Clinical resources
Challenging some of the common assumptions in headache, migraine and concussion care.
Medicine evolves because we continue to question what we think we know. Many concepts that were once considered established, such as migraine being purely vascular or prolonged rest being the best treatment after concussion, have been challenged by contemporary research.
The following questions explore areas where current evidence has changed our understanding, while also highlighting where important questions remain unanswered. Each summary outlines what we know today, where the evidence is heading, and what this may mean for clinical practice.
Migraine is no longer considered simply a vascular disorder.
Modern imaging studies have found little or no meaningful arterial dilation during migraine attacks, and current evidence suggests that blood-vessel changes alone cannot explain migraine pain.
Instead, migraine is understood as a disorder involving altered brain function, activation of the trigeminovascular system and abnormal sensory processing.
Rather than asking whether migraine is neurological or vascular, researchers increasingly view it as a neurological disorder involving complex interactions between the brain, trigeminal pathways and peripheral sensory input.
Understanding why some patients become sensitised—and what maintains that sensitisation—remains one of migraine research’s biggest questions.
This broader understanding helps explain why migraine presents with much more than headache and supports a multidisciplinary approach to assessment and management.
For much of the twentieth century, migraine was considered a vascular disorder. It was thought that constriction of blood vessels caused aura, followed by dilation of blood vessels that produced the headache. This theory shaped migraine research and treatment for decades and remains a common explanation given to patients today.
Over the past 30 years, however, advances in neuroimaging, neurophysiology and headache science have fundamentally changed our understanding. While blood vessels remain involved, migraine is now recognised as a complex neurological disorder involving altered sensory processing, activation of the trigeminal system and changes in brain network function. Rather than asking whether migraine is “vascular” or “neurological”, the current evidence suggests it is best understood as a neurovascular disorder, where the brain, trigeminal system and blood vessels interact.
Migraine affects approximately one in seven people and is one of the leading causes of disability worldwide. Despite its prevalence, many misconceptions remain, particularly around the idea that migraine is simply caused by blood vessels widening.
This matters because how we understand migraine influences how we assess, explain and manage it. If migraine is viewed purely as a vascular disorder, there is a risk of overlooking the broader neurological and sensory processes that contribute to symptoms such as nausea, dizziness, visual disturbance, sound sensitivity and altered movement tolerance.
The modern model encourages clinicians to consider migraine as a disorder of altered nervous system function, with multiple factors influencing an individual’s threshold for an attack.
The vascular theory was largely based on the pioneering work of Harold Wolff in the 1930s and 1940s. Wolff observed that some migraine patients appeared to have distended superficial temporal arteries during attacks and that compression of these vessels occasionally reduced pain. The effectiveness of early vasoconstrictor medications, such as ergotamine, further reinforced the belief that blood vessel dilation was the primary cause of migraine.
For many years, this explanation fit the available evidence and became widely accepted.
However, as imaging techniques improved, researchers were able to study the brain and cerebral blood vessels during spontaneous migraine attacks. The results challenged the traditional model.
One of the landmark studies in migraine research was published by Schoonman et al. (2008). Using high-resolution magnetic resonance angiography during spontaneous migraine attacks, the researchers found no significant dilation of intracranial arteries on the painful side of the head compared with the non-painful side.
Similarly, Amin et al. (2013) used advanced MRI techniques to examine migraine attacks and again found little evidence that arterial dilation could adequately explain the severity or timing of migraine pain.
These studies did not show that blood vessels are irrelevant. Rather, they demonstrated that blood vessel changes alone are insufficient to explain migraine.
Current evidence supports migraine as a disorder involving altered excitability of the brain and activation of the trigeminal system.
The trigeminal nerve supplies pain-sensitive structures around the meninges and cerebral blood vessels. During a migraine attack, activation of trigeminal afferents leads to release of neuropeptides such as calcitonin gene-related peptide (CGRP), substance P and PACAP. These molecules contribute to neurogenic inflammation, sensitisation and pain transmission.
The success of CGRP-targeted medications has provided further support for this model. Importantly, these treatments appear to work by modulating neural signalling rather than simply preventing vasodilation.
The neurological model also explains many of the symptoms that cannot be accounted for by blood vessel changes alone.
