Use of lateral femoral cutaneous nerve blocks by landmark technique is ineffective in decreasing narcotic usage after skin grafts: A retrospective case-control study.

INTRODUCTION: Cutaneous burns are commonly treated with autologous skin grafts. Following skin grafting, many patients complain of pain at the donor site. Donor sites are taken most commonly from the lateral thigh, which is innervated by the lateral femoral cutaneous nerve (LFCN). Use of a LFCN blocks should decrease nociception from the donor site. METHODS: Our group began utilizing LFCN blocks in 2019. Utilizing anatomic landmarks, LFCN blocks were performed on all patients who received autologous skin grafts to reduce perioperative pain. A retrospective cohort study was performed on all patients with 10% or less total body surface areas burns who received an autologous skin graft. A similar cohort from 2016, prior to use of any local or regional analgesia, was used as a historical control. Post-operative enteral and parenteral narcotic analgesics were collected for each post-operative day up to day 5 or discharge (whichever came first) and converted to morphine milligram equivalents (MME) to quantify analgesia after surgery. RESULTS: Chart review identified 55 patients in the 2020 cohort. Fifty-five patients from the 2016 cohort were matched based upon size of skin graft, total body surface area (TBSA) burned, gender, and age. There were no statistically significant differences between the two groups in terms of size of graft, TBSA burned, age, gender, or type of burn. When examining narcotics usage in the immediate perioperative period (days 0-2), we found no difference between the two groups for total MME (113 vs 133, p = 0.28) or IV MME (38 vs 33, p = 0.45). Similar relationships existed in the extended post-operative period (days 1-5) for total MME (149 vs. 188, t = 0.22) or IV MME (37 vs. 50, t = 0.25). Examining daily narcotic usage also yielded no statistically different values. CONCLUSION: Our data shows that use of LFCN block by landmark technique did not reduce narcotic usage in patients that undergo skin grafting procedures. Future studies should consider ultrasound-guided LFCN blocks.

Striatal Subregion-selective Dysregulated Dopamine Receptor-mediated Intracellular Signaling in a Model of DOPA-responsive Dystonia.

Although the mechanisms underlying dystonia are largely unknown, dystonia is often associated with abnormal dopamine neurotransmission. DOPA-responsive dystonia (DRD) is a prototype disorder for understanding dopamine dysfunction in dystonia because it is caused by mutations in genes necessary for the synthesis of dopamine and alleviated by the indirect-acting dopamine agonist l-DOPA. Although adaptations in striatal dopamine receptor-mediated intracellular signaling have been studied extensively in models of Parkinson's disease, another movement disorders associated with dopamine deficiency, little is known about dopaminergic adaptations in dystonia. To identify the dopamine receptor-mediated intracellular signaling associated with dystonia, we used immunohistochemistry to quantify striatal protein kinase A activity and extracellular signal-related kinase (ERK) phosphorylation after dopaminergic challenges in a knockin mouse model of DRD. l-DOPA treatment induced the phosphorylation of both protein kinase A substrates and ERK largely in D1 dopamine receptor-expressing striatal neurons. As expected, this response was blocked by pretreatment with the D1 dopamine receptor antagonist SCH23390. The D2 dopamine receptor antagonist raclopride also significantly reduced the phosphorylation of ERK; this contrasts with models of parkinsonism in which l-DOPA-induced ERK phosphorylation is not mediated by D2 dopamine receptors. Further, the dysregulated signaling was dependent on striatal subdomains whereby ERK phosphorylation was largely confined to dorsomedial (associative) striatum while the dorsolateral (sensorimotor) striatum was unresponsive. This complex interaction between striatal functional domains and dysregulated dopamine-receptor mediated responses has not been observed in other models of dopamine deficiency, such as parkinsonism, suggesting that regional variation in dopamine-mediated neurotransmission may be a hallmark of dystonia.