Another guest blog for you on a new look at pain by Katie Bigelow. This is based on a growing body of evidence and neuroscience regarding how to view pain.
Katie is a Z Health trainer level 3 trainer in GA and look for more excellent info from her in the next few years. . If you are in that area, I would highly recommend that you drop here at line at this email. kbigelo AT emory DOT edu
Take it away Katie!
Pain Perception and the Neuromatrix
By: Katelin Bigelow
Pain is a sensory output from the nervous system that has eluded scientists for many years. It is not clearly understood why pain can act as both a survival mechanism and a debilitating disorder in individuals. The mechanisms of how pain works in the brain and the significance of each structure and its affects on pain perception continues to be studied. Understanding the function of the basic structure of the nervous system, the neuron, has allowed for increased knowledge in how the signal begins and travels to the brain. Many aspects of the neural signaling pathway have been studied on how a stimulus reaches the brain, but it is what occurs in the brain that is least understood. This article will review the definition of pain, the structure and function of the neuron, the neural pathway a stimulus must travel, and the neuromatrix theory of pain in the brain.
What is Pain?
The International Association for the Study of Pain defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage (International Association for the Study of Pain 2007). Pain is a survival response that signals threat to the body resulting in an action signal being released and physical movement away from the harmful stimulus. As the International Association for the Study of Pain states, pain can be caused by a sensory or emotional stimulus. Pain does not have to come directly from a physical threat as it can be emotional or spiritual, but it is perceived as a danger by the brain. Thus any stimulus is painful if the brain interprets it as threatening to its survival. The amount of pain experienced does not directly relate to the amount of tissue damage sustained (Butler and Moseley 2003). Chronic pain may occur without any significant tissue damage, or with pain that is out of proportion to the amount of tissue damage suffered. The brain may not even receive the message that the threat is gone and continue to send the action signal of pain to the body.
Pain’s danger signal is a multi-system output event that can create changes throughout the entire body to meet the needs of any threat. Pain decreases cognitive accuracy and negatively influences memory, attention, and focus at the time of the event. Pain alters nervous system activity and modifies immune system activity usually reducing its functional capacity. Visuomotor systems are activated by painful stimuli as well as physiologic motor systems, which aid in the escape of the threat, promoting safety and survival. (Cobb 2007).
A neuron or nerve cell is the specific type of cell found only in the nervous system. A neuron contains sensory, chemical, thermal, electrical and other receptors that send and receive information to and from other cells in the body. A neuron’s receptors are the first to receive information regarding initial harmful stimuli. A nerve cell contains the same basic organelles as other cells in an organism. These organelles and their characteristic features of the cell allow the neuron to maintain plasticity and rapid responsiveness to environmental conditions (Lambert and Kinsley 2005). In addition to the organelles located in the soma, the neuron structure also contains dendrites and an axon. Dendrites are branching fibers that extend from the neuron cell body and retrieve information from surrounding neurons and cells. Dendrites increase the surface area of the neuron with branch-like extensions known as dendritic spines. Dendritic spines also increase communication between the surrounding cells. The axon of a neuron is a cylindrical extension of the cell body coming from the opposite side of the neuron’s dendrites. The axon of a neuron projects information out to surrounding cells via the action potential. Action potential is created when the threshold of positively charged particles is reached inside the cell and an electrical impulse is released to surrounding cells (Butler and Moseley 2003). The axon of a neuron can also have myelin sheath surrounding it to aid in protection and the speed at which signals are sent. The neuron’s distinctive structure as shown in Figure 1 from the National Institute on Drug Abuse allows for information to travel rapidly and efficiently throughout the nervous system. The nervous system governs all other body systems and maintaining homeostasis.
Neural Signal Pathway
The neural signal pathway describes the process of how a stimulus, painful or otherwise, is initiated and travels up to the brain where processing and output occur. A painful stimulus first occurs when the receptor site of a nocioreceptor or pain receptor on a neuron receives an activation signal. This causes the neuron to fire and send information via the axon to the peripheral nerve fibers, which become larger and larger as the message becomes closer and closer until the spinal nerve is formed (Wilkinson et al., 1994). The peripheral nerve fibers branch and send the message into the dorsal and ventral roots. The information then enters into the meninges on its way to spinal cord. The pain signal then travels into and up the spinal cord towards the brainstem. Once the brain receives the stimulus it then determines whether or not it is threatening. The threatening information enters clusters of nodes responsible for sensation, movement, emotions, and memory where the information is expressed. There is no pain center in the brain; instead there are many structures throughout the brain that play a role in the expression of pain. There is a specific pattern, theorized as the neurosignature by Dr. Ron Melzack that is responsible for painful output (Melzack 2001). The brain structures that are thought to be involved in the pattern are shown in Table 1, along with their functions. These brain structures play a role in processing the stimulus, and are responsible for the final output that is received as pain. The output travels back down the neural pathway to the area that initially received the threatening stimulus, and the individual responds with action and movement.
Brain Structures and Functions Involved in Pain Neurosignature
Organize and prepare to
Focus and concentration.
Memory and decision-making.
Addiction, fear, and the condition
Autonomic nervous system
regulation, motivation, and
Movement and cognition.
