Meralgia Paresthetica: A 5 Model Osteopathic Approach

Martin Torrents, DO, MPH, MBA | martin.torrents@touro.edu

AUTHOR DISCLOSURES:

No relevant financial affiliations.

INTRODUCTION

Meralgia paresthetica (MP) is the diagnostic term given to a patient presenting with a mononeuropathy of the lateral femoral cutaneous nerve (LFCN) and typically presents with numbness, tingling, paresthesias, or any other sign of nerve impingement along the anterior and lateral thigh. It is specifically due to compression of this nerve as it passes over the anterior superior iliac spine and then under the inguinal canal at the lateral end as it progresses. It may be more commonly seen in individuals who are obese, have diabetes, or wear their pants too tight at the waist. Presenting clinical signs and symptoms may be sufficient for obtaining the diagnosis, however, electrodiagnostic studies may be useful in confirming the diagnosis and quantifying the degree of nerve involvement.1 Treatment can vary from activity modification and a holistic approach to TENS unit applications, analgesics and local and/or systemic anti-inflammatories. Surgical interventions with neurolysis or neurectomies for those with significant weakness and atrophy or focal conduction blocks on electrodiagnostic examinations have also been used as treatment modalities.2 Given that this condition can be considered an inflammatory mononeuropathy based on its clinical presentation, relieving compression of the nerve along its course with osteopathic manipulation and behavioral modifications can provide symptomatic relief and restore normal functioning of the lateral femoral cutaneous nerve.

MP typically occurs in patients ranging from 30 to 60 years of age and has an approximate incidence of 4-10/10,000 people.3 The age group of 55-64 years old had the highest incidence of MP in both men and women.1 It is estimated that the actual incidence may be a little higher due to under-reporting of symptoms and physicians attributing MP to other causes of hip and/or thigh pain. The incidence rates are similar between men and women, ruling out gender as a determinant.

In addition to these factors, there are several behavioral and genetic causes that can contribute to the symptoms of MP. Consistent use of tight belts, tight sweat pants, corsets, or body armor have been associated with the development of symptoms of MP.4,5 It is suspected that any extra added weight applied to the waist belt can also contribute (i.e. keys, cell phone/pager holders, gun holsters, etc.). Chronic repetitive positioning of the lower extremity in an extended or externally rotated position may also impinge on the nerve. MP as a post-op complication after orthopedic hip surgery, hernia repairs, or being in a prone position during surgery has also been noted.6,7 In addition, pelvic crush fractures and pelvic osteotomies have also been linked with the prevalence of MP.7 Among common genetic causes, patients with diabetes mellitus type 2 (DMT2) are seven times more likely to develop MP and there is a strong association of MP as a precursor to DMT2.1 Obesity, pregnancy, and increased BMI have been associated with MP due to increased abdominal girth.1,8 Other causes of MP include benign pelvic masses, tumors along the iliac crests, and osteoid sarcomas.7

ETIOLOGY

A mononeuropathy of the lateral femoral cutaneous nerve (LCFN) is what brings about the symptoms of MP. Originating from the L2 and L3 spinal nerves, the lateral femoral cutaneous nerve enters the pelvic cavity lateral to the psoas muscle. It continues towards the ASIS over the iliacus muscle. Many variants can be found for its path as it makes a right angle to exit the pelvic cavity above, below, or through the inguinal canal. Whichever course it takes, it is usually within 5cm of the ASIS. Therefore, it passes through the lacuna muscularis, a passageway inferior to the inguinal canal that takes the nerve to the sartorius muscle. In this passageway it may travel along the iliopsoas muscle, which, if in a contracted state, may compress some nerve fibers. After passing this location, the nerve passes superficially over the sartorius muscle and branches into the anterior and posterior branches (Figure 1). There is also a common variant of the nerve piercing though the sartorius muscle. The anterior branch continues deep to the tensor fascia lata for about 5-10 cm down the lateral thigh and then pierces the fascia to become subcutaneous, where it may be subjected to mechanical stress. The lateral femoral cutaneous nerve takes a long and complicated pathway, which presents many opportunities for the nerve to become entrapped. As with any nerve, prolonged chronic repetitive trauma may lead to trophic changes of the skin, neuropathic pain, and underlying tissue changes.

FIGURE 1:

Anatomy of LCFN and Cutaneous Sensory Distribution

 

There are several pathological changes that may affect the LFCN under prolonged compression or entrapment. In addition to the disordered orientation of nerve fiber bundles intermixed with increased connective tissue components that can be present in compression neuropathies,9,10 an autopsy study of 12 nerves revealed that the LFCN demonstrated local demyelination and Wallerian degeneration. Greater relevance for this case were the additional findings of endoneurial vascular changes and polarized internodal swellings suggesting that mechanical factors are responsible for the symptoms of MP.10,11,12

These findings suggest that an osteopathic structural exam on the patient with MP should be considered an essential component of the physical examination in order to identify areas of mechanical compression on the LFCN by means of somatic dysfunctions of the lumbar spine, pelvis, sacrum, and lower extremities.

