Double Crush Syndrome in Surgically-Treated Lumbosacral Radiculopathy: Prevalence, Risk Factors, and Clinical Implications

Abstract

Introduction

Double crush syndrome (DCS) refers to compressive neuropathy at multiple sites along a peripheral nerve (PN), yet its relevance in the lower extremity remains poorly defined. This study aimed to (1) determine the prevalence of PN lesions in patients undergoing surgery for lumbosacral radiculopathy (LR), (2) identify commonly affected nerves, (3) assess associated risk factors, and (4) evaluate the DCS hypothesis by comparing the incidence of PN lesions in patients undergoing surgery for LR versus matched controls.

Methods

A retrospective cohort study was conducted using the PearlDiver database (2010-2022) to identify adult patients who underwent lumbar decompression and/or fusion for LR. PN lesions diagnosed within two years before or after surgery were categorized by nerve. Univariate logistic regression was used to identify risk factors. A matched control cohort without LR was created using propensity score matching to evaluate the DCS hypothesis.

Results

Of 650,562 patients undergoing surgery for LR, 32,909 (5.1%) were diagnosed with a PN lesion, with 60.6% occurring before and 38.4% after surgery. The most commonly affected nerves were the sciatic (31.7%), plantar (16.1%), and peroneal (11.2%). Risk factors for PN lesions included female gender (odds ratio [OR]: 1.22), age 50-59 years (OR: 1.23) and 60-69 years (OR: 1.17), and higher comorbidity burden with Elixhauser Comorbidity Index ≥5 (OR: 1.50). Comorbid conditions associated with increased risk included complex regional pain syndrome (OR: 3.33), fibromyalgia (OR: 1.73), and osteoarthritis (OR: 1.61). Compared to matched controls, patients with LR were significantly more likely to develop a PN lesion (OR: 3.10).

Conclusions

PN lesions affect over 5% of patients undergoing surgery for LR and are significantly more common than in controls, supporting the DCS hypothesis in the lower extremity. Clinicians should maintain a broad differential diagnosis when evaluating radicular symptoms, especially in patients with high comorbidity burden or recurrent postoperative pain.

Introduction

Double crush syndrome (DCS) represents a significant clinical challenge in the diagnosis and management of spinal pathology and peripheral nerve (PN) disorders¹⁾. Originally described by Upton and McComas in 1973, DCS refers to the compressive pathology at multiple sites along a PN that results in additive neurological dysfunction¹⁾. The DCS hypothesis suggests that a proximal nerve lesion may predispose the distal portion of the same nerve to injury, wherein minor nerve compression―that would otherwise remain asymptomatic―results in clinically significant symptoms^1-3).

The mechanistic basis of DCS has been extensively investigated in preclinical studies, which collectively suggest that proximal compression disrupts axoplasmic flow, leading to distal degenerative changes or impaired function^3-7). However, the clinical relevance of the DCS hypothesis remains controversial. For example, several studies have found no increased risk of carpal tunnel syndrome in patients with C6-C8 radiculopathy, challenging the fundamental premise of the DCS concept^8,9). Despite the lack of consensus about whether compression at one site predisposes to injury at another along the same nerve, clinicians generally acknowledge that patients can present with concomitant PN lesions at multiple sites¹⁰⁾.

Research on DCS has predominantly focused on the upper extremity, particularly the concurrent presentation of cervical radiculopathy and peripheral neuropathies involving the median or ulnar nerves¹¹⁾. In contrast, there has been relatively little investigation into DCS affecting the lower extremity¹²⁾. This knowledge gap is concerning given that lumbosacral radiculopathy (LR) represents one of the most common complaints evaluated by spine surgeons and a leading cause of disability in adults¹³⁾. Characterized by compression or irritation of lumbosacral nerve roots, this condition manifests as low back and buttock pain radiating to the lower extremities, often accompanied by numbness, weakness, and reflex changes¹³⁾. Similarly, peripheral mononeuropathies such as peroneal nerve entrapment or tarsal tunnel syndrome (TTS) can produce motor and sensory symptoms that mimic lumbar radiculopathy^14,15).