Memory, spacial cognition,
and fear conditioning.
Pain Neuromatrix in the Brain
The model of the neuromatrix of pain in the brain theorizes that pain is a multidimensional experience produced by patterns of nerve impulses. These patterns, called neurosignatures, are triggered by sensory or emotional stimulus that can be noxious or non-noxious. Pain is a warning signal produced by the brain when any danger is perceived. The pain neuromatrix seeks to explain the complex neural network involved in the interpretation of a stimulus and the resulting output. An individual’s neuromatrix is genetically determined and modified by the constant sensory experiences received from the environment (Melzack 2001).
The pain neuromatrix has four major components that determine the sensory output of pain. The first component is the input of stimulus from the surrounding environment that allows for bodily awareness and a sense of self. Second, the input travels up the neural pathway to the brain where it is processed and integrated to become a characteristic pattern, known as the neurosignature (Melzack 2001). The neurosigniture is imprinted into the brain’s neuromatrix as major sensory events are interpreted. The third component is the process of converting the patterns created by the neurosignature into self-awareness, which is accessed through the virtual body. The virtual body and the primary somatosensory homunculus are the most well known for spatial representation of both the internal and external physical environment. Both are significant in the conversion of neurosignature to awareness (Moseley 2003). The fourth component to the pain neuromatrix in the brain is the output stimulus of pain. The virtual body aids the brain in sending the pain signal to the most relevant body part that will result in action/movement and thus ensure survival.
Chronic pain has an added complexity to the activity of the pain neuromatrix. Chronic pain contributes two inter-dependent mechanisms, 1) nociceptive and 2) non-nociceptive mechanisms. Both increase the conviction of the nervous system that body tissue is in danger resulting in an increase of activity in the pain neuromatrix. Nociceptive mechanisms include immune system related dysfunction that stimulates nocioreceptors in the body’s tissues. The non-nocioceptive mechanism includes a cognitive-evaluative aspect. The increased neuromatrix activity results in the repetitive cycling of the given neurosigniture, which constantly produces a painful output regardless of any actual danger to the body’s tissue. (Moseley 2003).
Another factor in chronic pain is the stress the individual experiences. Pain disrupts regulatory systems throughout the body. Stress is produced to return the body back to homeostasis and thus also is important to pain. Stress is a biological system and like pain is activated by any threat to the biological homeostasis, psychological stability and the body-self image (Ader and Cohen 1993). When any significant traumatic event occurs in the body, cortisol is released. Cortisol is an essential hormone and responsible for producing and maintaining high levels of glucose for immediate response after any injury, threat, or emergency (Melzack 2001). While cortisol is meant to aid in the immediate survival process it can have adverse effects if it is constantly being released over long periods of time, like with chronic pain. Sustained cortisol release over extended periods of time can cause weakness, fatigue, decalcification of bone, and suppress the immune system (Woolf 2007). Prolonged immune suppression may diminish gradually and give way to excessive immune response. Sensitization of inflammatory cells can result in reducing the nocioceptor threshold and increasing the responsiveness of the immune system (Woolf 2007). The immune system’s attack on its own body’s tissue might produce autoimmune diseases that are chronic pain syndromes (Melzack 2001).
The pain and neuromatrix in the brain theory offers a paradigm shift for how pain is interpreted by the nervous system. Any stimulus coming from the receptors of a neuron can be perceived by the brain as pain regardless of whether body tissue damage is actually occurring. All pain is created and processed in the neuromatrix of the brain and is a result of the brain’s perception of the given event. There is no specific location in the brain where pain is located; rather it is affected by multiple structures and their functions. Pain is also individual and dependent upon a person’s genetics, experiences, emotional status, stress levels, and environmental factors. A better understanding of the pain neuromatrix will help advance our knowledge and ability to cope with pain.
Ader, R., and N. Cohen. “Psychoneuroimmunology: Conditioning and Stress.” Annual Review of Psychology, 1993, vol. 44, pp. 53-85.
Butler, D.S., and G.L. Moseley. Explain Pain. Adelaide, South Australia: Noigroup Publishers, 2003.
Cobb, W. E. “The T-Phase Approach to Pain & Performance Barriers.” T Phase Manual, 2007 pp. 1-5.
[IASP] International Association for the Study of Pain. 2007, Dec. 13. IASP home page.
Lambert, K., and C.H. Kinsley. Clinical Neuroscience; The Neurobiological Foundations of Mental Health. New York: Worth Publishers, 2005.
Melzack, R. “Pain and the Neuromatrix in the Brain.” Journal of Dental Education, 2001, vol. 65, pp. 1378-1382.
Moseley, G.L. “A Pain Neuromatrix Approach to patients with Chronic Pain.” Manual Therapy, 2003, vol. 8, pp. 130-140.
[NIDA] National Institute on Drug Abuse. 2006, Nov. 2. NIDA home page.
Wilkinson, S. V., M.T. Neary, R.O. Jones, and K.F. Sunchein. “The Neuroanatomy of Pain.” Pain Management, 1994, vol. 11, pp. 1-13.
Woolf, C.J., and Q. Ma. “Nocioceptors-Noxious Stimulus Detectors.” Neuron, 2007, vol. 55, pp. 353-364.