Updated May 2026. Written by the Upwell Health Collective clinical team. Clinically reviewed May 2026. Next review November 2026. For educational purposes only.
Related reading from Upwell Health:
• Lower Back Pain: Australia's Most Comprehensive Guide — the spinal pain science, imaging evidence, and exercise framework that underpins this guide.
• Pain Is Not Damage: The Most Important Distinction in Chronic Pain — essential for understanding why headache pain is not proportional to tissue damage.
• Central Sensitisation: Why Your Pain Won't Go Away — the neurological process that drives chronic migraine and medication overuse headache.
• The Sleep–Pain Connection — sleep disruption is one of the most consistent migraine triggers and recovery barriers.
• Stress, Anxiety & Chronic Pain — the nervous system dysregulation that drives both chronic headache and chronic pain.
Headache disorders are among the most prevalent neurological conditions on earth. They are also among the most undertreated, misunderstood, and stigmatised. In Australia, the picture is stark.
According to the Australian Institute of Health and Welfare (AIHW, December 2025) — its first comprehensive report compiling neurological condition data in one place — around 2.2 million Australians were living with a long-term neurological condition in 2022, and migraine was the most common, affecting 77% of all people with a neurological condition. Approximately 1.7 million Australians were living with migraine in 2022. Migraine disproportionately affects people of working age and females — females are more than twice as likely as males to be impacted.
Migraine & Headache Australia’s 2024–25 national perceptions survey (n = 1,335) found that over 4 million Australians live with migraine, yet most Australians — even those living with it — underestimate how common it is. The survey revealed persistent stigma, significant gaps in care, and widespread impact on work, study, and family life. A national study (QUT Statistical and Genomic Epidemiology Laboratory) estimated Australian prevalence at 19.3% overall — 26.5% of women and 11.7% of men.
The Jean Hailes 2025 National Women’s Health Survey on migraine in Australian women is the most current national estimate of migraine prevalence in Australian women specifically. Migraine is one of the leading causes of disability in Australia — and the condition in which the gap between the evidence base and common clinical practice is most striking.
This guide covers three connected conditions: migraine, headache (tension-type and cervicogenic), and neck pain. They frequently coexist, share neurobiological pathways, and respond to overlapping management strategies. Understanding all three as a system — rather than as isolated problems — is the foundation of effective management.
The International Headache Society’s International Classification of Headache Disorders (ICHD-3) classifies over 200 headache types. Clinically, the most important distinction is between primary and secondary headaches.
Primary headaches have no identifiable underlying structural cause — the headache itself is the condition. The three most common primary headaches are migraine, tension-type headache, and cluster headache. Managing them correctly requires understanding what type you have, because the treatments are often quite different.
Secondary headaches are symptoms of another condition — they have an identifiable cause. These include cervicogenic headache (caused by the cervical spine), medication overuse headache, headache due to infection, intracranial pathology, or vascular disorders. Secondary headaches require addressing the underlying cause, not just treating the headache symptom.
Red flags: when headache needs urgent medical assessment.
Seek urgent medical assessment if your headache is accompanied by any of the following:
• Thunderclap headache — sudden-onset severe headache reaching maximum intensity within seconds. This is a medical emergency (possible subarachnoid haemorrhage).
• New headache in a person over 50 with no previous headache history
• Headache with fever, neck stiffness, rash — possible meningitis
• Headache with neurological symptoms — new focal weakness, vision loss, speech difficulty
• Headache worsening progressively over days to weeks without fluctuation
• Headache after head trauma
• Headache with vision changes in an older person (giant cell arteritis risk)
• History of cancer or immunosuppression with new headache type
The vast majority of headache presentations in primary care and allied health are primary headaches — migraine, tension-type, or cervicogenic. Red flags are uncommon but must be assessed by a clinician before other management begins.
Migraine is a neurological disorder characterised by recurrent attacks of moderate to severe headache, typically unilateral (one-sided), pulsating in quality, lasting 4 to 72 hours, and accompanied by nausea and/or sensitivity to light and sound. These are the textbook features. In practice, migraine presents on a spectrum that is far more variable, and this variability is the primary reason it is underdiagnosed.
Many people with migraine do not have unilateral headache. Many do not have pulsating pain. Many have significant disability between attacks (the interictal burden) that is not captured by headache days alone. Many have attacks that begin without headache — aura without headache (previously called acephalgic migraine), or the prodrome alone. A significant proportion of people diagnosed with “sinus headaches” or “chronic tension headaches” actually have migraine.
