EMOTIONAL MODULATION OF PAIN PERCEPTION: NEUROBIOLOGICAL AND NEUROPSYCHIATRIC BASES

Abstract

Pain is a multidimensional experience resulting from the integration of sensory, emotional, cognitive, and behavioral components. The contemporary definition by the International Association for the Study of Pain (IASP) characterizes pain as an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage, emphasizing that its intensity cannot be inferred solely from peripheral nociceptive activity. In this context, emotional states such as anxiety, fear, stress, depression, and catastrophizing can substantially alter pain perception, whereas positive emotions, expectations of analgesia, distraction, and a sense of safety can reduce its intensity. These interactions are mediated by circuits involving the prefrontal cortex, anterior cingulate cortex, insula, amygdala, periaqueductal gray, rostroventromedial medulla, locus coeruleus, and the dorsal horn of the spinal cord. Endogenous opioid, serotonergic, noradrenergic, dopaminergic, glutamatergic, and GABAergic systems participate in the descending modulation of nociception. Persistent alterations in these circuits contribute to central sensitization, the chronification of pain, and the overlap between chronic pain and depressive and anxiety disorders. Understanding these mechanisms supports the biopsychosocial model and reinforces the need for an integrated assessment of the somatic, emotional, and cognitive components of pain. However, acknowledging emotional influence should not be confused with attributing pain exclusively to a psychological cause. The contemporary approach considers that nociceptive, neuropathic, and nociplastic mechanisms can coexist and interact with psychological and social factors.