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Pain empathy is a specific subgroup of empathy that involves recognizing and understanding another person’s pain. Empathy is the mental ability that allows one person to understand another person’s mental and emotional state and how to effectively respond to that person. When a person receives cues that another person is in pain, neural pain circuits within the brain are activated. There are several cues that can communicate pain to another person: visualization of the injury causing event, the injury itself, behavioral efforts of the injured to avoid further harm, and displays of pain and distress such as facial expressions, crying, and screaming. From an evolutionary perspective, pain empathy is beneficial for human group survival since it provides motivation for non-injured people to offer aid to the injured and to avoid injury themselves.
- 1 Initiating Pain Empathy
- 2 Pain processing areas of the brain (The Pain Matrix)
- 3 Detection Methods
- 4 Lack of pain empathy
- 5 In group racial bias
- 6 Physicians and pain empathy response
- 7 Pain synesthesia
- 8 References
Initiating Pain Empathy[edit | edit source]
Resonance[edit | edit source]
Perceiving another person's affective state can cause automatic changes in brain activity in the viewer. This automatic change in brain activity is known as resonance and helps initiate an empathetic response. The inferior frontal gyrus and the inferior parietal lobule are two regions of the brain associated with empathy resonance.
Self other discrimination[edit | edit source]
In order to have empathy for another person, one must understand the context of that person’s experience while maintaining a certain degree of separation from their own experience. The ability to differentiate the source of an affective stimuli as originating from the self or from other another is known as self-other discrimination. Self-other discrimination is associated with the extrastriate body area (EBA), posterior superior temporal sulcus (pSTS), temporoparietal junction (TPJ), ventral premotor cortex, and the posterior and inferior parietal cortex.
Response to painful facial expressions[edit | edit source]
A painful facial expression is one way in which the experience of pain is communicated from one individual to another. One study aimed to measure test subject’s related brain activity and facial muscle activity when they watched video clips of a variety of facial expressions including neutral emotion, joy, fear, and pain. The study found that when a subject is shown a painful facial expression, their late positive potential (LPP) is increased during the time period of 600-1000ms after the initial exposure of the stimulus. This increase in LPP for painful facial expressions was higher than the increase caused by other emotional expressions. 
Pain processing areas of the brain (The Pain Matrix)[edit | edit source]
One study used functional magnetic resonance imaging (fMRI) to measure brain activity while during the experience of painful stimuli or while observing someone else received a painful stimuli. The study group consisted of 16 couples since it was likely these individuals would have empathy for one another. One person would receive a painful stimulus via electrode to the back of their hand while their partner observed and brain activity was measured in both participants. The results from the fMRI are detailed below.
First hand experience of pain[edit | edit source]
The activated brain regions in the person experiencing the pain firsthand included: contralateral sensorimotor cortex, bilateral secondary sensorimotor cortex, contralateral posterior insula, bilateral mid and anterior insula, anterior cingulate cortex, right ventrolateral and mediodorsal thalamus, brainstem, and mid and right lateral cerebellum. One study used fMRI to observe brain activity of an individual receiving unpredictable laser pain stimuli. This study showed that the primary and secondary sensorimotor cortex, posterior insula, and lateral thalamus are involved in processing aspects of nociceptive stimuli such as location and intensity.
Observed pain in others[edit | edit source]
Several brain regions including the bilateral anterior insula (AI), rostral anterior cingulate cortex (ACC), brainstem, and cerebellum were activated both in instances of first person painful experience and observed painful experience. The bilateral anterior insula (AI) and rostral anterior cingulate cortex (ACC) are therefore hypothesized to take part in the emotional reaction evoked from witnessing another in pain. The samotosensory region of the brain was not shown by fMRI to be excited during pain observation, rather only when the pain was experience firsthand.
Detection Methods[edit | edit source]
Magnetoencephalography[edit | edit source]
fMRI studies were not able to detect activity in the somatosensory cortex during pain empathy. Neuromagnetic oscillatory activity was recorded from the primary somatosensory cortex in order to determine if it is involved in pain empathy. When the left medial nerve was stimulated, post-stimulus rebounds of 10 Hz of somatosensory oscillations were quantified. These baseline somatosensory oscillations were suppressed when the subject observed a painful stimulus to a stranger. These results show that the somatosensory cortex is involved in the pain empathy response even thought the activity could not be detected using fMRI techniques.
