TEMPOROMANDIBULAR JOINT PAIN & STIFFNESS

MIGRAINE

Patient Information

What You Should Know!

Pathophysiology

Migraines though disabling, are a common condition with many variations in presentation amongst those that suffer with it. Migraines are a recurrent primary headache disorder that is episodic in nature, resulting from dysfunction of the central nervous system (i.e. brain and neural system). This alteration leads to activation of the trigeminal vascular system which is located in the brain stem and essentially responsible for sensory and movement information from your mouth and face (Sonu, Kolsoum, Parvin and Houshang, 2013). The trigeminovascular system specifically, is a key pain-signaling pathway involved in the migraine attack (Schoene and Sandor, 2003). It is further characterized as a neurovascular event (i.e. involving the nerves and blood vessels) that is characterized by mostly unilateral (one-sided) throbbing head pain (Noseda and Burstein, 2013). A transient aura may be experienced (related to cortical malfunction). The brain disturbances (also known as cortical alterations) arise from what we term cortical spreading depression (CSD), which though spontaneous in nature can occur preemptively before you get a headache. There are also potential genetic factors involved in the predisposition to this process (Noseda and Burstein, 2013).

Information from the blood vessels, sinuses, and afferent information related to the upper cervical spine are all involved in the trigeminocervical complex,  which of course plays a collaborative role in migraine pathogenesis (Goadsby, Holland, Martins-Olivera, Hoffmann, Schankin and Akerman, 2017). The trigeminocervical nucleus is a well understood component in the referral pathway involving head pain originating from the neck. Input related to sensory information from the upper cervical nerve roots may be perceived in the head through a concept known as “convergence.” This is important to understand, as treatment of your neck may be appropriate depending on findings from a comprehensive musculoskeletal assessment (Hall, Briffa, Hopper and Robinson, 2010). Pain in the eye region for example may even be attributable to nerve fibers from the ocular region and sensory convergence of the trigeminal system and upper cervical region(Tseng, Cheng and Fu, 2017). There are also overlapping pathways that influence the generation, perception and regulation of your emotions and affective behaviours. Migraine can commonly co-exist with vertigo or balance disorders, and psychiatric conditions such as phobias and panic related disorders. Understanding these individual mechanisms and objective features is essentially key to determining the most effective treatment strategies for you. This will also help you prevent the development of chronic headache (Balaban, Jacob and Furman, 2011).

There are further pathophysiological considerations such as vascular changes,  neurogenic alterations with nociceptive afferents, blood vessel dilation in the dura and trigeminal neurovascular activation. Further genetic links exist with specific gene and environmental influences involved. Neurotransmitters (chemicals in the brain) are also involved and play a role in migraine pathogenesis such as monoamines (dopamine and 5-HT) which are essentially key chemicals in the pain involved in pain processing. Additional neocortical links are involved in addition to specific roles involving the hypothalamus and brainstem region. fMRI results have also specifically indicated activation in key areas of the brain, reinforcing the complexity of the system and pathophysiology involved. These areas include the dorsal rostral pons, periaqueductal gray, substantia nigra, prefrontal corte,x red nucleus, anterior cingulate, cerebellum, posterior cingulate, insula, thalamus, temporal lobes, cerebral peduncle and locus coeruleus. There are further changes involving the white and gray matter of the brain as well (Sonu, et al., 2013).

The underlying vascular and neural mechanisms involved with this condition remain unclarified, although there are certainly premonitory symptoms that seem to occur in the lead up to an attack which we will discuss in more detail later on! Migraines are ultimately characterized by altered excitability of the brain in response to preceding events with activation of the trigemino-vascular system in predisposed individuals (Noseda and Burstein, 2013). It is important to understand that there are more complicated neurobiological and neurophysiological processes involved in this experience, particularly if your headaches have already become chronic in nature. Understanding the pain neuroscience behind this however is important for modifying negative beliefs and fear avoidance in order to prevent migraine related disability and additional health care visits (Louw, Nijs, and Puentedura, 2017).