The diagnostic challenge of identifying PN lesions in patients presenting with radicular symptoms is substantial and frequently overlooked, even in cases of recurrent symptoms following lumbar decompression surgery¹²⁾. Early identification of PN lesions in these patients is critical for improving outcomes, enhancing patient satisfaction, and avoiding unnecessary spine surgery¹²⁾. Unfortunately, current literature on DCS in the lower extremities is limited to case reports and small single-institution studies focusing on specific PN compression syndromes (e.g., TTS), which fail to capture the full scope of this condition^16-22).

Using a comprehensive national insurance claims database, this study aimed to: (1) determine the prevalence of concomitant lower extremity PN lesions in patients undergoing surgery for LR, (2) identify the most common sites for lower extremity PN lesions in these patients, and (3) explore potential risk factors for the diagnosis of DCS. A secondary objective was to evaluate the DCS hypothesis by investigating whether patients with LR were at increased risk of developing PN lesions compared to matched controls without LR.

Methods

Data Source and Study Population

This retrospective study leveraged the PearlDiver Mariner Database (PearlDiver Technologies, Colorado Springs, CO, USA) to identify patients who underwent surgery for LR between 2010 and 2022. PearlDiver is a large nationwide insurance claims database encompassing roughly 157 million deidentified patients, offering demographic, diagnostic, and procedural data from various payer types across inpatient and outpatient settings. Given the use of anonymized data and the retrospective design, the study did not require informed consent or institutional review board approval.

Identification of Study Cohorts

Patients were identified using diagnostic codes from the International Classification of Diseases 9th (ICD-9) and 10th (ICD-10) editions, as well as Current Procedural Terminology codes. Records with diagnostic codes for LR were queried, and patients were included if they underwent lumbar decompression and/or fusion for LR to ensure the inclusion of individuals with sufficiently severe disease.

Patients were further categorized based on the presence of PN compression syndromes or lesions occurring within two years before or after lumbar spine surgery. A two-year timeframe was selected to capture patients with a high likelihood of concomitant PN lesions at multiple sites including: (1) patients who experienced treatment failure for a PN lesion and were subsequently referred to a spine surgeon and (2) patients who developed recurrent/persistent symptoms following lumbar surgery and were later diagnosed with a PN lesion, suggesting the latter was a primary contributor to their symptoms.

PN lesions were categorized by specific nerves, including the sciatic, lateral femoral cutaneous, femoral, peroneal, tibial, plantar, and other nerves (i.e., saphenous nerve, sensory nerves, and others not classified specifically by the ICD coding system). Posterior TTS was identified using tibial or plantar nerve lesions, and anterior TTS was identified using peroneal nerve lesions. A detailed list of diagnosis codes is provided in Supplemental Table 1.

PN lesions were identified solely through ICD-9 and ICD-10 diagnostic codes for PN lesion, compressive neuropathy, mononeuropathy, or injury. Confirmatory diagnostic modalities such as electromyography or nerve conduction studies were not required for inclusion, consistent with the constraints of insurance claims data. As such, diagnoses may reflect clinical impressions rather than objective testing. To focus exclusively on lower extremity pathology, patients with cervical or thoracic radiculopathy or PN lesions affecting the upper extremities were excluded from analysis.

Exclusion criteria included patients under 18 years of age, those with less than 90 days of follow-up before or after lumbar spine surgery, and cases involving surgical indications for trauma, malignancy, or infection. Continuous variables were reported as mean values with standard deviations, while categorical variables were presented as raw counts and percentages.

Primary Outcomes

The primary objective of this study was to determine the prevalence of concomitant PN lesions in patients undergoing surgery for LR. Additionally, we identified demographic risk factors for the diagnosis of PN lesions in patients with LR within two years of surgery. Risk factors analyzed included gender, age range, Elixhauser Comorbidity Index (ECI), and various individual comorbidities. The ECI was also transformed into a binary variable to identify a cohort of patients with a greater comorbidity burden (ECI ≥5 vs. ECI ≤4).

Patients with nerve lesions were also identified if they underwent PN decompression surgery; however, no further analysis was completed on this cohort since a small proportion of patients with lower extremity PN lesions undergo operative treatment.

