HEADACHE: and sensory sensitivities

Tinnitus, Tinnitus in my ear –

I hope you’ll soon, yes, disappear,

You’ve got my brain so nicely curled

I’ve got to get you from my world!

-Gerald B. Frank



Hypersensitivities are common in migraine and post-traumatic headache.

  • Remember, most post-traumatic headaches resemble migraines, clinically.
  • Diagnosing a migraine really just involves making sure you have all the checkboxes checked off on the migraine checklist
    • the post-traumatic headache checklist is even shorter
  • So, are they all really the same?
    • Many patients have different symptoms despite having the same diagnosis (i.e., migraine, post-traumatic headache, etc.)


Headaches are a more elaborate experience than just the part where your head hurts

  • The picture below illustrates the progression of a migraine attack from start to end



Attack Generation

We don’t know as much as we would like to know about this phase.


Premonitory Phase

  • Occurs in 80% of patients
  • It can last hours to a couple of days before a headache
  • It can occur without progressing to a headache
  • Symptoms patients can experience in this phase include:
    • Drowsiness, irritability, difficulty concentration, yawning, nausea, stiff neck/neck pain, changes in appetite, sensory hypersensitivities (light, sound, smell), food cravings, changes in mood for better or for worse,  etc.
  • If you can get to become aware of your premonitory symptoms, this is a great opportunity to use these signals as feedback to incorporate more balance and self-care into your day.



  • This happens in about 25% of patients, and they can happen frequently or just once, and anything inbetween
  • It is a transient neurological phenomenon, lasting 5-60 minutes. For example, these can be experienced as:
    • visual changes, i.e.,  spots or sparkles or geometric shapes in your visual field (which are typically black-and-white or silver and evolve over time), loss of vision (which can either affect a part, a corner of vision, half of the field, or even your entire field of vision)
    • Sensory symptoms like tingling or pins and needles which will start in one body part and will typically move over the body to involve other body parts over the course of minutes.


Headache Phase

  • This is the part of the headache that hurts your head and to which the diagnostic checklist relates



  • This can resemble the premonitory phase, but typically the patient feels washed out, “can’t think quite straight” sensation.
  • This phase usually doesn’t last longer than a day or two, but it can last much longer in those with chronic headache


It is not unusual for those who get chronic headache to have remodeling of the way their brains function. 


This is known as Sensitization.

  • The more you have headaches, the more you strengthen those networks in the brain that execute headaches
  • Headaches are longer lasting pain
  • Headaches are more severe
  • There is a lower threshold for triggering a headache
  • More likely to get more frequent headaches
  • Things that are typically nonpainful can hurt (e.g., lights, shaving, collars, ponytails, etc.) (Schwedt et al., 2014)


As such, many patients can experience symptoms even when they are not having a headache.

  • These are known as interictal symptoms (i.e., symptoms you get between headaches).
  • They are different from headache triggers because triggers tend to abruptly and intensely cause a headache where as interictal symptoms tend cause chronic smoldering symptoms.

How do you experience the headache?


Is there a way we can observe this experience?

  • Cortical hyperexcitability refers to when the brain is more active that is ideal, like having too much orange light up on this fMRI image above
    • Think of a computer, if it’s making too much noise and getting too hot, it’s not working as efficiently
  • fMRI has shown us some general information about the pain experience (Bingel et al., 2009)
  • Pain can be conceptualized as being experienced by a matrix in our brain called the “Pain Matrix”.
  • In this Pain Matrix, there sits a few “committees”:
    • Sensory-discriminative
    • Affective-motivational (i.e., relating to emotions)
    • Cognitive
    • Integrative



This concerns itself with:

  • where on the body the pain is felt
  • and what it feels like (i.e., burning, sharp)

Parts of the brain that sit on this committee include:

  • Primary sensory cortex
  • Posterior insula



This concerns itself with:

  • Realizing that it’s unpleasant
  • Being fearful of pain
  • Wanting to avoid pain

Parts of the brain that sit on this committee include:

  • Anterior Cingulate Cortex (ACC)
  • Anterior insula
  • Amygdala



This concerns itself with:

  • How much attention you pay to the pain
  • Expectations of being in pain
  • Memories of prior pain experiences

Parts of the brain that sit on this committee include:

  • Prefrontal cortex (PFC)
  • Hippocampus



This concerns itself with:

