stronger evidence for surgical recommendations. The inclusion of patient-reported functional outcomes would have enhanced the comprehensiveness of this study and provided more insight into the clinical significance of C5 palsy. Although efforts were made to collect these metrics, the available documentation was insufficient to yield analyzable or clinically meaningful data.
Lack of long-term follow-up for all patients with C5 palsy also represents a potential limitation. Notably, 3/6 patients who did not achieve full strength recovery only had follow-up for a 1-month period. This also contributes to our lack of ability to determine any risk factors for persistent weakness in this patient population. Among patients in this study who had a follow-up for 6 months or longer, the recovery rate was 80%. Thus, we are potentially underestimating the rate of C5 recovery in this patient population.
Another limitation is our reporting of laminectomy decompression width as a nonstandardized measurement. Individual lamina width depends on individual anatomy and is known to vary along with the size of the canal diameter, spinal cord diameter, cervical spine body, and lateral masses. Each of these factors may influence intraoperative laminectomy width during surgery. Future studies may consider standardizing laminectomy width by bony canal width or spinal cord diameter. We also acknowledge the somewhat arbitrary grouping of patients into laminectomy width categories (<18 mm, 18–22 mm, and >22 mm). Another noteworthy factor is the individual variation in myotome distribution. It is possible that surgical manipulation of the C3 to C4 and C5 to C6 joints could also possibly influence these outcomes. In the present study, to remove potential confounders, we only excluded patients with prior surgery on C5 to C6. This may represent a possible limitation. We also did not formally analyze the degree of postoperative decompression at that level; thus, we are unable to comment on decompression inadequacy as a factor to be formally analyzed.
Conclusion
In the present study, patients with C5 palsy had significantly wider laminectomies compared with those who did not develop C5 palsy. Patients in the groups with laminectomy width <22 mm were found to be independently associated with significantly lower odds of developing postoperative C5 palsy. In addition, preoperative MRI findings of cord signal change at C3 to C5 and severe foraminal stenosis at C4 to C5 were independently linked to a significantly increased risk of postoperative C5 palsy, even after adjusting for known radiographic risk factors. Prospective investigations are needed to establish causal relationships and improve the prediction of C5 palsy in patients undergoing PCDF for symptomatic cervical spondylosis.
Footnotes
Funding The authors received no financial support for the research, authorship, and/or publication of this article.
Declaration of Conflicting Interests The authors report no conflicts of interest in this work.
Previous Presentations A subset of these data was presented at the Spine Summit in Las Vegas, Nevada, on 25 February 2022 and at the Michigan Association of Neurological Surgeons Annual Meeting at Boyne Mountain in Boyne Falls, Michigan, on 27 August 2022.
Disclosures Peter Bono reports consulting fees from Globus Medical, Stryker, and Spinal Elements. The remaining authors have nothing to disclose.
Ethics Approval Institutional board approval and waiver of consent were obtained prior to study onset (IRB: 17700-64).
- This manuscript is generously published free of charge by ISASS, the International Society for the Advancement of Spine Surgery. Copyright © 2026 ISASS. To see more or order reprints or permissions, see http://ijssurgery.com.
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