Secondary Outcome

The secondary objective focused on evaluating the DCS hypothesis. This was done by examining whether patients with LR were at an increased risk of being diagnosed with PN lesions compared to matched controls without LR over the entire study period. Unlike the primary analysis, this evaluation did not impose a two-year timeframe for diagnosing PN lesions in the LR group, allowing for a more equal comparison with the control cohort.

Statistical Analysis

Statistical analyses were performed using RStudio (Version 4.4.2) within the PearlDiver Mariner Database platform. Continuous variables were compared using Student's t-test, while categorical variables were analyzed using Pearson's chi-squared test of independence. Univariate logistic regression was utilized to identify risk factors in patients with surgically treated LR for diagnosis of a PN lesion within 2 years before or after surgery.

To test the DCS hypothesis, propensity score matching was performed to create a control group without LR. Patients were matched based on age, gender, and ECI. A univariate logistic regression analysis was employed to assess whether patients with surgically treated LR were more likely to be diagnosed with a PN lesion compared to the general population during the study period. A p-value <0.05 was considered statistically significant for all analyses.

Results

Demographic Characteristics

A total of 650,562 patients who underwent lumbar decompression and/or lumbar fusion for LR between 2010 and 2022 were identified. Overall, 32,909 patients (5.06%) were diagnosed with a PN lesion within 2 years before or after surgery. Among these patients, 19,948 (60.62%) were diagnosed 2 years before surgery, and 12,961 (38.38%) were newly diagnosed within 2 years after surgery. Patients who were diagnosed with PN lesions before or after surgery were older (mean age: 58.77±12.82 years vs. 57.96±14.25 years), had a higher comorbidity burden (ECI: 5.05±3.61 vs. 4.30±3.47), were more likely to be female (56.52% vs. 50.48%), and were more frequently treated with lumbar fusion compared to lumbar decompression (45.11% vs. 40.68%) (all p<0.001). Complete demographic information is displayed in Table 1.

Table 1.

Demographics of Patients Undergoing Surgery for LR and Prevalence of PN Lesions.

LR surgery	No PN lesion		PN lesion		p-Value
	n=617,653		n=32,909
Age	57.96	±14.25	58.77	±12.82	<0.001
ECI	4.30	±3.47	5.05	±3.61	<0.001
Male	305,879	(49.52%)	14,310	(43.48%)	<0.001
Female	311,772	(50.48%)	1,599	(56.52%)	<0.001
Lumbar fusion	251,270	(40.68%)	14,845	(45.11%)	<0.001
Multilevel	96,193	(15.57%)	5,951	(18.08%)	<0.001
Decompression	369,058	(59.75%)	18,448	(56.06%)	<0.001
Multilevel	117,903	(19.09%)	6,326	(19.22%)	0.552

Statistical significance defined as p<0.05, significant values bolded.

ECI: Elixhauser comorbidity Index; LR: lumbosacral radiculopathy; PN: peripheral nerve

Nerves Affected

Among the 32,909 patients with PN lesions, the most affected nerves were the sciatic (10,419 patients, 31.66%), plantar (5,283 patients, 16.05%), lateral femoral cutaneous (3,697 patients, 11.23%), peroneal (3,669 patients, 11.15%), and distal tibial (2,542 patients, 7.72%). Additionally, 11,901 patients (36.16%) were diagnosed with other PN lesions not specifically recognized in the ICD diagnostic system.

When analyzing by anatomical region, 7,585 patients were identified with posterior TTS (23.05%), and 10,785 patients were identified with anterior or posterior TTS (32.77%). The anatomic breakdown of PN lesions can be seen in Table 2.

Table 2.

Anatomic Breakdown of PN Lesions in Patients Undergoing Surgery for LR.

Location of lesion		% of patients with PN lesions n=32,909	% of total patients undergoing surgery for LR n=650,562
Total	32,909	(100%)	(5.06%)
Other	11,901	(36.16%)	(1.83%)
Sciatic	10,419	(31.66%)	(1.60%)
Plantar	5,283	(16.05%)	(0.81%)
Lateral femoral cutaneous	3,697	(11.23%)	(0.57%)
Peroneal	3,669	(11.15%)	(0.56%)
Distal tibial	2,542	(7.72%)	(0.39%)
Femoral	666	(2.02%)	(0.10%)
Proximal tibial	261	(0.79%)	(0.04%)
Posterior tarsal tunnel	7,585	(23.05%)	(1.17%)
Anterior or posterior tarsal tunnel	10,785	(32.77%)	(1.67%)

Posterior tarsal tunnel defined as tibial or plantar nerve lesion; anterior tarsal tunnel syndrome defined as a peroneal nerve lesion.

