Why Is Cranio-facial Pain So Much Worse Than Everything Else?

Read time: 7-8 minutes

Outline:

  • Pain is weird
  • Chronic head and face pain and suicidality
  • Why head and face pain feels worse
  • The neuroscience of suffering

Pain is complicated. It’s even more complicated as a clinician because the expectation from years and years of conditioning is that when you have pain, then something about that painful body part must be damaged to cause it. When people are in pain, doctors are typically trained to identify things like a ruptured disc, broken bone, or torn muscle to validate a patients’ sense of suffering.

In this model, the more damage that is present = more pain. Less damage = less pain.

However, the experience of pain can be way more complex than finding damaged tissue. The experience of pain is an emotional response to ‘painful’ sensory receptors called nociceptors. While tissue damage can cause a lot of nociceptors to fire, and trigger increased pain, but it is far from the only factor in the pain equation. but it is taken into the context of cultural, social, cognitive, and experiential factors.

Which takes us to an important point.

The amount of pain you experience can also depend on what body part is injured. As we’ll see today, there are hardwired circuits in your brain that can make the experience of pain in the head/face a different and perhaps worse experience then pain from the body as a whole.

Chronic Facial Pain and Suicidality

Chronic pain is a known risk for suicidal ideation, and has been documented in numerous studies [source]. These thoughts have a higher chance of turning into behavior when you have chronic pain and a co-morbid mental health disorder [source].

This effect seems most pronounced when the source of the pain is coming from the head or face. Two disorders in particular are highly associated with suicidal thoughts and behavior; trigeminal neuralgia and cluster headaches. Trigeminal neuralgia has a high enough association that it was historically dubbed the suicide disease, while cluster headache has been known to be called the suicide headache.

Both of these illnesses are associated with some of the most intense pain that human beings can experience. The severity of the pain combined with the chronicity of the pain lead to a sense of despair because these disorders can be difficult to treat, so there is always a fear of the next attack.

Scientists have recently uncovered some neurological pathways that might explain why conditions like trigeminal neuralgia and cluster headaches can cause such disproportionate suffering compared to other body pains.

The Trigeminal Complex and the Limbic System

It’s been known that pain experienced in the head and face activate the emotional centers of the brain more than pain felt in the periphery of the body [source]. From an evolutionary standpoint, a higher state of pain in the head and neck region may have served a  purpose so that there would be extra vigilance in protecting this region of the body from injury. What was unknown was weather this heightened sense of protection was derived from a psycho-social factors, or if it was something that was hard wired into our nervous system.

Duke University scientists may have some answers. A 2017 study in Nature Neuroscience showed that sensory neurons in the head and face have a direct pathway to the emotional circuits in the brain.

Scientists identified a direct, monosynaptic connection between sensory fibers of the trigeminal nerve into a part of the brainstem called the parabrachial nucleus. The parabrachial nucleus has direct connections into the emotional hub of the brain in the amygdala, which is highly tied to fear and avoidance behavior.

Why is this important? Because monosynaptic connections are way more powerful sensory stimuli than indirect pathways.

Think of it this way:

Let’s say you were mailing a time-sensitive package that needed to get to it’s destination as soon as possible. Would you choose to overnight it by plane, or would you choose regular first-class mail?

Cranio-facial pain uses direct and indirect pathways that tap into the brain’s emotional responses to pain.

You probably chose to overnight it right? Why? Because it’s going to get there faster, and because the person receiving it is going to perceive that package as more important because it was sent with all of this overnight labeling implying it’s importance.

These monosynaptic pathways are like your overnight deliveries, where the indirect pathways are like ground shipping.

Our brains place a higher priority on signals coming from these monosynaptic pathways.

While other body regions only use an indirect path to the parabrachial nucleus, the trigeminal distribution uses both indirect AND direct pathways to stimulate this emotional hub.

That means that firing from nociceptive pain fibers in the trigeminal distribution, or even pathways that share trigeminal distribution will have a higher chance of driving an emotional response than pain fibers from the shoulder, back, hip, etc.

The Emotional Brain’s Influence On Pain

How big of an influence does emotion make in the experience of pain? In this study, the researchers stimulated pain receptors in the paw or in the face of mice using a chemical called formalin. Using a technique called optogenetics, researchers can selectively express brain activity in a mouse model using different light frequencies.

