Migraine specialist in Sydney

Migraine is a brain condition, not just a bad headache. The headache and the symptoms around it are the disease.

What is happening inside an attack. The brain briefly changes how it processes signals: it dials up sensitivity to light, sound and movement, and releases an inflammatory chemical called CGRPCGRPCalcitonin gene-related peptide. A neuropeptide released around the trigeminal nerve and meningeal blood vessels during a migraine attack. Blocking CGRP or its receptor with monoclonal antibodies or small-molecule gepants is the basis of the newest migraine therapies. around the nerves of the head. That is why migraine pain throbs, why it sits on one side, and why nausea and the urge to lie in a dark room come with it. The World Health Organization ranks migraine as one of the most disabling conditions in the world — not because it is dangerous, but because it costs people days they can’t get back.

Two clinically important categories drive almost every treatment decision:

• Episodic migraine — headache on fewer than 15 days per month. Most people with migraine sit here.
• Chronic migraine — headache on 15 or more days per month, for at least three months, with at least 8 of those days being migrainous (the International Classification of Headache Disorders definition). Chronic migraine is what unlocks Botox and (typically) CGRP monoclonal antibodies on the PBS, when other criteria are met — PBS eligibility usually requires this pattern sustained for at least six months before initiation.

A separate axis is whether you experience auraauraReversible neurological symptoms — usually visual (zigzag lines, blind spots), sometimes sensory (tingling, numbness) or speech — that develop over 5–20 minutes and last under an hour. Aura occurs in about a third of people with migraine. — reversible neurological symptoms (commonly visual zigzags or blind spots, sometimes tingling, numbness or speech disturbance) that build over 5–20 minutes and resolve within an hour. Aura matters clinically because it changes which acute medications are safe (see section IX).

A migraine attack is more than the headache itself. Most people move through some, though not always all, of four phases. Recognising where you are in the cycle is one of the most useful skills you can build.

1. Prodrome — hours to a day before

Subtle signals the brain is about to enter an attack: yawning, unusual tiredness, food cravings, neck stiffness, irritability or a sense that something is “off.” If you can recognise your prodrome, you can sometimes pre-empt the attack with hydration, rest, or an acute treatment.

2. Aura — about a third of people, lasting up to an hour

• Visual: zigzag lines, blind spots, flashing lights, shimmering crescents that drift across the visual field
• Sensory: tingling or numbness spreading up an arm or across the face
• Speech: difficulty finding words, slurring
• Rarely: weakness ( hemiplegic migrainehemiplegic migraineA rare migraine variant in which aura includes one-sided weakness. It changes treatment because triptans and ergots are contraindicated. There are familial and sporadic forms.) or brainstem symptoms (vertigo, double vision, ringing in the ears)

A first-ever aura, or aura with new neurological symptoms, deserves urgent assessment to rule out stroke or transient ischaemic attack.

3. Headache — 4 to 72 hours

• Throbbing or pulsating pain, often one-sided
• Worsening with movement, bending or routine activity
• Sensitivity to light, sound and sometimes smell
• Nausea, vomiting
• Difficulty thinking clearly, light-headedness

4. Postdrome — up to 24 hours after

The “migraine hangover.” Drained, foggy, tender on the side that hurt, mood changes, continued sensitivity to light and sound. Often dismissed as fatigue but a recognised part of the attack.

Most adults with recurrent headaches have migraine, tension-type headache, or both. A small minority have a secondary cause — something causing the headache — and it is the doctor’s job to look for it. The features below should prompt further investigation:

• Sudden onset — thunderclap headache reaching peak intensity within seconds; suspect subarachnoid haemorrhagesubarachnoid haemorrhageBleeding into the space surrounding the brain, most often from a ruptured cerebral aneurysm. Classic presentation is a sudden, ‘worst-ever’ thunderclap headache. Investigated urgently with non-contrast CT brain and, if negative within 6 hours of onset, sometimes lumbar puncture. until proven otherwise
• New focal neurological deficit — weakness, slurred speech, vision loss, persistent confusion
• Fever, neck stiffness or rash — suspect meningitis or encephalitis
• New headache after age 50 — especially with jaw claudication, scalp tenderness or visual loss; consider giant cell arteritisgiant cell arteritisAn inflammatory condition of medium and large arteries in older adults that can cause sudden permanent vision loss if untreated. Suggested by new headache after 50 with scalp tenderness, jaw claudication, or visual symptoms; investigated with ESR/CRP and managed urgently with corticosteroids.
• Progressive headache — getting worse over days or weeks despite treatment
• Postural headache — significantly worse standing, better lying down (suspect low CSF pressure) or vice versa (suspect raised intracranial pressure)
• Headache after head injury
• Headache in pregnancy or postpartum — new or atypical headache here always needs same-day assessment
• Cancer history, immunosuppression or HIV with a new headache pattern

Any of these is a reason to be seen sooner rather than later, and may justify imaging (typically MRI brain) that would not otherwise be needed.