Burdon of disease

Surprisingly, 16 percent of the population worldwide suffer migraine headache, of which 30 percent of these migraines follow neurological symptoms related to transient aura. Approximately 3 percent of worldwide disability attributable to disease is attributable to migraine. The public health outcome of headaches and migraines is a consolidated understanding, though further literature is needed to provide greater understanding across stakeholders and policy changes for chronic headache related disorders. Migraines are recognized as one of the more disabling diseases, the first amongst neurological disorders, with double the increase with respect to previous Global Burden of Disease (GBD) rankings (Leonardi, Raggi, and Leonardi, 2013).  

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Symptoms

There are ordinarily a myriad of neurological symptoms including nausea, light sensitivity and sensitivity to smell or sound. Cognitive (brain processing), emotional, autonomic, or motor (movement) disturbances may all occur. There are also a wide variety of triggers including hormonal changes, stress, sleep disruption, sensory overload or hunger depending on your individual predisposition (Noseda and Burstein, 2013).

Premonitory phase

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There is typically an initial stage referred to as the premonitory stage. During this phase you might start to suspect the onset of a migraine. Symptoms can occur up to 48 hours prior to the onset of your headache. This phase can be related to physical, emotional, or cognitive (mental processes). These symptoms might also include yawning, neck stiffness, food cravings, depression or hyperactivity, fatigue, irritability of poor concentration (Rosengren and Welgampola, 2018).

Aura

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The second stage usually involves an aura. Bear in mind that a migraine can present with or without aura, depending on whether the focal neurological symptoms occur prior to or during your headache (Sonu, Kolsoum, Parvin and Houshang, 2013). Nevertheless, the actual aura is temporary and includes neurological symptoms of a reversable nature just prior to or during your migraine attack. This stage involves sensory symptoms such as alterations in touch, smell or vision. The most common symptom during the aura is visual alterations in which you might experience blind spots (scotomas), flashes of light, bright spots, shapes or blurred vision. The second most common symptom is paresthesia, which involves numbness or tingling of the skin. Other less common features during an aura could include speech and language disturbances or limb weakness. Auras generally start to appear in the first 5 minutes but may last anywhere up to an hour (Rosengren and Welgampola, 2018).

Unfortunately, sometimes there can be more complicated symptoms at this point including vertigo, ataxia (compromised walking), nausea and vomiting, drowsiness or in more serious cases,  amnesia and altered consciousness. Uncommon variants may include visual field alterations, spacial distortion and altered perceptions of size and shape, or visual hallucination (Blumenfeld, Victorio, and Berenson, 2016).

Headache

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The third stage involves the headache which is usually of a moderate to severe intensity with a throbbing or pulsatile quality. It has a duration of between 4 to 72 hours. The headache typically starts at the base of the skull and progresses upwards and over. Symptoms such as nausea, vomiting, lightheadedness, blurred vision and sensitivity to light or sound (photophobia or phonophobia) may be experienced at this point. Be mindful that physical activity may actually aggravate the headache as well (Rosengren and Welgampola, 2018).  

Postdrome

The fourth stage involves resolution of the headache, though you may have symptoms similar to the those experienced during the premonitory phase. You might just feel fatigued or “washed out” at this point (Rosengren and Welgampola, 2018).

Are there different kinds of Auras?

Migraine with Aura

Auras are defined as recurrent attacks, lasting minutes of reversible visual, sensory or other neurological symptoms that gradually develop and are usually followed by a headache and other migraine related symptoms. Typically have one or more of the following reversible symptoms including:

1. Visual

2. Sensory

3. Speech and or language

4. Motor

5. Brainstem

6. Retinal

Note: It is possible to suffer both migraine attacks with aura and without. You may also experience an aura without a headache

Typical Aura

• Visual

• +/- sensory symptoms

• +/- speech/language symptoms  

• No motor weakness, brainstem or retinal symptoms

• Gradual development

• Hour in duration

• Mix of positive and negative neurological features that are fully reversible

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Brainstem Auras

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Brainstem aura – at least 2 reversible of dysarthria, vertigo, tinnitus, hypacucsis, diplopia, ataxia not attributable to sensory deficit, decreased level of consciousness but no motor or retinal symptoms

• Primary – Olfactory, auditory, visceral, kinesthetic, limb pain

• Vestibulocochlear – Vertigo, deafness, drop attacks

• Motor – Chorea, dystonia, hemiplegia

• Higher integrative functions – memory, mood, perception and planning

Hemiplegic Auras

This involves migraine aura with motor weakness that is fully reversible

• Fully reversible motor weakness, visual, sensory, speech/language symptoms

• Sometimes these motor symptoms can last upward of 72 hours

• Different variations of hemiplegic aura

Retinal migraine

Involves repeated attacks of monocular visual disturbance, including scotomata/blindness, scintillations all in association with a migraine headache

The aura consists of:

• Fully reversible symptoms lasting less than 60 minutes and is followed by a headache

What factors lead to my migraines becoming chronic?