LR: lumbosacral radiculopathy; PN: peripheral nerve

Of the 32,909 patients with PN lesions, a total of 2,150 (6.53%) underwent PN decompression surgery. The most frequently decompressed nerves were the plantar (930 patients, 43.25%), peroneal (631 patients, 29.35%), and distal tibial (536 patients, 24.93%). Among the patients who underwent PN decompression surgery, 776 (36.1%) had the procedure within two years prior to LR surgery, 434 (20.18%) underwent it on the same day as their LR surgery, and 940 (43.72%) had the procedure within two years following their LR surgery.

Risk Factors for Peripheral Nerve Lesions in Patients Undergoing Surgery for Lumbosacral Radiculopathy

Univariate logistic regression revealed that among patients with surgically treated LR, female gender (odds ratio [OR]: 1.22 [1.20-1.23]), age 50-59 years (OR: 1.23 [1.20-1.26]) and age 60-69 years (OR:1.17 [1.14-1.20]) were associated with increased odds of having a concomitant diagnosis of a PN lesion (all p<0.001) (Table 3). Conversely, male gender (OR: 0.78 [0.77-0.80]), age <40 years (OR: 0.66 [0.64-0.69]), and age >70 years (OR: 0.92 [0.89-0.94]) were associated with a lower likelihood (all p<0.001).

Table 3.

Risk Factors for Presence of OR Development of a PN Lesion in Patients Undergoing Surgery for Lumbosacral Radiculopathy.

	No PN lesion n=617,653		PN lesion n=32,909		p-Value	OR	[95% CI]
Female	311,772	(50.48%)	18,599	(56.52%)	<0.001	1.22	[1.20-1.23]
Male	305,879	(49.52%)	14,310	(43.48%)	<0.001	0.78	[0.77-0.80]
ECI ≥5	243,873	(39.48%)	16,255	(49.39%)	<0.001	1.50	[1.46-1.53]
ECI ≤4	373,780	(60.52%)	16,654	(50.61%)	<0.001	0.67	[0.65-0.68]
Age Range
Age <40	77,641	(12.57%)	2,854	(8.67%)	<0.001	0.66	[0.64-0.69]
Age 40-49	93,422	(15.13%)	4,968	(15.10%)	0.886	1.00	[0.97-1.03]
Age 50-59	138,677	(22.45%)	8,625	(26.21%)	<0.001	1.23	[1.20-1.26]
Age 60-69	161,612	(26.17%)	9,652	(29.33%)	<0.001	1.17	[1.14-1.20]
Age >70	154,479	(25.01%)	7,701	(23.40%)	<0.001	0.92	[0.89-0.94]
Comorbidities
Complex regional pain syndrome	6,101	(0.99%)	1,057	(3.21%)	<0.001	3.33	[3.11-3.55]
Drug induced peripheral neuropathy	2,717	(0.44%)	276	(0.84%)	<0.001	1.91	[1.69-2.16]
Fibromyalgia	111,817	(18.10%)	9,122	(27.72%)	<0.001	1.73	[1.69-1.78]
Osteoarthritis	273,799	(44.33%)	18,508	(56.24%)	<0.001	1.61	[1.58-1.65]
Rheumatoid arthritis	29,951	(4.85%)	2,320	(7.05%)	<0.001	1.49	[1.42-1.55]
Autoimmune	134,471	(21.77%)	9,406	(28.58%)	<0.001	1.44	[1.40-1.47]
Peripheral vascular disease	139,768	(22.63%)	9,695	(29.46%)	<0.001	1.43	[1.39-1.46]
Drug abuse	91,939	(14.89%)	6,535	(19.86%)	<0.001	1.42	[1.38-1.46]
Liver disease	117,545	(19.03%)	7,905	(24.02%)	<0.001	1.35	[1.31-1.38]
Obesity	281,645	(45.60%)	17,143	(52.09%)	<0.001	1.30	[1.27-1.33]
Chemotherapy	44,449	(7.20%)	2,973	(9.03%)	<0.001	1.28	[1.23-1.33]
Hypothyroidism	160,989	(26.06%)	10,023	(30.46%)	<0.001	1.24	[1.21-1.27]
Diabetes	243,534	(39.43%)	14,785	(44.93%)	<0.001	1.25	[1.23-1.28]
Diabetes complicated	135,710	(21.97%)	8,562	(26.02%)	<0.001	1.25	[1.22-1.28]
Renal disease	105,552	(17.09%)	6,389	(19.41%)	<0.001	1.17	[1.14-1.20]
Alcohol abuse	49,820	(8.07%)	2,944	(8.95%)	<0.001	1.12	[1.08-1.16]
Tobacco use	296,582	(48.02%)	16,458	(50.01%)	<0.001	1.08	[1.06-1.11]