Migraine is strongly heritable — about half of people with migraine have a first-degree relative who is also affected, and the risk is higher when both parents have migraine. The susceptibility is built in; what triggers an attack on a given day usually is not.

The best-established triggers are:

• Hormonal change — particularly the oestrogen drop around menstruation. Most women with migraine improve in the second and third trimesters of pregnancy and after menopause.
• Sleep change — either too little or too much, irregular bed and wake times
• Skipped meals and dehydration
• Stress — and stress relief. Many migraines land on the first day off, not during the busy week.
• Alcohol — particularly red wine
• Bright or flickering light, strong smells, weather change
• Some medications — certain oral contraceptives, vasodilators, nitrates

Two notes that often surprise patients. First: the much-publicised food triggers (chocolate, aged cheese, MSG) are real for some people but rare for most — do not eliminate foods speculatively. Second: caffeine is a friend in moderation and an enemy in withdrawal. If you drink coffee, drink it on a regular schedule.

Risk factors that cannot be changed: female sex (about three times the prevalence of men in adulthood — though pre-pubertal migraine is roughly equal between sexes), age (peak in the 30s and 40s), and a family history of migraine. Co-existing depression, anxiety, sleep disorders, and other pain conditions all raise frequency.

Migraine is a clinical diagnosis. There is no blood test or scan that confirms it — it is recognised by the pattern of symptoms, weighed against international diagnostic criteria, and checked against a careful list of features that should make you look for something else.

The shape of a first consultation:

• A structured history. The timeline, character, frequency and impact of your attacks; what you have tried; what worked, what didn’t; family history; comorbid conditions; current medications. We use validated brief questionnaires — the MIDASMIDASMigraine Disability Assessment — a brief 5-item questionnaire scoring how many days migraine has cost you in the last 3 months across work, household and social activities. Used to measure baseline disability and track change with treatment. (Migraine Disability Assessment) and HIT-6HIT-6Headache Impact Test, 6-item version — a brief questionnaire scoring how severely headaches affect your life, with ranges from little/no impact to severe impact. Used to track change with treatment. (Headache Impact Test) — to measure how migraine is affecting your life and track change with treatment.
• A neurological examination, where appropriate— what we look for depends on your presentation, but the point of it is to rule out signs of a secondary cause and to document a normal baseline.
• Review of your headache diary — if you have one, you have already done half of the diagnostic work.
• Imaging only when clinically indicated.Typical migraine in an otherwise well adult does not require an MRI or CT. We image when there are red-flag features (see section III), an atypical presentation, or another reason to look for a secondary cause.
• Bloods only when clinically indicated. Routine bloods (inflammatory markers, thyroid, vitamin levels) are not part of a primary-headache work-up and are reserved for specific suspicions — for example inflammatory markers if giant cell arteritis is being considered in someone over 50.

You leave the first consultation with a written plan: a likely diagnosis, an acute treatment that works for your attacks, a clear decision on whether you need a preventive (and if so, which one), a follow-up timeline, and an answer to the question you came in with.

The aim of acute treatment is to abort the attack early — ideally within 30 minutes of pain onset — and to do it without leaning on any one medication often enough to provoke medication-overuse headache.

Simple analgesics

For mild-to-moderate attacks, the best-evidenced simple analgesics are soluble aspirin 900 mg as a single acute dose, or an NSAID at full adult acute dose — ibuprofen 400–800 mg or naproxen 500–825 mg are typical — taken as early as possible in the headache, ideally with an anti-emetic (metoclopramide or prochlorperazine) when nausea is part of the picture. Aspirin should be avoided in active peptic ulcer disease, bleeding disorders, late pregnancy, and in those under 16 years (Reye syndrome risk). Paracetamol monotherapy has weaker evidence in migraine and is best reserved for situations where aspirin and NSAIDs are contraindicated. If simple analgesics are needed on more than 14 days a month, that is a flag (see section VIII).