These include:
Functional imaging studies have shown altered activity within multiple brain regions before, during and after migraine attacks, including the hypothalamus, brainstem, thalamus and cortical sensory networks.
Migraine is therefore increasingly understood as a disorder of altered sensory processing rather than simply a disorder of pain.
The trigeminovascular system forms the interface between the brain and peripheral sensory structures.
Activation of trigeminal afferents can lead to:
This system provides a biologically plausible explanation for why migraine symptoms extend well beyond the head and why factors such as sleep deprivation, stress, hormonal fluctuations, illness and sensory overload can influence migraine threshold.
One of the most exciting developments in headache research is the shift from asking “What causes migraine?” to “What lowers an individual’s threshold for migraine?”
Rather than viewing migraine as a single event, researchers increasingly describe it as a dynamic disorder involving interactions between multiple neural systems.
Emerging research is exploring how information arriving from the cervical spine, vestibular system, autonomic nervous system and visual system may influence central sensory processing within susceptible individuals.
This is particularly relevant because these systems converge within regions such as the trigeminocervical complex, an area known to integrate sensory information from both the head and upper cervical spine.
At The Headache Clinic, we view migraine as a neurological disorder involving multiple interacting systems rather than a condition arising from a single tissue or structure.
Our assessments are therefore designed to identify potentially modifiable contributors that may influence an individual’s migraine threshold. Alongside recognised neurological mechanisms, we routinely assess:
Over many years of clinical practice, we have observed that some patients experience meaningful reductions in migraine frequency and severity when these contributors are addressed, particularly where cervical impairments are identified.
The modern understanding of migraine encourages clinicians to think beyond a purely vascular explanation.
For patients with recurrent migraine, management may include:
A broader systems-based assessment does not replace evidence-based neurological care—it complements it by identifying additional factors that may influence symptom burden.
Although our understanding of migraine has advanced considerably, important questions remain.
We still do not know:
These questions represent some of the most exciting areas of contemporary headache research.
| Study | Why it matters |
|---|---|
| Wolff (1948) | Established the classical vascular theory of migraine. |
| Schoonman et al. (2008) | Demonstrated little evidence of significant intracranial vasodilation during spontaneous migraine attacks. |
| Amin et al. (2013) | Confirmed that arterial dilation alone does not explain migraine pain. |
| Noseda & Burstein (2013) | Comprehensive review of the trigeminovascular pathway and migraine neurobiology. |
| Goadsby et al. (2017) | Described CGRP biology and the rationale for targeted migraine therapies. |
| Brennan & Pietrobon (2018) | Reviewed migraine as a disorder of altered neuronal excitability and brain networks. |
BPPV is the most common cause of positional vertigo, but not every patient who becomes dizzy when moving their head has BPPV.
Vestibular migraine, persistent postural-perceptual dizziness (PPPD), cervical sensorimotor dysfunction and central vestibular disorders can all produce positional or movement-related dizziness.
Diagnosis should be based on the pattern of symptoms, examination findings and characteristic positional nystagmus—not positional dizziness alone.
Researchers increasingly recognise that dizziness often reflects interaction between vestibular, visual and cervical sensory systems.
Although cervical dizziness remains a diagnosis of exclusion, growing evidence supports the importance of cervical sensorimotor function in balance and spatial orientation.
Patients who do not fit the typical pattern of BPPV—or who fail to improve following appropriate repositioning—may benefit from broader vestibular and cervical assessment.
Benign Paroxysmal Positional Vertigo (BPPV) is the most common cause of positional vertigo, but it is not the only cause.
Patients who become dizzy when lying down, rolling over in bed or changing head position may instead have vestibular migraine, persistent postural-perceptual dizziness (PPPD), central vestibular disorders or, in selected cases, altered cervical sensorimotor function.
The diagnosis should therefore be based on the overall clinical picture, including symptom characteristics, examination findings and eye movement testing—not positional dizziness alone.
Positional dizziness is one of the most common reasons patients present to primary care.
Because BPPV is common, it is often considered first—and rightly so.
However, many patients labelled as having “BPPV” have:
For these patients, considering alternative diagnoses may prevent delayed diagnosis and inappropriate treatment.