  • Integrating the above components (middle cingulate)
    • take in stimuli from many different sensory systems and then co-process them so we get one unified perception of what’s going on in our environment
    • Example: What we see can affect what we hear and what we hear can affect what we see
  • This is important in migraine
    • migraine has symptoms in many different sensory domains
      • temporal pole: one of the most common areas injured in concussion
      • Temporo-parietal-occipital junction also have these sensory integration roles in the brain also
      • Somatosensory implications: which lead to the experience of pain and allodynia (the experience of pain to things that are not normally painful)
      • Visual implications: hypersensitive during an attack but being in bright light makes the headache pain worse as well (i.e., photophobia)
      • Auditory implications: hypersensitive to sound (i.e., phonophobia)
      • Olfactory areas: hypersensitivite to odours (i.e., osmophobia)

Parts of the brain that sit on this committee include:

  • Temporal cortex
  • Pulvinar


A visual representation of these committees of the Pain Matrix an be seen in the figure below,

  • where the paths between the 3 boxes can be imagined to represent the integrative pathways.

We have discussed avoidance, endurance and approach behaviours previously.


Obviously we are not saying that hypersensitivities exist because you continue to avoid them.

  • E.g., If you were to get burnt by a fire, you would rightfully do well to avoid it again in the future.


But we do know that with experiences that rely heavily on the Central Nervous System, the body can adapt to a “new normal”.

  • E.g., when you come out of a movie theatre, the lights seem so bright
  • E.g., when you come in from a ski hill, the lighting seems so dim.


E.g., There is research evidence that avoiding sound exacerbates one’s sensitivity to sounds.


Deciding on how to negotiate this fine line is easier if you employ:





Hyperacusis refers to when everyday sounds are experienced as louder than they ought to be.

  • This can be experienced as just “supersonic hearing”, annoyance, fear and pain. That is, the experience of the sound can also involve emotional and cognitive parts of the brain (see section above “cortical hyperexcitability and our experience of headache”.


While there are some different causes to hyperacusis, we will focus hyperacusis in the context of migraine.

  • Migraine likely accounts for over 90% of all cases of hyperacusis (Hain, 2021).
  • Dr. Hain has a nice diagram illustrating how hyperacusis in the context of migraine compares to “normal” people experience sound.
    • That is, migraineurs don’t hear better than non-migraine people, they just feel as if their hearing is “supersonic”. It may be because they simply pay more attention to it.


Many different conditions have been associated with hyperacusis

  • What they have in common is that they (e.g., fibromyalgia, complex regional pain syndrome, autism spectrum disorder, etc.) are marked by an increased sensitivity to sensory input.
  • Psychological conditions are correlated with hyperacusis.
    • When certain specific sounds (e.g., the sound of your husband brushing his teeth) set you off, it is known as misophonia, and is not related to the loudness of the sound, but of the sound pattern.
    • Misophonia is best treated with relaxation training and exposure therapy.


Psychological issues don’t cause phonophobia

  • But being highly vigilant or obsessive about it makes the experience more drastic
  • A challenging question to answer precisely is:


Are you avoiding because it hurts, or because you’re afraid of it, or a bit of both?

1. Devices

a) Ear plugs

      • While this can be useful in the short-term, it is not recommended to rely on this in the long-term because of what was mentioned in the section above “Approach vs. Avoidance Behaviour”.

b) Maskers/sound generators

      • These work by conditioning the nervous system to get used to sound. These involve hearing aid-like devices that are adjusted every month in a way to increase desensitization.
        • This is the same principle behind allergy shots.

2. Psychotherapy

a) “Tinnitus” Retraining Therapy (TRT)

      • The goal of sound therapy is to reduce the strength of tinnitus-related neuronal activity (Jastreboff, 2015).
        • It appears that part of it involves reclassifying the tinnitus as a neutral sensation and thus, relies on changing the relationship with which one relates to tinnitus, cognitively and emotionally.
      • Dr. Hain has a nice article on sound therapy (masking) where he points out that many cellphone “apps” do the same thing and that the main value of the TRT program as of 2020 is the psychotherapy piece as well as oversight by an experienced practitioner.

b) Auditory integration training

      • This consists of about 20 half-hour sessions over 10 days listening to specially filtered and modulated music.
      • It is an unproven technique, that seems unlikely to do any harm.
      • It is based on Guy Bernard’s book “Audition Égale Comportement” (Hearing Equals Behavior).

c) Psychotherapy for anxiety, depression, hypervigilance or obsessiveness


3. Lifestyle changes

    • Avoid loud noises
    • Minimize/eliminate stimulants like caffeine and nicotine.
    • manage migraine triggers
    • Focus on wellness
    • Stay motivated in living for the things you value


4. Medication

a) Anti-depressants may be helpful

      • These may especially be helpful if someone has a lot of anxiety and/or depression

b) Antiepileptic medications may be helpful

      • These are frequently used to treat migraine

What is tinnitus?