Triptans

Triptans — sumatriptan (oral, nasal, subcutaneous), rizatriptan, eletriptan, zolmitriptan and others — are the workhorse of moderate-to-severe migraine. They work best taken early in the headache phase. If one triptan fails, another often succeeds — this is one of the most common decisions we revisit.

Triptans should not be used in: uncontrolled hypertension, ischaemic heart disease, prior stroke or transient ischaemic attack, peripheral vascular disease, hemiplegic migraine or migraine with brainstem aura. They should be avoided in pregnancy except where the benefit clearly outweighs the risk (sumatriptan has the most reassuring pregnancy-exposure data among the triptans).

Gepants

GepantsgepantsSmall-molecule oral medications that block the CGRP receptor. Examples include rimegepant and ubrogepant. Useful for acute treatment and, in the case of rimegepant, also for prevention. Their advantage over triptans is that they have no vasoconstrictor activity, so they can be used in patients with cardiovascular contraindications to triptans. are an oral class that blocks the CGRP receptor. They are particularly useful when triptans have failed or are contraindicated — including in patients with cardiovascular disease, prior stroke, or hemiplegic migraine. Rimegepant (Nurtec ODT) is TGA-registered in Australia for both acute treatment and prevention of migraine, but is not currently PBS-subsidised— it is dispensed on private prescription. Cost is meaningful and worth discussing before prescribing.

Anti-emetics

Metoclopramide and prochlorperazine are first-line in migraine: they treat nausea, can improve absorption of oral analgesics, and have prokinetic effects useful when gastric stasis is part of the attack. Domperidone (prescription-only in Australia) is an alternative; it carries a QT-prolongation caution and is generally avoided in older patients or alongside other QT-prolonging medications.

What we do not recommend

Avoid combination painkillers containing codeine for migraine. They are a leading cause of medication-overuse headache, they are sedating, and they do not abort attacks. If you are using codeine-containing products several times a week, raise it specifically — we will help you taper.

A preventive is a daily treatment, taken whether or not you have a headache, that aims to reduce attack frequency, severity and duration. In randomised trials, around 40–50% of patients achieve at least a 50% reduction in monthly migraine days on a well-chosen preventive — the realistic goal is meaningful reduction, not zero, and finding the right agent often takes more than one trial. Most preventives need 8–12 weeks at a therapeutic dose before you can judge whether they have worked.

We typically consider a preventive when migraine costs you more than four days a month, when attacks are severe or prolonged, when acute medications are failing or being overused, or when the disability is unacceptable to you whatever the frequency.

Oral preventives — usually first line

• Beta-blockers — propranolol is the best-established. Contraindicated in asthma, second- or third-degree heart block, decompensated heart failure, and significant bradycardia or hypotension. Use with caution in depression and in athletes.
• Topiramate — effective; common adverse effects include cognitive slowing, paraesthesia, weight loss, and (rarely) renal stones or angle-closure glaucoma. Topiramate carries a risk of oral cleft and reduced fetal growth and requires effective contraception in women of childbearing potential. At doses ≥200 mg/day, topiramate can also reduce the efficacy of combined oral contraceptives (CYP3A4 induction) — an additional reason non-oestrogen contraception is preferred.
• Amitriptyline — a tricyclic antidepressant useful when migraine coexists with insomnia or chronic tension-type headache.
• Candesartan — an angiotensin-receptor blocker with growing evidence for migraine prevention; well tolerated.
• Venlafaxine — an SNRI used off-label for migraine where there is comorbid depression or anxiety.

Sodium valproate must not be prescribed for migraine prevention in women of childbearing potential — it is a known teratogen with high rates of major birth defects and developmental problems, and the Therapeutic Goods Administration has issued specific guidance restricting its use. SSRIs are not recommended for migraine prevention — the evidence does not support them.

CGRP monoclonal antibodies — for chronic and refractory migraine

Three are available in Australia, given as a self-injection: erenumab (Aimovig) targets the CGRP receptor; galcanezumab (Emgality) and fremanezumab (Ajovy) target the CGRP ligand. Erenumab and galcanezumab are dosed monthly; fremanezumab can be dosed monthly or quarterly. Many patients respond within the first 1–3 months — faster than oral preventives.

