Just the thought of it… (Image: Emmanuel Faure/Getty)

FOR some people, seeing pain in someone else is more than emotionally distressing: they feel the pain in their own body too. Now some of the pathways involved have been identified.

“Synaesthetic pain” occurs mainly in people who have lost a limb. Some amputees are already known to experience phantom limb pain – a feeling of pain in a limb that is no longer there – but synaesthetic pain is different. Rather than occurring spontaneously, it is triggered by observed or imagined pain.

“When I hear my husband’s power tools, or see a knife, I often get a sharp pain through my phantom leg,” says Jane Barrett, who has experienced synaesthetic pain since losing her leg in a motorcycle accident.


When we observe or imagine pain, it activates areas of the brain involved in the processing of real pain. This is called the mirror neuron system and is thought to help us to understand other people’s actions and emotions. But the activation is not as strong as that caused by real pain because inhibitory mechanisms normally dampen the response.

Bernadette Fitzgibbon at Monash University in Melbourne, Australia, and colleagues, think those inhibitory mechanisms are themselves inhibited in pain synaesthetes. They used EEG to record brain activity in eight amputees who experience both phantom and synaesthetic pain, 10 amputees who experience just phantom pain and 10 healthy people with no amputations while they looked at images of hands or feet in potentially painful and non-painful situations.

When viewing the images, pain synaesthetes exhibited decreased theta and alpha brainwaves compared with the other volunteers. Such a decrease reflects an increase in neural activity, suggesting that their mirror systems are activated more strongly (Social Cognitive and Affective Neuroscience, DOI: 10.1093/scan/nsr016).

Fitzgibbon says the traumatic experience associated with losing a limb may heighten the sensitivity of pain synaesthetes to others’ pain. When threatened, our body naturally becomes hypervigilant to pain: our pain threshold lowers, which can make even small triggers painful. Pain synaesthesia may be a symptom of an abnormal, ongoing hypervigilance.

Michael Banissy at University College London welcomes the new “building block” in our understanding of the condition. “The suggestion that acquired mirror-pain synaesthesia may be mediated by neural disinhibition is intriguing. It implies that plasticity in neural systems involved in our ability to process observed pain can trigger actual pain.”