Meralgia Paresthetica Successfully Treated with Palmithoylethanolamide

| July 1, 2020

by Rocco Salvatore Calabrò MD, PhD; Carmela Casella, MD;  Alfredo Manuli, MSc; David Militi, MD; and Giuseppe Gervasi, MD, PhD

Drs. Calabrò and Manuli are with IRCCS Centro Neurolesi “Bonino Pulejo” in Messina, Italy. Dr. Casella is with Policlinico University in Messina, Italy. Dr. Militi is with Stomato-dental Laboratory in Messina, Italy. Dr. Gervasi is with the Hygiene and Preventive Medicine Department at the University of Tor Vergata in Rome, Italy.

FUNDING: No funding was provided for this study.

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


ABSTRACT: Meralgia paresthetica (MP) is an uncommon entrapment mononeuropathy that is characterized by a sudden onset of paresthesia and numbness in the anterolateral surface of the thigh. Palmithoylethanolamide (PEA) is commonly used in the treatment of chronic pelvic pain and compressive neuropathies. Herein, we describe an otherwise healthy 28-year-old patient affected by posttraumatic MP for three months who was successfully treated with PEA (1200mg/day). Further studies are needed to better investigate the potential use of PEA as therapeutic drug in peripheral neuropathies, including MP, to avoid or delay more invasive surgical treatments.

Keywords: Polyneuropathy, nutraceuticals, inflammation

Innov Clin Neurosci. 2020;17(7–9):10–11


Meralgia paresthetica (MP) is an uncommon entrapment mononeuropathy characterized by a sudden onset of paresthesia and numbness in the anterolateral surface of the thigh. The main pathophysiological feature of MP is compression of lateral femoral cutaneous nerve (LFCN) as it exits the pelvis.1 Spontaneous recovery and conservative measures are the main therapeutic strategies in MP management, especially when the compression is related to increased intra-abdominal pressure.2

Palmithoylethanolamide (PEA) is an endogenous fatty acid amide analogue of endocannabinoid anandamide, which acts as a lipid mediator. It is commonly used as a nutritional supplement for specific medical conditions.3 In Italy, it is approved for the treatment of chronic pelvic pain and as an adjuvant treatment for neuropathies caused by endoneural edema. Here we describe a case of MP successfully treated with PEA.

Case Description 

An otherwise healthy 28-year-old male patient presented to our facility with persistent paresthesia in the lower limb. He reported a troublesome tingling and itch-like sensation on the anterolateral surface of the right thigh that had been present for 10 months. The patient had no history of neoplastic or metabolic illness (including diabetes). He reported being in a car accident, without any evidence of major trauma or medical consequences, prior to our evaluation. He reported wearing his seatbelt at the time of the accident. His general examination was normal, except for being mildly overweight (body mass index [BMI]=28kg/m2). Neurological examination, lumbosacral spinal cord computed tomography (CT), lower limb EMG (electromyography), and pelvic CT imaging were normal. Taking into account the medical history, including the car accident, and clinical examination, a diagnosis of MP was made. The patient was prescribed PEA up to 1200mg/day. At the one-month follow-up visit, the patient reported progressive improvement in his symptoms, with  complete resolution at the six-month follow-up visit.

Discussion

MP is a clinical syndrome caused by peripheral damage to LFCN, initially known as Bernhardt-Roth Syndrome.1 Typically, MP is divided into either spontaneous or iatrogenic, according to the underlying physiopathological process. The most common cause of spontaneous MP is the entrapment of LFCN or a compression process. Predisposing factors include medical conditions that cause an increase in intraabdominal pressure (e.g., overweight/obesity, pregnancy).1,2 Spontaneous cases of MP are related to peripheral C and A-delta nervous fiber damage of LFNC, which are responsible for pain and tingling symptoms, respectively.2

Nerve block with corticosteroid local infiltration and the option of surgery on the inguinal ligament are the main therapeutic strategies for spontaneous MP.  However, conservative measures with antiflammatory drugs or analgesic treatment (e.g., amtriptiline, phenytoine, carbamazepine, opioids) are effective optional strategies, given that MP might present a spontaneous recovery.2 Conservative therapeutic strategies are particularly important for pain and paraesthesia management.1,2

In our patient, MP was probably related to nerve compression caused by both the car accident and being overweight. The presence of overweight could cause increased intrabdominal pressure that produces permanent mechanical stress on the LFNC.1 The mild compression of the seat belt during the car accident may have been amplified by our patient’s excess weight.

Because the patient had been experiencing symptoms of MP for 10 months prior to visiting our clinic, we did not believe his MP would go into spontaneous remission, as many patients do. Thus, we decided to treat the patient with PEA based on its demonstrated efficacy for treatment of various pain conditions, including peripheral nerve disorders with inflammatory processes.1,4,5

PEA is thought to act on receptors located in the nociceptive pathway (e.g., cannabinoid receptor CB1, transient receptor potential channel of the vanilloid type 1 [TRPV1], peroxisome proliferator-activated receptor γ [PPARγ]) via an “entorouge effect,” as well as a more direct action on an exclusive target, namely the mast cells via an ALIA (autacoid local injury antagonism) mechanism.5

Tingling is a benign but troublesome symptom of MP, with a typically slow recovery following resolution of compression resolution for one year, plausibly due to LFNC damage caused by a demyelinating process of A-delta fibers.1 Recently, a neuroprotective role of PEA in demyelinating disorders has been described.3 Although the molecular target has not yet been clarified, PEA administration could compensate or amplify endogenous mechanisms to counteract neurodegenerative and neuro-inflammatory process.1–4

Paresthesia is another important symptom of peripheral nerve compression. Physical and mental impairments (as per 36-Item Short Form Survey [SF-36] score) in subjects with this symptom have both been described, with quick improvements in quality of life following surgical treatment of the entrapment.2 To this end, the potential absence of adverse events could support the routine clinical use of PEA in relieving pain due to nerve compression.

Conclusion 

PEA, an endogenous mediator, could potentially offer protection against neuropathic pain and be a valuable alternative to the most common used treatments in MP. However, further studies are needed to better investigate the potential use of PEA as a therapeutic drug in pheripheral neuropathies, including MP.

References

  1. Harney D, Patijn J. Meralgia paresthetica: diagnosis and management strategies. Pain Med. 2007;8:669–677
  2. Khalil N, Nicotra A, Rakowicz W. Treatment for meralgia paraesthetica. Cochrane Database Syst Rev. 2012;12:CD004159.
  3. Petrosino S, Di Marzo V. The pharmacology of palmitoylethanolamide and first data on the therapeutic efficacy of some of its new formulations. Br J Pharmacol. 2017;174:1349–1365.
  4. Calabrò RS, Gervasi G, Marino S, et al. Misdiagnosed chronic pelvic pain: pudendal neuralgia responding to a novel use of palmitoylethanolamide. Pain Med. 2010;11:781–784.
  5. Aloe L, Leon A, Levi-Montalcini R. A proposed autacoid mechanism controlling mastocyte behaviour. Agents Actions. 1993;39(Spec No):C145–147.

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Category: Case Report, Current Issue, Neurology

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