Pain is multidimensional. Pain is 100% produced by the brain in response to a perceived threat. The brain allocates a location using the cortical maps, hence why we feel pain in our backs or knees. The brain tries to make sense of the situation, scrutinising what is going on on the basis of past experience (learning) and comparing to the information being received from ALL body systems. This is the reason for the term ‘multisystem output’ as a way of describing what is happening when we are in pain.
The most obvious reason why the pain worsens is that we move, exercise or sit for too long. All of these activities are ‘physical’, asking the tissues to take the strain either rapidly or gradually. On reaching a certain level of strain, lower than normal in cases of sensitivity, nerves start sending danger signals to the spinal cord. From the spinal cord messages are relayed to the brain, still on the subject of danger. Theses are not pain signals. It is only when the brain interprets the information as threatening that the experience of pain is produced – an output from the brain. This is typical in acute situations when the injury or problem is new. The pain is vital, useful and motivates action.
A key point to understand is that the brain does not actually need the tissues to produce pain. Think about phantom limb pain. There is no limb. There are no tissues. But it hurts. It seriously hurts in may cases. So, there are other ‘triggers’ for pain besides actually moving or asking the tissues (muscles, tendons, ligaments, bones etc) to take the strain. Common ‘non-tissue’ circumstances that can amplify pain include stress, circadian rhythms, menstrual cycle, fatigue and thoughts. I think that to take this on board is an enlightening experience. To understand that your pain can be as a result of other reasons besides what you are doing physically can help to explain why it hurts at times when you have not done anything differently and you really cannot comprehend why the pain has increased.
A further influential player in our experiences is vision. I’m really interested in this as the process of ‘seeing’ is much aligned to the way pain is experienced. Information is received by the brain via the optic nerve. The brain must make sense of this data and create a credible outcome, again very much using past experience to judge the present. We still see a bird in his cage despite slender lines dividing his body (the struts of the cage). We don’t see ‘slices’ of a bird. Also consider optical illusions. A great deal of work has been done looking at the use of vision for therapeutic effect, i.e. the graded motor imagery programme. Clearly the mirror box is creating the illusion that the affected side is moving and appearing to be normal. Imagined movements requires us to ‘see’ and feel movement although we are keeping very still. The premotor cortex is very active during these imagined movements, and this part of the brain is involved in the production of pain.
What we are seeing is deemed to be an illusion in some quarters. We all have different experiences and backgrounds. Our beliefs about life and ourselves vary. This will influence what we ‘see’. If you have just watched a scary movie and then go outside into the dark to put the rubbish out, a shadow could be ‘seen’ as something more dangerous than if you have just laughed at a comedy show. Also consider when we see someone injure themselves, again on TV or watching sport. We often wince, grab our corresponding body part or take some other defensive action. Our brains are interpreting someone else’s danger and imprinting this onto our experience, perhaps as a way of helping us to learn that it is dangerous to be in their situation. This is likely due to the mirror neuron network and that when we watch someone else move or position themselves, our virtual body that exists in the brain mimics that position. There are also aspects of empathy in sharing someone’s pain. But, if that position is ‘threatening’ to our brain, we will hurt.
What do we do about that? We use strategies to desensitise and habituate, similar to dealing with any fear. The modern way of tackling pain states, especially those that persist, is using a biobehavioral approach. This means that as well as addressing tissue health with movement and treatment, we must concurrently target the brain and other systems that are involved in the pain experience, e.g. immune, endocrine. It is called ‘top-down’ – ‘bottom-up’. Top-down referring to the brain and our beliefs, understanding, thoughts, how the brain is controlling movement and protecting us; bottom-up signifying the need to nourish the tissues with movement. These exist on a spectrum and both are addressed in a contemporary biopsychosocial treatment programme – see www.specialistpainphysio.com/treatment
Below are some interesting abstracts in relation to this blog:
Pain. 2010 Feb;148(2):268-74. Epub 2009 Dec 11.
Pain sensation evoked by observing injury in others.
School of Psychology, University of Birmingham, Edgbaston, UK.
Observing someone else in pain produces a shared emotional experience that predominantly activates brain areas processing the emotional component of pain. Occasionally, however, sensory areas are also activated and there are anecdotal reports of people sharing both the somatic and emotional components of someone else’s pain. Here we presented a series of images or short clips depicting noxious events to a large group of normal controls. Approximately one-third of this sample reported an actual noxious somatic experience in response to one or more of the images or clips. Ten of these pain responders were subsequently recruited and matched with 10 non-responders to take part in an fMRI study. The subjects were scanned while observing static images of noxious events. In contrast with emotional images not containing noxious events the responders activated emotional and sensory brain regions associated with pain while the non-responders activated very little. These findings provide convincing evidence that some people can readily experience both the emotional and sensory components of pain during observation of other’s pain resulting in a shared physical pain experience.
