Meralgia Paresthetica: A Review

Abstract

Introduction

Meralgia paresthetica (MP) is a pain-and-paresthesia syndrome of the anterolateral thigh caused by compression of the lateral femoral cutaneous nerve (LFCN). The diagnosis is primarily clinical, while ultrasound, magnetic resonance imaging, and electrodiagnostic studies may assist in atypical cases.

Methods

We reviewed the most relevant publications on MP from 1979 to 2025, searching PubMed, SciELO, Cochrane, Scopus, ResearchGate, and Google with the descriptors: “meralgia paresthetica” and “lateral femoral cutaneous nerve of the thigh.” A total of 131 articles were considered; 37 references published within the last five years were highlighted.

Results

Multiple risk factors contribute to MP. First-line management is conservative; surgery is considered for refractory cases.

Conclusions

Diagnosis can be challenging, often delayed by variable presentation and low awareness. Evidence guiding the most effective non-surgical and surgical interventions remains limited. Further studies are needed to improve clinical diagnosis and clarify optimal treatment strategies.

Resumo

Introdução

A meralgia parestésica (MP) é uma síndrome de dor e parestesia da face ântero-lateral da coxa causada por compressão do nervo cutâneo femoral lateral (NCFL). O diagnóstico é principalmente clínico, enquanto a ultrassonografia, a ressonância magnética e os estudos eletrodiagnósticos podem auxiliar em casos atípicos.

Métodos

Revisamos as publicações mais relevantes sobre MP de 1979 a 2025, pesquisando no PubMed, SciELO, Cochrane, Scopus, ResearchGate e Google com os descritores: “meralgia parestésica” e “nervo cutâneo femoral lateral da coxa”. Um total de 131 artigos foi considerado; 37 referências publicadas nos últimos cinco anos foram destacadas.

Resultados

Múltiplos fatores de risco contribuem para a MP. O manejo de primeira linha é conservador; a cirurgia é considerada para casos refratários.

Conclusões

O diagnóstico pode ser desafiador, muitas vezes atrasado pela apresentação variável e baixa conscientização. As evidências que orientam as intervenções não cirúrgicas e cirúrgicas mais eficazes permanecem limitadas. Mais estudos são necessários para melhorar o diagnóstico clínico e esclarecer as estratégias terapêuticas ideais.

Keywords

Meralgia paresthetica - nerve compression syndromes - lateral femoral cutaneous nerve - neuralgia - pain management - neurolysis - neurectomy

Palavras-chave

Nervo cutâneo lateral femoral - meralgia parestésica - anterior thigh pain - lateral femoral cutaneous nerve

Introdução

Meralgia paresthetica (MP) is a relatively common but frequently underdiagnosed mononeuropathy of the lateral femoral cutaneous nerve (LFCN), also known as the lateral cutaneous nerve of the thigh (LCNT).[1] [2] [3] [4] [5] This condition produces dysesthesia and neuropathic pain over the anterolateral thigh, often leading to significant morbidity.

The first report associating compression of the LCNT with thigh pain was provided by Hager in 1855.[6] Later, in 1895, the German neuropathologist Martin Bernhardt and the Russian neurologist Vladimir Karlovich Roth offered detailed descriptions of this entity, which subsequently became known as the Bernhardt–Roth syndrome. The term meralgia is derived from the Greek words meros (thigh) and algos (pain), whereas paresthesia refers to abnormal sensations.[7] [8]

The clinical diagnosis and treatment of MP remain challenging due to its heterogeneous presentation and overlapping symptomatology with other neuropathies. Consequently, delayed diagnosis is common and frequently results in significant disability and decreased quality of life for affected individuals. The aim of this review is to provide a comprehensive synthesis of epidemiology, anatomy, etiology, clinical presentation, diagnostic approach (including differential diagnoses and complementary examinations), and treatment options for MP.

Methods

Design: Narrative Literature Review

Data sources and search strategy: We searched PubMed/MEDLINE, SciELO, Cochrane Library, Scopus, ResearchGate, and Google for studies from January 1, 1979, to September 5, 2025, using: “meralgia paresthetica” AND/OR “lateral femoral cutaneous nerve of the thigh”. We also hand-searched reference lists of included articles.