Osteopathic exam findings were consistent with the following: bilateral hypertonicity to the psoas muscles right sided more severe than left, L2 flexed, rotated, and sidebent right, positive ASIS compression test on right with innominate findings consistent with a posteriorly rotated and out-flared pelvis. A restriction in excursion of the right hemidiaphragm was noted during the inspiratory phase of thoracic respiration. In addition, a chronically hypertrophied tensor fascia lata muscle with tenderness to palpation and a taut iliotibial band were also noted on her right.

For the right out-flared innominate dysfunction: The patient laid supine while the physician stood on the left side of the table. The patient’s right hip and knee were flexed to approximately 75 degrees and the right foot was positioned just lateral to the left knee. The physician’s cephalad hand was placed under the patient’s right innominate, grasping the medial aspect of the right PSIS. The physician’s caudad hand was placed on the patient’s right knee and adducted it until the edge of the restrictive barrier was reached (Figure 3). The physician instructed the patient to abduct the right hip while the physician applied an equal counterforce. This isometric contraction was maintained for 3-5 seconds, then the patient was instructed to stop and relax. Once the patient completely relaxed, the physician further adducted the patient’s right knee to the edge of the new restrictive barrier and drew traction laterally on the right PSIS. Three to five repetitions of these directions were performed after which reassessment of the area was indicated.15

FIGURE 2:

Posterior Innominate Muscle Energy

 

FIGURE 3:

Outflare Innominate Muscle Energy

 

FIGURE 4:

Lumbar Spine Muscle Energy

 

FIGURE 5:

Diaphragmatic Lift Technique

 

FIGURE 6:

Peripheral Nerve OMT of LFCN

 

FIGURE 7:

Peripheral Nerve OMT of LCFN Perforating Branches

 

G. Sutherland, an original student of the founder of osteopathic medicine, Dr. Andrew T. Still, described a diaphragmatic lift technique in which the ultimate goal would be to “draw the diaphragm cranially, elevating the floor of the thorax, drawing upward on the abdominal contents, promoting venous and lymphatic drainage from the lower half of the body.”17 Based on his description of this technique, the physician can stand on the side that is easiest for them facing the patient. Then the physician’s thumbs were placed right inferior to the sternum at the costosternal junctions while the rest of the fingers were spread around the lateral edges of the ribs towards the patient’s head. A cephalad and lateral lift is then exerted by the physician, lifting the diaphragm. The patient was instructed to exhale while the physician continued to lift the diaphragm in a cephalad and lateral direction. Tension was maintained and held while the patient inspired and was slightly increased during exhalation (Figure 5). Concomitantly, the patient was instructed to exhale immediately after inhaling and to not hold the breath in, while the physician continued to engage new barriers with cephalad and lateral tractions. Finally, when no more advancement of fingers were noted, the patient was told to rapidly exhale, while simultaneously doing the valsalva maneuver (closing throat and increasing intrathoracic pressure) and expanding her chest.

FIGURE 8:

Standing Psoas and Achilles Stretch

 

Osteopathic structural evaluation at follow-up was only significant for a restricted right pelvic diaphragm which was not evident at the initial visit. This could be a new somatic dysfunction or a compensatory mechanism after other somatic dysfunctions were treated. A simple pelvic diaphragm release was performed in a supine position, which the patient tolerated very well. The patient was instructed to continue with the exercises and stretches and to return to the office if symptoms returned, persisted, or worsened.

CONCLUSION

The etiology of MP can be one that is multifactorial, ranging from musculoskeletal dysfunctions to genetic causes. Given this wide array of causes, the treatment of MP should encompass a multifactorial approach. Utilizing the tenets of osteopathic medicine which state that “structure and function are intimately related” as well as “the body is capable of self-healing, self-regulating mechanisms” can provide the physician with an in-depth manipulative treatment rationale for MP and other mononeuropathies. In addition, once this approach is combined with a motivated patient’s willingness to partake in a home exercise program and suggested behavioral modifications for relieving compression of the nerve, a successful outcome can be obtained. Empowering the patient with responsibility for their health by use of exercises and stretches also allows application of another tenet which is “the human is a combination of mind, body and spirit” at a deeper level of self-consciousness and self-realization. An osteopathic approach can be key in treating musculoskeletal causes and modifying behavioral contributions that has been refractory to other treatment options. Although both surgical and non-surgical approaches have been shown to be effective in treating the symptoms of MP, osteopathic manipulation should also be considered before more invasive treatment modalities.

REFERENCES

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