Historically, dizziness was often classified according to which movement provoked symptoms.
Modern vestibular medicine has shifted towards understanding why movement provokes symptoms.
Different disorders may produce dizziness during the same movement, but through entirely different mechanisms.
For example:
The movement itself is therefore not the diagnosis—it is simply the trigger.
BPPV results from displaced otoconia entering one of the semicircular canals.
Typical features include:
When these findings are present, the diagnosis is usually straightforward.
Vestibular migraine is now recognised as one of the most common causes of recurrent spontaneous or positional dizziness.
Patients may report dizziness triggered by:
Unlike BPPV, episodes often last minutes to hours, although shorter episodes can occur.
Many patients have a personal or family history of migraine, even if headache is absent during the dizzy episode.
Importantly, vestibular migraine and BPPV may coexist in the same patient.
Persistent Postural-Perceptual Dizziness is characterised by:
PPPD often develops following another vestibular disorder such as BPPV, vestibular neuritis or vestibular migraine.
Rather than representing ongoing damage to the vestibular system, PPPD reflects altered sensory processing and postural control.
The upper cervical spine contains a high density of proprioceptive receptors that contribute to balance, eye movement control and spatial orientation.
Studies demonstrate that altered cervical sensory input can influence vestibular reflexes and postural control.
Consequently, some patients with cervical dysfunction report dizziness associated with neck movement, sustained postures or following neck injury.
One of the biggest developments in dizziness research is the recognition that balance depends on the integration of information from multiple sensory systems.
The brain continuously combines input from:
to determine where the body is in space.
Researchers are increasingly investigating how dysfunction within one system influences the others.
Rather than viewing dizziness as arising from a single organ, modern research suggests many patients experience symptoms because of altered interaction between these sensory networks.
This systems-based understanding is particularly relevant in vestibular migraine, persistent post-concussion dizziness, cervical sensorimotor dysfunction and persistent dizziness following vestibular disorders.
At The Headache Clinic, we approach dizziness as a symptom rather than a diagnosis.
In our assessment we consider recognised vestibular disorders such as BPPV, vestibular migraine and PPPD.
However, we also assess:
Many of our patients present with overlapping conditions rather than a single diagnosis.
For example, it is not uncommon for someone with migraine to have cervical dysfunction, or for an individual recovering from concussion to have vestibular, cervical and autonomic impairments simultaneously.
Our clinical experience suggests that recognising these interacting contributors often provides a clearer explanation for persistent dizziness than searching for a single cause.
Although emerging evidence supports interactions between cervical, vestibular and central sensory pathways, high-quality research is still needed to determine which patients derive the greatest benefit from targeted cervical rehabilitation.
When assessing positional dizziness:
Several important questions remain.
We still do not know:
These remain active areas of vestibular and headache research.
| Study | Why it matters |
|---|---|
| Bhattacharyya et al. (2017) | AAO-HNS Clinical Practice Guideline for BPPV; emphasises accurate diagnosis with positional testing and appropriate use of repositioning manoeuvres. |
| Lempert et al. (2022) | Bárány Society/International Headache Society diagnostic criteria for vestibular migraine. |
| Staab et al. (2017) | Defines PPPD and explains its pathophysiology as a functional disorder of sensory integration. |
| Treleaven (2017) | Reviews cervical sensorimotor dysfunction and its potential role in dizziness following neck disorders. |
| De Hertogh et al. (2007) | Highlights the challenges in diagnosing cervicogenic dizziness and the lack of a gold-standard test. |
The International Classification of Headache Disorders recognises several childhood episodic syndromes associated with migraine, including abdominal migraine, cyclic vomiting syndrome, benign paroxysmal vertigo and benign paroxysmal torticollis.
Infantile colic is also associated with an increased likelihood of developing migraine later in life.
These conditions suggest that migraine may affect sensory, autonomic and gastrointestinal systems before the typical headache phenotype develops.
Migraine is increasingly viewed as a disorder affecting multiple neural networks rather than simply a headache disorder.
Understanding these childhood syndromes may allow earlier recognition of inherited migraine susceptibility.
When recurrent gastrointestinal or vestibular symptoms occur in children without red flags, migraine should remain part of the differential diagnosis.