Transcranial magnetic stimulation (TMS)[edit | edit source]
Single-pulse transcranial magnetic stimulation (TMS) has been used to stimulate the motor cortex of a person observing another person’s actions, and this has been shown to increase the corticospinal excitability of associated with their motor resonance. TMS studies have shown that frontal structures of the motor resonance system are used to process information about other people’s physical actions.
Motor evoked potential (MEP)[edit | edit source]
Sensorimotor contagion is an automatic reduction in corticospinal excitability due observing another person experiencing pain. In a study by Avenanti on pain empathy in racial bias, it was shown that when a person sees a needle being poked into the hand of another person, there is a reduced motor evoked potential (MEP) in the muscle of the observer’s hand.
Lack of pain empathy[edit | edit source]
Lack of empathy occurs in several conditions including autism, schizophrenia, sadistic personality disorder, psychopathy, and sociopathy. One recent view is that an improper ratio of cortical excitability to inhibition causes empathy defects. Brain stimulation is being investigated for its potential to alter motor resonance, pain empathy, self-other discrimination, and mentalizing as a way to treat empathy related disorders.
Sadistic personality disorder[edit | edit source]
Psychopathy is thought to be caused by normal processing of social and emotional cues, but abnormal use of these cues. One study used fMRI to look at the brain activity of youth with aggressive conduct disorder and socially normal youth when they observed empathy eliciting stimuli. The results showed that the aggressive conduct disorder group had activation in the amygdala and ventral striatum, which lead the researcher to believe that these subjects may get a rewarding feeling from viewing pain in others.
Autism[edit | edit source]
Austism spectrum disorders are characterized by an impairment in the processing of social and emotional affective cues.
Juvenile psychopathy[edit | edit source]
Young individuals who have callous and unemotional traits (CU) exhibit an overall lack of empathy. It has been thought that if a person experiences pain empathy they will be less likely to hurt others, since people that experience pain empathy have distress when another person is hurt.
One study involved showing juvenile psychopaths video clips of strangers experiencing painful stimuli. The results of the study showed that the juvenile psychopaths had atypical processing of these pain empathy eliciting stimuli in comparison with the normal juvenile controls. The central late positive potential (LPP), a late cognitive evaluative component of pain, was decreased in subjects with low CU traits. Subjects with high CU traits had both a decrease in central LPP and in frontal N120, an early affective arousal component of pain. There were also differences in the pain thresholds between normal test subjects, subjects with low CU traits, and subjects with high CU traits. The subjects with CU traits had higher pain thresholds than the controls, which suggests they were less sensitive to noxious pain. The results of the study show the CU trait juvenile’s lack of pain empathy was due to a lack of arousal due to another person’s distress rather than a lack of understanding of the other’s emotional state.
In group racial bias[edit | edit source]
An experiment utilizing transcranial magnetic stimulation (TMS) was performed in order to determine if another person’s race affected pain empathy by measuring inhibition of corticospinal excitability. Caucasian and black participants watched video clips of a needle penetrating a muscle in the right hand of a stranger who either belonged to their racial group or the other racial group. TMS was used to stimulate the left motor cortex and motor-evoked potentials (MEPs) were measured in the observer’s first dorsal interosseus (FDI) muscle of the right hand. The results of the experiment showed that when the video clip showed a hand belonging to a person of the same racial group, the measured corticospinal excitability to the right hand of the observer was reduced. This inhibition effect was not present when a subject viewed a clip of an a hand belonging to a stranger outside of their racial group. This corticospinal inhibition occurs in first hand experience of pain, and suggests that there is activation of the observer's sensorimotor system while witnessing painful stimuli.