It is important to consider risk factors for modifying migraine management, with emphasis on relieving the current pain and disability, whilst preventing chronificiation of the condition. Reducing attack frequency, preventing medication overuse, and employing appropriate use of preventative medication and therapeutic intervention is key for improving your current pain and disability. Genetic factors also contribute to the risk of developing episodic migraine, though the role of genic influence on migraine chronificiation is not well understood. Repeated migraine episodes may lead to central sensitization with associative chemical and anatomical changes in the areas that control pain. This can result in pain experienced in relation to nonpainful stimuli (i.e sensory information that would not ordinarily trigger you may begin to do so). Further risk factors for the chronificiation of migraine include snoring, sleep apnea, weight gain or obesity, psychiatric comorbidities, and stressful life events. Other factors that influence the progression to chronicity include concurrent temporomandibular disorders (jaw problems), medication overuse, caffeine overuse or additional head trauma (Bigal and Lipton, 2011). Fear avoidance and pain catastrophizing are also predisposing factors for further disability and functional decline associated with migraine (Gil-Martinez, Navarro-Fernandez, Mangas-Guijarro, Lara-lara, Lopez-Lopez, Fernandez-Carnero and La Touche, 2017).

Preventative pharmaceuticals

Preventative therapy is important for reducing the frequency, duration, and severity of your migraines. It also helps to reduce disability and improve responsivity to your usual acute medications. This is important for improving your quality of life and functionality, whilst reducing your overall health care utilization. Preventative therapy is applicable in your case when the attacks begin to significantly interfere with your quality of life, and daily function despite trigger management and acute medication implementation or lifestyle modification. It is also indicated when you experience greater than 4 or more episodes of migraines per month or rather 8 or more headache days over that time in order to prevent the headaches from becoming chronic in nature. Further instances where this applies is if there is failure to respond to acute medication or there is overuse, contraindications or side effects from this medication. Sometimes the migraines can be particularly debilitating with subtypes such as hemiplegic migraine, basilar migraine or prolonged aura. The following medications are used in preventative treatment  including antiepileptic drugs, antidepressants, beta blockers, calcium channel antagonists, botulinum neurotoxins, NSAIDs and serotonin antagonists/other (Silberstein, 2015). These essentially work at a neural and chemical level to reduce the frequency and severity of your headaches.  It is important for the risks and the benefits to be considered to ensure you feel informed and in control of your choices on the matter. Interventions including Topiramate and Onabotulinum toxin A for example are both considered safe and effective medications. In the case of drug over-use, it is only secondary to detoxification (medication cessation) that a prophylaxis medication regime can be commenced, which would otherwise be ineffective from the start. The more appropriate regime for chronic migraine based treatment now consists of the implementation of pharmacogenics, with avoidance of medication abuse related to non-responsivity of the previously implemented medication (Farinelli, Dionisi, and Martelletti, 2011).     

What other conservative management options do I have in order to prevent chronicity?

Physiotherapy

Spinal manipulations, mobilization, therapeutic exercises, and soft tissue interventions or needle therapy are all potential lines of treatment modalities depending on your individual structural and joint mechanisms. If there are appropriate features on your objective assessment indicating mechanisms related to your neck and the joints involved, then there are certainly potential grounds for physiotherapy management (Fernandez-de-las-Penas and Cuadrodo, 2015).

Psychological strategies and behavioral modification

It is also important to identify and manage dietary, environmental and behavioural triggers which can be effective for preventing your migraines. However, exposure of triggers and trigger avoidance where applicable needs to be handled with scrutiny. For example, short term exposure to anxiety producing stimuli will result in increased anxiety, whilst prolonged exposure to the same stimuli actually encourages reductions in subsequent anxiety responses. Graduated exposure to triggers can therefore help with desensitization (Martin, Reece, Callan, Macleod, Kaur, Gregg and Goadsby, 2013). Headache triggers, dietary exposure, stress, physical activity, hormonal fluctuations, and sleep disruptions should all be addressed (Millstine, Chen and Bauer, 2017). Improvements in self-efficacy positively reduces the impact of stress on your overall headache frequency.

