Introduction
Sciatica is most commonly attributed to lumbosacral radiculopathy secondary to intervertebral disc disease or spinal stenosis. However, extraspinal causes of sciatic nerve irritation should be considered when symptoms persist despite unrevealing lumbar imaging or when conventional spine-directed interventions fail to provide sustained relief[1]. Among these, piriformis syndrome (PS) – often categorized within deep gluteal syndrome (DGS) – represents an important but frequently underrecognized cause of extraspinal sciatic neuropathy resulting from irritation or compression of the sciatic nerve within the deep gluteal space[2].
Despite its clinical relevance, PS remains diagnostically challenging due to overlap with spinal disorders and the absence of standardized diagnostic criteria. It may account for approximately 5–8% of sciatica cases, although estimates vary widely[1–3]. Structural causes such as piriformis hypertrophy remain poorly characterized, with evidence mainly from case reports and imaging studies[4].
Typical features include deep gluteal pain radiating to the posterior leg, sciatic notch tenderness, and symptom provocation with piriformis tension maneuvers[3].HIGHLIGHTSPiriformis hypertrophy is a rare but important structural cause of refractory extraspinal sciatica.Persistent sciatica with nondiagnostic lumbar imaging should prompt evaluation for deep gluteal syndrome.Pelvic MRI identified unilateral piriformis hypertrophy after multiple unsuccessful spine-directed treatments.A multimodal diagnostic approach integrating clinical, imaging, and electrodiagnostic findings improves diagnostic accuracy.
Congenital variations and acquired changes, such as piriformis hypertrophy, may alter the sciatic nerve–muscle relationship, causing extraspinal nerve irritation. Advanced imaging, including pelvic MRI and magnetic resonance neurography, can identify structural abnormalities suggestive of deep gluteal pathology; however, linking these findings to symptoms remains challenging, especially in chronic, refractory cases[4].
We present a 42-year-old man with refractory sciatica despite normal lumbar imaging and unsuccessful interventions, in whom a pelvic MRI revealed marked unilateral piriformis hypertrophy. This case highlights the importance of considering deep gluteal causes when spinal evaluation fails to explain persistent symptoms.
This case report has been reported in line with the SCARE checklist[5].
Case presentation
A 42-year-old male pharmacist presented with chronic mild low back pain accompanied by severe left lower extremity pain radiating along the sciatic distribution. The pain was described as positional, electric-like, and exacerbated by specific postures, resulting in substantial functional limitation and distress. At baseline, the patient reported a Visual Analog Scale (VAS) pain score of 8/10 for lower extremity pain and an Oswestry Disability Index (ODI) score of 54% (indicating severe disability).
Family history was unremarkable, with no known similar neurological or musculoskeletal conditions, and the patient had no relevant past medical history.
Neurologic examination was largely nonfocal, demonstrating no objective motor weakness, sensory loss, or reflex asymmetry in the lower extremities. Pain-limited movement was present, but muscle strength was preserved at 5/5 on the Medical Research Council (MRC) scale in the lower extremities. Straight-leg raise testing was non-diagnostic, and no focal lumbar radicular signs were elicited.
Despite the severe symptom burden, the absence of clear neurologic deficits contributed to prolonged diagnostic uncertainty.
Initial lumbar MRI demonstrated only mild L4–L5 degenerative disc changes and did not reveal significant nerve root compression sufficient to explain the severity of symptoms. Over the subsequent 4 years, the patient underwent multiple spine-directed interventions, including interlaminar and transforaminal epidural steroid injections, without sustained clinical benefit. Lumbar discectomy was recommended at one point but was declined by the patient.
Additional peripheral diagnostic and therapeutic interventions were pursued. A lateral femoral cutaneous nerve block produced only transient relief, while an empiric piriformis injection failed to yield meaningful improvement. Fluoroscopy-guided platelet-rich plasma (PRP) injection targeting the piriformis produced partial but temporary symptom reduction, with maximal improvement estimated at approximately 40–50% before symptom recurrence (VAS pain score decreased from 8/10 to 4/10 at 4 weeks post-injection, before returning to 7/10 by 3 months).
