6.3.4: Modulation

Pain Is Necessary for Survival, but Our Brain Can Stop It if It Needs To

In April 2003, the climber Aron Ralston found himself at the floor of Blue John Canyon in Utah, forced to make an appalling choice: face a slow but certain death—or amputate his right arm. Five days earlier he fell down the canyon—since then he had been stuck with his right arm trapped between an 800-lb boulder and the steep sandstone wall. Weak from lack of food and water and close to giving up, it occurred to him like an epiphany that if he broke the two bones in his forearm he could manage to cut off the rest with his pocket knife. The thought of freeing himself and surviving made him so exited he spent the next 40 minutes completely engrossed in the task: first snapping his bones using his body as a lever, then sticking his fingers into the arm, pinching bundles of muscle fibers and severing them one by one, before cutting the blue arteries and the pale “noodle-like” nerves. The pain was unimportant. Only cutting through the thick white main nerve made him stop for a minute—the flood of pain, he describes, was like thrusting his entire arm “into a cauldron of magma.” Finally free, he rappelled down a cliff and walked another 7 miles until he was rescued by some hikers (Ralston, 2010). How is it possible to do something so excruciatingly painful to yourself, and still manage to walk, talk, and think rationally afterwards? The answer lies within the brain, where signals from the body are interpreted. When we perceive somatosensory and nociceptive signals from the body, the experience is highly subjective and malleable by motivation, attention, emotion, and context.

Figure 3: Pain processing pathways

Left - Ascending pain pathways: An injury is signaled simultaneously via fast-conducting Aα or Aβ-fibres and slow-conducting C-pain or Aδ-fibres. The fast A-fibres signal pressure, stretching and other tissue movements to the somatosensory cortex via the dorsal column nuclei. The C-pain and Aδ-fibres sends pain information from nociceptors in the tissue or skin, and transmits these signals to second order neurons in the dorsal horn of the spinal cord. The second order neurons then cross over to the opposite side, where they form the ascending spinothalamic tract. This tract projects signals to nuclei in the medulla and midbrain on the way up to the thalamus (T). The thalamus relays the information to the somatosensory and insular cortex, as well as cortical regions mediating different aspects of the pain experience such as affective responses in the cingulate cortex.

Right - Descending pain modulation pathways: Information from the environment and certain motivational states can activate this top–down pathway. Several areas in the limbic forebrain including the anterior cingulate and insular cortex, nuclei in the amygdala and the hypothalamus (H), project to the midbrain periaqueductal grey (PAG), which then modulates ascending pain transmission from the afferent pain system indirectly through the rostral ventromedial medulla (RVM) in the brainstem. This modulating system produces analgesia by the release of endogenous opioids, and uses ON- and OFF-cells to exert either inhibitory (green) or facilitatory (red) control of nociceptive signals at the spinal dorsal horn.

The Motivation–Decision Model and Descending Modulation of Pain

According to the motivation–decision model, the brain automatically and continuously evaluates the pros and cons of any situation—weighing impending threats and available rewards (Fields, 2004, 2006). Anything more important for survival than avoiding the pain activates the brain’s descending pain modulatory system—a top-down system involving several parts of the brain and brainstem, which inhibits nociceptive signaling so that the more important actions can be attended to (Figure 3b). In Aron’s extreme case, his actions were likely based on such an unconscious decision process—taking into account his homeostatic state (his hunger, thirst, the inflammation and decay of his crushed hand slowly affecting the rest of his body), the sensory input available (the sweet smell of his dissolving skin, the silence around him indicating his solitude), and his knowledge about the threats facing him (death, or excruciating pain that won’t kill him) versus the potential rewards (survival, seeing his family again). Aron’s story illustrates the evolutionary advantage to being able to shut off pain: The descending pain modulatory system allows us to go through with potentially life-saving actions. However, when one has reached safety or obtained the reward, healing is more important. The very same descending system can then “crank up” nociception from the body to promote healing and motivate us to avoid potentially painful actions. To facilitate or inhibit nociceptive signals from the body, the descending pain modulatory system uses a set of ON- or OFF-cells in the brainstem, which regulates how much of the nociceptive signal reaches the brain. The descending system is dependent on opioid signaling, and analgesics like morphine relieve pain via this circuit (Petrovic, Kalso, Petersson, & Ingvar, 2002).

The Analgesic Power of Reward

Social rewards, like holding the hands or just seeing the picture of a loved one, can reduce sensations of pain. [Image: rogerl01, CC0 Public Domain, https://goo.gl/m25gce]

Thinking about the good things, like his loved ones and the life ahead of him, was probably pivotal to Aron’s survival. The promise of a reward can be enough to relieve pain. Expecting pain relief (getting less pain is often the best possible outcome if you’re in pain, i.e., it is a reward) from a medical treatment contributes to the placebo effect—where pain relief is due at least partly to your brain’s descending modulation circuit, and such relief depends on the brain’s own opioid system (Eippert et al., 2009; Eippert, Finsterbusch, Bingel, & Buchel, 2009; Levine, Gordon, & Fields, 1978). Eating tasty food, listening to good music, or feeling pleasant touch on your skin also decreases pain in both animals and humans, presumably through the same mechanism in the brain (Leknes & Tracey, 2008). In a now classic experiment, Dum and Herz (1984) either fed rats normal rat food or let them feast on highly rewarding chocolate-covered candy (rats love sweets) while standing on a metal plate until they learned exactly what to expect when placed there. When the plate was heated up to a noxious/painful level, the rats that expected candy endured the temperature for twice as long as the rats expecting normal chow. Moreover, this effect was completely abolished when the rats’ opioid (endorphin) system was blocked with a drug, indicating that the analgesic effect of reward anticipation was caused by endorphin release.

For Aron the climber, both the stress from knowing that death was impending and the anticipation of the reward it would be to survive probably flooded his brain with endorphins, contributing to the wave of excitement and euphoria he experienced while he carried out the amputation “like a five-year-old unleashed on his Christmas presents” (Ralston, 2010). This altered his experience of the pain from the extreme tissue damage he was causing and enabled him to focus on freeing himself. Our brain, it turns out, can modulate the perception of how unpleasant pain is, while still retaining the ability to experience the intensity of the sensation (Rainville, Duncan, Price, Carrier, & Bushnell, 1997; Rainville, Feine, Bushnell, & Duncan, 1992). Social rewards, like holding the hand of your boyfriend or girlfriend, have pain-reducing effects. Even looking at a picture of him/her can have similar effects—in fact, seeing a picture of a person we feel close to not only reduces subjective pain ratings, but also the activity in pain-related brain areas (Eisenberger et al., 2011). The most common things to do when wanting to help someone through a painful experience—being present and holding the person’s hand—thus seems to have a measurably positive effect.

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Touch and Pain by Guro E. Løseth, Dan-Mikael Ellingson, and Siri Leknes is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Permissions beyond the scope of this license may be available in our Licensing Agreement.