(Workbook Page 26, 27)
Wind-up pain is caused by a series of events in synapses and in nerve cells. NMDA receptors are activated when Substance P attaches to NK-1 receptors and then incorporated into the cell, activating Protein Kinase-C. This then removes the magnesium blocking the actuation of the NMDA receptor. Glutamate attaches to internal receptor sites in the NMDA receptor and Calcium floods into the cell, causing the pain signal to increase and fire more frequently.
Wind-up pain is one of the hallmarks of the neuroplastic changes that create persistent pain. Persistent pain is not just a longer lasting acute pain. There are several changes that happen in brain and body. Wind-up can happen anywhere in the spinal cord or brain. It means that the pain signal that comes into the central nervous system becomes stronger and longer lasting. This is a physiologic process that involves activation of receptors that are normally dormant on post synaptic nerve endings. The result is that the nerve fires more frequently and with greater strength. It also means that the nerves fired this way keep firing even without an ongoing stimulus. Hence people may heal, but the pain circuit remains activated.
Part of the wind-up process involves nerves sprouting into pain processing areas that normally transmit signals that do not lead to pain. The result is that nerve signaling for touch, movement, pressure, temperature or vibration signal for pain. These sprouts also grow into different levels up and down the spinal cord. This accounts for pain starting in a discreet area and progressing to occurring in an entire region. In this way an injury to the finger causing local pain can gradually involve the entire hand.
Look at the graphic on page 26 of the Neuroplastic Transformation workbook and read the accompanying text. The graphic shows an incoming signal that winds up at the dorsal horn of the spinal cord. This signal is not yet felt as pain, because it has not reached the thinking and perceiving part of the brain. When it does so, it will wind up at each of these levels due to activation of NMDA receptors on post-synaptic nerve endings. This is one of the reasons that persistent pain is so powerful.
Persistent pain can be caused by injury to a nerve and happen in the moment of that injury. It is not related to the length of time it has been present, for example, six months or a year. It relates the pathological process that causes it. Here we see a lumbar disc herniating into a nerve root. In that instant the pain transforms from acute pain to persistent pain. This is marked by injury to the nerve root, made up of tens of thousands of nerve cell axons. These release massive amounts of Substance-P into the spinal cord where these nerve roots enter the central nervous system. The pain signal spreads out to a greater area, activates specialized receptors (NMDAR) and causes the pain signal to become greater in strength and persistent firing (Long-Term Potentiation). This is known as wind-up. The wound-up signal crosses to the opposite side of the spinal cord and travels up to the brain, where it causes more Substance-P release and winds up at each of 16 regions of the brain. When it gets to the Amygdala, the signal is transformed into the perception of pain. The signal fires on its own with or without further stimulus from the area of injury. The brain's normal analgesic mechanisms are overwhelmed and attempts to stop this signal fail.
In persistent pain there are many signals sent to the brain, including touch, temperature, movement, position and vibration that are all being interpreted by the brain as pain. See if you can distinguish these normally non-painful signals and separate them from your pain. Instead of viewing your pain as a danger to avoid, look at it as something that is no longer dangerous and instead as a signal to do something, in order to come up with new ways to reduce it. By doing this the pain can be reduced from a threat to an opportunity to change your brain in relationship to your body.