When light activated the direct pathway, the mice showed more intense avoidance behavior to the formalin on the face. When light was used to knock out this pathway, the mice didn’t react as strongly.

So you have the same amount of pain stimulus, the same mouse, and it experiences pain differently because the path to the parabrachial nucleus was turned off.

It suggests that our emotional brain’s connection to a painful stimulus plays a substantial role in the experience of pain.

Biology vs Psychology

There’s always a debate about nature vs nurture when confronted with the struggles of human existence. In recent years, it has evolved into a debate between biomechanical/orthopedic search to treat identifiable lesions vs a biopsychosocial approach which generally tends to lean heavily on the psycho and social components of the pain experience.

Here is some evidence that suggests that the two are inseparably linked together.

The experience of pain is intimately tied to our thoughts, memories, expectations, and current mental state. If the experience of pain is tied to some of these neural circuits, then changing our mind activating our different neural circuits in the brain can change our experience of pain.

It also means that fear/avoidance behavior, and repetitive responses to painful stimuli may create plasticity in the neural circuits that may reinforce the same pain over and over again.

Changing thoughts and behavior can have a significant impact on the perception of pain and the feelings of suffering for a persistent pain patient.

That doesn’t mean that we are just telling people in the midst of a terrible trigeminal neuralgia or cluster headache attack that they have to suck it up and think differently about their pain.

It means that when people have persistent pain disorders, in the process of treating patients with various interventions, we have to help and guide a patient through the process of re-framing their pain and illness.

This is really hard for patients with persistent pain. It means that sometimes we are walking a line where a patient may feel like we are telling them that the pain is just in their head. Sometimes it means that the patient is going to ask the same question, or tell you the same symptom over and over again because they’re looking for you to just understand that what they are feeling and that know that they’re being heard.

Trying to help a patient disassociate themselves from their chronic pain emotionally is challenging. After all, most of us didn’t become doctors and therapists to be a patient’s psychologist. However, empowering a patient with a stronger belief in the resilience of their body can be extremely fulfilling, and in my opinion puts people on the path to recovery while they’re in the process of receiving quality care.

 

Looking at the Brain in Chronic Whiplash Injury

Injuries occurring after a motor vehicle collision can lead to chronic head and neck pain long after the damage of the injury is done repairing. These patients are generally classified as having chronic whiplash associated disorder (cWAD). A problem with cWAD is that we don’t really have a strong sense of why some people will get chronic pain after the injury while most will recover seemingly unphased.

Years of research studying biomechanical changes, ligament studies, and MRI changes in the neck have yet to show a diagnostic lesion that is predictive of a poor prognosis in whiplash patients. A number of studies have shown that psychosocial factors like work status, gender, and attorney retention appear to have a stronger correlation to chronic pain than any current medical diagnostics. This has allowed critics to say that chronic whiplash may be more psychosomatic than a true pathology. 1

How Whiplash Can Change the Brain

Conventional thought on whiplash has linked the pain of whiplash to a soft tissue injury in the cervical spine. When the neck undergoes rapid acceleration and deceleration, then the ligaments, muscles, and tendons of the cervical spine can be sprained and strained with varying levels of severity.

Instability of the cervical ligaments can lead to chronic pain in some trauma cases, but many patients who have chronic pain after an accident don’t have this level of injury. Many of these patients may even have close to normal imaging findings. Even in patients that have positive imaging findings, there’s not much difference between the imaging findings of those that will get better on their own and those that will have long lasting pain. 2

It’s easy to understand how injuries to muscular and ligamentous tissue can cause pain, but chronic whiplash injury is about more than just neck pain. Chronic whiplash often includes things like migraine headache, vertigo, and cognitive decline which are similar symptoms to mild traumatic brain injury. At least one study has shown that whiplash and concussion are indistinguishable based on symptoms alone. 3

When pain is poorly related to tissue injury, then it becomes more helpful to start thinking about pain as it relates to the brain itself. It’s easy to understand how the whipping of the head can tear and injure ligament and muscle tissue, but we have to dig a little deeper to see how whiplash can affect the brain.