J Cogn Neurosci. 2007 Jan;19(1):42-58.
The neural substrate of human empathy: effects of perspective-taking and cognitive appraisal.
INSERM Unit 280, France.
Whether observation of distress in others leads to empathic concern and altruistic motivation, or to personal distress and egoistic motivation, seems to depend upon the capacity for self-other differentiation and cognitive appraisal. In this experiment, behavioral measures and event-related functional magnetic resonance imaging were used to investigate the effects of perspective-taking and cognitive appraisal while participants observed the facial expression of pain resulting from medical treatment. Video clips showing the faces of patients were presented either with the instruction to imagine the feelings of the patient (“imagine other”) or to imagine oneself to be in the patient’s situation (“imagine self”). Cognitive appraisal was manipulated by providing information that the medical treatment had or had not been successful. Behavioral measures demonstrated that perspective-taking and treatment effectiveness instructions affected participants’ affective responses to the observed pain. Hemodynamic changes were detected in the insular cortices, anterior medial cingulate cortex (aMCC), amygdala, and in visual areas including the fusiform gyrus. Graded responses related to the perspective-taking instructions were observed in middle insula, aMCC, medial and lateral premotor areas, and selectively in left and right parietal cortices. Treatment effectiveness resulted in signal changes in the perigenual anterior cingulate cortex, in the ventromedial orbito-frontal cortex, in the right lateral middle frontal gyrus, and in the cerebellum. These findings support the view that humans’ responses to the pain of others can be modulated by cognitive and motivational processes, which influence whether observing a conspecific in need of help will result in empathic concern, an important instigator for helping behavior.
Hum Brain Mapp. 2009 Oct;30(10):3227-37.
Empathic neural responses to others’ pain are modulated by emotional contexts.
Department of Psychology, Peking University, Beijing 100871, People’s Republic of China. [email protected]
Recent brain imaging studies indicate that empathy for pain relies upon both the affective and/or the sensorimotor nodes of the pain matrix, and empathic neural responses are modulated by stimulus reality, personal experience, and affective link with others. The current work investigated whether and how empathic neural responses are modulated by emotional contexts in which painful stimulations are perceived. Using functional magnetic resonance imaging (fMRI), we first showed that perceiving a painful stimulation (needle penetration) applied to a face with neutral expression induced activation in the anterior cingulate cortex (ACC) relative to nonpainful stimulation (Q-tip touch). However, when observation of the painful stimuli delivered to a neutral face was intermixed with observation of painful or happy faces, the ACC activity decreased while the activity in the face area of the secondary somatosensory cortex increased to the painful stimulation. Moreover, the secondary somatosensory activity associated with the painful stimulation decreased when the painful stimulation was applied to faces with happy and painful expressions. The findings suggest that observing painful stimuli in an emotional context weakens affective responses but increases sensory responses to perceived pain and implies possible interactions between the affective and sensory components of the pain matrix during empathy for pain.
Neuron. 2007 Aug 2;55(3):377-91.
The cerebral signature for pain perception and its modulation.
Centre for Functional Magnetic Resonance Imaging of the Brain, Clinical Neurology and Nuffield Department of Anaesthetics, Oxford University, OX3 9DU Oxford, England, UK. [email protected]
Our understanding of the neural correlates of pain perception in humans has increased significantly since the advent of neuroimaging. Relating neural activity changes to the varied pain experiences has led to an increased awareness of how factors (e.g., cognition, emotion, context, injury) can separately influence pain perception. Tying this body of knowledge in humans to work in animal models of pain provides an opportunity to determine common features that reliably contribute to pain perception and its modulation. One key system that underpins the ability to change pain intensity is the brainstem’s descending modulatory network with its pro- and antinociceptive components. We discuss not only the latest data describing the cerebral signature of pain and its modulation in humans, but also suggest that the brainstem plays a pivotal role in gating the degree of nociceptive transmission so that the resultant pain experienced is appropriate for the particular situation of the individual.
Neuroimage. 2009 Sep;47(3):987-94. Epub 2009 May 28.
The influence of negative emotions on pain: behavioral effects and neural mechanisms.
Nuffield Department of Anaesthetics, University of Oxford, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK. [email protected]
The idea that pain can lead to feelings of frustration, worry, anxiety and depression seems obvious, particularly if it is of a chronic nature. However, there is also evidence for the reverse causal relationship in which negative mood and emotion can lead to pain or exacerbate it. Here, we review findings from studies on the modulation of pain by experimentally induced mood changes and clinical mood disorders. We discuss possible neural mechanisms underlying this modulatory influence focusing on the periaqueductal grey (PAG), amygdala, anterior cingulate cortex (ACC) and anterior insula as key players in both, pain and affective processing.
Disclaimer: this blog is for informational purposes only. If you are concerned or unsure about your pain or condition, you must consult with your GP or a health professional.