Pharmacologic therapies – including gabapentin, pregabalin, duloxetine, nonsteroidal anti-inflammatory drugs, muscle relaxants, and corticosteroids – also failed to provide durable benefit.
Given persistent symptoms despite an unrevealing conventional lumbar evaluation, an expanded diagnostic assessment was pursued. MRI studies of the brain and entire spine did not identify significant central nervous system or compressive spinal pathology sufficient to explain the chronicity or severity of symptoms. Electrodiagnostic testing demonstrated preserved tibial and peroneal motor conduction with normal F-wave latencies and intact sural sensory responses; however, an asymmetric reduction in the left superficial peroneal sensory amplitude and chronic neurogenic motor unit remodeling in the left L5/S1-predominant musculature were identified (Tables 1–2).
Notably, the asymmetric superficial peroneal sensory abnormality and chronic unilateral neurogenic remodeling broadened the diagnostic consideration beyond isolated lumbar root pathology and raised suspicion of a more distal or multifactorial process.Table 1Nerve conduction study findings.NerveSideSite/segmentLatency (ms)Amplitude (mV/µV)Conduction velocity (m/s)InterpretationPeroneal motorLeftAnkle6.02.5 mV–Low-normal amplitude; no conduction blockPeroneal motorLeftFibular head–ankle12.72.4 mV45Normal conduction velocityPeroneal motorLeftPopliteal fossa–fibular head14.62.5 mV47Normal conduction velocityTibial motorLeftAnkle4.012.8 mV–NormalTibial motorLeftPopliteal fossa–ankle12.210.7 mV46Normal conduction velocityPeroneal F-waveLeft–46.9a––NormalTibial F-waveLeft–45.4a––NormalSuperficial peroneal sensoryLeftAnkle4.21 µV47Markedly reduced amplitude compared with the contralateral sideSuperficial peroneal sensoryRightAnkle4.222 µV44NormalSural sensoryLeftLower leg3.029 µV57NormalaF-wave latency. Amplitude values are reported in mV for motor studies and µV for sensory studies. F-wave values represent F-wave latency in milliseconds.Motor conduction studies demonstrated preserved distal latencies, conduction velocities, and F-wave latencies without evidence of focal demyelination or conduction block.
Sensory studies revealed preserved sural response with marked left-right asymmetry of superficial peroneal sensory amplitude, suggesting asymmetric peripheral sensory involvement not fully explained by isolated root pathology.Table 2Needle electromyography findings.MuscleInsertional activityFibrillation potentialsPositive sharp wavesFasciculationsMUAP durationMUAP amplitudePolyphasiaRecruitmentMaximal volitional activityLeft tibialis anteriorNormalAbsentAbsentAbsent++++++Reduced+Left extensor hallucis longusNormalAbsentAbsentAbsent+++++++++Reduced+Left medial gastrocnemiusNormalAbsentAbsentAbsent+++++++Reduced+Left vastus lateralisNormalAbsentAbsentAbsentNormalNormalNormalNormal+Right tibialis anteriorNormalAbsentAbsentAbsentNormalNormalNormalNormal+Right extensor hallucis longusNormalAbsentAbsentAbsentNormalNormalNormalNormal+Right medial gastrocnemiusNormalAbsentAbsentAbsentNormalNormalNormalNormal+Right vastus lateralisNormalAbsentAbsentAbsentNormalNormalNormalNormal+Right lumbar paraspinalsNormalAbsentAbsentAbsentNormalNormalNormalNormal+MUAP, motor unit action potential. The symbols+, ++, and +++ indicate increasing degrees of abnormality where applicable.Chronic neurogenic motor unit remodeling characterized by prolonged duration, increased amplitude, polyphasia, and reduced recruitment was identified predominantly within left L5/S1-distribution musculature without active denervation. These findings support chronic unilateral neurogenic dysfunction while reducing evidence for ongoing acute radiculopathy.
Pelvic MRI ultimately demonstrated marked unilateral hypertrophy of the left piriformis muscle, with clear asymmetry compared with the contralateral side on axial and coronal sequences (Fig. 1). Quantitative measurements demonstrated increased piriformis dimensions on the symptomatic side, with associated narrowing of the deep gluteal space and no alternative intrapelvic compressive lesion.