Migraine is increasingly recognised as a disorder of the nervous system rather than simply a headache disorder. Long before a child develops the typical migraine headache, they may experience recurring episodes of abdominal pain, vomiting, vertigo or episodic torticollis. These conditions are recognised by the International Classification of Headache Disorders (ICHD-3) as episodic syndromes associated with migraine and often represent the earliest expression of an inherited migraine disorder.
When most clinicians hear the word migraine, they immediately think of a severe one-sided headache associated with nausea and sensitivity to light or sound.
While this is the classic presentation in adults, migraine in childhood often looks very different.
Many children first present with recurrent episodes of abdominal pain, unexplained vomiting, vertigo or transient episodes of head tilt—sometimes years before they ever experience a migraine headache.
Recognising these presentations can prevent unnecessary investigations, reduce family anxiety and help clinicians identify children with an underlying migraine predisposition much earlier.
Historically, migraine was viewed almost exclusively as a headache disorder.
However, long-term follow-up studies demonstrated that many adults with migraine recalled experiencing seemingly unrelated episodic illnesses during childhood.
As research accumulated, it became clear that these conditions shared common characteristics:
This evidence led the International Headache Society to formally recognise these conditions as episodic syndromes associated with migraine within the ICHD-3 classification.
Rather than being separate diseases, they are now considered early manifestations of migraine biology.
Migraine is now understood as a disorder involving widespread sensory, autonomic and brainstem networks.
This helps explain why migraine can present with gastrointestinal, vestibular and autonomic symptoms without headache, particularly during childhood.
Recognised childhood episodic syndromes include:
Recurrent episodes of moderate to severe central abdominal pain lasting between two and 72 hours, often accompanied by nausea, vomiting and pallor.
Children are completely well between episodes.
Many later develop typical migraine headaches during adolescence or adulthood.
Repeated stereotyped episodes of intense vomiting separated by completely symptom-free intervals.
Although the exact relationship remains incompletely understood, substantial overlap exists between cyclic vomiting syndrome and migraine, with many patients responding to migraine-directed therapies.
Brief spontaneous episodes of vertigo occurring in otherwise healthy young children.
Children recover completely between attacks and frequently develop migraine later in life.
Episodes of intermittent head tilt beginning during infancy.
Episodes may last hours to days and often resolve spontaneously with age.
Although uncommon, this syndrome has one of the strongest recognised associations with later migraine.
Infantile colic is not formally classified within ICHD-3, but growing evidence suggests it may represent one of the earliest manifestations of migraine susceptibility.
Systematic reviews have demonstrated that infants with colic are more likely to develop migraine later in childhood, while mothers with migraine are more likely to have infants affected by colic.
Although causation has not been established, these findings support an important association between the two conditions.
Perhaps the biggest shift in migraine research is moving from asking:
“Where is the headache?”
to asking:
“How is this person’s nervous system expressing migraine?”
Researchers increasingly recognise migraine as a disorder involving multiple interconnected neural systems, including the sensory, vestibular, autonomic and gastrointestinal networks.
This broader understanding helps explain why children may initially present with symptoms that appear unrelated to headache.
Rather than viewing abdominal migraine, cyclic vomiting syndrome or benign paroxysmal vertigo as isolated disorders, they are increasingly understood as different clinical expressions of an underlying migraine predisposition.
Future research aims to better understand why different children express migraine biology in different ways, and whether early recognition may improve long-term management.
At The Headache Clinic, we view migraine as a neurological disorder that can present in many different ways across the lifespan.
For children, this means looking beyond headache alone.
When assessing recurrent episodes of abdominal pain, dizziness, unexplained vomiting or episodic torticollis, we consider whether these symptoms may reflect an underlying migraine predisposition, particularly where there is a family history of migraine and no alternative medical explanation.
Recognising these syndromes does not replace appropriate medical investigation. Many gastrointestinal, neurological and vestibular disorders can present with similar symptoms, and serious pathology must always be excluded when clinically indicated.
Once alternative diagnoses have been excluded, recognising migraine as a potential explanation can help families better understand the condition, reduce unnecessary investigations and support appropriate management.
Our assessment extends beyond establishing the diagnosis.