Eligibility criteria: Peer-reviewed human studies (randomized and non-randomized trials, observational studies, case series/reports), reviews, anatomical/cadaveric studies of the LFCN, and imaging/interventional technique papers relevant to MP. Animal studies and reports not focused on MP were excluded. No language restrictions (Portuguese, English, and Spanish sources included).

Study selection and data handling: Titles/abstracts were screened for relevance to MP; full texts were reviewed when necessary. A total of 131 articles were retained; 37 publications from the last five years were emphasized for contemporary practice.

Outcomes of interest: Epidemiology and risk factors[9] [10] [11] [12]; anatomical variants and potential entrapment sites[2] [3] [4] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27]; diagnostic criteria and adjunct tests—clinical maneuvers, ultrasonography, MR neurography, and electrodiagnostics[28] [29] [30] [31] [32] [33] [34] [35] [36] [37] [38] [39] [40] [41] [42] [43] [44] [45] [46] [47] [48] [49] [50] [51]; conservative treatments and ultrasound-guided perineural injections[43] [44] [45] [46] [47] [52] [53] [54] [55] [56] [57] [58] [59] [60] [61] [62] [63] [64] [65]; interventional pain procedures (pulsed radiofrequency, radiofrequency ablation, peripheral nerve stimulation)[54] [66] [67] [68] [69] [70] [71] [72]; and surgical options (neurolysis, neurectomy, transposition) with outcomes and complications.[2] [5] [13] [42] [53] [55] [73] [74] [75] [76] [77] [78] [79] [80] [81] [82] [83]

Synthesis: Due to heterogeneity of designs and outcomes, we performed qualitative synthesis without meta-analysis. As a review of published literature, no ethics approval was required.

Anatomy

A precise understanding of the anatomy of the LFCN is essential for both diagnosis and treatment planning.[13]

The LFCN is a purely sensory nerve that originates from the lumbar plexus, typically arising from the ventral rami of L2 and L3, although anatomical variants may derive from L1–L2 or from L2 alone.[3] [13] [14] [15] [16] [17] [18] [19] [20] The nerve emerges from the lateral border of the psoas major muscle (30% of cases), above (27%) or below (43%) the level of the iliac crest.[21] From this point, it courses between the iliac fascia and the iliacus muscle toward the anterior superior iliac spine (ASIS). It then crosses either beneath or through the inguinal ligament to enter the anterior compartment of the thigh.[4]

Distal to the inguinal ligament, the LFCN divides into anterior and posterior branches, both of which pierce the fascia lata to provide cutaneous innervation.[2] [4] The anterior branch innervates the anterolateral thigh down to the knee, while the posterior branch supplies the skin from the greater trochanter to the mid-lateral thigh.[23]

The anatomical course of the LFCN is highly variable.[2] [24] In up to 90% of cases, it passes below or through the inguinal ligament medial to the sartorius muscle and the ASIS.[14] [23] [25] Alternative pathways include passing above the inguinal ligament, lateral to the ASIS, or even through the sartorius muscle—variations that may or may not predispose to entrapment.[14] [23] [25]

Pokharel et al.[1] identified four potential entrapment sites for the LFCN:

1. Near the ASIS at the inguinal ligament, where the nerve changes its course from nearly horizontal to vertical.

2. At its emergence from the psoas muscle.

3. During its passage through the fascia lata.

4. At the site where the fascia lata exits distally.

Most authors agree that entrapment at the level of the inguinal ligament is the predominant mechanism in MP.[26] [28] Pearce[27] further emphasized that the region between the fascia lata and the inguinal ligament is the most frequent compression site.

Epidemiology

MP occurs more frequently in men, with peak incidence between 41 and 60 years of age.[9] [10] [11] [12] [26] [84] [85] [86] Although less common, pediatric cases have been reported in the literature.[1] [87] [88] [89] [90]

Several risk factors are associated with the development of MP, including obesity, elevated body mass index (BMI), pregnancy, diabetes mellitus, hypothyroidism, and advanced age.[9] [10] [11] [12] In a large population-based study, van Slobbe et al.[12] reported an incidence rate of 4.3 per 10,000 patients per year. Similarly, Parisi et al.,[11] analyzing cases between 1990 and 1999, found an incidence of 32.6 per 100,000 patients per year. Importantly, the incidence was 7.5 times higher among patients with diabetes mellitus compared to the general population, underscoring the role of metabolic disorders as significant contributors to MP.

