Figure 1. There are many types of sensory receptors located in the skin, each attuned to specific touch-related stimuli.

The skin can convey many sensations, such as the biting cold of a wind, the comfortable pressure of a hand holding yours, or the irritating itch from a woolen scarf. The different types of information activate specific receptors that convert the stimulation of the skin to electrical nerve impulses, a process called transduction. There are three main groups of receptors in our skin: mechanoreceptors, responding to mechanical stimuli, such as stroking, stretching, or vibration of the skin; thermoreceptors, responding to cold or hot temperatures; and chemoreceptors, responding to certain types of chemicals either applied externally or released within the skin (such as histamine from an inflammation). For an overview of the different receptor types and their properties, see Table 1. The experience of pain usually starts with activation of nociceptors—receptors that fire specifically to potentially tissue-damaging stimuli. Most of the nociceptors are subtypes of either chemoreceptors or mechanoreceptors. When tissue is damaged or inflamed, certain chemical substances are released from the cells, and these substances activate the chemosensitive nociceptors. Mechanoreceptive nociceptors have a high threshold for activation—they respond to mechanical stimulation that is so intense it might damage the tissue. Sensory information collected from the receptors and free nerve endings travels up the spinal cord and is transmitted to regions of the medulla, thalamus, and ultimately to the somatosensory cortex, which is located in the postcentral gyrus of the parietal lobe.

Action Potentials in the Receptor Cells Travel as Nerve Impulses with Different Speeds

Figure 2. The Homunculus: Homunculus means “little man”, and here you see a scale model of the human body distorted to reflect the relative space that body parts occupy in the somatosensory cortex. As you can see, the lips, hands, feet, and genitals send more somatosensory projections to the brain than do any other body parts.

When you step on a pin, this activates a host of mechanoreceptors, many of which are nociceptors. You may have noticed that the sensation changes over time. First, you feel a sharp stab that propels you to remove your foot, and only then you feel a wave of more aching pain. The sharp stab is signaled via fast-conducting A-fibers, which project to the somatosensory cortex. This part of the cortex is somatotopically organized—that is, the sensory signals are represented according to where in the body they stem from (see homunculus illustration, Figure 2). The unpleasant ache you feel after the sharp pin stab is a separate, simultaneous signal sent from the nociceptors in your foot via thin C-pain or Aδ-fibers to the insular cortex and other brain regions involved in the processing of emotion and interoception (see Figure 3 for a schematic representation of this pathway). The experience of stepping on a pin is, in other words, composed of two separate signals: one discriminatory signal allowing us to localize the touch stimulus and distinguish whether it’s a blunt or a sharp stab; and one affective signal that lets us know that stepping on the pin is bad. It is common to divide pain into sensory–discriminatory and affective–motivational aspects (Auvray, Myin, & Spence, 2010). This distinction corresponds, at least partly, to how this information travels from the peripheral to the central nervous system and how it is processed in the brain (Price, 2000).

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 excited 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, as Aron Ralston did, and still manage to walk, talk, and think rationally afterward? 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 send 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.

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

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 a 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 thing 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.

The Power of the Mind

The context of pain and touch has a great impact on how we interpret it. Just imagine how different it would feel to Aron if someone amputated his hand against his will and for no discernible reason. Prolonged pain from injuries can be easier to bear if the incident causing them provides a positive context—like a war wound that testifies to a soldier’s courage and commitment—or phantom pain from a hand that was cut off to enable life to carry on.

The relative meaning of pain is illustrated by a recent experiment, where the same moderately painful heat was administered to participants in two different contexts—one control context where the alternative was a non-painful heat; and another where the alternative was an intensely painful heat. In the control context, where the moderate heat was the least preferable outcome, it was (unsurprisingly) rated as painful. In the other context, it was the best possible outcome, and here the exact same moderately painful heat was actually rated as pleasant—because it meant the intensely painful heat had been avoided. This somewhat surprising change in perception—where pain becomes pleasant because it represents relief from something worse—highlights the importance of the meaning individuals ascribe to their pain, which can have decisive effects in pain treatment (Leknes et al., 2013). In the case of touch, knowing who or what is stroking your skin can make all the difference—try thinking about slugs the next time someone strokes your skin if you want an illustration of this point.

Pain and pleasure not only share modulatory systems—another common attribute is that we don’t need to be on the receiving end of it ourselves in order to experience it. How did you feel when you read about Aron cutting through his own tissue, or “Thomas” destroying his own bones unknowingly? Did you cringe? It’s quite likely that some of your brain areas processing affective aspects of pain were active even though the nociceptors in your skin and deep tissue were not firing. Pain can be experienced vicariously, as can itch, pleasurable touch, and other sensations. Tania Singer and her colleagues found in an fMRI study that some of the same brain areas that were active when participants felt pain on their own skin (anterior cingulate and insula) were also active when they were given a signal that a loved one was feeling the pain. Those who were most “empathetic” also showed the largest brain responses (Singer et al., 2004). A similar effect has been found for pleasurable touch: The posterior insula of participants watching videos of someone else’s arm being gently stroked shows the same activation as if they were receiving the touch themselves (Morrison, Bjornsdotter, & Olausson, 2011).