We also assess whether there are potentially modifiable contributors that may influence a child’s symptoms or future migraine burden.
Depending on the child’s age and presentation, this may include assessment of:
Our clinical experience suggests that identifying and addressing modifiable cervical, vestibular and sensorimotor impairments may assist some children as part of a broader multidisciplinary management approach. However, further high-quality research is required to determine which children benefit, why they benefit and how these findings should be integrated into evidence-based paediatric migraine care.
For children presenting with recurrent episodic symptoms:
Despite growing recognition of childhood migraine syndromes, several important questions remain.
We still do not know:
These remain active areas of paediatric headache research.
| Study | Why it matters |
|---|---|
| ICHD-3 (2018) | Officially recognises childhood episodic syndromes associated with migraine. |
| Romanello et al. (2013) | Meta-analysis demonstrating the association between infantile colic and later migraine. |
| Gelfand (2015) | Comprehensive review of childhood episodic syndromes and migraine. |
| Rome IV Criteria (2016) | Standardised diagnostic criteria for abdominal migraine and related functional gastrointestinal disorders. |
| Tarantino et al. (2020) | Reviews the evolving understanding of paediatric migraine phenotypes. |
Current evidence shows that cervical musculoskeletal impairments can be present in people with headache and migraine even when neck pain is absent.
The International Classification of Headache Disorders does not require neck pain for the diagnosis of cervicogenic headache, and cervical assessment should be guided by the overall clinical picture rather than a single symptom.
Researchers are increasingly investigating how cervical sensory input may influence trigeminal processing and central sensitisation.
Although it has not been established that cervical dysfunction drives migraine in all patients, identifying which patients may have a clinically meaningful cervical contribution is an important area of ongoing research.
The absence of neck pain should not automatically exclude cervical assessment when other clinical features suggest potential involvement.
The absence of neck pain does not necessarily exclude cervical musculoskeletal dysfunction.
Current evidence demonstrates that patients with headache and migraine may exhibit measurable cervical impairments—including reduced movement, impaired muscle performance and altered sensorimotor control—even when neck pain is not their primary complaint.
This suggests that cervical assessment should be guided by the overall clinical presentation rather than the presence or absence of neck pain alone.
One of the most common reasons clinicians choose not to assess the cervical spine is because the patient says,
“My neck doesn’t hurt.”
Historically this has seemed reasonable. If the patient has no neck symptoms, why would the neck be relevant?
However, over the past two decades, research has increasingly shown that cervical dysfunction and neck pain are not synonymous.
In other musculoskeletal conditions, clinicians readily accept that movement dysfunction may exist without pain. Emerging headache research suggests the same principle may apply to the upper cervical spine.
The important clinical question is therefore not:
“Does the patient have neck pain?”
but
“Could cervical dysfunction be contributing to this patient’s symptoms?”
Traditionally, headaches were divided into:
This sometimes led to the misconception that the cervical spine is only relevant in patients with cervicogenic headache.
Modern neuroscience paints a more complex picture.
The upper cervical spine shares close anatomical and physiological connections with the trigeminal system through the trigeminocervical complex (TCC) within the upper cervical spinal cord and lower brainstem.
This convergence provides a biological mechanism by which nociceptive and sensorimotor information arising from the upper cervical spine may influence head pain, facial pain and dizziness.
Systematic reviews consistently report that people with headache disorders demonstrate:
These findings are observed across cervicogenic headache, tension-type headache and even in migraine.
Importantly, these impairments are not always accompanied by significant neck pain.
The International Classification of Headache Disorders (ICHD-3) recognises neck movement and examination findings as part of the diagnosis of cervicogenic headache.
Neck pain is common but is not an essential diagnostic criterion.
Similarly, recent observational studies have demonstrated cervical musculoskeletal impairments in patients whose primary complaint is migraine despite relatively mild cervical symptoms.
These findings suggest that relying solely on neck pain risks overlooking potentially relevant physical impairments.
Current evidence demonstrates an association between cervical dysfunction and several headache disorders.
It does not conclusively establish that cervical dysfunction initiates or maintains migraine.
Several explanations remain possible.
Cervical dysfunction could represent:
Current research has not yet determined which explanation is correct, and different mechanisms may apply to different patient subgroups.
