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Intracranial Atherosclerosis

Stroke-prevention care from a stroke and interventional neurology team — medical optimisation first, with intracranial stenting at affiliated Sydney hospitals when medical therapy alone isn’t enough.

Most people with intracranial atherosclerosis avoid further stroke when treated with optimised medical therapy. Stenting is a focused option for the smaller group whose strokes recur despite that — and we can deliver both arms of care under the same roof. The emergency notice below is for people experiencing stroke symptoms right now.

The emergency notice below applies only if you currently have stroke symptoms. If your symptoms are stable, you can scroll past it.

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At a glance
  • Optimised medical therapy is the backbone of stroke prevention in intracranial atherosclerosis. Dual antiplatelet for the first 90 days then aspirin long-term, a high-intensity statin to a low LDL target, tight blood-pressure and glucose control, and stopping smoking together cut the early recurrent-stroke risk steeply (Chimowitz et al., SAMMPRIS, NEJM 2011; Kleindorfer et al., AHA/ASA Stroke 2021).
  • Symptomatic intracranial atherosclerotic stenosis carries an elevated early recurrent-stroke risk that is highest in the first weeks and falls with optimised treatment. The first three months are the highest-risk window and shape the dual-antiplatelet plan.
  • Stenting is reserved for selected patients whose strokes recur despite optimised medical therapy. The 2011 SAMMPRIS trial established that elective stenting was not better than aggressive medical therapy in unselected patients; later registry data (WEAVE 2019, WOVEN 2021) supports a more selective modern role.
  • Three of our stroke and interventional neurologists perform the stenting procedure personally — Dr Hugh Stephen Winters, Dr Timothy Ang, and Dr Emma Harrison — at affiliated Sydney hospitals. The consult, the decision and the long-term follow-up sit with CURA.
  • Risk-factor optimisation is actively owned at CURA via 6–12-week follow-ups for the first year — lipids, blood pressure, HbA1c, antiplatelet review, smoking, weight and sleep apnoea. Not handed back to your GP after a single visit.
Directory

You’ve just been told you might have intracranial atherosclerosis — what now?

Today

  • Confirm you don’t have active stroke symptoms. FAST signs — face droop, arm weakness, slurred speech — need 000, not a clinic appointment, even if they seem to come and go.
  • Do not stop your antiplatelet, statin, or blood-pressure medication on your own. If you’ve been started on aspirin or clopidogrel after a TIA or stroke, even a short break increases your recurrent-stroke risk in the highest-risk window.
  • Ask your hospital, GP, or imaging provider for copies of any recent vascular imaging — CT angiography (CTA), MR angiography (MRA), carotid ultrasound — and the radiology reports. These are the most useful single pieces of information for the first appointment.

This week

  • Ask your GP for a current 12-month referral to a stroke neurologist. Mention any recent TIA or minor stroke and any imaging that shows narrowing of an artery inside the brain — these trigger urgent triage at CURA.
  • Make a list of your medications, recent blood pressure readings, and any recent HbA1c and cholesterol results. If you don’t have these, your GP can run them before the consult so we can set the plan in one visit.
  • Note any cardiac history — atrial fibrillation, recent cardiac monitoring, echocardiogram — or arrange a baseline ECG with your GP. Cardio-embolic stroke needs ruling out before the antiplatelet plan is finalised.

This month

  • If you smoke, this is the highest-impact thing you can change for stroke prevention. Ask reception about the smoking-cessation supports we routinely use; nicotine replacement and/or varenicline are available through your GP and are far more effective than going it alone.
  • If you snore loudly, have witnessed apnoeas, or wake unrefreshed, mention this at the consult — obstructive sleep apnoea increases recurrent-stroke risk and a sleep study is part of the routine workup.
  • Bring a family member or friend to the first appointment if you can. There is a lot of new information and a second pair of ears is invaluable.

Recent symptomatic ICAD is triaged urgently. Stable incidental findings on imaging are seen routinely.

I.