Migraine is not “just a headache.” It is a whole-brain neurological condition with four phases — prodrome, aura, headache, and postdrome — that can span 1 to 3 days even when the headache itself is brief. The disability associated with severe migraine attacks is comparable to the disability of quadriplegia on the days attacks occur. It is the second leading cause of years lived with disability globally (WHO), and the leading cause of disability in women under 50.
Multiple factors contribute. Stigma is significant — the 2024–25 Migraine & Headache Australia national survey found persistent misunderstanding even among people living with the condition. Many people attribute migraine to lifestyle choices or personal sensitivity rather than recognising it as a genetic neurological disorder. Many do not seek diagnosis. Many who do seek diagnosis are misclassified. And until the CGRP-targeted therapies arrived, there was relatively little treatment that was specific to migraine pathophysiology — which reduced the urgency of precise diagnosis.
That has now changed. Migraine-specific preventive therapies exist that are more effective and better tolerated than anything previously available. Getting the diagnosis right now directly changes what treatment is available. The stakes of accurate diagnosis are higher than they have ever been.
Migraine pathophysiology has been one of the most actively researched areas in neuroscience over the past 30 years. The current understanding involves a complex interaction between a sensitised, hyperexcitable brain, cortical spreading depression, the trigeminovascular system, and the neuropeptide calcitonin gene-related peptide (CGRP).
People with migraine have a brain that responds more intensely to stimuli than neurotypical brains. This is not a flaw — it is a feature of the neurology. The migraine brain processes sensory information more acutely, generates stronger cortical responses to light, sound, smell, and motion, and has a lower threshold for triggering pain-generating cascades. This hyperexcitability is largely genetically determined — migraine has a strong hereditary component, with family history a significant risk factor.
The implication: migraine is not caused by triggers. Triggers lower the threshold for an attack in a brain that is already predisposed to attack. This is a critical distinction for patient education and management.
In approximately one-third of people with migraine, attacks are preceded by aura — transient neurological symptoms (most commonly visual, such as a shimmering arc of light or blind spot) that develop gradually over 5 to 20 minutes and resolve within an hour. The mechanism underlying aura is cortical spreading depression (CSD): a slow wave of neuronal and glial depolarisation followed by suppressed neural activity that propagates across the cortex at approximately 3 to 5 mm per minute.
CSD was first linked to migraine aura through the classic observation by Karl Lashley (1941) of his own visual aura, whose speed of spread across the visual field corresponded precisely to the known speed of a disturbance propagating across the visual cortex. Modern fMRI imaging has confirmed this in humans. CSD triggers the trigeminal pain pathway — activating meningeal afferents of the trigeminal nerve and driving the release of pain-mediating neuropeptides including CGRP.
Calcitonin gene-related peptide (CGRP) is a vasoactive neuropeptide widely expressed throughout the nervous system. It was first found to be elevated in extracerebral circulation during migraine attacks by Goadsby et al. in 1990. Since then, its role in migraine pathophysiology has been comprehensively established:
The discovery of CGRP’s central role in migraine pathophysiology led directly to the development of the most significant advance in migraine treatment in decades: CGRP-targeted therapies. A 2025 review (PMC, Current Pain and Headache Reports) confirmed that the 2024 American Headache Society consensus statement now recommends CGRP monoclonal antibodies be considered first-line preventive treatment in episodic migraine — a major shift from their previous positioning as second or third-line options.
As migraine attacks become more frequent, the nervous system undergoes changes that lower the threshold for subsequent attacks. This central sensitisation — the same process that drives chronic pain in other conditions — is why episodic migraine (less than 15 days per month) can transform into chronic migraine (15 or more days per month) if not adequately managed. Cutaneous allodynia — pain from normally non-painful skin stimulation, such as wearing glasses during an attack, or brushing hair becoming painful — is a marker of central sensitisation and correlates with the transformation to chronicity.
Understanding the full migraine attack — not just the headache phase — transforms how patients and clinicians approach management.
Up to 80% of people with migraine experience premonitory symptoms before the headache begins. These include yawning (one of the most consistent), fatigue, neck stiffness, food cravings (classically for carbohydrates), mood changes (irritability, depression, or euphoria), cognitive difficulty, and increased sensitivity to light and sound. These symptoms are driven by hypothalamic activation — the hypothalamus appears to be an early participant in migraine initiation, not just the trigeminal system.
The clinical importance: many people mistake prodrome symptoms for triggers. Food cravings in the prodrome lead patients to eat chocolate and then attribute the subsequent headache to chocolate. The chocolate did not cause the migraine — the migraine caused the chocolate craving. This distinction is important for reducing self-blame and misguided dietary restriction.
