MBS

PRIMER

You can think of MBS symptoms as a warning signal. Our brains are constantly scanning our environments, bodies, and minds for signs of danger. When they identify one, they produce a warning signal, such as pain, to motivate us to take action to protect ourselves (see pain 101).

While we are programmed to interpret pain and other physical symptoms as a warning of injury or disease, the brain can produce such symptoms in the absence of a physical problem (see psychogenic pain). In MBS, the brain produces symptoms in response to dangers that are psychological in nature (see dangers from within).

MBS symptoms are “fueled” by fear (see fear is the fuel) and “learned” via the establishment of symptom-producing neural pathways (see neural pathways are the infrastructure).

Q: Why do our brains use physical symptoms to warn us about psychological issues?

A: Because physical symptoms get results. They scare the shit out of us; they motivate us to take action when nothing else will. Our brains can learn that creating physical symptoms is an effective way to (a) distract us from challenging emotions, (b) force us back into bed (away from the stressors of the world), or (c) land us needed care, and thereby keep us “safe.”

Pain 101

Pain is the warning signal that the brain produces in response to the presence or threat of tissue damage. It’s an important survival mechanism; it teaches us to avoid harmful activities (e.g., touching a hot stove) and motivates us to protect an injury while it heals (e.g., stop running on a sprained ankle). 

When we are injured, damaged cells release chemical signals that bind to and activate receptors on pain-sensing neurons called nociceptors. The activated nociceptors respond by transmitting a warning signal to the brain. The brain evaluates the warning signal and, if it deems it worthy of action, it translates it into a sensation of pain at the site of the injury (i.e., so that you know where the problem is). So while the pain feels like it’s coming from the injury, it’s really produced by the brain, which dictates when, where, and how much pain to produce in response to signals from the body.

Psychogenic pain

We’re biologically programmed to believe that any pain that we experience is caused by a physical problem in our body, but sometimes it isn’t. Nociceptors can be activated in the absence of tissue damage, and your brain can create pain in the absence of nociceptor signaling (Garland, 2012). A well-known example of the latter phenomenon is phantom pain, wherein people feel pain in a part of the body that is no longer there (i.e., a place where they have no nociceptors). The brain can also learn to produce pain in response to innocuous stimuli from the body as a result of “central sensitization,” a process in which the neurons in a pain-sensing pathway become hyper-sensitive, such that they have a lower activation threshold for transmitting pain signals (Volcheck, 2023).

Pain that is produced in the absence of an illness or injury is sometimes referred to as “psychogenic pain,” “neuroplastic pain,” or “centralized pain.” It’s helpful to think of this type of pain as a false alarm. It sounds just like a “real” alarm, but it was tripped in the absence of a legitimate emergency. The most beloved example of psychogenic pain is the legend of boot nail guy.

Boot nail guy

Boot nail guy is/was a construction worker who jumped down onto a nail such that it pierced through his boot and caused him agonizing pain. (The poor guy had to be sedated with both fentanyl and midazolam.) However, when doctors took his boot off, they found that he was completely uninjured; the nail had passed between two of his toes (Fisher et al., BMJ 310(70), 1995). Boot nail guy’s pain was created by his brain simply because it believed that he was in danger.

Dangers from within

To recap, our brains create pain to warn about a perceived threat, and sometimes the perceived threat is not a physical problem. The strange truth is that sometimes the perceived threat is a psychological problem. It could be stress, overwhelm, an internal conflict, a feeling of being trapped, a shameful secret, a negative thought pattern (e.g., putting pressure on yourself, beating yourself up), fear, anger, guilt, shame, or another challenging emotion; anything that makes the brain feel unsafe.

We all understand that stress and emotions can cause physiological changes. For example, we accept that our pits get sweaty and our stomachs get squirrely when we are nervous. Yet, the idea that stress and emotions can cause debilitating pain (and a bizarre collection of other symptoms) sounds like magical thinking. There is, however, a growing body of scientific research that demonstrates that our pain is tied to our stress and emotions. Click on the dropdown menu for the details.

  • Stress increases the sensitivity of our nervous systems to pain (Crettaz, 2013). One way it does so is by triggering the production of certain cytokines (i.e., intercellular chemical messages) that cause our nerve endings to become more sensitive (Aubert, 2008). As a result, people who are chronically stressed can develop a hyperactive nervous system that is prone to misinterpreting benign signals from the body as dangerous and producing pain in response. 

    Muscle tension is one example of a benign signal that could be misinterpreted by the nervous system. Stress triggers the flight-or-fight response, which causes our muscles to tense up to prepare us to deal with a threat. So if we are chronically stressed, we may be living with our muscles perpetually on guard. Negative emotions, such as anger, have also been shown to increase muscle tension. For example, one study found that anger increases muscle tension specifically in the low back of people with chronic low back pain (Quartana, 2007).