  • This refers to a noise you hear that others can’t hear
  • It is experienced differently by different people, e.g., ringing, whooshing, roar
  • it affects about 15-20% of the population (Adjamian et al, 2009)
  • 90% of persons with chronic tinnitus have some form of hearing loss (Davis and Rafaie, 2000; Lockwood et al., 2002) but only 30-40% of people with hearing loss get tinnitus
  • There are other things that are correlated with tinnitus (i.e., anxiety, stress, sleep disturbances, depression) (Holmes and Padgham, 2009)
    • Persistent tinnitus is associated with changes in the way sound is processed by the brain (Adjamian et al, 2009)
  • It should be investigated as it could herald a more serious disorder like an 8th nerve tumour
  • Tinnitus becomes more tolerated as time goes on (Andersson et al, 2001)
  • Tinnitus can adversely affect peoples’ sleep and their ability to focus


While there are some different causes to hyperacusis, we will focus hyperacusis in the context of migraine.

  • Migraine likely accounts for over 90% of all cases of hyperacusis (Hain, 2021).
  • Dr. Hain has a nice diagram illustrating how hyperacusis in the context of migraine compares to “normal” people experience sound.
    • That is, migraineurs don’t hear better than non-migraine people, they just feel as if their hearing is “supersonic”. It may be because they simply pay more attention to it.


Causes of tinnitus

  • There are many causes of tinnitus, however we will limit our discussion to a few common conditions seen in our patients that could be contributing to their tinnitus.
  • People with head, neck and TMJ injuries can have more tinnitus (Folmer and Griest, 2003; Park and Moon, 2014; Lee et al, 2016).
    • It is believed that some of the somatosensory nerves “cross-talk” with the hearing pathways
  • Patients with anxiety and/or depression tend to be more annoyed by the tinnitus (Pinto et al, 2014).
  • B12 deficiency is common in tinnitus patients.
  • Fibromyalgia is often associated with tinnitus (Cil et al, 2020).
  • Schecklmann et al (2014) suggested that tinnitus is associated with alterations in motor cortex excitability

A good overview of the management of tinnitus can be found at https://dizziness-and-balance.com/disorders/hearing/tinnitus/tinnitus_treat.html.


However, a brief summary of treatments approaches follows:


1. Psychotherapy


2. Devices

a) Hearing aids

      • reasonable to try if your tinnitus is associated with hearing loss



3. Diet

  • Low salt, avoid stimulants (caffeine, nicotine, etc.)


4. Complementary and Integrative Medicine (CIM)

  • Some patients find Ginkgo-Biloba, Zinc and acupuncture helpful.
  • Although there is little evidence that these work, there is little risk to them.


5. Antidepressants

  • these have shown evidence to be helpful in tinnitus


6. Bottom Line

  • The more you focus on tinnitus, the worse it gets
  • Remember that 10-15% of the population have tinnitus but only 20% of these (1% of the population) actually seek medical care (Adjamian et al, 2009).
  • Most people “get used” to tinnitus, and learn to “tune it out”.
    • When this doesn’t happen, the treatments that work the best for tinnitus are those that make you happier about your life and improve your sleep.

Motion sickness is a normal human experience.

  • nearly everyone (except for those without a functioning vestibular system) can experience motion sickness under certain conditions.


What causes motion sickness that is disruptive in day-to-day life?

  • We have previously discussed how the brain “sizes up” its environment by using sensory information (from the visual system, vestibular system, somatosensory system) to move and use the body effectively (Learn more in our article “Visual Vestibular Mismatch“)
  • Under most circumstances, the sensory input coming into the brain gives information that agrees with each other (i.e., about the way the world is situated and the way you are situated within your environment)
  • When the sensory input coming in to the brain gives information that doesn’t agree with each other (each sense says something different), there is a “conflict”
  • This is what causes motion sickness
  • e.g., a lot of people get “car sick” when they read in the car.
    • your eyes are telling you that nothing is moving (as they are fixed on the text in your book)
    • but your inner ears (vestibular system) are telling your brain that you are moving.
    • conflict sets in between the two systems’ input and the brain in trying to reconcile the discrepant signals experiences motion sickness.


Motion sickness and migraine

  • About 50% of those with migraine have motion sickness, and migraineurs have about a 5 times increased risk of motion sickness when compared to non-migraineurs (Marcus et al, 2005).
  • Migraineurs tend to have sensory hypersensitivity which would be expected to amplify the discrepancy between the signals.