Aura occurs in approximately one-third of migraine patients. It is most commonly visual (flashing lights, scintillating scotoma, zigzag patterns, blind spots) but can be sensory (tingling or numbness, typically spreading from one hand up the arm and into the face), language-related (difficulty finding words), or motor (rare — hemiplegic migraine). Aura symptoms develop gradually over 5 to 20 minutes (distinguishing them from the sudden onset of TIA symptoms) and resolve completely within 60 minutes. A patient who only experiences aura without headache may not realise they are having a migraine at all.
The headache phase is what most people associate with migraine. Typical features include unilateral (one-sided) location, moderate to severe intensity, pulsating quality, and worsening with physical activity. Nausea (sometimes vomiting), photophobia (light sensitivity), and phonophobia (sound sensitivity) are common. Osmophobia (smell sensitivity) is less commonly discussed but highly characteristic of migraine when present. Not all migraine headaches are unilateral or pulsating — the diagnosis does not require all typical features.
The “migraine hangover” is underappreciated and undertreated. After the headache resolves, many people experience fatigue, cognitive difficulty (“brain fog”), mood changes, and residual head tenderness for 24 to 48 hours. The postdrome represents a real phase of the attack with its own neurobiological signature — it is not imagined and not a medication side effect. Understanding it helps patients plan their recovery and reduces the frustration of feeling unwell long after the pain has resolved.
The concept of migraine triggers is one of the most clinically misused concepts in headache medicine. Triggers are stimuli that lower the attack threshold in a predisposed brain — they do not cause migraine in the way a virus causes infection. A trigger that provokes an attack in one person at one time may have no effect at another time, or in another person, because whether a threshold is crossed depends on the cumulative load of multiple simultaneous inputs.
Common triggers include: sleep disruption (both too little and too much sleep), skipping meals, dehydration, stress and stress let-down (the “weekend migraine” after a stressful week), hormonal fluctuation (particularly falling oestrogen), weather changes (barometric pressure drops), alcohol (particularly red wine and beer), strong sensory stimuli (bright lights, strong smells), and caffeine both excess and withdrawal.
The evidence on dietary triggers is far less robust than commonly believed. Chocolate, cheese, and red wine are frequently cited but weakly supported by controlled evidence — and the prodrome-trigger confusion (craving the food before the attack rather than the food causing the attack) inflates perceived trigger rates substantially. Eliminating large numbers of foods based on uncontrolled observation produces dietary restriction that reduces quality of life without clear benefit.
The most consistent, evidence-supported migraine triggers:
• Sleep irregularity — both too little and too much. Consistent sleep timing is one of the highest-yield lifestyle interventions.
• Skipping meals — hypoglycaemia lowers threshold. Regular meal timing is anti-migraine behaviour.
• Dehydration — inadequate fluid intake is a consistent trigger. The evidence supports 7–8 glasses of water daily.
• Stress and stress let-down — both the stress itself and the relaxation after it. Managing the stress cycle, not just the stress.
• Hormonal fluctuation in women — particularly the oestrogen drop around menstruation.
• Caffeine — both excess and withdrawal. Consistent moderate intake is safer than variable intake.
The 3:1 female-to-male prevalence ratio of migraine after puberty reflects a hormonal driver that is one of the most clearly established factors in migraine biology. Oestrogen plays a significant role in modulating the sensitivity of the trigeminal pain pathway — and fluctuating oestrogen levels are a powerful migraine threshold modulator.
Menstrual migraine occurs in the perimenstrual window — defined as two days before menstruation to three days after — and is driven by the sharp fall in oestrogen that precedes menstruation. Menstrual migraines tend to be more severe, longer-lasting, and less responsive to triptans than attacks at other times of the cycle. A 2025 review (Taylor & Francis Group, PMC11901366) confirmed that the steep decline in oestrogen during menstruation destabilises brain pain pathways, making predisposed women more vulnerable to attack at this specific time.
Management of menstrual migraine may include: acute treatment at onset (triptans remain most effective), mini-prevention (short courses of NSAIDs or triptans taken around the perimenstrual window), hormonal strategies (discussed with a GP or gynaecologist — maintaining stable oestrogen levels through certain contraceptive approaches), and addressing the underlying migraine frequency through standard prevention.