Etiology

The causes of MP can be broadly divided into idiopathic and iatrogenic forms. Idiopathic cases are further subdivided into mechanical and metabolic origins.[1] [4] Pokharel et al.[1] proposed a tripartite classification: (1) mechanical, (2) metabolic, and (3) iatrogenic.

Mechanical Causes

Direct mechanical compression is considered the principal cause of MP.[1] [4] Contributing anatomic and biomechanical factors include limb length discrepancy and degenerative disease of the pubic symphysis.[91] Conditions that increase intra-abdominal pressure—such as pregnancy, obesity, retroperitoneal or pelvic tumors, and ascites—may also precipitate nerve entrapment.[1] External mechanical factors, including seat belts, corsets, and tight garments, can exert sustained pressure on the inguinal region, leading to symptomatic compression of the LFCN.[92]

Metabolic Causes

Metabolic factors such as lead intoxication, diabetes mellitus, and chronic alcoholism have been implicated in the pathogenesis of MP, often mediated by free radical formation, inflammatory processes, and microvascular damage to the nerve.[28] [93] [94] The use of statins has also been associated with MP.[95] [96] Statin-induced neuropathy, with an estimated incidence of 12 per 100,000 person-years, typically manifests as an axonal sensorimotor neuropathy with predominant sensory involvement, thought to result from impairment of mitochondrial respiratory chain function.[96]

Iatrogenic Causes

MP is also well recognized as a post-surgical complication. Reported associations include:

• Orthopedic procedures: iliac crest bone graft harvesting, pelvic fixation or osteotomy, hip surgery, pelvic fracture repair, and lumbar spine surgery.[86] [97] [98] [99] [100] [101]

• Spinal surgery positioning: the use of Jackson or Relton-Hall frames during prone positioning has been associated with MP, likely due to external compression and compromised blood flow to the vasa nervorum of the LFCN.[102] MP has also been reported after prolonged prone positioning in the intensive care unit, particularly during mechanical ventilation for respiratory failure, including in COVID-19-related Acute Respiratory Distress Syndrome (ARDS).[103] [104] [105]

• Abdominal and pelvic surgeries: laparoscopic procedures such as myomectomy, inguinal hernia repair, cholecystectomy, cesarean section, and bariatric surgery have all been linked to MP.[26] [106] [107] [108] [109] [110]

• Obstetric and gynecologic surgeries: cesarean delivery after attempted vaginal birth, gynecologic oncologic procedures, and surgeries requiring prolonged lithotomy positioning can directly or indirectly injure the LFCN.[94] [111] [112] In such cases, retractors or hematomas in the psoas muscle may further exacerbate compression.

Thus, MP represents a multifactorial neuropathy with a broad spectrum of intrinsic and extrinsic etiological factors. Recognition of these mechanisms is fundamental for both diagnosis and prevention in high-risk populations.

Clinical Presentation

MP typically presents as a constellation of neuropathic sensory symptoms localized to the anterolateral thigh. Patients often describe unpleasant sensations such as burning, tingling, stabbing pain, numbness, or a sensation of vibration (“cell phone buzz”).[1] [4] [113] [114]

Symptoms are frequently exacerbated by prolonged standing or walking, particularly at the level of the inguinal ligament, whereas sitting may relieve discomfort. However, in some cases, sitting itself worsens symptoms.[85] The lateral aspect of the thigh is the most affected region, followed by the anterior thigh.[115]

MP is usually unilateral, but bilateral involvement has been reported in 10–20% of patients.[26] [105] [115] [116] [117] Symptoms are purely sensory, without associated motor deficits, distinguishing MP from other neuropathies or radiculopathies.

Differential Diagnosis

In some cases, MP may represent a diagnosis of exclusion due to overlapping symptomatology with other neurological and musculoskeletal disorders.[4] [29] [85] [113] [118] [119] The hallmark is localized sensory disturbance over the anterolateral thigh, in the absence of back pain, motor weakness, or reflex changes. Delays in diagnosis of several months to years are not uncommon.