What intracranial atherosclerosis is

Intracranial atherosclerosis is the build-up of cholesterol plaque inside the arteries that carry blood through the brain itself.

The brain is fed by a ring of arteries called the and the major branches that come off it — the middle cerebral, anterior cerebral, posterior cerebral, basilar and intracranial vertebral arteries. When narrows one of these intracranial vessels, blood flow downstream can fall — or, more commonly, plaque rupture triggers a clot that blocks the vessel and causes a stroke or transient ischaemic attack.

Intracranial atherosclerotic disease (ICAD) is sometimes called intracranial atherosclerotic stenosis (ICAS) when imaging shows significant narrowing. Both terms describe the same biology — plaque inside the brain’s own arteries — in contrast to extracranial carotid disease, which is plaque in the neck arteries before they enter the skull.

The distinction matters because the two conditions are managed differently. Significant extracranial carotid stenosis often warrants surgical endarterectomy or carotid stenting; intracranial disease, by contrast, is treated medically first in almost every case — a position established by the SAMMPRIS trial in 2011 (see Section VI).

ICAD is responsible for around 8–10% of ischaemic strokes in Western populations, and a meaningfully higher share — up to a third or more — in people of Asian, Hispanic, and African ancestry. It is more common with age, in smokers, and in people with hypertension, diabetes, or high cholesterol.

II.

Symptoms and warning signs

Intracranial atherosclerosis announces itself through and ischaemic strokes. The symptoms map to whichever part of the brain has lost its blood supply.

FAST recognition — the public message

The simplest way to catch a stroke or TIA early is the FAST sign set:

  • Face — one side of the face droops; ask the person to smile.
  • Arm — one arm is weak or numb; ask the person to raise both arms.
  • Speech — speech is slurred or hard to find words for; ask the person to repeat a simple sentence.
  • Time — if any of these are present, call 000 immediately, even if the symptom seems to be improving.

Other emergency presentations include sudden loss of vision in one eye or one half of the visual field, sudden severe vertigo with unsteadiness, sudden double vision, and the worst headache of your life. None of these belong in an outpatient appointment; they belong in an emergency department, where hyperacute stroke care is decided and delivered.

TIA — the warning shot

A TIA looks like a stroke but the symptoms typically resolve within minutes to an hour. Because the symptoms have gone, TIAs are frequently dismissed by the person who has them as “a funny turn”.

Don’t. The single most important fact about TIAs is that they are warning shots: a meaningful proportion of people who have a TIA go on to have a completed stroke in the days and weeks afterwards, and the risk is concentrated in the first 48 hours. A TIA is treated as a medical urgency. If your symptoms have settled but you suspect you have had one, call your GP, our reception, or go to an emergency department on the same day.

III.

Causes and risk factors

The risk factors for intracranial atherosclerosis are largely the same as the risk factors for atherosclerosis anywhere else — and most of them are modifiable. This is why the rest of this page spends so much time on medical management. Most of the work of preventing your next stroke is done in this list.

Modifiable — what we work on with you

  • High blood pressure is the single largest modifiable risk factor for stroke worldwide. The treatment target in secondary stroke prevention is below 130/80 mmHg where tolerated.
  • Diabetes and pre-diabetes. Glycaemic control is individualised; an HbA1c target is set in collaboration with your GP and (where relevant) your endocrinologist.
  • High cholesterol — specifically the LDL-cholesterol fraction. The secondary-prevention target at CURA is LDL below 1.4 mmol/L (in line with current European Society of Cardiology guidance for very-high-risk patients), achieved with a high-intensity statin and, if needed, ezetimibe.
  • Smoking. Stopping smoking is the single highest-impact thing most patients can change. Pharmacological supports (nicotine replacement, varenicline) plus structured counselling roughly triple quit rates compared with willpower alone.
  • Obstructive sleep apnoea independently increases recurrent-stroke risk. A sleep study is part of the workup for anyone who snores loudly, has witnessed apnoeas, or wakes unrefreshed.
  • Excess weight and physical inactivity compound each of the above. Sustained weight reduction and structured cardiovascular activity (broadly aiming for around 150 minutes of moderate activity per week, where safe) reduce stroke risk independently of the other targets.
  • Excess alcohol increases stroke risk; the pragmatic target is consistent with national low-risk drinking guidance.