Univariate logistic regression was utilized. Statistical significance defined as p<0.05, significant values bolded.

CI: confidence interval; ECI: Elixhauser Comorbidity Index; OR: odds ratio; PN: peripheral nerve

A higher comorbidity burden, analyzed as patients with an ECI ≥5, was associated with increased odds of having a concomitant diagnosis of a PN lesion (OR: 1.50 [1.46-1.53], p<0.001). Individual comorbidities associated with the highest odds of being diagnosed with a PN lesion included complex regional pain syndrome (OR: 3.33 [3.11-3.55]), drug-induced peripheral neuropathy (OR: 1.91 [1.69-2.16]), fibromyalgia (OR: 1.73 [1.69-1.78]), osteoarthritis (OR: 1.61 [1.58-1.65]), rheumatoid arthritis (OR: 1.49 [1.42-1.55]), and other autoimmune conditions (OR: 1.44 [1.40-1.47]) (p<0.001). The complete analysis of risk factors is displayed in Table 3 and Fig. 1.

Figure 1.

Forest plot of odds ratios: Factors associated with the presence or development of peripheral nerve lesions in patients undergoing surgery for lumbosacral radiculopathy.

Double Crush Hypothesis

To test the double crush hypothesis, a control group without LR was created through 1:1 exact propensity matching based on age, gender, and ECI, resulting in 133,350 patients in each cohort. Patients with operatively treated LR were significantly more likely to develop a PN lesion during the study period (OR: 3.10 [2.98-3.23]) than patients without LR.

Discussion

DCS has been widely studied in the upper extremity, but its manifestation in the lower extremity remains less understood. This study demonstrates that 5.06% of patients undergoing surgical treatment for LR were also diagnosed with lower extremity PN lesions within two years before or after surgery. These patients exhibited a significantly higher likelihood (OR: 3.1) of developing PN lesions compared to matched controls without LR. These findings underscore the substantial prevalence of PN lesions in this population, their potential to complicate the diagnosis of LR, and their likely contribution to failed back surgery syndrome due to undiagnosed preoperative PN compression.

This study represents the first large-scale, nationwide analysis of the prevalence of DCS in the lower extremity. Previous studies on lower extremity DCS have been limited to case reports and single-institution studies focusing predominantly on TTS^16-22). For instance, Zheng et al.¹⁶⁾ reported a 4.8% prevalence among 581 patients with concomitant anterior or posterior TTS and LR, while Golovchinsky¹⁸⁾ found a prevalence of 5.3% among 169 patients. When investigating anterior and posterior TTS (tibial, plantar, and peroneal nerves), the present study found a prevalence of 1.66%, lower than previous literature, which may reflect differences in methodology and diagnostic mechanisms. However, the overall prevalence of 5.06% reported here likely underestimates the true prevalence of symptomatic PN lesions in this population due to reliance on billing codes, as they are often underdiagnosed in clinical practice compared to studies that use universal diagnostic testing²³⁾. Notably, the prevalence observed in this study is lower than that reported in the upper extremity, where institutional studies have found rates ranging from 10.29% to 33%, and a similar national database study reported a prevalence of 9.98% in patients with cervical radiculopathy^{8,10,11,24-26)}.