This is perhaps one of the most exciting areas of contemporary headache research.
Increasingly, researchers are asking whether persistent sensory input from the upper cervical spine could influence central pain processing in susceptible individuals.
Experimental studies have demonstrated convergence between cervical and trigeminal afferents within the trigeminocervical complex.
Functional imaging studies continue to improve our understanding of central sensitisation and altered pain modulation in migraine.
At the same time, researchers are beginning to investigate whether reducing abnormal cervical input may influence central nervous system excitability.
The next generation of research is likely to focus on identifying:
At The Headache Clinic, we regard the cervical spine as a potential contributor within a broader systems-based assessment of headache and migraine.
Our assessment aims to determine whether cervical dysfunction may represent one of several modifiable factors influencing an individual’s symptom burden.
Alongside cervical assessment, we also evaluate vestibular function, visual integration, autonomic regulation, sleep, exercise tolerance and recognised migraine triggers.
Over many years of clinical practice, we have observed that some patients experience substantial improvements in headache frequency, intensity and disability following targeted cervical rehabilitation.
These observations are consistent with the emerging understanding of interactions between cervical and trigeminal pathways.
We believe the challenge for future research is not to ask whether the cervical spine causes migraine, but rather:
Which patients have clinically meaningful cervical contributions, and how can they be identified?
Answering that question has the potential to significantly advance personalised headache management.
Current evidence supports considering the cervical spine as part of a comprehensive headache assessment when clinically indicated.
Clinicians may consider cervical assessment where patients demonstrate:
The absence of neck pain alone should not automatically exclude further assessment.
Several important questions remain unanswered.
We still do not know:
These questions represent some of the most important research priorities in headache medicine.
| Study | Why it matters |
|---|---|
| ICHD-3 (2018) | Diagnostic framework for cervicogenic headache; neck pain is common but not essential. |
| Di Antonio et al. (2023) | Systematic review showing cervical musculoskeletal impairments in people with migraine, including those without prominent neck pain. |
| Getsoian et al. (2020) | Demonstrated the value of combining cervical examination findings to identify cervicogenic headache, highlighting that no single feature is sufficient. |
| Bogduk (2001 onward) | Established the anatomical basis of the trigeminocervical complex and cervical referral patterns. |
| Watson & Drummond | Experimental studies showing that stimulation of upper cervical structures can reproduce familiar head pain in selected patients, supporting biological plausibility but not proving causation. |
International concussion guidelines no longer recommend prolonged rest.
After an initial period of relative rest (24–48 hours), symptom-limited physical activity and individually prescribed aerobic exercise are associated with faster recovery and reduced risk of persistent symptoms.
Research is increasingly shifting from protecting the brain through prolonged rest to actively promoting recovery through graded rehabilitation.
Exercise, vestibular rehabilitation, cervical assessment and psychological support are increasingly recognised as complementary components of concussion management.
The goal is not to avoid exercise but to prescribe the right type, intensity and timing for the individual patient.
Current international guidelines no longer recommend prolonged rest after concussion. Following an initial period of 24–48 hours of relative rest, gradual, symptom-limited physical activity is encouraged and, for many patients, is associated with faster recovery than prolonged inactivity.
For many years, complete physical and cognitive rest was considered the cornerstone of concussion management. Patients were advised to avoid exercise, school, work and even normal daily activities until they became symptom free.
While well intentioned, research over the past decade has shown that prolonged rest may actually delay recovery in some individuals. Today, concussion is increasingly viewed as an active rehabilitation process, where carefully prescribed activity helps restore normal brain function rather than simply waiting for symptoms to disappear.
This change represents one of the most significant shifts in modern concussion management.
Earlier concussion guidelines recommended “rest until symptom free” because it seemed logical that an injured brain should be protected from further stress.
However, clinicians began noticing that patients who rested for prolonged periods often developed:
At the same time, researchers demonstrated that the physiological disturbances following concussion are dynamic rather than static. While the brain initially requires protection, it also appears to benefit from gradual re-exposure to normal activity as recovery progresses.
This prompted researchers to investigate whether carefully prescribed exercise could actually assist recovery.
The 6th International Consensus Statement on Concussion in Sport (Amsterdam, 2022) recommends relative rest for the first 24–48 hours following injury.