In the absence of spinal pathology sufficient to explain the symptoms, these findings supported a probable structural extraspinal source of sciatic nerve irritation, consistent with PS. Figure 1.Pelvic MRI demonstrating unilateral left piriformis hypertrophy with deep gluteal asymmetry. (A) Axial T2-weighted image (T2WI) demonstrates asymmetric enlargement of the piriformis muscle on the affected side (arrows), with relative signal heterogeneity.
(B) Coronal T2-weighted image (T2WI) demonstrates the craniocaudal extent of piriformis hypertrophy and associated asymmetry of the deep gluteal region (arrows). (C) Axial T1-weighted image (T1WI) provides a quantitative assessment of piriformis muscle thickness, confirming unilateral hypertrophy compared with the contralateral side. (D) Axial short tau inversion recovery (STIR) image demonstrates increased intramuscular signal intensity within the affected piriformis muscle, with associated narrowing of the deep gluteal space.
(E) Coronal oblique fat-suppressed T2-weighted image (T2 SPAIR) highlights a hyperintense signal within the hypertrophied piriformis muscle (arrows), supporting an abnormal signal alteration within the affected muscle. (F) Axial post-contrast fat-suppressed T1-weighted image (T1WI SPIR) demonstrates enhancement of the affected piriformis muscle (green arrows), indicating post-contrast signal enhancement.
Given persistent refractory symptoms, multimodal treatment resistance, and concordant pelvic imaging findings, the patient’s presentation was considered most consistent with refractory extraspinal sciatica, likely related to deep gluteal muscular pathology. A surgical referral was recommended but was declined.
At the 6-month follow-up, the patient continued to experience fluctuating positional left-sided sciatic pain with partial, temporary improvement after piriformis-targeted interventions, suggesting a modifiable extraspinal pain source. Conservative management with physiotherapy, activity modification, and analgesics was continued, although functional limitations persisted with prolonged sitting and hip flexion.
The chronological sequence of symptom onset, diagnostic investigations, therapeutic interventions, pelvic imaging, and subsequent follow-up is summarized in Table 3.Table 3Timeline.Time pointClinical event/investigationFindings or outcomeApproximately 4 years before final diagnosisOnset of symptomsChronic mild low back pain accompanied by severe left-sided sciatic pain, described as positional and electric-like.Initial evaluationLumbar MRIMild L4–L5 degenerative changes without significant nerve root compression sufficient to explain the severity of symptoms.Subsequent months/yearsSpine-directed treatmentInterlaminar and transforaminal epidural steroid injections and other spine-directed interventions were performed without sustained clinical benefit.During the subsequent evaluationAdditional interventionsLateral femoral cutaneous nerve block provided only transient relief. An empiric piriformis injection did not provide meaningful improvement.During the subsequent treatment coursePiriformis-targeted PRP injectionFluoroscopy-guided PRP injection produced partial temporary improvement, estimated at approximately 40–50%, followed by recurrence of symptoms.Over the 4-year coursePharmacological treatmentGabapentin, pregabalin, duloxetine, nonsteroidal anti-inflammatory drugs, muscle relaxants, and corticosteroids were used without durable symptom relief.Later diagnostic evaluationBrain and whole-spine MRINo significant central nervous system or compressive spinal pathology sufficient to explain the patient’s symptoms was identified.Later diagnostic evaluationElectrodiagnostic testingPreserved tibial and peroneal motor conduction and normal F-wave latencies were observed, with intact sural sensory responses; asymmetric left superficial peroneal sensory abnormality and chronic L5/S1-predominant neurogenic remodeling were also identified.Subsequent pelvic evaluationPelvic MRIMarked unilateral hypertrophy of the left piriformis muscle with deep gluteal asymmetry and no alternative intrapelvic compressive lesion was demonstrated.After pelvic MRIMultidisciplinary/clinical assessmentThe findings were considered most consistent with probable piriformis-related extraspinal sciatica. Surgical referral was recommended but declined by the patient.6-month follow-upClinical outcomePersistent but fluctuating positional left-sided sciatic pain remained, with partial temporary improvement after piriformis-targeted interventions.