Important differential diagnoses include:

1. Lumbar Radiculopathy. Patients with lumbar radiculopathy usually present with low back pain, often accompanied by motor weakness, reflex changes, and sensory deficits extending below the knee. In contrast, MP produces isolated sensory changes confined to the LFCN distribution without spinal symptoms. When the two conditions coexist, diagnostic uncertainty increases.[30] [118] [120] [121] [122]

2. Trochanteric Bursitis. This painful hip girdle disorder produces diffuse pain around the buttock and lateral thigh, often mimicking MP. However, pain from bursitis typically improves after local anesthetic injection into the bursa.[123]

3. Femoroacetabular Impingement (FAI). FAI is a frequent cause of anterior hip pain, which may be mistaken for MP. Clinical examination reveals tenderness along the anterior hip joint line, with pain provoked by hip flexion, adduction, and internal rotation (FADIR test) or flexion, abduction, and external rotation (FABER test). Unlike MP, FAI does not involve cutaneous sensory changes.[124]

4. Femoral Neuropathy. Although femoral neuropathy may cause pain radiating along the anterior thigh, its etiology differs, often related to abdominal surgery, iatrogenic trauma during hip or pelvic surgery, lithotomy positioning, or local ischemia. In diabetic femoral neuropathy, a history of diabetes mellitus is typically present. Importantly, femoral neuropathy produces motor weakness and reflex changes, absent in MP.

Complementary Examinations

The diagnosis of MP is primarily clinical, supported by history and physical examination findings.[28] [31] [32] Most patients show no motor or reflex abnormalities, though localized hypoesthesia or alopecia may be observed in the distribution of the LFCN. Laboratory testing for diabetes mellitus and thyroid dysfunction may be warranted to exclude metabolic causes.[1]

Clinical Tests

Several bedside maneuvers have been proposed to support the diagnosis:

1. Tinel's Sign at the Inguinal Ligament: Percussion or pressure over the inguinal ligament, medial and inferior to the ASIS, or extension of the thigh may reproduce or aggravate paresthesias.[33] [85]

2. Neurodynamic Tests: With the patient supine, the examiner stabilizes the pelvis cranially and flexes the knee with hip adduction to the LFCN. Reproduction of symptoms indicates a positive test.[85]

3. Pelvic Compression Test: With the patient in the lateral decubitus position, the examiner applies downward compression on the pelvis for ∼45 seconds. Symptom relief occurs because the inguinal ligament slackens. Reported sensitivity and specificity are 95% and 93%, respectively.[30] [32] [34]

4. Diagnostic Nerve Block: Injection of lidocaine near the ASIS, 1 cm medial and inferior to the ligament or at the site of maximal tenderness, may yield immediate temporary pain relief, confirming the diagnosis.[31] [34] [89] [125]

Imaging Modalities

1. Ultrasonography (US): High-resolution ultrasonography has become a valuable tool for the diagnosis of MP. Findings include hypoechogenicity, abrupt caliber change, indistinct perineurium, increased intraneural vascularity, or enlargement of cross-sectional area.[1] [9] [32] [35] [36] [37] [38] [39] [40] US can also reveal underlying mechanical causes of entrapment and guide targeted nerve blocks.[35] [41] [42] [43] [44] [45] [46] [47]

2. Magnetic Resonance Neurography (MRN): MR neurography provides accurate and reproducible evaluation of the LFCN, detecting increased signal intensity, caliber changes, and course abnormalities. It is considered a reliable adjunct in atypical or complex cases.[29] [48] [49] [50]

3. Electrophysiological Studies: Electromyography (EMG) and nerve conduction studies (NCS) can help differentiate MP from lumbar radiculopathy or femoral neuropathy and may provide prognostic insights.[51] [126] [127] These tests are particularly useful in cases where clinical diagnosis is uncertain.

Treatment

MP may represent a challenging condition to manage, and therapeutic options range from conservative measures to invasive surgical procedures. While many cases resolve spontaneously or with simple interventions, a subset of patients requires more advanced treatment.[66] [85] [113]

Conservative Treatment

Conservative management is recommended as the first-line approach for MP.[52] [113] Spontaneous resolution occurs in up to 85% of cases,[53] [54] and other authors have also demonstrated high efficacy of conservative measures.[47] [55] [125]

General measures include:

• Weight reduction in obese patients.

• Avoidance of tight clothing, belts, or corsets.

• Protection of the affected region.

• Abdominal muscle strengthening.

• Physical therapy.

Pharmacological therapy:

• Neuropathic pain agents: pregabalin, gabapentin, or tricyclic antidepressants.