Non-modifiable — the context, not your fault

  • Age. Atherosclerotic disease becomes commoner with age, with most clinically significant ICAD presenting after the age of 50.
  • Family history of premature stroke or cardiovascular disease.
  • Ancestry. Intracranial atherosclerosis is substantially more common in people of Asian, Hispanic, and African ancestry than in those of European ancestry — for reasons that are not fully understood and that include both genetic and environmental contributors.
  • Male sex at younger ages, although the difference narrows after midlife.
IV.

How it is diagnosed

Intracranial atherosclerosis is most often picked up after a TIA or minor stroke, on the imaging that follows it. Sometimes it is found incidentally on a scan ordered for another reason. Either way, the first job is to confirm the imaging finding and put it in context with the rest of the workup.

The vascular imaging that shows it

  • is the usual first-line vascular imaging test after a TIA or stroke. It is widely available and gives a clear picture of any narrowing in the major intracranial arteries.
  • images the same arteries with magnetic resonance instead of X-rays. It is the alternative when CTA isn’t appropriate — for example, in patients with significant kidney impairment or iodinated-contrast allergy.
  • gives the most detailed view of the cerebral arteries. It is reserved for situations where CTA or MRA leaves a real question, or as the diagnostic half of a stenting procedure when one is being considered.

The severity of any stenosis is reported in your imaging report as mild, moderate, or severe (often quoted as a percentage — for example “~70% narrowing”). At consultation we walk you through what the report says and what it means for your treatment plan; we don’t expect you to interpret radiology language on your own.

Read the full workup detail (cardiac source, blood tests, sleep study) ↓

Why imaging on its own isn’t the whole workup

Finding intracranial atherosclerosis on a scan after a TIA or stroke does not, on its own, prove the atherosclerosis caused the event. Up to a quarter of TIAs and minor strokes are caused by a clot from the heart, not the cerebral arteries themselves. The antiplatelet plan and the long-term prevention plan are different depending on the answer, so the workup is broader than the vascular imaging alone.

Cardiac source workup

  • 12-lead ECG on the day, looking for atrial fibrillation or evidence of past cardiac injury.
  • Echocardiogram (usually transthoracic in the first instance, with a transoesophageal study reserved for specific questions) to look at the heart structure and any source of clot.
  • Holter monitor or longer-duration ambulatory cardiac monitoring (often 7–14 days, sometimes longer) to catch paroxysmal atrial fibrillation that a single ECG would miss.

Bloods and metabolic profile

  • Lipid panel (total cholesterol, LDL, HDL, triglycerides) to set the statin target.
  • HbA1c to screen for diabetes or pre-diabetes.
  • Renal function (eGFR, urea, electrolytes), with implications for both contrast use and antihypertensive choice.
  • Inflammatory markers and an autoimmune screen where the clinical picture raises a question of vasculitis or a non-atherosclerotic cause for the imaging appearance.

Sleep study where indicated

Obstructive sleep apnoea is common, frequently undiagnosed, and an independent driver of recurrent-stroke risk. A home-based sleep study (or a laboratory polysomnogram where indicated) is part of the routine workup for patients who snore loudly, have been told they stop breathing in their sleep, or wake unrefreshed.

What you leave the consultation with

By the end of the first appointment you have a clear picture of which tests are still needed, who orders each one (we coordinate referrals), and a working plan that can be tightened as the results come back.

V.

Aggressive medical management — the backbone of stroke prevention

For almost every patient with intracranial atherosclerosis, the single most important treatment is not a procedure. It is a coordinated, intensive, and sustained medical-management plan. This is what the SAMMPRIS trial proved in 2011, and it remains the starting point in 2026.