Conservative management was continued.Chronological timeline of the patient’s clinical course, including symptom onset, diagnostic investigations, therapeutic interventions, identification of piriformis hypertrophy, and clinical outcome at 6-month follow-up.
Discussion
PS, a form of DGS, is an extraspinal cause of sciatic nerve irritation due to compression within the deep gluteal space[1,2]. It commonly mimics lumbosacral radiculopathy, presenting with deep gluteal pain radiating to the posterior leg and worsening with sitting or hip maneuvers[1–3]. Limited deep gluteal space and sciatic nerve excursion may contribute to nerve irritation[2,6].
Due to overlapping symptoms and often nonspecific neurologic findings, PS is frequently misdiagnosed as spinal pathology, sometimes leading to unnecessary lumbar interventions[2,3].
The prevalence of PS varies due to the absence of universally accepted diagnostic criteria, but evidence suggests it contributes to a notable proportion of chronic buttock and sciatic pain syndromes[1]. Historically, PS has been estimated to account for 5–6% of low back, buttock, and leg pain cases and up to 17% of chronic low back disorders[7,8]. Structural factors, including anatomical variations, fibrous bands, and piriformis muscle hypertrophy, can alter the sciatic nerve–muscle relationship and contribute to extraspinal nerve irritation[4].
Advanced imaging techniques, such as ultrasound with shear wave elastography, have demonstrated increased piriformis muscle thickness and stiffness in affected patients compared with healthy controls[9]. Recent systematic reviews indicate that fibrovascular bands and sciatic nerve anatomical variations are the most common structural causes, while piriformis hypertrophy accounts for approximately 7.5% of confirmed extraspinal entrapments[10].
Pelvic MRI identified unilateral piriformis hypertrophy and deep gluteal asymmetry in a patient with persistent sciatica despite normal lumbar imaging, supporting a piriformis-related pathology when combined with clinical findings and treatment response[11,12], while MR neurography further supports the diagnostic value of identifying piriformis and sciatic nerve abnormalities in extraspinal sciatica[13].
Electrodiagnostic testing supports diagnostic refinement by suggesting a possible extraspinal component in the presence of compatible pelvic imaging. Although specialized techniques, such as FAIR maneuver–induced H-reflex assessment, may demonstrate dynamic sciatic nerve compression[14,15], electrodiagnostic studies are mainly complementary and are more useful for excluding alternative diagnoses than for confirming PS[8].
Pelvic MRI and MR neurography are valuable in refractory sciatica when lumbar evaluation is inconclusive, identifying findings such as piriformis hypertrophy, asymmetry, and sciatic nerve changes[4,16]. Structural assessment of DGS should extend beyond the piriformis muscle to include adjacent musculoskeletal abnormalities, such as piriformis enthesopathy and ischiofemoral impingement, which may contribute to sciatic nerve irritation[6,17]. A comprehensive evaluation is essential because abnormalities of other deep external rotator muscles, particularly the quadratus femoris, may mimic deep gluteal nerve entrapment[18].
Imaging findings should be integrated with clinical and complementary assessments rather than interpreted alone.
Management of piriformis-related sciatica typically begins with conservative approaches, including medications, physical therapy, and image-guided injections[7]. In refractory cases, regenerative therapies such as ultrasound-guided dextrose prolotherapy and PRP injections may provide minimally invasive options to reduce gluteal pain and improve function[17]. Botulinum toxin type A injections may provide longer-lasting symptom relief than local anesthetic injections by relaxing the piriformis muscle and reducing sciatic nerve compression in refractory cases[8,19].
In the present case, targeted botulinum toxin injection was considered as a potential minimally invasive treatment option, given the suspected piriformis-related sciatic nerve irritation. However, it was not pursued prior to surgical consideration, as the patient had already undergone extensive conservative and interventional treatments without satisfactory or sustained improvement, and clinical decision-making subsequently focused on definitive decompression as a potential treatment for persistent symptoms and the structural abnormality.