• Topical agents: lidocaine patches, capsaicin patches.

• Analgesics: tramadol or nonsteroidal anti-inflammatory drugs (NSAIDs).[52] [56] [57] [58] NSAIDs are primarily used for acute pain and for a short duration, given their side effects.

• Other drugs: cannabinoids, antiepileptics, and antidepressants have been investigated but showed inconclusive benefit in MP.[59]

Physical therapy aims at:

• Pain reduction.

• Improving range of motion.

• Manual therapy.

• Functional training.

• Patient education.

Infiltration with corticosteroids: Local steroid injection around the LFCN has shown important short-term benefits in reducing pain and improving function.[60] [61] [62] [63] Ultrasound-guided perineural injections have further improved accuracy and outcomes, with multiple reports supporting their efficacy.[43] [44] [46] [64] [65]

Interventional Treatments

For refractory cases, interventional pain techniques have been employed.

• Pulsed radiofrequency (PRF) lesioning of the LFCN has demonstrated promising results in retrospective studies.[54] [67] [70] Although evidence remains limited, PRF may be considered in cases of chronic, refractory neuropathic pain.

• Radiofrequency ablation has been reported with favorable outcomes in select patients.[68] [69]

• Peripheral nerve stimulation (PNS): This modality has shown benefit in multiple neuropathic pain syndromes, including MP, improving both pain and functional outcomes.[60] [71] [72] PNS can be performed under local anesthesia, does not necessarily require permanent implants, and avoids more invasive surgical procedures.[66]

• Other approaches: acupuncture and kinesio-taping performed by trained specialists have shown encouraging results as complementary therapies for pain control and functional improvement.[128] [129] [130]

Surgical Treatment

Surgical management is indicated when conservative and interventional therapies fail, or when symptoms are severe and disabling.[5] [53] The two principal surgical procedures are:

1. Neurolysis: decompression of the LFCN at the inguinal ligament.

2. Neurectomy: transection of the nerve.

Both techniques have demonstrated efficacy in improving symptoms.[2] [13] [42] [53]

• Neurolysis is often favored as the initial surgical procedure, as it preserves sensory function and avoids the risk of deafferentation pain associated with neurectomy.[15] [75]

• Neurectomy, however, has been reported to provide higher rates of long-term pain relief, particularly in iatrogenic MP.[2] [76] [77]

Other surgical options include nerve transposition, considered a technical variation of neurolysis, with favorable results reported.[73] [74]

Comparative studies:

• De Ruiter et al.[76] [77] compared neurolysis versus neurectomy and found both effective, but with slightly higher success rates in neurectomy.

• Khalil et al.[15] reported similar outcomes with both procedures.

• Other authors have suggested that neurectomy may provide more definitive relief but at the cost of permanent numbness.[55] [78] [79] [80] [81] [82]

Indications and contraindications: According to Finerty et al. [9], surgical treatment should be considered in:

• Patients with failed conservative management.

• Individuals with abdominal obesity.

• Patients with MP symptoms following anterior hip surgery or arthroscopy.

Relative contraindications include:

1. Concomitant lumbar radiculopathy or imaging evidence of nerve root compression.

2. Intraperitoneal or intrapelvic masses compressing the proximal LFCN, in which case distal neurectomy may be ineffective.

Berini et al.[83] emphasized that patients with chronic, intractable MP benefit most from neurectomy at the inguinal ligament compression site.

Despite multiple comparative studies, the optimal surgical approach remains debated, with no definitive consensus.[2] [85]

Conclusion

MP is a sensory mononeuropathy of the lateral femoral cutaneous nerve that is most often diagnosed clinically within the spectrum of nerve compression syndromes. Although frequently benign and self-limiting, MP may cause significant disability and reduction in quality of life.

Most patients respond well to conservative measures, while refractory cases may benefit from image-guided nerve blocks, interventional pain procedures, or surgical options. To date, there is no clear consensus on the optimal surgical strategy, with both neurolysis and neurectomy showing favorable outcomes.

High-quality, prospective studies are still needed to refine diagnostic pathways, establish evidence-based treatment algorithms, and improve the overall management of this condition.

Conflicts of Interest

The authors declare no conflicts of interest.

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Publikationsverlauf

Eingereicht: 17. September 2025

Angenommen: 10. November 2025

Artikel online veröffentlicht:
29. Dezember 2025