Surgery for Meralgia Paresthetica
- Author: Ira Kornbluth, MD, MA, FAAPMR; Chief Editor: William L Jaffe, MD more...
Meralgia paresthetica is a common but underrecognized condition that is manifested by pain, numbness, and tingling in the anterior and lateral parts of the thigh. Bernhardt first described symptoms corresponding to meralgia paresthetica in 1878. In 1885, Hagar correctly suggested that lateral femoral cutaneous nerve compression was the source of this symptom complex; surgical correction of meralgia paresthetica also dates back to Hagar at this time. (See the image below.) A decade later, Roth coined the term meralgia paresthetica from the Greek words meros (thigh) and algos (pain). Anecdotally, Sigmund Freud is said to have diagnosed himself and his son with this condition.
Entrapment of the lateral femoral cutaneous nerve results in pain and sensory abnormalities in the anterolateral thigh. The lateral femoral cutaneous nerve is a pure sensory nerve that typically receives its innervation from the L2-3 lumbar nerve roots and includes sudomotor fibers. Sudomotor changes, such as mild sweating in the nerve distribution, may be evident, although this is uncommon. Because the lateral femoral cutaneous nerve is purely sensory, no associated motor or reflex findings should be present.[1, 2]
As physicians and patients become increasingly aware of meralgia paresthetica and as new medications and surgical techniques develop, the diagnosis and initiation of a treatment plan will be made more rapidly. Patients and physicians alike would benefit from an algorithm guiding diagnosis and treatment.
The lateral femoral cutaneous nerve typically arises from lumbar nerve roots, specifically those at the L2-3 levels, although the nerve can arise from different combinations of the L1-3 nerve roots. The lateral femoral cutaneous nerve pierces the psoas, travels across the iliacus toward the anterior superior iliac spine, and then enters the anterolateral thigh by passing under, through, or above the inguinal ligament.
In most individuals, the lateral femoral cutaneous nerve crosses into the anterolateral thigh approximately 1 cm medial to the anterior superior iliac spine. However, the relation of the lateral femoral cutaneous nerve to the anterior superior iliac spine is quite variable. The nerve may cross into the anterolateral thigh as much as 2 cm lateral or 6 cm medial to the anterior superior iliac spine. A bifurcation into anterior and posterior divisions occurs approximately 5-12 cm below the anterior superior iliac spine.
Cadaver dissections have demonstrated that anatomic variations are also found in the origin of the lateral femoral cutaneous nerve. As many as 30% of lateral femoral cutaneous nerves may be derived partially or entirely from adjacent genitofemoral or femoral nerves.
Along its course, the lateral femoral cutaneous nerve is vulnerable to compression at several sites. The nerve emerges from the psoas muscle, intersects with the inguinal ligament, curves around the anterior superior iliac spine, and exits from the fascia lata. Meralgia paresthetica most commonly occurs from compression of the nerve as it exits the pelvis.[3, 4]
Peripheral nerve injuries are described in terms of the nature of the insult and the associated prognosis. Thus, a compressive force results in a neuropraxic injury to the nerve, which is characterized by the loss of myelin without affecting the axon or its axonal sheath. Neuropraxic injuries have the best prognosis and may heal over hours to months, depending on the severity. Loss of the axon or its axonal sheath constitutes a more severe nerve injury and a worse prognosis for healing, because the nerve undergoes wallerian degeneration or destruction of the nerve fibers distal to the injury site.
If the injury involves only the axons and spares the axonal sheath (axonotmesis), the patient may make a full, but likely slow, recovery. If the axonal sheath is affected such that the nerve is in discontinuity (neurotmesis), then the prognosis for spontaneous recovery is poor. Most commonly, compressive forces tend to result in neuropraxic injuries, and relief of the compressive force initiates the healing process.
Metabolic conditions, such as diabetes, alcoholism, and thyroid disorders, can contribute to the development of a neuropathy in the lateral femoral cutaneous nerve and other peripheral nerves. In most instances, the etiology of meralgia paresthetica involves excessive pressure on the nerve at various sites of possible entrapment. Pressure may be from internal causes such as obesity, pregnancy, or pelvic tumors.
There is a higher incidence of obesity in patients with meralgia paresthetica, which strongly suggests that obesity is an independent risk factor. Alternatively, external causes such as tight belts worn around the waist may be identified as the culprit.[7, 8] In addition, the lateral femoral cutaneous nerve may be injured iatrogenically from local trauma during surgical procedures. Hip replacement, iliac crest bone grafting, appendectomy, inguinal lymph node dissection, aortofemoral bypass, uterine surgery, cesarean section, and quadriceps surgery have all been implicated as causative for meralgia paresthetica.
The prevalence of meralgia paresthetica has been estimated at 3 cases per 10,000 individuals, and this condition has been reported in up to 35% of patients referred for evaluation of leg discomfort. However, these symptoms are often not recognized or they may be mistaken for other conditions such as lumbar radiculopathy. In a large case series, the presumptive diagnosis by the referring physician was meralgia paresthetica in 47 of 120 patients (39%). This condition has been described in toddlers and elderly persons, but most cases occur in patients aged 30-65 years. Whether a sex predominance exists is unclear. Meralgia paresthetica is usually unilateral but may be bilateral in as many as 50% of cases.
The outcome of meralgia paresthetica depends largely on whether the diagnosis and treatment plan are achieved within a reasonable time frame. The prognosis from conservative management alone is quite good because the condition often is self-limited. In 277 patients treated conservatively by Williams and Trzil, 91% had satisfactory symptom relief. In the worst-case scenario, patients treated conservatively had persistent symptoms such as pain, numbness, burning, hyposensitivity, and tingling in the anterolateral thigh.
Controversial issues include the efficacy of surgery and the selection of a surgical procedure. van Eerten et al noted complete symptom relief in 3 of 10 patients who underwent neurolysis and in 9 of 11 patients who had a transection. Similarly, 23 of 24 patients who had a transection in Williams and Trzil's series had complete relief of their presenting symptoms. Ivins reported results for 8 patients who underwent neurolysis; 4 experienced relief of symptoms, of which 2 had recurrence of their symptoms. Siu and Chandran reported results from a case series of 45 decompressive procedures in 42 patients who underwent neurolysis: 43% reported complete relief, 40% reported partial relief, and 17% reported no relief.
Although transection is more likely to produce complete relief, it likely will cause permanent anesthesia of the anterolateral thigh.
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