Extended pulsed radiofrequency as a part of multimodal pain management in a refractory case of Bernhardt-Roth syndrome

Discussion

LFCN is a pure sensory nerve that can originate from L2 to L3 or L3 alone. This nerve is susceptible to compression as it traverses down the lumbar plexus, through the abdominal cavity, under the inguinal ligament and into the subcutaneous tissue in thigh, resulting into BRS (figure 1). The possible aetiologies can be mechanical, iatrogenic, metabolic, neuropathic or idiopathic. The risk factors associated are tight belts, corset, trousers, obesity, diabetes and pregnany.2 The incidence rate of BRS has been found to be 7.5-fold higher in the diabetic population as compared with general population.3 The aetiology in a diabetic patient is proposed by myo-inositol-dependent protein kinase C agonist deficiency in diabetic nerve, which regulates the Na⁺K⁺-ATPase. Another theory postulated is an increased swelling of the LFCN in diabetics due to reduced axoplasmic transport, making it more susceptible to compression.4 Elaborate workup is essential to rule out the various differentials for BRS, namely lumbar radiculopathy, pelvic mass compressing the nerve, femoroacetabular impingement, iliac crest malignancy, avulsion fracture of the anterior superior iliac spine and trochanteric bursitis.5 We also performed an elaborate biochemical evaluation and ruled out abnormal thyroid function, vitamin B12, folate deficiency and anaemia. HbA1C was 8.4 in our patient signifying poorly controlled diabetes. First line of approach is always to treat the underlying cause like losing weight, not wearing tight belts, and in our case, good glycaemic control. After endocrine consultation, his medication was changed to metformin 1000 mg two times per day with vildagliptin 25 mg two times per day. Medical nutrition therapy, exercise and pharmacotherapy resulted in good glycaemic control in subsequent blood sugar charting. The other treatments include physiotherapy, pharmacotherapy like non-steroidal anti-inflammatory drugs, anticonvulsants, antidepressants, LFCN blocks, PRF and surgery. Pain has been found to be refractory to oral pharmacotherapy in 10%–15% of these patients.6 PRF is employed once the conservative management for neuropathic pain fails. It uses radiofrequency current in high-voltage, short pulses of 20 ms followed by a silent phase, conventionally performed for 120 s while keeping the maximum tissue temperature below 42°C.7 There have been previous documentations of use of extended PRF ranging from 5 to 10 min for genicular nerve, gasserian ganglion, trigeminal nerve and saphenous nerve, which stated that prolonging the duration of PRF resulted into considerable analgesia without any adverse effects.8 9 However, after extensive research, we could only find a single case series by Ghai et al, regarding successful use of extended PRF for treatment of LFCN compressive neuropathic pain. Employing 8 min of PRF, they found good pain relief on follow-up period of 2 years without any complication.10 We, in concurrence to their finding, got significant analgesia with extended PRF in our patient who was refractory to all other therapies. The surgical management in such a case includes constriction tissue neurolysis, neurolysis with transposition of the LFCN and transection with excision of LFCN segment.2 To the best of our knowledge, this is one of the rare documentations of pain management in a diabetic patient of BRS with successful extended PRF. However, larger-scale research needs to be carried out to establish the validity, efficacy and safety of extended PRF in refractory neuropathic pain.