Objective: Many pieces of research have focused on pain within individuals, but little attention has been paid to whether pain can change an individual's empathic ability and affect social relationships. The purpose of this study is to explore how chronic low back pain changes empathy. Methods: Twenty-four chronic low back pain patients and 22 healthy controls were recruited. We set up an experimental pain-exposed model for each healthy subject. All subjects received a painful-empathic magnetic resonance scan. After the scan, all subjects rated the pain intensity and multiple empathy-related indicators. The clinical assessment scale was the 20-item Basic Empathy Scale in Adults. Result: The chronic low back pain patients reported lower scores on the total scores of BES-A, the subscale scores of emotional disconnection and cognitive empathy, and the discomfort rating. The fMRI results in the chronic low back pain patients showed that there were multiple abnormal brain pathways centered on the anterior insula. The DTI results in the chronic low back pain patients showed that there were reduced fractional anisotropy values in the corpus callosum, bilateral anterior thalamic radiation (ATR), right posterior thalamic radiation (PTR), right superior longitudinal fasciculus (SLF), and left anterior corona radiate (ACR). Conclusion: Our study found that patients with chronic low back pain have impaired empathy ability. The abnormal functional connectivity of multiple brain networks, multiple damaged white matter tracts, and the lower behavioral scores in chronic low back pain patients supported our findings.

Objective: Automatic detection of auditory stimuli, represented by the mismatch negativity (MMN), facilitates rapid processing of salient stimuli in the environment. The amplitude of MMN declines with ageing. However, whether automatic detection of auditory stimuli is affected by visually perceived negative emotions with normal ageing remains unclear. We aimed to evaluate how fearful facial expressions affect the MMN amplitude under ageing.Methods: We used a modified oddball paradigm to analyze the amplitude of N100 (N1) and MMN in 22 young adults and 21 middle-aged adults.Results: We found that the amplitude of N1 elicited by standard tones was smaller under fearful facial expressions than neutral facial expressions and was more negative for young adults than middle-aged adults. The MMN amplitude under fearful facial expressions was greater than neutral facial expressions, but the amplitude in middle-aged adults was smaller than in young adults.Conclusion: Visually perceived negative emotion promotes the extraction of auditory features. Additionally, it enhances the effect of auditory change detection in middle-aged adults but fails to compensate for this decline with normal ageing.Significance: The study may help to understand how visually perceived emotion affects the early stage of auditory information processing from an event process perspective.

Mlxipl regulates glucose metabolism, lipogenesis and tumorigenesis and has a wide-ranging impact on human health and disease. However, the role of Mlxipl in neuropathic pain remains unknown. In this study, we found that Mlxipl was increased in the ipsilateral L4–L6 spinal dorsal horn after Spared Nerve Injury surgery. Knockdown of Mlxipl in the ipsilateral L4–L6 spinal dorsal horn by intraspinal microinjection aggravated Spared Nerve Injury-induced mechanical allodynia and inflammation in the spinal dorsal horn, on the contrary, overexpression of Mlxipl inhibited mechanical allodynia and inflammation. Subsequently, the rat Mlxipl promoter was analyzed using bioinformatics methods to predict the upstream transcription factor cJun. Luciferase assays and ChIP-qPCR confirmed that cJun bound to the promoter of Mlxipl and enhanced its expression. Finally, we demonstrated that Mlxipl inhibited the inflammatory responses of lipopolysaccharide-induced microglia and that Mlxipl was regulated by the transcription factor cJun. These findings suggested that cJun-induced Mlxipl upregulation in the spinal dorsal horn after peripheral nerve injury provided a protective mechanism for the development and progression of neuropathic pain by inhibiting microglial-derived neuroinflammation. Targeting Mlxipl in the spinal dorsal horn might represent an effective strategy for the treatment of neuropathic pain.