Beliefs (Locus of control) and headache related cognitions (Catastrophizing) are also thought to influence the development of chronic headache and disability. It is therefore important to address any anxiety or depression. Poor locus of control i.e. the belief that there will be no improvement or control over the onset and course of your attacks is also more correlative with migraine chronicity (Seng, Buse Klepper, Mayson, Grinberg, Grosberg, Pavlovic, Robbins, Vollbracht, and Lipton, 2017). Acceptance and coping strategies should be implemented in the management of your migraines. Acknowledging and modifying maladaptive cognitive and behavioral responses can also help prevent migraine-related disability and support your overall quality of life (Seng, and Holroyd, 2014).

It is important that you feel safe, respected and validated with your concerns during this process. I will do my best to ensure attentive and careful history taking so that we can collaboratively ensure the restoration of your social life, normal activities, and overall quality of life. Our goal should be to achieve optimal self-efficacy and restore the confidence to fully participate in life again.  

References

- Too many references! All available on request however so please feel free to reach out :) 

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Whiplash

Whiplash

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“Whiplash-associated disorders” (WAD) is the name given to myriad of symptoms related to a acceleration/deceleration involving the neck, usually most commonly acquired in road traffic accidents. Having said this, it could actually occur with sporting related injuries, bicycle accidents or more traumatic falls and head injuries.

The cardinal symptom is most commonly neck pain, though the following features may be reported:

·        Neck stiffness

·        Paraesthesia/anesthesia

·        Dizziness

·        Headache

·        Upper limb pain

Assessment

Neck pain from WAD can be associated with significant disability, reduced quality of life and psychological impact. It is also a compensable injury, with a extenuating evidence of the psychological and physical manifestations involved with resultant implications for treatment. Your physiotherapist is ultimately responsible for identifying and being involved the classification of your whiplash injury (severity dependent). Sometimes there are complaints of neck pain, tenderness, and stiffness only but no physical signs evident at assessment. In cases of WAD II however, there is complaint of pain with associative musculoskeletal signs including reduced range of motion (in the neck) and tenderness to the touch. WAD III however, is more severe with respect to functional compromise neck complaints and neurological compromise. This includes reduced or absent deep tendon reflexes, sensory deficits, and muscle weakness. WAD IV in contrast, includes compromise with fracture or dislocation. Your physio will have specific tests and protocols that help to solidify your risk factors and where they think you are in relation to healing times and of course what level of injury you have!

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Diagnostics

The diagnosis is largely dependent on patient report, symptomology with respect to neck pain and additional report following the traumatic event. In contrast to reduced progress in assessment of peripheral pathology, there has been great progress with respect to understanding the condition from a physical and psychological perspective. This has resultant implications for clinical assessment of WAD. In some cases, people will need to be referred on for further imaging and additional management.

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Physiotherapy

The Physiotherapy Management of whiplash depends largely on which stage of the condition is involved and whether it is acute in nature (i.e. 0-12 weeks) or more chronic (>12 weeks). The time frames are consistent with more current guidelines for WAD management. Timeframes help to guide management and therefore prevent chronicity. Both the psychological and physical variables are important when predicting chronicity in this respect, and management therefore needs to be handled in accordance with this. Some of the main points for physiotherapy include:

• Reassurance and encouragement for active participation

• Maintenance of normal life activities as much as possible and ensuring the recovery process is supported through movement and focus on functionality

• Exercise is effective in early treatment if WAD with specific neck exercises including range of motion, postural endurance, low load isometric and strengthening exercises

• Manual therapy also has evidence for acute WAD

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References

Whiplash Guidelines (nsw.gov.au)

Sterling M. Physiotherapy management of whiplash-associated disorders (WAD). J Physiother. 2014 Mar;60(1):5-12. doi: 10.1016/j.jphys.2013.12.004. Epub 2014 Apr 24. PMID: 24856935.