Migraine frequently improves during the second and third trimesters of pregnancy, when oestrogen levels remain consistently elevated. The first trimester — with significant hormonal flux — can see worsening. Post-partum, falling oestrogen levels after delivery can trigger severe attacks. Perimenopause, with its erratic hormonal fluctuation, commonly worsens migraine frequency and severity in women who have a prior migraine history. After menopause, when oestrogen levels stabilise at a new lower level, many women experience improvement — though this is not universal and hormone replacement therapy can either improve or worsen migraine depending on its form and delivery.
The Jean Hailes 2025 National Women’s Health Survey on migraine in Australian women provides the most current Australian data on how migraine affects women across the lifespan. For women whose migraine is significantly hormonally driven, a multidisciplinary approach involving their GP, gynaecologist, and physiotherapist produces the best outcomes.
Tension-type headache (TTH) is the most prevalent headache disorder globally — the lifetime prevalence is estimated at 30 to 78%. Despite this, it is the headache type that receives the least specific clinical attention, partly because it is often mild and self-limiting, and partly because it lacks the dramatic symptom profile of migraine.
Tension-type headache is characterised by bilateral (both-sides) headache of mild to moderate intensity, pressing or tightening quality (not pulsating), not worsening with routine physical activity, and without the prominent nausea, photophobia, and phonophobia of migraine. It typically lasts 30 minutes to 7 days. Episodic TTH is defined as fewer than 15 days per month; chronic TTH is 15 or more days per month for more than 3 months.
The mechanisms of tension-type headache involve both peripheral (myofascial) and central sensitisation components. Pericranial muscle tenderness — particularly of the suboccipital muscles, trapezius, and sternocleidomastoid — is a consistent finding and correlates with headache intensity in episodic TTH. In chronic TTH, central sensitisation of pain pathways becomes more prominent, explaining why the headache can persist even when the peripheral muscle component is addressed.
A 2025 systematic review and meta-analysis (Journal of Oral and Facial Pain and Headache, Onan et al., searches to June 2024) confirmed that physiotherapy approaches are effective for chronic tension-type headache across multiple outcomes: headache intensity, duration, frequency, disability, and headache impact. Physiotherapy combined with exercise and transcutaneous electrical stimulation was effective for headache severity and frequency. Manual therapy targeting the cervical and thoracic spine, trigger point therapy, and deep cervical flexor strengthening all have supporting evidence.
A 2025 component network meta-analysis of 12 RCTs found that resistance exercise significantly reduces headache frequency in tension-type headache. The same analysis found that stretching alone was not superior to usual care. This is clinically important: the intervention type matters. Not all exercise is equal for headache management.
The distinction matters because the treatments are different. Key differentiating features: TTH is bilateral; migraine is often unilateral. TTH is pressing/tightening; migraine is pulsating. TTH is not aggravated by activity; migraine typically is. TTH causes minimal nausea and mild light/sound sensitivity at most; migraine causes significant nausea and prominent sensory sensitivity. Many patients with frequent TTH actually have migraine — re-evaluation with a headache specialist or neurologically trained physiotherapist is worthwhile if tension-type headache is frequent and disabling.
Cervicogenic headache (CGH) is a secondary headache — pain referred from the cervical spine and its structures — that is frequently misdiagnosed as tension-type headache or migraine. It accounts for approximately 2.5 to 4% of headaches in the general population but a significantly higher proportion in clinical settings, particularly in people with a history of neck trauma, whiplash, or prolonged poor cervical posture.
The mechanism: structures in the upper cervical spine (C1, C2, C3 levels — facet joints, intervertebral discs, ligaments, muscles) refer pain to the head via the trigeminocervical nucleus — the region of the brainstem where trigeminal and cervical afferent nerve fibres converge. This anatomical convergence means that pathology in the upper cervical spine can genuinely produce head pain that is clinically indistinguishable from primary headache by pain location alone.
The diagnostic hallmark of cervicogenic headache: head pain that is reproduced or significantly modulated by cervical spine assessment — by manual pressure on the upper cervical joints, by specific movement provocation, or by diagnostic anaesthetic block of the cervical structures. If cervical examination does not reproduce the familiar headache, cervicogenic origin is unlikely.
The evidence for physiotherapy in cervicogenic headache is among the strongest for any headache type. A 2025 systematic review and network meta-analysis (Frontiers in Neurology, Xu & Ling, May 2025, searches to July 2024) evaluated spinal manipulation, mobilisation, and massage for CGH. The review confirmed meaningful reductions in pain, disability, and headache frequency with manual therapy interventions. A 2024 systematic review and network meta-analysis (Physical Therapy, Jung et al.) confirmed physiotherapy interventions reduce headache intensity, frequency, and duration in CGH.
