PS252 - Factors Leading to Pain

Pain

• Complex psychological and physiological experience that serves an essential adaptive function, alerting us to actual or potential tissue damage.

• However, the experience of pain is not simply a direct result of sensory input. Instead, it arises from the interaction of biological, psychological, and social factors.

• Theories and research in behavioural neuroscience and health psychology have shown that pain perception is shaped by physiological processes in the nervous system, cognitive appraisal, emotions, and contextual influences.

Early explanations of pain: specificity theory

• Specificity theory (Descartes, 17th century) and later elaborated by von Frey (1895), suggests that pain results from direct activation of specialised pain receptors that transmit signals to a specific pain centre in the brain. This treated pain as a simple, one-way process from stimulus to perception.

• However, couldn’t explain why people report pain without obvious physical damage, or why the same injury can produce different levels of pain in different people.

Early explanations of pain: pattern theory (Goldscheider, 1894)

• Proposed that pain results not from specific receptors but from the pattern and intensity of neural stimulation. Even this model could not explain the psychological modulation of pain.

• A major shift occurred with the development of the Gate Control Theory of Pain (Melzack & Wall, 1965). This theory proposed that pain signals from peripheral nerves are modulated at the level of the spinal cord, specifically in the substantia gelatinosa of the dorsal horn.

• According to this model, a neural “gate” can either allow or inhibit pain signals before they reach the brain. Input from large-diameter (touch) fibres can close the gate, reducing pain, whereas small-diameter (pain) fibres open it.

• Critically, cognitive and emotional factors, such as attention, expectation, and mood, can also influence the gate through descending pathways from the brain. Thus, psychological processes directly affect physiological pain transmission.

Neuromatrix Theory of Pain (1999)

• Builds on GTT, emphasises that pain is produced by a distributed network of neurons: the “neuromatrix”, that integrates sensory, emotional, and cognitive information.

• Pain is thus an output of the brain, not a direct reflection of injury. This framework helps explain phantom limb pain.

• Even without sensory input, the neuromatrix can generate pain when body representations in the brain are disrupted. This demonstrates that pain is constructed by the central nervous system rather than merely transmitted from the periphery.

Psychological factors shaping pain: cognitive appraisal

• How an individual interprets meaning of pain

• Athletes often report less pain during competition than at rest, because the pain is interpreted as part of effort or achievement. Conversely, catastrophising—an exaggerated negative focus on pain—predicts higher pain intensity and disability.

• Emotional states such as fear, anxiety, and depression are also powerful amplifiers of pain, partly due to shared neural pathways involving the amygdala and anterior cingulate cortex.

Psychological factors shaping pain: learning and expectation

• Classical conditioning can cause previously neutral cues to elicit pain responses if they have been repeatedly paired with painful stimuli.

• Expectancy effects also play a role, as seen in the placebo effect, where believing a treatment will reduce pain can activate endogenous opioid systems in the brain. Conversely, the nocebo effect, where negative expectations increase pain, highlights the powerful top-down influence of cognition on sensory experience.