ABSTRACT
BACKGROUND: Rebound pain as a side effect of regional anaesthesia is an excessive sensation of pain after the effect of local anaesthesia has subsided. This sensation goes well beyond the normal wound pain following a surgical intervention. This phenomenon has entered focus of research in the past 10 years now, but the specific causes are so far unclear and there are still no targeted treatment recommendations. OBJECTIVE: This review article is intended to give the readership an overview of the current state of research about rebound pain. The theories of pathophysiology are presented and prophylaxis as well as treatment strategies are explained. MATERIAL AND METHODS: For this review article, the publications about rebound pain that appeared from 2005 up to May 2021 in PubMed were reviewed and the authors' definitions of rebound pain as well as the assumptions on pathophysiology and treatment recommendations were summarized. RESULTS AND DISCUSSION: A total of 22 original papers from the years 2005-2021 were evaluated regarding the differences between the definitions of rebound pain, the assumption of its occurrence as well as possible treatment options. It turns out that there is no uniform definition by the professional societies, the pathophysiology has not yet been clearly identified and no clear recommendations for prophylaxis or treatment can be given to date; however, early administration of pain medication (e.g. NSAIDs) before the end of the nerve block has proven to be helpful. Likewise, dexamethasone as an adjuvant to regional anaesthesia shows positive effects regarding the occurrence of rebound pain. In any case, it makes sense to provide patients with comprehensive information about this special side effect of regional anaesthesia so that those affected can correctly classify the excessive pain reaction. Targeted studies to avoid severe pain after regional anaesthesia, e.g. through the addition of adjuvants, are necessary in order to keep side effects as low as possible and thereby improve patient comfort and the acceptance of regional anaesthesia.
Subject(s)
Anesthesia, Conduction , Nerve Block , Anesthesia, Conduction/adverse effects , Anesthesia, Local , Anesthetics, Local/therapeutic use , Humans , Nerve Block/adverse effects , Pain, Postoperative/etiologyABSTRACT
Physiological reactions to psychological stress are positively associated with several important chronic conditions including cardiovascular and neurodegenerative diseases and are linked to increased mortality. As such, the identification of cellular and molecular pathways that act to reduce stress responding may represent important targets for therapeutic intervention. Here we report that acute treatment with the peroxisome-proliferator activated receptor-γ (PPARγ) agonist rosiglitazone (RSG) blunts systemic responses to acute psychological stress in rats. Rats that had previously received oral RSG for 5 d exhibited a 40% reduction in the initial heart rate response to an acute restraint stress, compared with vehicle-treated controls, suggesting that increased PPARγ signaling blunts the acute autonomic response to stress. Rats previously treated with RSG likewise had a blunted hormonal response to this stressor, exhibiting a 30% reduction in peak corticosterone levels compared with controls. Moreover, stress-induced expression of c-Fos, a marker of early neuronal activation, was similarly reduced in the paraventricular hypothalamus, a key site for brain stress integration, facilitating both autonomic and hypothalamic-pituitary-adrenocortical responses to stress. Taken as a whole, these data suggest that PPARγ stimulation potently inhibits physiological responses to psychological stress, prescribing a novel role for PPARγ signaling in the regulation of brain stress integration.