TEMPOROMANDIBULAR JOINT PAIN & STIFFNESS
Temporomandibular Joint Disorders (TMJ) - JAW PAIN & DYSFUNCTION
Temporomandibular Joint Disorder (TMD) is a heterogeneous set of neuromuscular and musculoskeletal conditions involving the temporomandibular joint site, osseous (bony components) and surrounding musculature components. TMD affects approximately 15 percent of the adult population with peak cases at 20 to 40 years. It can be classified as intrarticular (inside the joint) or extra-articular (outside the joint). Common symptoms include headache, earache and facial pain.
Classification of intra-articular joint disorders
Congenital or developmental including condylar hyperplasia, first and second brachial arch disorders and idiopathic condylar resorption
Degenerative joint disorders
Inflammatory: synovitis, capsulitis, polyarthritides (RA, ankylosing spondylitis, psoriatic arthritis, reiter syndrome and gout)
Disc derangement disorders: Disc displacement without reduction (closed lock), disc displacement with reduction and perforation
Trauma: fracture, intracapsular hemorrhage and contusion
Hypermobility disorders: Dislocation, joint laxity, subluxation
Temporomandibular hypomobility: ankylosis, post radiation fibrosis
Cautious assessment and critical screening questions are a necessity for appropriate management of these conditions and referral on for further assessment and surgical intervention in some cases. Treatment depends on a variety of factors including their presenting symptoms, medical history, previous trauma, orthodontic and dental history. The presence of sleep and breathing disorders may also be a relevant feature in their history. There may also be the presence of additional injuries and concurrent pain conditions.
The diagnosis of TMD is largely determined by physical and historical examination findings. Symptoms are commonly related to jaw movements including opening and closing or chewing. Pain usually presents in the masseter, temple regions or preauricular areas (sometimes there is another reason for orofacial pain) and referral should be made.
Restrictions in opening
Deviation/deflections in the range
Jaw discomfort and dysfunction
Neck, arm, eye or even back pain
Ear pain/ hyperacusis sensation, fulness or stuffiness feeling
When to refer to us:
Any of the above signs and symptoms!
Pre and post dental procedures which may include tooth extractions/splinting/braces or wisdom teeth procedures particularly if there is functional compromise related to positioning or sustained opening.
General parafuntional orofacial habits
Signs and indications for TMD
Any signs of obvious dizziness, tooth pain ear or sinus not accounted for by other condition/pathology.
Alterations in bites/joint positioning with associative muscle parafunction regardless of prior dental or orthodontic history could potentially benefit from the support of physiotherapy to help build up motor control and strength. It is important to ensure they have the adaptive strategies in place to cope with, and benefit from further intervention including splints for example, or additional dental procedures for that matter.
Physio helps support and improve symptoms associated with TMD. These techniques involve both active (involving you!) and passive approaches to improve your overall muscle strength, coordination, range of motion and ability to relax the joint structures and muscles that are causing discomfort.
Joint disorders could involve disc pathology, internal derangements, displacements of the disc (with or without reduction), capsulitis/synovitis, osteoarthritis/arthrosis, masticatory parafunction, myalgia or trismus which can also be post procedural in some instances.
Disc displacements without reduction
Disc displacement without reduction may be symptomatic particularly with myalgic contribution and inflammation present including capsulitis or synovitis. Disc displacements without reduction could involve painful limitation with related changes in their movement patterns which can be observed through objective assessment.
Disc Displacements with reduction
Disc displacements with reduction are also suspected in the presence of either asymptomatic or a painful click (depending on the individual and presence of inflammation or irritability of the system. Associated inflammation through the retro-discal tissue region or in relation to subluxations could occur with capsular synovitis or capsulitis. Osteoarthritic changes could also result in changes to the articular surfaces which could be progressive in nature particularly in the presence of systemic disease.
Tuz HH, Onder EM, Kisnisci RS. Prevalence of otologic complaints in patients with temporomandibular disorder. Am J Orthod Dentofacial Orthop. 2003 Jun;123(6):620-3. doi: 10.1016/s0889-5406(03)00153-7. PMID: 12806339.
Feteih R. M. (2006). Signs and symptoms of temporomandibular disorders and oral parafunctions in urban Saudi Arabian adolescents: a research report. Head & face medicine, 2, 25. https://doi.org/10.1186/1746-160X-2-25
Gauer, R., & Semidey, M. (2015). Diagnosis and Treatment of Temporomandibular Disorders. American Family Physician, 91(6), 378–386B.