Physicians and pain empathy response[edit | edit source]
Physicians are frequently exposed to people experiencing pain due to injury or illness, or have to inflict pain during the course of treatment. Physicians have to regulate their emotional response to this stimuli in order to effectively help the patient and maintain their own personal well being. Pain empathy can motivate an individual to help someone who is in pain, but repeated exposure to individuals in pain with no ability to regulate emotional arousal can cause distress. One study sought to determine if physicians had an altered response to viewing painful stimuli. Physicians and control subjects watched video clips of a stranger being poked with a needle into the hands or feet. fMRI was used to measure the hemodynamic activity within the brain while viewing the painful stimuli. The fMRI revealed that brain areas involved in the pain matrix: somatosensory cortex, anterior insula, dorsal anterior cingulated nucleus (dACC), and the periaqueductal gray (PAG) were activated in the control subject population when viewing the needle penetration videos. The physicians had activation of higher order executive functioning in the brain as shown by activation of the dorsolateral and medial prefrontal cortex, both involved in self-regulation, and activation of the precentral, superior parietal, and temporoparietal junction, involved with executive attention. The physicians did not have activation of the anterior insula, dorsal anterior cingulated nucleus (dACC), or the periaqueductal gray (PAG). The study concluded that physicians adapt to the healthcare environment by down regulating their automatic empathetic response to patient’s pain.
Pain synesthesia[edit | edit source]
Synesthesia occurs when sensory information in one cognitive pathway causes a sensation through another cognitive pathway. One form of synesthesia will cause a person to see certain colors when triggered by certain numbers, letters, or words. Pain synesthesia is a form of synesthesia that causes a person to experience pain when seeing pain empathetic eliciting stimuli. The most common group for reporting pain synesthesia are patients with phantom limb syndrome.
References[edit | edit source]
- Jean Decety, W. I. (Ed.). (2009). The Social Neuroscience of Empathy: MIT Press.
- Hetu, S., Taschereau-Dumouchel, V., & Jackson, P. L. (2012). Stimulating the brain to study social interactions and empathy. [Article]. Brain Stimulation, 5(2), 95-102.
- Reicherts, P., Wieser, M. J., Gerdes, A. B. M., Likowski, K. U., Weyers, P., Muhlberger, A., & Pauli, P. (2012). Electrocortical evidence for preferential processing of dynamic pain expressions compared to other emotional expressions. [Article]. Pain, 153(9), 1959-1964. doi: 10.1016/j.pain.2012.06.017
- Singer T, S. B., O'Doherty J, Kaube H, Dolan RJ, Frith CD. (2004). Empathy for pain involves the affective but not sensory components of pain. Science, 303(5661), 1157-1162.
- Bingel, U., Quante, M., Knab, R., Bromm, B., Weiller, C., & Buchel, C. (2003). Single trial fMRI reveals significant contralateral bias in responses to laser pain within thalamus and somatosensory cortices. [Article]. Neuroimage, 18(3), 740-748. doi: 10.1016/s1053-8119(02)00033-2
- Cheng, Y., Yang, C. Y., Lin, C. P., Lee, P. L., & Decety, J. (2008). The perception of pain in others suppresses somatosensory oscillations: A magnetoencephalography study.
- Avenanti, A., Sirigu, A., & Aglioti, S. M. (2010). Racial bias reduces empathic sensorimotor resonance with other-race pain. Current Biology: CB, 20(11), 1018-1022.
- Decety, J., Michalska, K. J., Akitsuki, Y., & Lahey, B. B. (2009). Atypical empathic responses in adolescents with aggressive conduct disorder: A functional MRI investigation. Biological Psychology, 80, 203-211.
- Cheng, Y. W., Hung, A. Y., & Decety, J. (2012). Dissociation between affective sharing and emotion understanding in juvenile psychopaths. [Article]. Development and Psychopathology, 24(2), 623-636. doi: 10.1017/s095457941200020
- Decety, J., Yang, C. Y., & Cheng, Y. W. (2010). Physicians down-regulate their pain empathy response: An event-related brain potential study. [Article]. Neuroimage, 50(4), 1676-1682. doi: 10.1016/j.neuroimage.2010.01.025
- Fitzgibbon, B. M., Giummarra, M. J., Georgiou-Karistianis, N., Enticott, P. G., & Bradshaw, J. L. (2010). Shared pain: From empathy to synaesthesia. [Review]. Neuroscience and Biobehavioral Reviews, 34(4), 500-512. doi: 10.1016/j.neubiorev.2009.10.007
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