The most effective interventions for CGH based on current evidence:
Medication overuse headache (MOH) is the most common secondary headache disorder and one of the most underrecognised clinical traps in headache management. It is the paradoxical result of taking too much acute headache medication: the medication that relieves individual attacks increases the overall frequency of headaches, creating a cycle where the patient needs more medication to treat more headaches, which causes more headaches.
MOH develops when acute headache medications are taken on more than 10 days per month (for triptans, opioids, and combination analgesics) or more than 15 days per month (for simple analgesics such as paracetamol or NSAIDs) for more than 3 months. Any acute headache medication can cause MOH, but triptans and opioids carry the highest risk. The neurobiological mechanism involves changes in descending pain modulation — the brain’s own pain-suppressing systems become dysfunctional, and the central pain threshold drops, making headaches more frequent and severe.
A 2025 network meta-analysis (Journal of Headache and Pain) of 16 RCTs involving 3,000 participants evaluated the comparative efficacy of different strategies for managing MOH. The findings: withdrawal of overused medication is the essential first step, and adding preventive treatment to withdrawal produces better outcomes than withdrawal alone. Education about MOH is itself therapeutic — patients who understand the mechanism are more motivated to manage withdrawal.
One of the most significant clinical findings in recent migraine research is that anti-CGRP therapies (CGRP monoclonal antibodies and gepants) not only do not cause MOH but actively reduce medication overuse without requiring specific guidance for acute medication withdrawal. A 2025 ScienceDirect review found that erenumab, galcanezumab, and fremanezumab prompt significant interruption of drug overuse in real-world studies. This is clinically transformative for patients with MOH — the preventive medication itself addresses the overuse cycle rather than requiring the patient to first withdraw from all acute medication.
The essential steps in MOH management: first, establish the diagnosis and educate the patient about the mechanism — the self-blaming, confusing experience of headaches becoming more frequent despite (or because of) taking more medication makes sense once MOH is understood. Second, initiate withdrawal of the overused medication — this can be done abruptly (most patients) or gradually. Withdrawal symptoms (increased headache, nausea, restlessness) peak within 48 to 72 hours and typically resolve within 7 to 10 days, though may last up to 4 weeks for opioids. Third, initiate preventive treatment concurrently to address the underlying migraine frequency that led to overuse in the first place. For suitable patients, CGRP-targeted therapy should be considered. Fourth, address the psychosocial and behavioural patterns that drove overuse — anxiety about attacks, catastrophising, over-reliance on acute medication as the only coping strategy.
Neck pain is one of the most prevalent musculoskeletal conditions globally. It is the fourth leading cause of disability worldwide after lower back pain, stroke, and falls. Point prevalence estimates range from 10 to 15%, with lifetime prevalence approaching 50%. Like lower back pain, the majority of neck pain is non-specific — no single identifiable structural cause can be attributed.
The distribution of neck pain presentations mirrors the lower back pain framework:
Bilateral arm or leg symptoms, gait disturbance, bladder or bowel dysfunction, severe progressive neurological deficit, unexplained weight loss, history of cancer with new neck pain, fever with neck pain, or neck pain following significant trauma.
A 2025 systematic review and meta-analysis (Calafiore et al., searches January 2010 to January 2024, PROSPERO CRD42024499937) of 11 RCTs examining manual therapy and therapeutic exercise for chronic non-specific neck pain confirmed that both approaches reduce pain intensity in chronic neck pain. The combination of manual therapy and exercise is consistently superior to either alone.
The 2025 JOSPT systematic review and meta-analysis (Rossettini et al., searches to October 2024) specifically examined cervical joint mobilisation techniques for nonspecific neck pain and found significant improvements in pain and disability, with mobilisation superior to no treatment and comparable to manipulation for most outcomes.
Key evidence statements from the current literature:
The relationship between posture and neck pain is more complicated than the “straighten up” advice suggests. Forward head posture is associated with neck pain in some populations, but the relationship is neither universal nor strongly causal. Prolonged static posture in any position is more harmful than the specific posture adopted. The clinical goal is movement variety and muscular endurance, not a specific held position. Screen height, chair ergonomics, and regular movement breaks matter because they enable variety — not because they maintain the “correct” posture.
Triptans (sumatriptan, rizatriptan, eletriptan, zolmitriptan, and others) are selective serotonin 5-HT1B/1D agonists that work by constricting dilated intracranial blood vessels and blocking trigeminal pain signalling. They are the most effective class of oral acute migraine medication available. In clinical practice, triptans are significantly underused — many patients with moderate to severe migraine remain on simple analgesics when triptans are appropriate and superior.