Altered Cerebral Blood Flow

One of the best ways to see how a brain is changing is to monitor the way your brain uses blood. These studies are done using things like PET scans that help to identify areas of the brain that are gobbling up more glucose which tells us how active that part of the brain is at a given time.

Patients with chronic whiplash symptoms showed differences in blood flow in the brain in specific areas that play a role in how we perceive pain. These areas include the anterior cingulate cortex, insular cortex, medial prefrontal gyrus, and parahippocampus. 5

This is important because it tells us that the regions of the brain that are affected are NOT just the regions that perceive pain. Areas like the insular cortex and medial prefrontal gyrus are areas that aren’t directly responsible for feeling pain but are related to the limbic system and help us build context around pain.

If there are changes to the way these brain regions are wired, then we may also lose some of our ability to contextualize and inhibit our conscious perception of pain.

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The belief amongst these authors is that there is a mismatch between the incoming pain stimulus and the level of activation in the pain processing centers of the brain.

Axon Injury

This mechanism is pretty similar to what can happen with a concussion. When the head and neck accelerate and decelerate during a collision, the force of the head and neck moving can be stopped by a seatbelt, but it won’t not stop the brain from moving inside the skull. As the brain shifts forward and back, it can create a shearing force in the brain and damage the neurons deep within the brain. The forces from an accident like this have been shown to be similar with the forces associated with a football concussion. 4

Whiplash and the Brain

While the force may not be enough to cause a concussion, the force profiles of a concussion and whiplash are likely high enough to cause some axon injury in the brain.

Although axonal injury doesn’t really correlate well to pain, it can impact our balance, postural control, vision, and other systems that help to keep us upright in a healthy way. Breakdown of these systems can help make sense of why whiplash patients can have vertigo, concentration problems, and headaches.

Central Hyperexcitability

Imagine if you sprained your ankle playing basketball one day, but weeks later after your ankle should have healed, you start to feel pain in other areas of your body that had nothing to do with the ankle sprain. This is the phenomenon of central sensitization which is caused by hyperexcitability of the neurons in your spinal cord. Although just one part of the body was injured, the effects of a central hyperexcitability is that you may feel increased pain throughout your body as a whole.

When we describe the injury of a whiplash as a sprain/strain, then it should have more in common with a sprained ankle in terms of tissue damage and repair. We expect sprains and strains to feel close to normal again in 4-6 weeks for minor sprains. However, the pain of a minor whiplash can last months. Why?

The way the body reacts to injury of a central structure like the spine can be a lot different than the way it responds to a distal structure like the ankle or wrist. When you injure your neck and back, your nervous system perceives movement as more catastrophic because there’s a chance that injury can occur to the spinal cord. Your CNS brings your pain neurons closer to their firing threshold so that they fire easier. By doing this, it is more likely to make movement more painful and immobilize you because your pain receptors will fire more easily. Immobilizing an area of injury is one of the main purposes for pain, because tissue repair is harder for the body if you have  a cut or broken bone moving around all the time.

That’s why when you go down with a neck or back injury, you can be really cautious or apprehensive about any type of movement. Your brain is playing defense against you out of fear that your next movement may be catastrophic to your survival. This may be your body’s wave of keeping you immobilized until the inflammatory and repair response is over.

This becomes very problematic when your central nervous system retains this hyperexcitability AFTER the injured tissues have healed. It leads to a condition where you are feeling pain everywhere, but there’s no blood test or imaging to point to why you are hurting.

This is probably the most important reason for chronic pain, not just in whiplash, but we see this in conditions like fibromyalgia or post-surgical pain syndromes. This isn’t a new idea either. Researchers have shown that central sensitization is a player in whiplash dating back to the early 2000’s. 5, 6

Changing How the Brain Perceives Pain

We know now that the brain and central nervous system can be re-wired in a way to cause chronic pain through a concept known as neural plasticity. We also know that neural plasticity can be used therapeutically to help make the brain more resilient and sometimes undo this maladaptive pain response.