Dibble et al.¹²⁾ hypothesized that the most common presentations of DCS in the lower extremity involve L5/S1 radiculopathy with TTS or L5 radiculopathy with peroneal entrapment. Our results align with this pattern, as lesions involving the plantar nerve, peroneal nerve, and distal tibial nerve were most frequently observed in the distal lower extremity. Identifying these lesions is critical since they can mimic LR but may be successfully treated with PN decompression, potentially delaying or avoiding lumbar decompression surgery. Our findings also suggest that DCS is prevalent in the proximal lower extremity, with sciatic nerve (1.60%) and lateral femoral cutaneous nerve (0.57%) lesions among the most diagnosed. Although there are no case reports of DCS including concomitant lumbar radiculopathy and sciatic nerve compression, these syndromes can be difficult to differentiate as piriformis syndrome may be responsible for 0.5-6% of sciatic syndromes, and there is evidence that piriformis syndrome is common after lumbar surgery²⁷⁾. Meralgia paresthetica is especially common in the lumbar degenerative population, likely due to similar associations with obesity, and has also been associated with L2 and L3 radiculopathy^28,29).

The primary challenge in managing lower extremity DCS lies in recognizing the second site of compression rather than treating it¹²⁾. Patients often present with symptoms of radiculopathy or mononeuropathy that are attributed solely to lumbar pathology, and a concomitant PN lesion may only become apparent when symptoms persist or recur after lumbar decompression^19,22,30). In our cohort, 1.20% of patients received a new diagnosis of a PN lesion within two years postoperatively, suggesting that distal compression is frequently overlooked during initial evaluation. Clinicians should maintain a high index of suspicion in patients whose symptoms are out of proportion to lumbar imaging, especially when distal complaints, such as foot numbness, burning, or focal paresthesias, predominate. Particular attention should be given to patients with chronic overlapping pain syndromes like complex regional pain syndrome and fibromyalgia, which were among the strongest risk factors identified in this study¹²⁾.

Preoperative evaluation for LR should include thorough physical examination with provocative maneuvers, such as Tinel's sign at common entrapment sites (e.g., tarsal tunnel, fibular head), to screen for PN involvement¹²⁾. Electrodiagnostic studies can provide objective confirmation and are especially valuable in complex or ambiguous cases. Advanced imaging modalities, including magnetic resonance imaging or high-resolution ultrasound, may help identify nerve edema or entrapment and guide further testing^12,31). Clinicians should also assess systemic risk factors such as diabetes, autoimmune disease, or hypothyroidism, which predispose to multifocal neuropathy³²⁾. However, diagnosing DCS remains challenging due to often mild evidence of compression at multiple sites and the absence of standardized diagnostic criteria¹²⁾.

This study found that patients with operatively treated LR are at a higher risk of lower extremity PN lesions (OR: 3.10) compared to matched controls in the general population without LR, supporting the DCS hypothesis. While proposed mechanisms for DCS include impaired axonal transport, immune-mediated inflammation, ion channel dysregulation, and neuroma formation, its pathophysiology remains debated⁷⁾. Some argue that DCS may reflect a clinical syndrome influenced by altered gait mechanics or systemic conditions like osteoarthritis, autoimmune conditions, or diabetes that increase the risk of nerve damage rather than a distinct neurophysiological phenomenon along a single PN¹⁶⁾. However, this study cannot fully assess DCS pathophysiology due to database limitations, such as the inability to determine laterality or specific nerve root involvement of the LR. Because of this, the actual prevalence of anatomically defined DCS along the same PN is likely lower than the 5.06% of patients reported here who were diagnosed with any lower extremity PN lesion.

Female sex, age 50-69 years, and higher comorbidity burden emerged as significant risk factors for PN lesions in our analysis. These associations likely reflect a combination of biological susceptibility, degenerative change, and chronic disease burden. For example, hormonal influences, greater prevalence of fibromyalgia, and increased healthcare utilization may contribute to higher diagnosis rates among women^33,34). Advancing age is associated with neural degeneration, impaired repair capacity, and microvascular insufficiency, all of which may predispose to nerve compression³⁵⁾. A higher ECI may capture a cumulative vulnerability to neuropathy, including conditions such as diabetes, autoimmune disease, and vascular insufficiency, that act as additional “hits” predisposing nerves to injury³²⁾. The strongest associations were seen in patients with complex regional pain syndrome, drug-induced peripheral neuropathy, and fibromyalgia, suggesting that in many cases, symptoms may reflect a broader clinical syndrome rather than a discrete double compression mechanism. Cohen et al.²³⁾ have proposed reframing DCS as “multifocal neuropathy,” emphasizing systemic drivers of nerve dysfunction over strictly anatomical entrapment. This interpretation is further supported by elevated risk in patients with osteoarthritis and rheumatoid arthritis, where joint degeneration and osteophyte formation can contribute to both lumbar and PN compression, particularly in anatomically constrained regions such as the tarsal tunnel³⁶⁾.