Relative rest means avoiding activities that significantly worsen symptoms while continuing light activities of daily living, gentle walking and reducing unnecessary physical or cognitive overload.
Complete bed rest is no longer recommended.
Several high-quality randomised controlled trials have demonstrated that individually prescribed, symptom-limited aerobic exercise can reduce recovery time.
The work of John Leddy and colleagues has been particularly influential. Their studies showed that adolescents prescribed sub-symptom threshold aerobic exercise recovered several days faster than those undertaking stretching or prolonged rest.
Importantly, exercise was introduced early but remained below the level that significantly exacerbated symptoms.
Rather than “pushing through” symptoms, the goal is to gently challenge the recovering nervous system while avoiding sustained symptom escalation.
Concussion affects multiple interacting systems including:
This explains why recovery often benefits from a multidisciplinary approach rather than a single intervention.
Different patients recover through different rehabilitation pathways depending on the impairments identified during assessment.
One of the biggest changes in concussion research is the move away from viewing concussion as an isolated brain injury towards understanding it as a disorder involving multiple interacting physiological systems.
Researchers are increasingly investigating how impairments involving:
may contribute to persisting symptoms after concussion.
Rather than asking “How long should this person rest?”, clinicians are increasingly asking:
“Which systems are limiting this person’s recovery?”
This systems-based approach aims to identify modifiable impairments that can be targeted through rehabilitation rather than waiting for spontaneous recovery alone.
Although many questions remain regarding the optimal timing and combination of rehabilitation strategies, current evidence strongly supports active, individualised management over prolonged inactivity.
At The Headache Clinic, we view concussion recovery as an active rehabilitation process rather than a passive waiting period.
Every concussion is different. While the diagnosis may be the same, the factors contributing to ongoing symptoms often vary considerably between individuals.
Alongside recognised neurological recovery, we routinely assess:
Where impairments are identified, rehabilitation is tailored to the individual rather than relying on time alone.
One area of particular interest is the cervical spine. Many patients with concussion experience neck pain, headache, dizziness or movement-related symptoms. Emerging research suggests that cervical dysfunction may contribute to these symptoms through altered sensorimotor input and interactions within the trigeminocervical complex.
Current best practice encourages clinicians to:
For patients whose symptoms persist beyond the expected recovery period, a systems-based assessment may identify modifiable contributors that would not be addressed through rest alone.
Despite significant advances, several important questions remain.
We still do not know:
These remain active areas of international concussion research.
| Study | Why it matters |
|---|---|
| McCrory et al. (2017) | Established the shift away from prolonged rest in the Berlin Consensus Statement. |
| Amsterdam International Consensus Statement (2022) | Current international best-practice guidance recommending relative rest and early activity. |
| Leddy et al. (2019) | Randomised trial demonstrating faster recovery with prescribed sub-symptom aerobic exercise. |
| Leddy et al. (2021) | Further evidence supporting early exercise following sport-related concussion. |
| Schneider et al. (2014) | Demonstrated benefits of combined cervical and vestibular rehabilitation for persistent symptoms. |
| Silverberg & Iverson (2013) | Critiqued prolonged rest and highlighted active rehabilitation approaches. |
| Kontos et al. (2020) | Provides evidence that early specialist concussion assessment is associated with faster recovery and a lower likelihood of prolonged symptoms, supporting a shift away from “wait and see” management towards early education, active rehabilitation and identification of modifiable impairments. |
Headache, migraine, dizziness and concussion have traditionally been viewed as disorders of individual organs, whether the brain, inner ear or cervical spine. Increasingly, however, research suggests these conditions are better understood as involving interactions between multiple neural systems.
At The Headache Clinic, our assessments reflect this evolving understanding. Alongside established neurological diagnoses, we assess cervical, vestibular, temporomandibular (TMJ), visual and autonomic function, as well as sleep and exercise tolerance, to identify potentially modifiable contributors that may influence an individual’s symptoms.
Our clinical experience suggests many patients improve when these contributors are identified and addressed. While these observations are consistent with emerging research, further high-quality studies are needed to determine which patients benefit most, why they improve, and how these findings can best be integrated into evidence-based care.
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