In the past, pain was regarded as a simple stimulus-response relationship. In other words, an injury occurred (stimulus) and a message was sent to the brain to respond. This theory did not explain why pain sometimes continues after the initial damage had healed, or why two people respond differently to the same type of injury with different levels of pain. More recent research has shown that there are many pathways that can send a pain signal to the brain. There are multiple interacting peripheral (spinal cord, trigeminal nerve) and central (brain) mechanisms involved with pain perception. The detection of pain first requires activation of one or more tiny sensory organs (called nociceptors) located throughout our skin, muscles, and within our organs. The nociceptor converts the painful stimulation into an electrical signal that is sent to the spinal cord (for skin, muscle, joints, organs, and meninges) or to the trigeminal nerve ganglion (head, mouth, neck). From there the signal is transmitted to the brain where the pain is perceived. If the painful stimulus continues, the threshold for activating the nociceptor becomes less, and painful stimulation becomes easier. In other words, if the pain continues, it becomes easier to experience the same amount of pain with less of a stimulus. This increase in sensitivity to pain is called peripheral sensitization, or primary hyperalgesia. There are also a complex array of descending (from the brain to the spinal cord) pain pathways that contribute significantly to altering the painful signals. These pathways can cause either a reduction or an increase in pain perception within the brain. This is where previous psychological problems (depression, anxiety) and prior painful experiences may play an important role in how much pain an individual patient experiences. Alterations in an individual patient’s ability to modulate pain via these descending pathways may convert an acute pain problem into a chronic pain state. It is believed that chronic pain may travel along larger, slower nerve fibers and is characterized by dull and aching sensations. Although research is still being done to understand these pathways, it seems that the brain uses them to send chemical substances and nerve impulses to combat the pain signals being sent to the brain. The Gate Control Theory, developed by Melzack and Wall, is one theory about how pain signals are sent in the body. It states that there are “gates” on the nerve fibers of the spinal cord that can either allow a pain signal through or close off to stop the pain signal. The gates can be closed off when there is enough alternative stimulation or a signal from the brain. When the gates are open, pain signals get through more easily and pain can be intense. When the gates close, pain messages are stopped from reaching the brain and may not even be noticed. For example, rubbing your arm after you bump it creates a fast pain signal that crowds out the slower transmission of sharp pain from the bump. Gate control theory also takes into account the psychological factors that are related to pain and how they can impact the pain response.