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Purpose of Review Acute facial pain presents a complex challenge in medical practice, requiring a comprehensive and interdisciplinary approach to its management. This narrative review explores the contemporary landscape of treating acute facial pain, delving into pharmacological, non-pharmacological, and advanced interventions. The significance of tailored treatment strategies, rooted in the diverse etiologies of facial pain, such as dental infections, trigeminal neuralgia, temporomandibular joint disorders, sinusitis, or neurological conditions like migraines or cluster headaches, is underscored. We particularly emphasize recent advances in treating trigeminal neuralgia, elucidating current treatment concepts in managing this particular acute facial pain. Recent Findings Recent research sheds light on various treatment modalities for acute facial pain. Pharmacotherapy ranges from traditional NSAIDs and analgesics to anticonvulsants and antidepressants. Non-pharmacological interventions, including physical therapy and psychological approaches, play pivotal roles. Advanced interventions, such as nerve blocks and surgical procedures, are considered in cases of treatment resistance. Moreover, we explore innovative technologies like neuromodulation techniques and personalized medicine, offering promising avenues for optimizing treatment outcomes in acute facial pain management. Summary Modern management of acute facial pain requires a nuanced and patient-centric approach. Tailoring treatment strategies to the individual's underlying condition is paramount. While pharmacotherapy remains a cornerstone, the integration of non-pharmacological interventions is essential for comprehensive care. Advanced interventions should be reserved for cases where conservative measures prove inadequate. Furthermore, leveraging innovative technologies and personalized medicine holds promise for enhancing treatment efficacy. Ultimately, a holistic approach that considers the diverse needs of patients is crucial for effectively addressing acute facial pain.
Purpose of Review Acute facial pain presents a complex challenge in medical practice, requiring a comprehensive and interdisciplinary approach to its management. This narrative review explores the contemporary landscape of treating acute facial pain, delving into pharmacological, non-pharmacological, and advanced interventions. The significance of tailored treatment strategies, rooted in the diverse etiologies of facial pain, such as dental infections, trigeminal neuralgia, temporomandibular joint disorders, sinusitis, or neurological conditions like migraines or cluster headaches, is underscored. We particularly emphasize recent advances in treating trigeminal neuralgia, elucidating current treatment concepts in managing this particular acute facial pain. Recent Findings Recent research sheds light on various treatment modalities for acute facial pain. Pharmacotherapy ranges from traditional NSAIDs and analgesics to anticonvulsants and antidepressants. Non-pharmacological interventions, including physical therapy and psychological approaches, play pivotal roles. Advanced interventions, such as nerve blocks and surgical procedures, are considered in cases of treatment resistance. Moreover, we explore innovative technologies like neuromodulation techniques and personalized medicine, offering promising avenues for optimizing treatment outcomes in acute facial pain management. Summary Modern management of acute facial pain requires a nuanced and patient-centric approach. Tailoring treatment strategies to the individual's underlying condition is paramount. While pharmacotherapy remains a cornerstone, the integration of non-pharmacological interventions is essential for comprehensive care. Advanced interventions should be reserved for cases where conservative measures prove inadequate. Furthermore, leveraging innovative technologies and personalized medicine holds promise for enhancing treatment efficacy. Ultimately, a holistic approach that considers the diverse needs of patients is crucial for effectively addressing acute facial pain.
Chronic orofacial pain disorders are common debilitating conditions, affecting the trigeminal system. Its underlying pathophysiological mechanisms are still unclear and the therapy is often unsatisfactory, therefore, preclinical models are crucial to identify the key mediators and novel treatment options. Complete Freund’s adjuvant (CFA)-induced orofacial inflammatory allodynia/hyperalgesia is commonly used in rodents, but it has not been validated with currently used drugs. Here we tested the effects of the adjuvant analgesic/antiepileptic voltage-gated Na+ channel blocker complex mechanism of action topiramate in comparison with the gold standard antimigraine serotonin 5-HT1B/D receptor agonist sumatriptan in this model. CFA was injected subcutaneously into the right whisker pad of male Sprague-Dawley rats (250–300 g), then mechanonociceptive threshold values were investigated with von Frey filaments (3, 5, and 7 days after CFA injection). Effects of topiramate (30 mg/kg per os) and sumatriptan (1 mg/kg subcutaneous) on the adjuvant-induced chronic inflammatory orofacial allodynia were investigated 60, 120, and 180 min after the treatments each day. To determine the optimal concentration for drug effect analysis, we tested the effects of two different CFA-concentrations (1 and 0.5 mg/mL) on mechanonociceptive thresholds. Both concentrations of CFA induced a chronic orofacial allodynia in 60% of all rats. Although, higher CFA concentration induced greater allodynia, much more stable threshold reduction was observed with the lower CFA concentration: on day 3 the thresholds decreased from 18.30 g to approximately 11 g (low) and 5 g (high), respectively, however a slight increase was observed in the case of higher CFA concentration (on days 5, 7, and 11). In all investigation days, topiramate showed significant anti-allodynic effect comparing the pre and post drug dose and comparing the vehicle treated to the drug treated groups. Sumatriptan also caused a significant threshold increase compared to pre dose thresholds (day 3) and also showed a slight anti-allodynic effect compared to the vehicle-treated group (day 3 and 5). In the present study CFA-induced chronic orofacial allodynia was reversed by topiramate in rats validating the model with the adjuvant analgesic. Other than establishing a validated orofacial pain-related syndrome model in rats, new ways are opened for the repurposing of topiramate.
Neuropathic pain (NeP) is a complex and debilitating condition that impacts millions of people globally. Although various treatment options exist, their effectiveness is often limited, and they can be accompanied by significant side effects. In recent years, there has been increasing interest in targeting the N-methyl-D-aspartate receptor (NMDAR) as a potential therapeutic approach to alleviate different types of neuropathic pain. This narrative review aims to provide a comprehensive examination of NMDAR antagonists, specifically ketamine, memantine, methadone, amantadine, carbamazepine, valproic acid, phenytoin, dextromethorphan, riluzole, and levorphanol, in the management of NeP. By analyzing and summarizing current preclinical and clinical studies, this review seeks to evaluate the efficacy of these pharmacologic agents in providing adequate relief for NeP.
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