PBS Authority is required. All three are PBS-listed for chronic migraine (commonly defined as ≥15 headache days per month, with at least 8 of those being migrainous, for at least 6 months), when prescribed by a neurologist and after prior trial (or clear contraindication / intolerance) of multiple oral preventives from different therapeutic classes, each at adequate dose and duration. Continuation requires a documented ≥50% reduction in monthly migraine days measured from your headache diary. Eligibility for CGRP mAbs in high-frequency episodic migraine has been the subject of evolving PBS criteria — specific criteria are agent-dependent and should be confirmed against the current PBS schedule. Our team checks current criteria against your history at consultation and prepares the Authority application for you.

Common adverse effects are mild — injection-site reactions, and (with erenumab in particular) constipation and a small rise in blood pressure that should be monitored. CGRP monoclonal antibodies are generally not recommended in pregnancy or breastfeeding due to long half-lives and limited human data.

Botox (onabotulinumtoxinA) for chronic migraine

Botox for chronic migraine is delivered using the PREEMPT protocol: 155 units of onabotulinumtoxinA across 31 fixed injection sites in the head and neck, repeated every 12 weeks, with up to 40 additional units across 8 optional “follow-the-pain” sites. PBS subsidy is available for chronic migraine when prescribed by a neurologist and when eligibility is met — including documented chronic-migraine frequency over months, prior preventive failure, and demonstrated response (again, typically a 50% headache-day reduction) at continuation. Our team prepares the PBS Authority application.

Greater occipital nerve blocks

A targeted injection (lidocaine, sometimes with a small dose of corticosteroid) at the back of the head. We use it most often as a short-term bridging treatment during medication-overuse headache withdrawal, in pregnancy where systemic options are limited, and in chronic migraine with prominent occipital pain.

Lifestyle, behavioural and complementary approaches

These are not a substitute for medication in chronic migraine, but the evidence for them in episodic migraine is real and the cost profile is favourable:

• Aerobic exercise — 150 minutes a week of moderate exercise reduces migraine frequency in randomised trials.
• Cognitive behavioural therapy and biofeedback— particularly when migraine coexists with anxiety or sleep disturbance.
• Magnesium glycinate and riboflavin (vitamin B2) — well-tolerated supplements with reasonable evidence in episodic migraine prevention. We prefer magnesium glycinate (better absorbed and less likely to cause loose stools than other magnesium salts) — brands such as Magzorb are widely stocked at Australian pharmacies and health-food retailers. Riboflavin is equally available. Coenzyme Q10 is a reasonable third option. We will confirm sensible doses at consultation.
• Acupuncture — small but real benefit in randomised trials for episodic migraine.

Neuromodulation devices (single-pulse transcranial magnetic stimulation; non-invasive vagus nerve stimulation) have international regulatory approval but are not widely PBS-funded in Australia. We mention them where relevant.

If a single section in this guide changes the next year of someone’s life, it is this one. Medication-overuse headache (MOH) is the most common reason an episodic migraine becomes a chronic one, and the most common reason a previously useful preventive stops working.

MOH is defined as headache occurring on 15 or more days per month in someone with a pre-existing primary headache, where there has been regular overuse, for more than three months, of:

• Simple analgesics (paracetamol, aspirin, NSAIDs) on 15 or more days a month
• Triptans, ergots, opioids, or combination analgesics (e.g. paracetamol-codeine) on 10 or more days a month

The mechanism is not fully understood, but the practical consequence is: more reliever, more headache. The reliever feels essential because each dose helps the next attack, but the cumulative pattern drives the daily headache.

What MOH treatment looks like

• Withdraw the overused agent — under medical supervision. The approach depends on the agent: simple analgesics and triptans can usually be stopped abruptly; opioids and codeine-containing combinations should be tapered. Do not stop opioids or codeine-containing analgesics on your own — we will plan the withdrawal with your GP and provide bridging cover.
• Bridge. A short course of an alternative (sometimes an anti-emetic, sometimes a steroid taper, sometimes a greater occipital nerve block) covers the predictable rebound week or two.
• Start — or restart — a preventive. MOH frequently masks an underlying chronic migraine that was never properly preventively treated. Treating it well is the point of going through the withdrawal.
• Cap acute-medication days going forward. A useful rule of thumb after recovery: keep simple analgesic days under 15 a month and triptan / opioid / combination days under 10 a month, indefinitely.

