Editorial: Exploring the interplay between stress, neuropeptides, and alcohol use disorder.

Herpetic neuralgia (HN), which is caused by reactivation of the varicella-zoster virus (VZV), is a type of neuropathic pain. Its clinical subtypes include postherpetic neuralgia (PHN), which has a prevalence of up to 30–50% among individuals older than 50 years (), with an incidence that increases with age. It is a chronic pain syndrome with typical features, such as burning pain and electric-shock-like paroxysms, which are commonly associated with the development of so-called “pain shadow memory” (PSM), defined as the consolidation of painful experiences in the central nervous system (CNS) through neuroplastic processes. These processes lead to the formation of conditioned reflex-like memories, including situation association, action avoidance behavior, and verbal response (). Recent studies have suggested that pain memory is an important mechanism underlying the transition from acute pain to chronic pain. Pain-related experiences can induce long-term neuroplastic changes in brain regions involved in sensory processing, emotional regulation, and behavioral responses, including the anterior cingulate cortex, the amygdala, the hippocampus, and the prefrontal cortex (). These changes contribute to the formation and persistence of pain-related memories, which may be reactivated by environmental cues, sensory stimuli, or emotional triggers even after the original nociceptive stimulus has diminished. Emerging evidence indicates that pain memory not only amplifies pain perception but also promotes fear-avoidance behaviors, negative emotional states, and functional impairment. Consequently, the modulation of pain memory has become an increasingly important research focus in chronic pain management and rehabilitation. Although the concept of pain memory has been widely discussed in chronic pain research, studies specifically focusing on pain shadow memory in patients with herpetic neuralgia remain limited. Existing evidence suggests that patients with herpetic neuralgia frequently exhibit fear-related avoidance behaviors, heightened pain vigilance, and persistent negative emotional responses even after the acute phase of the disease (). These manifestations are considered to be closely associated with pain memory processes. Previous studies have primarily focused on pharmacological treatment, pain control, and psychological support, whereas the behavioral characteristics, recurrence mechanisms, and nursing management of pain shadow memory have received relatively little attention. Therefore, further investigation is needed to better understand the behavioral manifestations of pain shadow memory and to identify effective nursing strategies for its management in patients with postherpetic neuralgia. In humans, aberrant PSM activity is known to enhance pain sensitivity, promote the consolidation of maladaptive behaviors, and increase the risk of comorbid emotional disorders. The incidence of anxiety and depression in PHN patients was 40–60% higher than that in simple neuralgia patients, severely affecting their day-to-day activities and quality of life (). Existing clinical nursing interventions in the management of HN are limited to passive treatment that includes monitoring adverse drug reactions and simple skin care, without much focus on the mechanisms underlying PSM formation or their subsequent behavioral repetition ().