For patients with persistent symptoms despite exhaustive conservative management, surgical interventions, including piriformis release and sciatic neurolysis, may be considered[12]. Selected patients with confirmed structural abnormalities may achieve favorable outcomes after decompression, emphasizing the importance of accurate diagnosis before additional invasive procedures[10]. In this case, failure of multiple interventions highlighted the diagnostic challenges of chronic sciatica and the need to identify the true pain generator.
The patient’s occupation as a pharmacist may be relevant when considering potential mechanical or postural contributors to his symptoms. Although no evidence currently establishes pharmacy work as a specific occupational risk factor for PS, professional activities that involve prolonged sitting or other sustained postures may be clinically relevant. Prolonged sitting is a commonly reported aggravating factor in PS and DGS, with symptoms often worsening during sustained sitting or positions that increase mechanical stress within the deep gluteal space[1].
More broadly, systematic evidence suggests that sedentary behavior and occupational sitting may be associated with musculoskeletal pain, although the strength and direction of these associations vary across occupational settings and available studies[20]. Accordingly, this patient’s occupation should be considered a potential source of prolonged or static postural exposure rather than evidence of a direct occupational cause of piriformis hypertrophy or sciatic nerve irritation. Future studies should investigate specific occupational exposures, including sitting duration, hip position, postural demands, physical activity, and work-related mechanical loading, to determine whether particular occupational patterns are associated with DGS.
The differential diagnosis of chronic sciatica includes spinal and extraspinal causes. In this case, lumbosacral radiculopathy, plexopathy, and peripheral neuropathies were considered, but were less likely based on imaging findings and clinical features. DGS, particularly piriformis-related sciatic entrapment, was favored based on positional symptoms, pelvic imaging abnormalities, and response to targeted intervention.
Other considerations included ischiofemoral impingement, hip pathology, sacroiliac dysfunction, and proximal hamstring disorders. Overall, the findings supported an extraspinal deep gluteal source as the most likely cause.
Strengths and limitations
The primary strength of this case report lies in its comprehensive, multimodal diagnostic approach – incorporating extensive neuroimaging and electrophysiological testing – over a 4-year longitudinal follow-up period. This thorough workup effectively highlights common diagnostic blind spots in the evaluation of chronic sciatica and emphasizes the clinical value of targeted pelvic imaging in preventing unnecessary spine-directed interventions. Furthermore, the report adheres to the SCARE guidelines, ensuring a structured and transparent presentation.
However, there are notable limitations to consider. As a single case report, the findings have inherent limitations regarding broad generalizability. Additionally, because the patient ultimately declined surgical intervention, there is a lack of direct intraoperative visualization or histopathological confirmation of the piriformis hypertrophy and its precise mechanical impingement on the sciatic nerve.
Finally, while structural asymmetry was clearly identified on static pelvic MRI, the evaluation did not utilize advanced dynamic imaging modalities – such as functional magnetic resonance neurography or dynamic ultrasound during provocative maneuvers – which could have provided more definitive, real-time evidence of sciatic nerve entrapment.
Conclusion
Piriformis hypertrophy is an uncommon but important cause of extraspinal sciatica that can mimic lumbosacral radiculopathy. This case highlights the need to consider alternative diagnoses when severe symptoms persist despite nondiagnostic spinal imaging and failed spine-directed treatments. A comprehensive approach integrating clinical assessment, pelvic imaging, and electrodiagnostic evaluation can improve diagnosis, guide targeted therapy, and reduce unnecessary spinal interventions.
Patient perspective
The patient described a 4-year course of severe left-sided sciatic pain as significantly affecting his daily activities, his ability to sit for prolonged periods, and his overall quality of life. He reported frustration with the persistence of symptoms despite multiple pharmacologic, interventional, and rehabilitation approaches. He considered the identification of the piriformis abnormality on pelvic MRI helpful in providing a possible explanation for his symptoms after previous spinal investigations had been unrevealing.
Although surgical treatment was discussed, he preferred to continue conservative management and declined surgical intervention. He expressed a preference for treatments that could improve pain and function while avoiding unnecessary invasive spinal procedures.