Key clinical points about triptans: they should be taken early in the attack (in or soon after the headache phase begins) rather than waited on until the headache is severe; early treatment produces better response rates. Response rates vary between individuals and across different triptans — non-response to one triptan does not predict non-response to all. Triptans are contraindicated in cardiovascular disease, certain vascular conditions, and in pregnancy. They are most effective in migraine without aura and migraine with aura after the aura phase has resolved.
NSAIDs (ibuprofen, naproxen, aspirin, diclofenac) are effective for mild to moderate migraine and are appropriate first-line treatments. They are less effective than triptans for severe migraine. Combination of a triptan with an NSAID is superior to either alone. Paracetamol alone has minimal efficacy for migraine and is generally not recommended as a standalone acute treatment. Anti-emetics (metoclopramide, prochlorperazine) enhance absorption of oral medications during attacks when gastric stasis slows absorption, and have intrinsic pain-modulating effects.
Gepants (CGRP receptor antagonists) represent a new class of migraine-specific acute treatments. Ubrogepant and rimegepant are available in some markets. Unlike triptans, gepants do not cause vasoconstriction and are not contraindicated in cardiovascular disease. They do not appear to cause medication overuse headache with regular use — an important advantage. They are currently less broadly available in Australia than triptans but represent the emerging standard for patients who cannot use triptans.
Acute treatment needs to be matched to the severity of the individual attack and taken early. Under-treatment — taking inadequate medication too late, or progressively stepping up when the attack is already severe — is one of the most common patterns in people with poorly controlled migraine. A stratified approach — using triptan-class treatment from the outset for moderate-to-severe attacks, rather than starting with simple analgesics and escalating — produces better outcomes and reduces the risk of MOH.
Migraine prevention is indicated when attacks are frequent (typically 4 or more per month), prolonged, significantly disabling, or when acute treatment is overused or ineffective. Prevention is substantially underutilised — many patients who would benefit remain on acute treatment alone.
Beta-blockers (propranolol, metoprolol), anti-epileptics (topiramate, valproate), and tricyclic antidepressants (amitriptyline) have been the historical mainstay of migraine prevention. They were developed for other conditions and repurposed for migraine prevention. They are effective for some patients but are associated with significant side effects, limited tolerability, and poor long-term adherence. The AHS 2024 consensus statement notes that CGRP-targeted therapy is now better tolerated than these non-specific options.
Four CGRP-targeted monoclonal antibodies are now approved for migraine prevention: erenumab (Aimovig), fremanezumab (Ajovy), galcanezumab (Emgality), and eptinezumab (Vyepti). Erenumab targets the CGRP receptor; the others target the CGRP peptide itself. A 2025 comprehensive review (Current Pain and Headache Reports, PMC11861264) examining clinical evidence from 2023 to 2024 confirmed that long-term studies reveal ongoing safety and efficacy for all four monoclonal antibodies, with the 2024 AHS consensus statement recommending they be considered first-line preventive treatment in episodic migraine.
What the CGRP monoclonal antibody evidence shows:
In clinical trials, approximately 40–60% of patients experienced a ≥50% reduction in monthly migraine days — comparable to what the best traditional preventives achieved, but with significantly superior tolerability and adherence. They are subcutaneous injections given monthly (erenumab, fremanezumab, galcanezumab) or intravenous infusions every 3 months (eptinezumab). A 2025 systematic review (searches 2018–2024, n > 50,000) found pooled 12-month adherence of approximately 55% — significantly higher than adherence to traditional preventives. They do not cause medication overuse headache and can actually resolve existing MOH. They are better tolerated than non-specific preventives. They can be considered first-line.
Access in Australia: CGRP monoclonal antibodies are available in Australia through specialist (neurologist) prescription. They are listed on the PBS for chronic migraine (15+ migraine days per month) in patients who have failed two previous preventive therapies. For episodic migraine, access is currently more restricted and may require private prescription. This access landscape is evolving as the evidence base grows and cost-effectiveness data matures.
OnabotulinumtoxinA (Botox) injected across 31 injection sites in the head and neck is approved for chronic migraine prevention. It reduces monthly migraine days by approximately 8 to 9 days in responders. It is PBS-listed in Australia for chronic migraine in patients who have failed two or more oral preventives. Combination of Botox and CGRP monoclonal antibody is an emerging strategy with supporting evidence for patients who have partial response to either alone.