Motion sickness and visual disorders

  • Many people who have had to break in a new pair of glasses, especially progressive lenses or multifocal lenses,  will tell you that there was some motion sickness experienced until they got used to it.
  • This can also be experienced by people who have high visual demands, like long hours in front a computer

Motion sickness is usually effectively treated. Treatment approaches can be classified into the following 3 categories:


1. Behavioural

  • This can involve things that make reduce or delay the onset of motion sickness
    • not reading while in the car
    • sitting in the front seat so you can see the horizon, or take in more of a panoramic view
    • If you are driving a car, you will be able to anticipate movements
    • eating bland well before you will be in a situation that normally provokes motion sickness


2. Medication

  • Medication focuses on reducing vestibular input and/or reducing your brain’s reaction to the signal.
  • This is an option you should discuss with your doctor if you’re interested.


3. Exercise (Habituation)

  • This follows the principles laid out in the article Exposure Hierarchy
  • It often involves retraining the way your brain weighs/organizes your sensory inputs:
    • reducing the reliance on the visual system for information regarding your internal map of where you are and how you use this information to control your posture
    • retraining neuromuscular control
    • retraining the vestibular system
    • increasing your awareness of your peripheral vision and integrating that efficiently in the a well functioning somatosensory system and vestibular system
    • Getting people to “practice” these skills regularly through regular participation in athletics
  • This is discussed more in our Post-Concussion Syndrome Dizziness & Imbalance Group Counselling Session

Dizziness and migraine is a big topic, with the most common of dizziness cited as being migraine.

We will provide a brief overview of the relationship between dizziness and migraine.


Relationship between Migraine and Dizziness

  • In addition to photophobia, phonophobia, nausea, and visual changes, dizziness and vertigo are common symptoms in migraine, occurring in 25 to 30% of the individuals with migraine (Furman et al., 2005)
  • Approximately 60-80 % of patients who have recurrent vertigo without hearing loss suffer from migraine (Furman et al., 2005; Brantberg et al., 2005)
  • The pathophysiology of migrainous vertigo is not well understood, buy may be a result of neuroanatomical connections between the trigeminal nuclei and vestibular nuclei (Furman et al., 2005).
  • 22% of migraneurs get Benign Paroxysmal Positional Vertigo (BPPV).
  • Benign Paroxysmal Positional Vertigo is a common occurrence following head trauma.
  • BPPV following traumatic brain injury has been estimated to account for 28% of all cases of post-traumatic vertigo (Hoffer et al., 2004).
  • About 18% of BPPV is said to be due to concussions (Baloh et al., 1987).



The rehabilitation approach includes:

  1. Treat the migraine using behavioural, lifestyle and medical management
  2. Treat BPPV if identified (Examples can be seen in our Concussion Rehab Videos Library in the section “BPPV Exercises”)
  3. Optimizing our senses (vision, vestibular, somatosensory systems, etc.)
  4. Retraining the way our brain organizes the signals from these systems (if needed).



Allodynia refers to when normal non-painful stimuli like brushing your hair, touching your face, shaving, etc. are felt to be painful. This usually happens during a migraine attack, but also can happed between headaches.

While patients with chronic headache have the same thresholds to detect somatosensory sensation (touch, temperature, pressure) when compared to non-chronic headache people, they have lower pain thresholds (Castien et al., 2018)

Headache is commonly the cause of neck pain

  • This has been discussed in another article “Migraine: and neck pain“, but as a brief recap…
  • Many experts think that in the majority of headache patients with neck pain – that is, patients that have neck pain along with other typical migraine symptoms – the neck pain is almost always a symptom of the migraine (just like light sensitivity and nausea).
  • Some people experience migraine exclusively as neck pain, without any headache
  • Migraine is episodic, so if it were caused by neck issues, you would expect that those neck issues should also be episodic, which is not the case for structural problem in the neck (e.g., disc herniations, wry neck, etc. are there constantly)
  • Many people have anatomical issues of their necks on MRI (even in many people who don’t have chronic headache) but it doesn’t mean, and usually doesn’t mean, that it is the cause for headache.
  • If you treat the migraine and the neck pain gets better, then we know that the neck pain was mostly due to the migraine.