The plan has five pillars: antiplatelet therapy, lipid control, blood-pressure control, glucose control, and lifestyle change. Each pillar is set at the first visit and titrated at follow-up.

Read the full medical-management detail ↓

Antiplatelet therapy

For patients with a recent symptomatic event (TIA or minor stroke attributable to intracranial atherosclerosis), we use — aspirin plus clopidogrel — for the first 90 days. Long-term aspirin then continues indefinitely as a single antiplatelet. The 90-day DAPT window is supported by CHANCE (Wang et al., NEJM 2013) and POINT (Johnston et al., NEJM 2018), which established that the early recurrent-stroke benefit is concentrated in the first three months and that longer DAPT increases bleeding without further reducing stroke. SAMMPRIS used the same regimen as the medical-therapy backbone in its trial of stenting.

For patients in whom the cardio-embolic workup turns up atrial fibrillation, the antiplatelet plan is replaced or supplemented by an oral anticoagulant — a different conversation handled at consultation in coordination with cardiology.

Lipid control

A high-intensity statin is started on the day of diagnosis (in practice, usually atorvastatin 40–80 mg or rosuvastatin 20–40 mg, with the dose individualised to your liver function, kidney function and tolerance). The target we titrate to is an LDL cholesterol below 1.4 mmol/L — in line with current European Society of Cardiology guidance for very-high-risk vascular patients. Where a statin alone doesn’t reach target, ezetimibe is added; for the small group still above target, PCSK9-inhibitor therapy is considered.

Blood-pressure control

The secondary-prevention blood-pressure target is below 130/80 mmHg, where it is tolerated. Lower is generally better for stroke prevention up to the point where it is causing dizziness, falls, or kidney impairment. We review BP at each follow-up; titration of antihypertensive doses may be done by us, by your GP, or jointly — the plan is set so that everyone working with you is on the same page.

Glucose control

HbA1c is reviewed at every visit. The target is individualised — tighter in younger patients, more relaxed in older patients with hypoglycaemia risk — and management is coordinated with your GP and endocrinologist where one is involved.

Lifestyle

  • Smoking cessation. Nicotine replacement, varenicline, and structured behavioural support roughly triple quit rates compared with willpower alone.
  • Sustained weight reduction where BMI is elevated. Even a 5–10% reduction has measurable effects on blood pressure, glucose, and lipids.
  • Regular cardiovascular activity, where safe — broadly around 150 minutes per week of moderate activity. The right starting plan after a stroke depends on residual deficit and is discussed at consultation.
  • Mediterranean-style diet — the dietary pattern with the strongest evidence base for cardiovascular risk reduction.
  • Treatment of obstructive sleep apnoea where it is found.
  • Moderation of alcohol intake, in line with national low-risk drinking guidance.
VI.

When stenting is considered

Stenting is not a first move. It is a focused option for the smaller group of patients whose strokes recur despite optimised medical therapy.

What SAMMPRIS established — and why it shapes care

In 2011, a landmark randomised trial called SAMMPRIS (Chimowitz et al., NEJM 2011) compared elective intracranial stenting plus aggressive medical therapy against aggressive medical therapy alone in patients with recently symptomatic high-grade (70–99%) intracranial stenosis. The trial was stopped early because the stenting arm was doing worse: the 30-day stroke-or-death rate after stenting was substantially higher than expected, and the medical-therapy arm did better than expected because the trial used a particularly aggressive medical regimen.

The conclusion that has shaped care ever since is that aggressive medical management is the right starting position for almost every patient, and that elective stenting should not be offered as a first move.

What WEAVE/WOVEN added — the more selective modern role

The story didn’t end there. Two later registry studies of the same stent device under tighter selection — WEAVE (Alexander et al., Stroke 2019) and the one-year follow-up WOVEN (Alexander et al., JNIS 2021) — reported much lower peri-procedural complication rates than SAMMPRIS, in patients selected for failed medical therapy with recurrent symptoms. The modern interpretation is that intracranial stenting is a useful tool when:

  • you have had recurrent stroke or TIA despite optimised medical therapy, and
  • imaging shows a high-grade stenosis (typically at least 70%) that is anatomically suitable, and
  • the procedure is performed by an experienced operator at an experienced centre.