Physiotherapy has a well-established, evidence-based role in headache management — particularly for cervicogenic headache, tension-type headache, and migraine with a significant musculoskeletal contribution. The 2025 systematic review (Frontiers in Neurology) on manual therapy for CGH and the 2025 systematic review on physiotherapy for chronic TTH both confirm meaningful clinical benefit.
What physiotherapy does for headache:
A 2025 RCT (Journal of Headache and Pain, February 2025, Ernst et al.) found that adding pain neuroscience education to standard physiotherapy reduced headache frequency in adults with migraine beyond standard care alone. This aligns with the evidence in lower back pain: understanding the neuroscience of pain changes how the nervous system processes it.
Exercise is one of the most evidence-supported, most underutilised interventions in headache management. A 2025 systematic review (Healthcare, Río et al., searches November 2024, 10 studies, 848 subjects) examining exercise for chronic tension-type headache and chronic migraine found exercise produced significant improvements in both conditions. For headache, the specific type of exercise matters:
The most important caveat about exercise and migraine: exercise can be a migraine trigger in some people, particularly at high intensity. This does not mean exercise should be avoided — it means exercise intensity should be titrated carefully, hydration should be maintained, and the exercise programme should be built progressively. Most patients with exercise-triggered migraine can exercise regularly at moderate intensity without provoking attacks when they are appropriately conditioned and hydrated.
The SEEDS framework — Sleep, Exercise, Eating, Diary, and Stress management — provides a practical structure for the lifestyle interventions with the strongest evidence for migraine management. Regular lifestyle behaviour (RLB) is not complementary to medical treatment: it is evidence-based treatment that reduces attack frequency and, in some cases, reduces the medication burden needed for control.
Psychological factors are significant drivers of headache chronification and treatment outcomes. Fear of headache, anticipatory anxiety about attacks, catastrophising about pain severity, and avoidance behaviour (restricting activities to prevent attacks) are associated with worse outcomes and higher headache frequency.
A 2024 randomised controlled study found that intensive short-term dynamic psychotherapy for tension-type headache improved both emotional regulation and headache symptoms. Cognitive behavioural therapy for headache has evidence support from multiple systematic reviews, particularly when combined with standard care rather than as a standalone intervention.
The relevance of the Whole Person Pain™ framework (Upwell’s clinical approach to chronic pain) to headache is significant: chronic headache involves the same interaction of biological, psychological, and social factors as other chronic pain conditions. Addressing only the biological component — medications and physical treatments — without attention to the psychological and social drivers produces inferior outcomes. Catastrophising about headache, avoidance of activity for fear of provoking attacks, anxiety about the next attack, and the social isolation that severe migraine can produce all require deliberate clinical attention.
Related reading: The Fear-Avoidance Trap, Pain Is Not Damage, and The Three Buckets: Why Chronic Pain Needs a Whole-Person Framework.
Clinical Pilates is particularly well-suited to cervical spine rehabilitation and headache management because of its emphasis on deep stabiliser activation, proximal control, and proprioceptive awareness. The cervical spine is not anatomically isolated — its mechanics are directly influenced by thoracic mobility, scapular position, shoulder girdle function, and lumbopelvic posture. The Pilates Reformer allows progressive loading of the deep cervical and thoracic stabilisers in supported positions that reduce cervical compressive load while building the endurance and motor control needed for long-term postural change.
For patients with cervicogenic headache driven by deep neck flexor weakness and upper cervical joint dysfunction, a clinical Pilates programme that integrates cervical retraining, thoracic extension mobility, and scapular stabilisation provides a comprehensive rehabilitation framework that extends beyond what individual exercise prescription alone achieves.
Related reading: Why Clinical Pilates Should Be Your Go-To Workout.
Upwell Health Collective at 436 Burke Road, Camberwell manages neck pain, headache, and migraine across our physiotherapy, exercise physiology, and clinical Pilates team. Our clinical approach combines evidence-based manual therapy and exercise with pain neuroscience education — because for headache conditions, understanding the neurology of pain is as important as the physical treatment.
We do not prescribe or manage CGRP monoclonal antibodies, triptans, or other pharmaceutical migraine treatments — those conversations belong with your GP or neurologist. What we can do is comprehensively assess the musculoskeletal and lifestyle contributors to your headache burden, provide evidence-based physical treatment where indicated, and help you build the lifestyle framework that reduces your overall headache frequency and improves your response to medical treatment.
Book an assessment online or contact our team directly. We are in Camberwell, with early morning and evening appointments available.
Q: How do I know if I have migraine or tension-type headache?