Neck pain is commonly the cause of headache

  • There are patients that undeniably get a migraine within minutes to hours of having “work” done on their necks or straining their necks.
  • There are also those who get what is called a “cervicogenic headache” (a headache of neck origin).
    • Cervicogenic: Many of the structures in the neck can refer pain along muscles and nerves that travel all over the head. For example, even neck structures at the back of your neck can cause pain to be referred to around the top of your head or even around the eyes; this surprises a lot of patients.
  • Occipital neuralgia (these are nerves at the back of the head) and other cranial neuropathy (nerve irritation) are comprised of the 2nd and 3rd cervical nerve roots.
    • Many migraine people get sensitive nerves (as discussed in the section “Introduction: What is hypersensitivity? > What is a migraine headache?” & “Skin/Muscles: Allodynia & Pain > Allodynia), and this can occur also in the nerves around the neck.
    • C1 to C3 nerve roots land in the same part of the Central Nervous System as the nerves of the head, and the part of the Central Nervous System that is part of the migraine pathway ⇒ the TCC (trigeminal cervical complex)
  • Ultimately, if you treat the neck pain, and the headache gets better, then you know that the headache was mostly due to the headache.


Migraine is commonly the cause of dizziness.

  • This has been discussed in the section above “Ears: Hearing & Balance > Dizziness”
  • If you treat the headache, and the dizziness gets better, then the mechanism at play was likely that the dizziness was caused by migraine.


Neck pain/tension is commonly the cause of dizziness.

  • The neck is rich of nerve fibers that send signals to the brain.
  • When the neck is stiff, painful, or doesn’t move in a coordinated way, the information it relays to brain has clinical consequences.
  • Sensory information from the neck is combined with vestibular and visual information to determine the position of the head on the neck (Brandt 1996); the relationship between the somatosensory system, vestibular system and visual system was discussed in our article Visual Vestibular Mismatch.
  • It is believed that the same somatosensory information from the neck helps in stabilizing vision. There are many tests (physical exam maneuvers and electrodiagnostic tests) that show a reflexive relationship between the neck and vestibular and visual systems (Kobayashi et al, 1991).
  • Say you are visually tracking a moving object, and you move your neck by a certain amount to help track it, if you don’t move your neck as much as you expected (this is a training drill we do where we put a laser on top of peoples’ heads, and get them to move a certain amount but without their vision, just on feel, and some people are way off), there will be a mismatch between what your brain expects to have seen and what it actually saw. This mismatch has been correlated with motion sickness (Brandt and Huppert, 2016).
  • If you treat the neck pain the dizziness gets better, then it likely points to these mechanisms to having been at play in the patient’s dizziness.


All of the above shows a chicken-and-egg relationship between three of the most common symptoms in patients with post-concussion syndrome and migraine.


As often, in chicken-and-egg situations, figuring out the conundrum becomes an academic endeavour.


Clinically, we just start rehabilitating one, usually the one that gives us the most returns for our effort.

We have previously discussed treatment of neck issues in the context of migraine and/or headache in another article.


We have also discussed neuromuscular control retraining of neck issues that can result in headaches in another article which can be accessed here.


However, if you can develop a healthy relationship with your neck symptoms, you will see them as messengers trying to tell you something about your stress level, your ergonomics, your activity level, etc.


They can be interpreted as cues to take some sort of adaptive action like dialing up on self-care, etc.



What is osmophobia?

  • This is an aversion or intolerance to odours.
  • The prevalence of osmophobia ranges from 25–86% among adult migraineurs and from 25–35% among children and adolescents with migraine (Rocha-Filho et al., 2015).
  • Migraineurs may have increased sensitivity to odors even between headache attacks (Silva-Neto et al., 2014).
  • Osmophobia is more common in migraineurs than non-migraineurs.
  • However, osmophobia is not very common other than in migraineurs or those with psychological conditions.
    • There are some other conditions in which it’s common too (e.g., multiple chemical sensitivity [Alobid et al, 2014].
    • Increased sensitivity to smell as well as other irritants may be related to a “sensitivity” personality type – Bell et al. (1994) suggested that sensitivity to environmental chemical odors was associated with high ratings for stress in the first 4 decades of life, as well as increased likelihood that a physician diagnosed the following: nasal allergies, breast cysts, hypothyroidism, sinusitis, food sensitivities, irritable bowel, and migraine headache.
  • Smell sensitivity ordinarily goes down with age. (Seow et al, 2016).


How is osmophobia treated?

Management of osmophobia is similar to the management of other hypersensitivities:

  1. Treat the migraine using behavioural, lifestyle and medical management
  2. Aim to use approach behaviours so that you are not unnecessarily punishing yourself with bothersome odours, but also, that you are not disrupting your life too much in avoiding pervasive odours.
  3. Psychotherapy
  4. Medical health
    • Consultations with your dentist, GP, allergist, ENT, Gastroenterologist can be helpful in identifying and treating other medical conditions that can contribute to osmophobia.
    • Quitting smoking can help.

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Last update: April 2021