This study has several limitations. As an insurance claims-based analysis, it relies on the accuracy of diagnostic and procedural coding, which introduces potential for misclassification and human error. The use of administrative codes does not provide information on how PN lesions were diagnosed, whether through electrodiagnostic testing, imaging, or clinical evaluation, so some cases may reflect nonspecific symptoms rather than confirmed compressive neuropathies. However, the concern that residual postoperative LR symptoms were miscoded as PN lesions is mitigated by the use of distinct diagnostic codes for radiculopathy and peripheral mononeuropathies, reducing the likelihood of diagnostic overlap. The database also lacks information on laterality and specific nerve root involvement, which prevents assessment of whether proximal and distal lesions occurred along the same nerve distribution and limits our ability to identify anatomically defined DCS. We did not evaluate outcomes in the small subset of patients who underwent PN decompression, and data on symptom resolution were not available. Despite these limitations, this study represents the largest national analysis of lower extremity DCS and provides meaningful insight into its prevalence, risk factors, and clinical relevance.

In conclusion, the prevalence of PN lesions in patients undergoing surgery for LR is 5.06% within 2 years before or after surgery. Patients with LR are at an increased risk of developing PN lesions compared to controls (OR: 3.10). Given the challenges in diagnosing DCS in the lower extremity, clinicians should maintain a broad differential diagnosis and consider PN lesions as contributors to radicular symptoms. These findings are highly relevant to spine surgeons and general orthopedic surgeons alike, as LR represents one of the most common presenting symptoms, and lower extremity PN lesions should always be included in the differential diagnosis. Future research should prioritize electrophysiological testing and high-quality prospective studies to better define DCS prevalence, pathophysiology, diagnostic guidelines, and optimal treatment in the lower extremity.

Author Contributions: Conceptualization: William J. Karakash, Jeffrey C. Wang, Raymond J. Hah, and Ram K. Alluri. Formal Analysis: William J. Karakash, Henry Avetisian, and Matthew C. Gallo. Data Curation: William J. Karakash and Henry Avetisian. Methodology: William J. Karakash, Henry Avetisian, Matthew C. Gallo, and Chimere O. Ezuma. Project Administration: William J. Karakash, Jeffrey C. Wang, Raymond J. Hah, and Ram K. Alluri. Writing - Original Draft: William J. Karakash, Henry Avetisian, Matthew C. Gallo, and Chimere O. Ezuma. Writing - Review & Editing: William J. Karakash, Matthew C. Gallo, Chimere O. Ezuma, Jeffrey C. Wang, Raymond J. Hah, and Ram K. Alluri.

Conflicts of Interest: Henry Avetisian, William J. Karakash, Matthew C. Gallo, and Chimere O. Ezuma have nothing to disclose. Jeffrey C. Wang has received intellectual property royalties from Zimmer Biomet, NovApproach, SeaSpine, Bioretec, and DePuy Synthes; and stock options from Bione Biologics, Electrocore, PearlDiver, Surgitech, and Illuminant. Raymond J. Hah has received grant funding from ATEC and Nuvasive; consulting fees from Medtronic, Globus, Orthofix, SI-Bone, Cerapedics, and Evolution Spine; and support from the North American Spine Society to attend meetings. Ram K. Alluri has received grant funding from NIH; consulting fees from Medtronic, Orthofix, and Globus; payment from Eccential Robotics for lectures and presentations; and stock options from HIA technologies, NeoOnc, and Globus.

Ethical Approval and Informed Consent Statement: Informed consent was waived due to the retrospective nature of the study, and institutional review board (IRB) approval was not required as the database is de-identified.

Data Availability Statement: Data is not publicly available but can be made available upon request.