Migraine in pregnancy

Most women with migraine improve in the second and third trimesters, although a minority worsen. Treatment is more constrained:

• Acute: paracetamol is first-line throughout pregnancy. NSAIDs may be considered for short courses between weeks 12 and 20 only after discussion with your obstetric team — avoid NSAIDs from 20 weeks’ gestation onwards because of risks of oligohydramnios and premature closure of the fetal ductus arteriosus (TGA and international regulator guidance), and many clinicians also avoid NSAIDs in the first trimester. Sumatriptan has the most reassuring pregnancy-exposure data among triptans but is used only where the benefit clearly outweighs the risk; ergots are contraindicated.
• Preventive: low-dose propranolol and magnesium are reasonable options; topiramate and valproate are contraindicated(teratogenicity); CGRP monoclonal antibodies are generally not recommended; greater occipital nerve blocks are a useful drug-light option.
• A new or atypical headache in pregnancy or postpartum is a red flag and warrants same-day assessment — pre-eclampsia, cerebral venous sinus thrombosis and other serious causes are over-represented in this group.

Migraine with aura, contraception and stroke risk

Migraine with aura roughly doubles ischaemic stroke risk, and the risk is amplified by smoking and by oestrogen-containing contraception. Australian guidance classifies migraine with aura as a contraindication to combined hormonal contraception at any age, regardless of smoking status — this includes combined oral contraceptive pills, the combined vaginal ring and the combined patch. Safer alternatives include the progestogen-only pill, the contraceptive implant, copper or hormonal IUDs, and the depot injection. We routinely review contraception and vascular risk factors at consultation, and we are happy to write back to your GP with shared-care recommendations.

Hemiplegic migraine

A rare migraine variant in which aura includes one-sided weakness. Triptans and ergots are contraindicated. Acute treatment relies on simple analgesics, anti-emetics, and (in appropriate patients) gepants. Preventive options are available.

Vestibular migraine

A high-prevalence migraine variant defined by recurrent vestibular symptoms (dizziness, vertigo) lasting minutes to days, in someone with a current or past history of migraine. It often presents to ENT or balance clinics first; the diagnosis frequently sits with neurology. Treatment mirrors migraine more broadly.

Cluster headache and the trigeminal autonomic cephalalgias

Cluster headache is a separate, much rarer primary headache disorder that is often misdiagnosed as migraine for years. The pain is excruciating, strictly one-sided, around or behind one eye, comes in clusters lasting weeks to months, and is accompanied by tearing, nasal congestion or eyelid drooping on the affected side. It needs different treatment — high-flow oxygen, subcutaneous sumatriptan, verapamil, occipital nerve blocks and (in some patients) galcanezumab. If your headaches sound like this, please flag it specifically.

Beyond medication, three habits move the needle for almost everyone with migraine:

• Regular sleep. Same time to bed and same time up, weekdays and weekends. Sleep change is one of the most consistent triggers.
• Regular meals and hydration. Skipped meals, dehydration and caffeine swings are the cheapest triggers to fix.
• Aerobic exercise on most days. Walk, swim, cycle, run — the evidence is that 150 minutes a week of moderate exercise reduces migraine frequency.

Practical rules of thumb that we go through at consultation: keep a headache diary indefinitely, identify your two or three most consistent triggers and act on those (rather than eliminating long lists of foods you enjoy), and treat early when an attack starts — the longer a triptan or gepant is delayed, the less it works.

Knowing what to expect helps the appointment go further. A typical first migraine consultation at CURA looks like this:

1. Detailed history (about 30 minutes). The headache timeline, character and frequency; what you have tried; what is working and what is not; family history; comorbid conditions; full current medication list.
2. Targeted neurological examination.
3. Review of your headache diary and prior imaging— if you have them.
4. A written plan — diagnosis, acute treatment, whether a preventive is indicated and which one, follow-up timeline. We write back to your GP within five business days of your consultation.

What to bring:

• Your GP referral (required for Medicare rebates)
• Your headache diary (paper or app screenshots)
• A list of every preventive and acute medication you have tried, with dose, duration and reason for stopping
• Your current medication list
• Any prior brain imaging (USB, CD or portal access)
• Your Medicare card

A GP referral is required for the Medicare rebate on a specialist consultation. For current consultation fees, the Medicare rebate and the typical out-of-pocket gap, please call our reception on (02) 7906 8356.