How the decision is made at CURA

The decision is never made on imaging alone. We look at:

  • How your symptoms are behaving on optimised medical therapy — specifically, whether you are having further TIAs or strokes despite the plan being tight.
  • The grade and location of the stenosis on CTA or MRA, and what catheter angiography adds where it is needed.
  • The anatomy of the artery and its branches — some locations are technically more favourable than others.
  • Your overall vascular health, your bleeding risk, and your preferences after a candid discussion of risks and likely benefit.
VII.

Intracranial stenting at affiliated Sydney hospitals

Intracranial stenting is performed by Dr Hugh Stephen Winters, Dr Timothy Ang, and Dr Emma Harrison at affiliated Sydney hospitals — the consult, decision-making, and follow-up sit with the practice; the procedure itself is inpatient.

Read stenting detail (procedure, recovery, outcomes, risks) ↓

What the procedure involves

Intracranial stenting is a minimally invasive endovascular procedure performed under general anaesthesia at an affiliated Sydney hospital. A catheter is passed through a small puncture in the groin (or, less commonly, the wrist) and navigated up through the vascular system to the brain’s arteries. Detailed angiography is performed to confirm the stenosis and assess the surrounding anatomy. If the appearance and the clinical picture justify proceeding, a stent — a small expandable metal mesh tube — is deployed across the narrowing to hold the artery open.

Hospital stay is typically 1–2 nights with close neurological monitoring after the procedure. Most patients are discharged the day after the procedure if their post-procedure imaging and examination are reassuring.

Antiplatelet cover around the procedure

Patients are placed on dual antiplatelet therapy (aspirin plus clopidogrel) commencing before the procedure and continuing for several months afterwards, with a long-term aspirin tail. The specific timing and duration are individualised; the rationale is to minimise the risk of clot forming on the new stent while it endothelialises.

Recovery and the first few weeks

Most patients return to gentle daily activity within days of discharge and to full activity within several weeks, with the specific recovery plan tailored to the procedure, your overall health, and any neurological deficit you started with. A post-procedure follow-up at the practice within the first two weeks confirms the wound is healing, the antiplatelet plan is being tolerated, and there have been no new neurological symptoms.

Outcomes

In appropriately selected patients — those who meet the modern WEAVE-style criteria of failed medical therapy with recurrent symptoms and high-grade stenosis — intracranial stenting can substantially reduce the risk of further stroke attributable to the treated artery. Long-term durability depends on careful adherence to the antiplatelet and risk-factor plan; a stent is not a substitute for the medical management, it is added to it.

Risks — named honestly

Intracranial stenting is a serious procedure on a serious artery. The principal procedural risks are:

  • Stroke at the time of the procedure, from dislodged plaque, dissection of the artery, or clot forming on the new stent. The peri-procedural stroke risk has been substantially lower in modern series (WEAVE/WOVEN) than in the SAMMPRIS era, but it is not zero, and is the main risk we weigh against the recurrent-stroke risk you would carry without the procedure.
  • Intracranial bleeding, including hyperperfusion-related haemorrhage where flow is restored to a previously underperfused region.
  • Stent thrombosis or restenosis over time, which is why the antiplatelet plan and the surveillance imaging schedule both matter long after the procedure.
  • Access-site complications at the groin or wrist puncture — bruising is common, more significant complications are rare.
  • The general risks of general anaesthesia.

These risks are discussed in detail at consultation in the specific context of your imaging, your medical-therapy response, and your bleeding risk. A written summary is provided so you have time with the information before deciding.

VIII.

Long-term monitoring and surveillance

Intracranial atherosclerosis is a chronic vascular condition. The surveillance plan is designed to do three things: keep the medical therapy tight, catch any change in the imaging early, and step the intensity down as the picture stabilises.