  • Pain and emotions have a complicated, bidirectional relationship. Pain triggers negative emotions, and negative emotions can trigger, perpetuate, and/or exacerbate pain (Lumley, 2011). Functional magnetic resonance imaging (fMRI) studies have shown that the same areas of the brain (i.e., the anterior insula and the anterior cingulate cortex) are activated when people feel physical pain as when they feel emotional pain (Eisenberger, 2003; Kross, 2011). Thus, when you are distressed, your brain may more readily produce pain because those areas are already engaged. 

    Both a lack ofawareness of negative emotions and a failure to express them are thought to contribute to chronic pain. Conditions in which one has difficulty recognizing emotions (i.e., alexithymia) or in which one wishes to express an emotion but is afraid to do so (i.e, ambivalence over emotional expression) are associated with increased pain severity (Lumley, 2011); and suppression of anger has been shown to increase the perception of pain in both healthy people (Quartana, 2007) and people with chronic back pain (Burns, 2008).

Fear is the fuel

People tend to react to MBS symptoms with negative emotions, such as fear, frustration, and despair. Unfortunately, these reactions increase our perception of pain and reinforce the brain’s notion that the stressor that it’s responding to is actually dangerous (Kirwilliam, 2007; Bunzli, 2017). Our beliefs (e.g., that something is physically wrong with us) and expectations (e.g., that a particular stimulus will trigger a symptom) can pile onto the problem by increasing our stress and fear (Gilam, 2020). Together, our symptoms and our negative reactions to them can create a hellish spiral: the more we agonize over a symptom, the more we feel it; and the more we feel it, the more we agonize over it.

When these concepts are applied to chronic pain, it is easy to see how this can get out of hand. People with chronic pain truly have much to fear. In addition to the pain itself, there are all its potential life-disrupting consequences (e.g., job loss, social alienation, substance abuse, suicide). Thus, their pain becomes a harbinger of ruin and despair. Doctors can’t satisfactorily explain the cause of their pain or make it stop, so they come to believe that it is incurable, which leaves them feeling trapped and hopeless. This can lead to pain catastrophizing and hypervigilance, which have both been shown to exacerbate pain (Quartana, 2009; Herbert, 2014). As a result, people with chronic pain end up with an overburdened, trigger-happy internal warning system. 

Neural pathways are the infrastructure

Neural pathways are the connections that form between neurons when we learn new things. When we first experience a stressor (e.g., an injury, an emotional event), the brain establishes a new neural pathway that allows it to produce a warning signal (e.g., pain) in response. When we later experience another stressor that resembles the original “priming” stressor, the same neural pathway is automatically activated because the brain has “learned” this response.

With repeated use, neural pathways become more ingrained. Pairs of neurons that frequently communicate with each other develop stronger connections and become more responsive to each other (i.e., they fire in response to lower amounts of stimulation). As neuropsychologist Donald Hebb famously put it, “neurons that fire together, wire together.” Thus, the more you use a symptom-producing neural pathway, the more sensitive the nerves in the pathway become, and the more readily your brain produces the symptom in response to stress.

I like to imagine this process using a sledding metaphor put forth by neuroscientist Mendel Kaelen and quoted by Michael Pollan in his book How to Change Your Mind: “Think of the brain as a hill covered in snow, and thoughts as sleds gliding down that hill. As one sled after another goes down the hill, a small number of main trails will appear in the snow. And every time a new sled goes down, it will be drawn into the preexisting trails, almost like a magnet. Those main trails represent the most well-traveled neural connections in your brain. In time, it becomes more and more difficult to glide down the hill on any other path or in a different direction.”

On location

MBS symptoms can appear seemingly out of nowhere, but it’s fairly common for people to get MBS symptoms in an area of the body in which they have previously experienced a physical problem such as an injury, infection, or disease.

In some cases, the symptoms of the physical problem morph directly into MBS because they are perpetuated by fear. Classic examples of this phenomenon include whiplash and long COVID, which are both suspected to be caused by negative expectations spread via social contagion (Joffe, 2023; Ferrari, 2002; Ferrari, 2005).

In other cases, the MBS symptoms appear at a later time. The idea here is that once you’ve built the neural infrastructure to produce a particular symptom, your body remembers how to produce that symptom in the same way that it remembers how to ride a bike. Your brain may latch onto using a previously afflicted body part simply because you are more likely to believe that something is wrong with that part and freak-the-fuck-out when you experience symptoms there.