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Meralgia Paresthetica in Patients with Obesity

| April 1, 2016

This column is written by medical students and is dedicated to reviewing the science behind obesity and bariatric surgery.

Column Editor: Daniel B. Jones, MD, MS, FASMBS
Professor of Surgery, Harvard Medical School, Vice Chair, Beth Israel Deaconess Medical Center, Boston, Massachusetts

This month: Meralgia Paresthetica in Patients with Obesity

by David J. Lee
Medical Student, Harvard Medical School, Boston, Massachusetts

Meralgia paresthetica is a mononeuropathy due to entrapment of the lateral femoral cutaneous nerve (LFCN) and disproportionately affects obese individuals. Compression of the LFCN most commonly occurs where the nerve passes through the inguinal ligament; however, anatomic variations have been reported. Patients experience dysesthesias, yet meralgia paresthetica is often underdiagnosed. While the mechanism remains unclear in bariatric patients, meralgia paresthetica is postulated to occur due to mechanical nerve compression in anatomically predisposed patients. Research also suggests that diabetes mellitus, a common comorbid condition of obesity, also has an etiological role. Conservative treatment includes weight reduction and repetitive nerve blocks, while surgical approaches of decompressing or sectioning the LFCN are reserved for severe, chronic cases. With greater awareness, clinicians may effectively address symptoms and facilitate a favorable outcome for this underdiagnosed condition.

Bariatric Times. 2016;13(4):14–17.

The lateral femoral cutaneous nerve (LFCN) is a purely sensory nerve branch of the lumbar plexus to innervate the skin at the antero-lateral aspect of the thigh. Entrapment of this nerve often occurs at its pelvic exit site, where the nerve passes under the inguinal ligament just medially to the anterior iliac process and pierces the fascia lata. Compression at this location causes distinct dysesthesia in the distribution of that nerve. This condition has been termed Bernhardt-Roth syndrome for Martin Bernhardt (1844–1915), a German neuropathologist who first depicted this condition in 1878,[1] and Vladimir Karlovich Roth (1848–1916), a distinguished Russian neurologist who in 1895 named the syndrome meralgia paresthetica (MP) from the Greek words meros, meaning “limb,” and algos, meaning “pain.”[2,3]

Patients with MP experience symptoms ranging from numbness and tingling (hypesthesia) to burning pain (paresthesia) in the anterolateral thigh, often limiting sleep and daily activities.[4]  Or, in the words of Sigmund Freud, who in the same year that Roth had coined the term, described its symptoms in self-observation as a “furry sensation, a feeling of ‘alien skin,’ usually almost imperceptible at rest but exacerbated by walking, and also frequently accompanied by a painful short pricking at right angles to the skin surface, as well as a disagreeable sensitivity to the rubbing of underclothes ….”[5]

The association of MP with obesity has been frequently recorded in the literature and is also often cited as a possible neurologic complication of bariatric surgery.[6,7] Incidence of MP is highest in individuals with overweight between 40 and 60 years of age with a male predominance. Rates have also uptrended in recent years as the population continues to age and become afflicted with obesity.[4,8] Furthermore, in one study, the incidence of MP among individuals with type 2 diabetes mellitus (T2DM), a common comorbid condition of obesity, is seven times the incidence of MP in the general population (247 vs. 32.6 per 100,000 patient years, respectively).[4] At the same time, due to the nonspecific nature of symptoms, MP is often a missed or underdiagnosed problem.[2,9,10]

This article reviews the latest literature in the etiology, diagnosis, and management of MP, providing a practical guide for bariatric surgeons caring for patients with obesity with this neurological disorder.

Anatomic Characteristics
The lateral femoral cutaneous nerve (LFCN) is part of the lumbar plexus and usually originates from the spinal nerve roots of L2 and L3 (sometimes also L1) and forms a distinct nerve at the level of the psoas muscle, where it emerges laterally to cross the iliac muscle between its fascial layers before it leaves the pelvis near the anterior superior iliac spine (ASIS). On its way, the nerve passes under the tendineous fibers of the inguinal ligament (IL) laterally in the lacuna musculorum and shifts then from a horizontal to a more vertical course while passing under the IL through a small opening in the lateral attachment of the IL to the ASIS. The nerve subsequently enters and courses through subcutaneous tissues of the thigh, dividing into its anterior and posterior branches about 10cm below the ASIS, innervating the anterolateral and posterolateral skin of the thigh, respectively.[2,10]

Entrapment (Figure 1) commonly occurs where the LFCN passes through the inguinal ligament where the LFCN bends at an angle about 90 degrees.[2,11] However, several case reports have shown that nerve entrapment may occur distal to the inguinal ligament, such as at the insertion site of the fascia lata of the thigh or the sartorius muscle.[11–13] Upon entrapment, irritation, friction, and tension occur along the entire nerve course that is worsened with adduction of the thigh. Pseudoganglions may eventually form in the nerve, also resulting in MP.[2]

MP may also occur from proximal compression (e.g., by retroperitoneal hematomas or tumors), but this is rare. It has occasionally been observed following iliac bone graft harvesting, pelvic surgery via an ilioinguinal approach, laparoscopic appendectomy, femoral artery catheterization, and hip or lumbar spinal surgery in the prone position. Furthermore, entrapment can be caused by tight clothing or seatbelts, long-distance walking, or certain sports that require forward-bent positions like cycling.[14]