Part of this means that we have to change our mindset about the nature of pain. Our patients yearn for a specific lesion with tissue damage to point to as the culprit for their pain. That way, if we get rid of the lesion, then the pain should follow suit. The obvious problem with this is that there may be no lesion at all. For some this will lead to despair and hopelessness, but for others it may lead to unnecessary procedures to cut or inject areas that are NOT the reason someone is hurting.

 

So if someone’s chronic pain is not coming from a pinched nerve, strained muscle, or injured ligament what is a doctor supposed to do for an ailing patient?

We have to engage patients in things that will change how the brain interacts with pain stimuli. Here’s a short list of useful strategies:

  1. Flip the script – Patients in pain are scared of movement because they think they are creating more injury. We can talk to our patients about this. If we have a level of confidence that pain is coming centrally, then we can teach patients not to fear their MRI or fear their movement. We can teach patients that moving their bodies may be painful right now, but they are NOT causing greater injury despite their pain. By giving patients a better sense of control over their bodies, their pain status can start dropping just by changing their mind.
  2. Lean into it – Patients consistently surprise themselves with how much pain they can tolerate as long as they know they aren’t harming themselves. Exercise and movement therapies can be powerful ways to affect central pain issues. Lots of people focus on doing exercise that help you avoid pain, but people with sensitization issues may benefit from leaning into the pain a bit. By gradually exposing the nervous system to movement with tolerable amounts of pain, you can train your body to tolerate that movement by desensitizing the fear response to that pain
  3. Adjust the Brain – most people and even many chiropractors attribute the benefits of chiropractic care to removing physical pressure on pinched nerves. This might be true in some cases, but it’s not the reason people with chronic pain syndromes get relief. A focus of chiropractic research in the past 10 years has studied how adjustments can change the way the brain processes sensory information.7, 8, 9When we combine these central changes from adjustments with movement therapies, we can make a big change in the way a person’s brain responds to movement.
  4. Biofeedback Tools– A unique way of addressing sensitization after whiplash is to use tools that provide real time feedback as a way to shift the brain’s attention on a painful area. Things like neurofeedback therapy with EEG, visual feedback with attached lasers, and wearable biofeedback devices allow the brain to shift it’s focus to another powerful stimuli. This provides a positive reinforcement to the patient to show that they can gain greater control over how pain shows up in their lives.

Closing Thoughts

The ability of our brains to change and adapt is an important piece of the rehabilitation process. While the above therapies are things I use in clinical practice on a day to day basis, these aren’t the only things that can help you recover. Our brain changes and adapts to ALL stimuli, and finding the right fit that works for you is the job of a good clinician.

  1. Dufton JA, Bruni SG, Kopec JA, Cassidy JD, Quon J. Delayed recovery in patients with whiplash-associated disorders. Injury. 2012 Jul;43(7):1141-7. doi: 10.1016/j.injury.2012.03.006. Epub 2012 Apr 2. PubMed PMID: 22475071.
  2. Curatolo M, Bogduk N, Ivancic PC, McLean SA, Siegmund GP, Winkelstein BA. The role of tissue damage in whiplash-associated disorders: discussion paper 1. Spine (Phila Pa 1976). 2011 Dec 1;36(25 Suppl):S309-15. doi: 10.1097/BRS.0b013e318238842a. Review. PubMed PMID: 22020601; PubMed Central PMCID: PMC3248632.
  3. Leddy JJ, Baker JG, Merchant A, Picano J, Gaile D, Matuszak J, Willer B. Brain or strain? Symptoms alone do not distinguish physiologic concussion from cervical/vestibular injury. Clin J Sport Med. 2015 May;25(3):237-42. doi: 10.1097/JSM.0000000000000128. PubMed PMID: 25051194.
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  7. Bialosky JE, George SZ, Horn ME et al. Spinal manipulative therapy-specific changes in pain sensitivity in individuals with low back pain. J Pain. 2014 Feb; 15(2):136-148.
  8. Lelic D, Niazi IK, Holt K, et al. Manipulation of dysfunctional spinal joints affects sensorimotor integration in the prefrontal cortex: a brain source localization study. Neural Plast. 2016; 2016:3704964.
  9. Haavik-Taylor H, Murphy B. Cervical spine manipulation alters sensorimotor integration: a somatosensory evoked potential study. Clin Neurophysiol. 2007 Feb; 118(2): 391-402.