As humans age, everyone's spine develops the degeneration of their vertebrae, discs, facet joints and ligaments as described above. Fortunately, most of the time, the presence of spinal degeneration does not greatly interfere with the movements of the spine, the function of the spinal muscles, the function of the spinal cord or nerve roots, nor does it stimulate the pain neurons that monitor the spine structures. Therefore, despite the presence of degeneration, most people can bend, twist and rotate their spine normally, can lift and carry anything they desire, and are without any pain or neurological symptoms.
Everyone's Pain System is Different
A key factor that determines whether or not one has symptoms, the type of symptoms that one experiences, as well as the duration of symptoms seems to be the unique interaction of one's own nervous system with the degeneration process. Much of a person's pain experience is likely determined by genetic differences in pain sensitivity and the ability of the pain systems that monitor the spine to adapt to the developing degeneration.
Did You Know?To date, several genes are under study that may play a significant role in the development and persistence of spinal pain. As knowledge of the genetics of pain sensitivity develops, this may help us identify the neurochemical pathways that cause individual differences in pain sensitivity. It may also allow us to predict who is most likely to experience persistent pain, and of great importance, who is likely to respond to specific treatments. Large studies of identical twins have found that many twin pain have similar spinal pain experiences.
It appears that some people have insensitive spines, and the pain neurons that monitor their spines are resistant to chemical and mechanical stimulation generated during the degenerative processes. Other people have modest pain sensitivity and experience brief episodes of spinal pain when the pain neurons are intensely stimulated by sudden breakdown of degenerating spine structures, such as progression of anular tears or acute disc herniation. Rapid resolution of spinal pain suggests that the pain neurons quickly adapted or adjusted to the degenerative event and return to their quiet state.
Low-threshold Pain
Unfortunately, some people experience daily neck or back pain that lasts for months, or even years. Despite extensive study, nothing unique has been noted about the spinal degeneration of most of these individuals to explain their chronic pain. What appears to be unique is the persistence of a heightened sensitivity of pain neurons that monitor their spines resulting in low threshold pain. This refers to pain that is generated by stimuli that are not harmful, nor of adequate intensity to stimulate the pain neurons when they are functioning normally.
Did You Know?Temporary development of low threshold pain is part of the normal neurological response to injuries, and accounts for the sensitivity that makes pressure or touch (non-harmful stimuli) painful at the site of a cut or bruise. This temporary low threshold pain sensitivity usually disappears with healing.
Examples of low threshold pain are many, and can include pain generated by a touch or pressure stimulation of the soft tissues of the spine, shoulders or pelvis; pain stimulated by normal movements of the spine such as bending or rotating the spine; and pain produced during prolonged positions such as sitting or standing. None of these actions are dangerous or harmful, but all produce stimulation of sensory neurons that monitor touch, joint movement or muscle function. Low threshold pain occurs when these stimuli are falsely translated by the nervous system into pain signals.
The mechanisms of persistent low threshold pain are complex and under intense study. Some research suggests that dysfunction of specialized sensory neurons in the spinal cord called wide dynamic range neurons may be involved in this phenomenon. Apparently, low threshold pain is produced when wide dynamic range neurons become "sensitized" and produce nerve impulses that stimulate the pain system in response to all input they receive from the primary sensory neurons that monitor the spine, regardless of whether the primary sensory neurons were reporting touch, movements, muscle activity or actual pain.
Through neurological connections between neurons, pain sensitized wide dynamic range neurons can sensitize neighboring neurons. This may cause pain sensitivity to touch and discomfort with movements to spread to wider and wider areas in the absence of injury to the newly painful areas. In some people with chronic spinal pain, a generalized lowering of pain threshold can develop throughout the body. In this situation, called central sensitization, harmless pressures, heat or cold stimulation applied to non-painful parts of the body produce are experienced as painful. These same stimuli do not produce pain in people without chronic pain. This central sensitization phenomenon is noted in many types of chronic pain in addition to chronic spinal pain.
The consequences of persistent low threshold pain and central sensitization associated with chronic spinal pain are profound. First, as this type of pain results from a dysfunction of the pain system, and does not alert us to damage or harm, the experience of low threshold pain does not serve any physiological purpose. Second, since this type of pain does not serve any physiological purpose, continuing activities in the presence of low threshold pain is safe. Third, since the problem is a neurological problem to a much greater degree than it is a problem of spine degeneration, treatment should be understood in terms of it neurological mechanisms.
The Effects of the Brain on Pain
The brain also appears to play a strong role in chronic spinal pain. Wide dynamic range neurons receive some direct control from the brain, which can inhibit or enhance their function. When attention is focused away from pain, brain centers that directly connect with the spinal cord can suppress wide dynamic range neuron function, which lessens their ability to stimulate the pain system. In contrast, when attention is focused on pain, inhibition of these neurons stops, and their full input into the pain system is allowed. This regulation of the wide dynamic range neurons by the brain may be one of several mechanisms through which thoughts, fears and focus may influence pain experience.
In addition to brain and spinal cord interactions, ongoing brain research is now uncovering complex interactions between pain processing centers in the brain and other brain centers concerned with thoughts and emotions. It has long been reported by people with chronic pain that periods of negative emotions, stress, fears and anger increase the severity of their symptoms. Conversely, many people have remarked that periods of positive emotions lessen their pain. Until recently, the mechanisms of interactions between the brain and pain have been elusive. By using brain imaging that show neuron (brain cell) metabolic activity, several areas of the brain involved with processing pain are noted to have heightened neuron activity when pain and emotional stimulations are combined. These findings give evidence to support the experiences reported by people with pain, and highlight the participation of the mind in the pain experience. The implications of the brain - pain interaction also support the importance of improved cognition (thoughts) in the management of chronic pain. Improved cognition can result from replacing misinformation with knowledge, developing a positive approach towards managing pain, having successful life experiences in the presence of pain, and striving to maintain optimum mental health.