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Orofacial pain conditions can be highly variable in nature but ultimately the name encompasses some of the most prevalent and debilitating pain conditions. These conditions may arise from structures innervated by the trigeminal structures including the face, head, jaw/masticatory system, temporomandibular joints, and related structures. Orofacial Pain (OFP) may arise from different areas with different etiology. Temporomandibular joint disorders are the most common of orofacial pain conditions sought after that are sought after for medical attention. These conditions involve a number of clinical implications for the masticatory muscles (Chewing) and temporomandibular joint (TMJ) or both. Trigeminal neuropathic pain conditions may arise from injury to or secondary to dental procedures, infection, disease or dysfunction, neoplasms and or peripheral or central nervous system disorders. Notably, there is a relationship between TMJ dysfunction management implementation and reductions in neck pain, with respect to cervical spine mobility.
Neurovascular disorders including primary headaches, may also present as orofacial pain; including facial migraine, where pain is localized to the second and third trigeminal nerve divisions. Collectively these conditions of the trigeminal system have a considerable impact on quality of life for the individual and suffering may be quite severe. This is why careful assessment and mindful treatment with an integrative approach towards screening is necessary for the individual to have safe and appropriate directive for their management. The orofacial region is very complex, with many variables involved in the onset of the pain. It is therefore important to assess and discuss functionality and have a thorough assessment conducted in order to elicit appropriate diagnosis and management. Early assessment and identification of red flags is key particularly if the person requires further referral and assessment from another colleague. This helps to optimize the care provided and overall functional outcomes. Often times, a multidisciplinary focus is required and should be encouraged from the start.
Conditions may include:
1. Temporomandibular disorders (TMD) which may include any conditions of the temporomandibular joint (TMJ) and surrounding musculoskeletal system
2. Masticatory clenching muscles and associative neck muscles and neural structures
3. Neural related conditions – trigeminal neuralgia TN or other conditions related to pain conditions of peripheral and central origin
4. Concurrent psychological disorders
Physiotherapy plays a considerable role in the conditions related to TMD, and muscle related parafunction. This may be particularly relevant in situations where there is a myalgic (muscle related) component, atypical facial pain/ear/tooth or sinus related pain and headaches where red flags have been identified and ruled out in assessment. It is important to ensure these patients have the opportunity to receive tools to restore their function and become empowered in the prevention of flare ups to ensure self-efficacy and prevent chronicity. There is certainly application for manual therapies related to cervico-mandibular techniques in addition to education and exercise prescription.
Goals of physiotherapy:
Restore normal function of the TMJ (both), muscles of mastication (chewing function), cervical muscles (neck)
Motor control and awareness
Romero-Reyes, M., & Uyanik, J. M. (2014). Orofacial pain management: current perspectives. Journal of pain research, 7, 99–115. https://doi.org/10.2147/JPR.S37593
Delgado de la Serna P, Plaza-Manzano G, Cleland J, Fernández-de-Las-Peñas C, Martín-Casas P, Díaz-Arribas MJ. Effects of Cervico-Mandibular Manual Therapy in Patients with Temporomandibular Pain Disorders and Associated Somatic Tinnitus: A Randomized Clinical Trial. Pain Med. 2020 Mar 1;21(3):613-624. doi: 10.1093/pm/pnz278. PMID: 31665507.
Karolina Walczyńska-Dragon, Stefan Baron, Aleksandra Nitecka-Buchta, Ewaryst Tkacz, "Correlation between TMD and Cervical Spine Pain and Mobility: Is the Whole Body Balance TMJ Related?", BioMed Research International, vol. 2014, Article ID 582414, 7 pages, 2014. https://doi.org/10.1155/2014/582414
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Headache & Migraines
Headaches & Migraines
Cervicogenic headaches as the name suggests refer to headaches originating from the neck. These headaches were originally difficult to diagnoses and manage due to poorly understood etiology. There are also many different reasons for the development of CHG. They are actually a commonly reported type of headache in weightlifting athletes, but in more common cases it is seen in those that have sustained whiplash injuries or concussion as they are more at risk of developing neck pain and resultant CGH. Headaches that occur more than 3 months after a concussion are more likely to be related to cervical spine etiology as appose to brain or head injury.
Whiplash, TMJ disorders and postural related conditions should all be understood in the context of cervical related positioning, load and the potential for onset of headaches in response to alterations in this movement patterning.
Headaches can be categorized as primary or secondary. Primary includes vascular related origin (which can include vascular, and some forms of migraine) in addition to those of muscular origin including tension-type headaches. Secondary headaches occur as a result of inflammation or other head and neck related injuries or etiology. Cervicogenic headaches are understood to be more unilateral in nature, with pain originating from one side of the neck/head and travelling into the front region with ipsilateral arm discomfort in some instances. It may also be bilateral (meaning both sides of the head can be involved) and neck included. These neck positions may be irritated by driving, carpentry work, hair-dressing, office work etc. Neck pain usually precedes or will co-exist with the onset of a headache. It is also aggravated through specific movements or sustained postures.
