THE NEUROMATRIX OF PAIN

When you stub your toe on a rock, you feel a pain at that specific spot on your body. The pain is often so sharp and so localized that you might be tempted to believe that it’s your toe itself that’s experiencing the pain. But that’s not really the case at all. First the nociceptive fibres in your toe send nerve impulses to your spinal cord, which relays them to your brain. And it is the neural activity of certain parts of your brain that then makes you feel the pain in your toe, jump back from the rock, shout a few choice words, and rub your toe vigorously. What are these parts of the brain, and how do they work together to make you feel the multiple properties of pain, such as the type of pain and its location, intensity, and negative emotional charge? These are complex questions that have been hotly debated over the past few decades and continue to be so today. Reticular formation (red), ventral posterolateral nucleus (VPL) of the thalamus (green), and somatosensory cortex (blue) But one thing seems certain: there is no single “pain centre” whose activity alone could account for all the multiple aspects of pain. In other words, there is no one part of the brain that could be surgically removed to eliminate all pain. That said, experiments conducted with brain imaging and other technologies do clearly show that when you are experiencing pain, the activity of many specific areas of your brain is altered. These areas are interconnected and form a network that some neuroscientists call the pain matrix. And from what is already known about these areas, they are often associated with different aspects of pain. One such area, located in the brainstem, is the reticular formation, one of the first brain structures that receives connections from the ascending pain pathways in the spinal cord. The activation of the reticular formation contributes to the reactions of awakeness and alertness associated with pain. The neurons of the reticular formation can alter your heart rate, arterial blood pressure, respiration, and other vital functions that can be affected by pain. It is also the reticular formation that allows a pain stimulus to go unnoticed if your attention is focused on some compelling task. The next stop along the ascending pain pathways is the thalamus, a brain structure that acts like a giant switchbox for sensory signals. There the pain pathways make connections to various sub-regions of the thalamus, in particular the ventral posterolateral (VPL) nucleus, which, as its name implies, is located in the ventral, posterior, lateral portion of the thalamus. The VPL nucleus then plays a major role in the sensory discrimination of pain. Its neurons project their axons into the somatosensory cortex, a brain structure known for its ability to locate pain and assess its intensity. Signals for the sense of touch also pass through the VPL nucleus and on to this same cortex, but information about pain and touch is handled in separate subregions of this nucleus. The medial portion of the thalamus also receives connections from the reticular formation. This part of the thalamus displays a more tenuous somatotopic organization (see sidebar) that prevents it from playing as much of a role in discriminating the bodily location of a stimulus. The neurons of the medial thalamus make connections to the motor cortical areas of the frontal lobe, whereby this part of the thalamus plays a role in generating the motor and emotional reactions associated with pain. The intralaminar nuclei of the thalamus, located quite close to the medial portion, are also part of this “non-specific” area of the thalamus, which participates in the alertness response to pain. In addition to connecting to the frontal lobe, the intralaminar nuclei also project to various parts of the limbic system. And because the frontal cortex itself sends numerous projections to the limbic system, these two structures taken together with the intralaminar nuclei unquestionably constitute a system that is involved in the unpleasant emotional component of pain and the behavioural responses designed to reduce it. Once nociceptive messages reach the cerebral cortex, the abundance of reciprocal connections there make the path of these messages much harder to follow. But brain-imaging studies have confirmed that the primary and secondary somatosensory cortexes, as well as the anterior cingulate cortex and the insular cortex, are all involved in the perception of pain.