A: The key distinguishing features: migraine is typically one-sided, pulsating, moderate to severe, worsened by activity, and accompanied by significant nausea and/or photophobia and phonophobia. Tension-type headache is bilateral, pressing or tightening, mild to moderate, not worsened by activity, and has minimal nausea and mild sensory sensitivity at most. Many people have both — a clinical assessment is the most reliable way to differentiate. Note that many patients diagnosed with “chronic tension headache” actually have migraine.
Q: What is cervicogenic headache and how do I know if I have it?
A: Cervicogenic headache is head pain referred from the cervical spine. The hallmark is that clinical examination of the upper cervical spine reproduces or significantly modifies your familiar headache. It is typically unilateral, starts from the posterior neck and radiates forward, and is triggered or worsened by specific neck positions or movements. A physiotherapist with headache expertise can assess this specifically. If your headache does not respond to cervical examination, cervicogenic origin is unlikely.
Q: Can physiotherapy help my migraine?
A: Physiotherapy does not treat the migraine brain directly. What it can do is identify and address musculoskeletal contributions to headache burden — particularly upper cervical dysfunction that lowers the migraine threshold — and provide pain education that changes how the nervous system processes pain. For migraine with significant cervical involvement (neck pain, restricted cervical movement, headache reproduced by cervical assessment), physiotherapy can meaningfully reduce headache frequency. For pure migraine with no cervical component, physiotherapy plays a supporting role through exercise prescription, lifestyle guidance, and pain education.
Q: What is medication overuse headache and do I have it?
A: MOH develops when you take acute headache medication on more than 10 days per month (triptans, opioids, combination analgesics) or 15 days per month (simple analgesics) for more than 3 months. The paradoxical result is more frequent, often daily, headache. If your headaches have gradually increased in frequency and you find yourself taking more medication to control them, MOH should be evaluated. Discuss with your GP or neurologist. The good news: modern CGRP-targeted preventive therapies can address MOH without requiring complete acute medication withdrawal first.
Q: I’ve tried several migraine preventives and nothing works. Is there anything new?
A: Yes — the CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab, eptinezumab) represent a genuine clinical advance. They are migraine-specific, work through the CGRP pathway that underlies migraine pathophysiology, and are better tolerated than traditional preventives. The 2024 American Headache Society now recommends them as first-line prevention for episodic migraine. In Australia, they are currently PBS-listed for chronic migraine after failing two preventives. Ask your GP for a referral to a neurologist if you haven’t explored this option.
Q: Can exercise trigger my migraine?
A: Yes, in some people, particularly at high intensity. But this does not mean you should avoid exercise. Regular moderate-intensity aerobic exercise consistently reduces migraine frequency in well-designed trials. The key is building exercise tolerance gradually, maintaining hydration, exercising at consistent times, and avoiding high-intensity exercise during vulnerable periods (perimenstrually, when stressed, when sleep-deprived). Most people with exercise-triggered migraine can develop a sustainable exercise programme with appropriate guidance.
Q: My neck is always stiff and I get headaches. Are they related?
A: Possibly. The upper cervical spine refers pain to the head via the trigeminocervical nucleus — a well-established anatomical pathway. If your headaches are reproduced by clinical assessment of your upper cervical joints, if they are associated with specific neck movements or positions, and if they are one-sided and start from the posterior neck, there is likely a cervicogenic component. A physiotherapy assessment that includes upper cervical examination will clarify the contribution of your cervical spine to your headache burden.
Q: Is migraine hereditary?
A: Yes — significantly so. Migraine has a strong genetic component. First-degree relatives of people with migraine have approximately a threefold higher risk than the general population. The genetic predisposition relates to the hyperexcitability of the migraine brain rather than to any single gene. The 2024–25 Migraine & Headache Australia survey found widespread confusion about migraine causes, with many patients blaming lifestyle choices — understanding the genetic, neurological nature of migraine is important for reducing self-blame and stigma.
Q: How many headache days per month mean I should consider preventive treatment?
A: Generally, prevention is considered when attacks occur 4 or more times per month, when attacks are significantly disabling even at lower frequency, when acute medications are used more than 10 days per month (risk of MOH), or when acute treatment is ineffective or contraindicated. If any of these apply, discuss preventive options with your GP or neurologist. Prevention is substantially underutilised — many people who would benefit are not offered it.
This article is for educational purposes only and does not substitute for individual clinical assessment or medical advice about prescription medications. For migraine prevention including CGRP therapies, consult your GP or neurologist. For physiotherapy assessment and management, book with the Upwell Health Collective team at 436 Burke Road, Camberwell VIC 3124. Information last reviewed May 2026.