There are several features that concern CGH:
Unilateral pain and facet lock (irradiating from behind the head in some cases)
Presence of cervical dysfunction (neck) observed during manual examination with your physiotherapist
Trigger point palpation of the head or neck may be precipitating of the headache
Aggravation of headache through sustained neck positions
Often times – NORMAL imaging.
Our physiotherapists are highly experienced in identifying red flags and ensuring immediate referral on in cases where sinister pathology is suspected.
Some of the Red flag symptoms we look for may include:
Worsening headache overtime
Sudden onset of severe head pain
Headaches in combination with stiff neck/rash and high fever
Onset of headaches following a head injury
Problems with profound dizziness or visual disturbances
Worth noting: Up to 44 % of those with “cervicogenic” headache may potentially have temporomandibular joint (TMJ) dysfunction. The convergence of sensory information underpins the pathophysiology involved with input from the upper cervical spine into the trigeminal spinal nucleus with resultant pain generation. Pain could arise from the upper cervical facets, cervical muscles, intervertebral discs, vertebral and internal carotid arteries, posterior cranial fossa and dura mater of the spinal cord.
Page P. (2011). Cervicogenic headaches: an evidence-led approach to clinical management. International journal of sports physical therapy, 6(3), 254–266.
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What You Should Know!
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).
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).
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).
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).
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).
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:
Speech and or language
Note: It is possible to suffer both migraine attacks with aura and without. You may also experience an aura without a headache
+/- sensory symptoms
+/- speech/language symptoms
No motor weakness, brainstem or retinal symptoms
Hour in duration
Mix of positive and negative neurological features that are fully reversible
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
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
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 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?
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.
- Too many references! All available on request however so please feel free to reach out :)
“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
· Upper limb pain
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!
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.
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
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.
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The implications of posture for neck and jaw pain
The effects of Posture for headache, neck and jaw conditions
Postural implications related to cervical postural positions have been demonstrated with TMJ disorders involving the stomatognathic system. Forward head posture and cervical spine positioning are also indicated with TMJ disorders.
The American Academy of Orofacial Pain highlight the direct correlation between the cervical spine (neck) and TMJ dysfunction. The cervical spine has an intimate connection between the masticatory system and the cranium, as demonstrated through joint articulations, muscular attachments, vascular structures and neural innervations. Postural coordination between these structures is fundamental in ensuring the functionality of the system!
More people are of course starting to realize the presence of of signs and symptoms related to cervical spine issues in patients with TMJ dysfunction. Despite multifactorial variables in the development of TMJ dysfunction, there has also been some indication for more severe TMJ problems involving that of more prominent lordosis in the cervical spine (neck). The TMJ disorders encompasses a multitude of clinical problems including the masticatory system and actual temporomandibular joint complex. The etiology is multifactorial and can be related to occlusal issues, anatomical, neuromuscular, and psychological variables and relatable structural dysfunction involving the neck. The TMJ can be adversely affected from a biomechanical perspective through alterations in the position of the head and body. Head positioning can implicate mandibular positioning, and the masticatory system. Changes in head positioning may alter patterns of habitual mouth closing.
Forward head posture potentially alters mandibular positioning through reducing the physiological space (joint space) which is thought to occur from displacement of the mandible backwards and upwards with excessive contracting of the clenching muscles. In summary: abnormal head positioning and poor posture CAN influence the development of many myofascial pain disorders.
“learning home” is important in addition to understanding the implications of postural compromise and sustained loading positions. Control and awareness in addition to strength and specific strategies to address this is therefore key! Our physiotherapists are very thorough when assessing for inappropriate movement patterns and sustained positioning in your daily routine which could be responsible for your pain.
Matheus, Ricardo Alves et al. “The Relationship Between Temporomandibular Dysfunction and Head and Cervical Posture.” Journal of applied oral science 17.3 (2009): 204–208. Web
Jaeger, J. O., Oakley, P. A., Moore, R. R., Ruggeroli, E. P., & Harrison, D. E. (2018). Resolution of temporomandibular joint dysfunction (TMJD) by correcting a lateral head translation posture following previous failed traditional chiropractic therapy: a CBP® case report. Journal of physical therapy science, 30(1), 103–107. https://doi.org/10.1589/jpts.30.103
Strini, P. J., Machado, N. A., Gorreri, M. C., Ferreira, A., Sousa, G., & Fernandes Neto, A. J. (2009). Postural evaluation of patients with temporomandibular disorders under use of occlusal splints. Journal of applied oral science : revista FOB, 17(5), 539–543. https://doi.org/10.1590/s1678-77572009000500033
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