The exact reason for LFCN entrapment in patients who have undergone bariatric surgery specifically remains unclear, however. While other mononeuropathies often occur after bariatric surgery due to losing the fat pad that protects the nerve from compression, MP occurs too soon post-surgery (e.g., as early as within 48 hours) for rapid weight loss to be its mechanism.[2,15] Furthermore, while it has been proposed that LFCN compression occurs due to the use of the Gomez abdominal retractor during bariatric surgeries,16 MP has also been observed when this device was not used.[2] Hence, it is likely that LFCN entrapment in MP may be due to mechanical compression from obesity itself.[15]

Since not all patients with obesity have MP, anatomic variations in the course of the LFCN may predispose some patients to nerve compression from pannicular traction on the inguinal ligament. Ghent described four predisposing anatomic variants: 1) the classical “split” ligament (i.e., LFCN passing through rather than deep to the inguinal ligament), 2) the “bow-string” deformation of the LFCN where it crosses the iliacus fascia, 3) passing of the LFCN through the sartorius, and 4) passing of the LFCN postero-laterally to ASIS.2,17 Since then, cadaveric investigations have revealed five distinct anatomic variants (Table 1), which may predispose the nerve to compression in certain positions, such as hip flexion (e.g., lithotomy position) and recumbence (e.g., as needed for an operation performed with the patient supine).[18]

Patients with obesity may also incur MP more frequently due to T2DM. MP has interestingly been suspected to be a preclinical expression of T2DM since MP tends to develop before T2DM manifests clinically.[4] Chronic hyperglycemia and inflammation may be underlying mechanisms, with inflammation possibly playing a role even in non-diabetic patients.[2,19] Magnetic resonance imaging (MRI) may prove helpful in future studies differentiating between inflammatory versus mechanical etiologies of MP.[20]

An evaluation of MP in a patient with obesity begins with a careful history and physical, most importantly ruling out other similarly presenting conditions in the differential diagnosis, such as lumbar disc herniation and metastasis in the iliac crest.
MP patients present with reports of pain, numbness, itching, or tingling in the thigh. Paresthesias or dysesthesias of abnormal light touch and pinprick on the anterolateral thigh may be present on exam. Such signs and symptoms may be exacerbated with hip extension or prolonged standing. Comparably to Tinel’s sign, palpation of the lateral inguinal ligament may also produce pain and paresthesias. Hair loss in the dermatomal LFCN area may be observed in patients who constantly rub this region.

However, patients will have a negative straight leg raise and show no tenderness over the sciatic notch.[7,21,22]

Additional testing may aid in the diagnosis of MP. Electrophysiologic tests have been used for diagnosing MP and include sensory nerve conduction velocity and somatosensory-evoked potentials.[22,23] However, these methods are considered superfluous by most neurologists and experienced physicians given the distinct presentation of this syndrome. Conduction studies have also been reported to be limited in individuals with obesity due to difficulty in measuring sensory nerve action potentials through adipose tissue. Lately, however, an ultrasound-guided technique of surface electrode placement has been shown to aid in eliciting action potentials.[24] In addition, some clinicians conduct a nerve block test of the LFCN with 8 mL of bupivacaine 0.25%, which can confirm a diagnosis of MP if the patient experiences symptomatic relief post-injection.[7,22,25]

Initial approaches should be aimed toward weight reduction, the underlying cause in patients with obesity. Patients with persistent pain have been successfully treated with repetitive nerve blocks, which have been postulated to reduce the hyperexcitability of neurons and c-fibers, thus allowing a break in the afferent-efferent loop at the spinal segmental level.[22,25,26] Anticonvulsants, tricyclic antidepressants, or antiarrhythmics may also be helpful for persistent pain, and topical lidocaine or capsaicin for epidermal dysesthesia.[21] With such conservative management, one report shows that 85 percent of patients experience a resolution of symptoms within 10 weeks of initiating treatment.[25]

Surgical options include decompression or sectioning of the LFCN; however, these are rarely necessary and reserved for severe, chronic cases of MP. Ivins suggests the following criteria: 1) Adults with less than 1 year of symptoms and all pediatric patients should undergo simple decompression; 2) patients in the first group who have persistent or recurrent symptoms should be considered for resection; 3) adult patients with symptoms present more than one year should be considered for primary resection.[27] Resection will result in an area of permanent painless numbness within the territory of the nerve, but no weakness or disabling feature should occur.[28]

Less invasive interventional options include pulsed radiofrequency treatment or spinal cord stimulation, both of which have been documented to be effective for MP refractory to conservative treatment with minimal to no complications.[21]

MP is not a rare disease and disproportionately affects bariatric patients. MP likely occurs due to mechanical compression from obesity in individuals who are anatomically predisposed. T2DM, a common comorbid condition, also seems to play an etiological role via inflammatory and hyperglycemic mechanisms. Though MP patients may be difficult to diagnose due to vague signs and symptoms, the great majority of patients recover with conservative treatment. With greater awareness of this disease, therefore, clinicians may facilitate more favorable outcomes.

Mr. Lee would like to thank Ekkehard Kasper, MD, PhD, for his assistance with reviewing this article. Dr. Kasper is on staff in Neurosurgery at Beth Israel Deaconess Medical Center (BIDMC ) and as such is Co-Director of the Brain Tumor Center at BIDMC, Director of Neurosurgical Oncology and Program Director in the BIDMC Cancer Center, and Co-Director of the CyberKnife Center. He also serves as Associate Professor at Harvard Medical School, Boston, Massachusetts.

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FUNDING: No funding was provided.

FINANCIAL DISCLOSURES: The author reports no conflicts of interest relevant to the content of this article.

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