Clinic follow-up cadence

  • First year: review every 6–12 weeks while we tighten lipids, blood pressure, HbA1c, antiplatelet response, smoking status and weight. The cadence is matched to how much is changing — patients on a stable plan are seen less often than patients still being titrated.
  • Second year: typically every 3–6 months, depending on stability.
  • Beyond two years: typically annually if the picture is stable, with the option to step down to GP-led review with as-needed neurology input where everything is on target and steady.

Surveillance vascular imaging

  • For most patients: CTA or MRA at 6 and 12 months after diagnosis or after stenting, then annually if stable. The imaging modality is matched to the clinical question and to your kidney function and contrast tolerance.
  • For patients with a stent: imaging at the same cadence, with the specific protocol chosen to look at both the treated artery and the rest of the cerebral vasculature.
  • Repeat imaging is brought forward if you have recurrent symptoms, a new TIA-like episode, or any change that raises a fresh question. A planned imaging schedule is a scaffold, not a ceiling.

Bloods at follow-up

Lipid panel and HbA1c are reviewed at the follow-up cadence above, with renal function checked alongside any antihypertensive change. Liver function is reviewed when statins are started or up-titrated.

When to come back urgently

Outside the planned follow-up schedule, please contact our reception — or, where appropriate, your GP or an emergency department — if you have:

  • Any new FAST-positive symptoms (call 000 first)
  • A new TIA-like episode, even if it has fully resolved
  • New side effects from your medication you suspect are causing you to skip doses
  • A planned procedure or operation where the antiplatelet or anticoagulant plan needs reviewing in advance
IX.

At your consultation

A first ICAD consultation usually takes 45–60 minutes. The consultation itself is the first appointment; vascular imaging, cardiac source workup, blood tests and any sleep study are organised as separate bookings — either ahead of the consult (so we can review the results with you) or shortly after, depending on what’s needed.

Bring

  • Your GP referral letter
  • All vascular imaging on USB or via secure link — CTAs, MRAs, carotid ultrasound — plus the radiology reports
  • Any cardiac investigations: ECG, echocardiogram report, recent Holter or ambulatory monitor results
  • A current medication list including the exact doses of any antiplatelet, anticoagulant, statin, antihypertensive or diabetes medication
  • Recent blood pressure readings if you have them, and recent HbA1c and cholesterol results if available
  • Medicare card and any private health insurance details
  • A family member or friend — a second pair of ears is invaluable when there’s a lot of new information

What the consult typically covers

Specifics depend on your presentation and what’s already been done. Where appropriate, we’ll:

  • Review your history, examine you, and review your imaging
  • Confirm or refine the diagnosis; identify whether the imaging finding likely caused the recent event or is incidental
  • Coordinate any further tests still needed — cardiac source workup, longer cardiac monitoring, sleep study, repeat imaging — as separate bookings; we coordinate the referrals and consolidate the results
  • Set or refine the medical-management plan: antiplatelet, statin, BP target, HbA1c target, smoking cessation, weight and sleep apnoea
  • Set the follow-up cadence and the trigger points that would move us toward considering stenting
  • Send a written letter to your GP with a clear shared-care plan

Fees and wait time

Consultation fees and out-of-pocket gaps depend on consultation type and your Medicare and private-health eligibility. Vascular imaging, cardiac source workup, lipid panels, HbA1c and sleep studies are Medicare-rebatable when ordered for a clinical indication. Wait times depend on triage urgency — recent symptomatic ICAD is triaged urgently. See our current fees → or call reception / use the online booking page.

Q&A

Frequently asked questions

Who treats intracranial atherosclerosis at CURA?

At CURA Medical Specialists in Drummoyne, Sydney, intracranial atherosclerosis is managed by three stroke and interventional neurologists: Dr Hugh Stephen Winters (FRACP, CCINR), Dr Timothy Ang (FRACP, CCINR), and Dr Emma Harrison (FRACP, CCINR). All three are dual-trained in stroke medicine and interventional neuroradiology, so the same team holds the diagnosis, the medical-management plan, the decision about whether stenting is needed, and the procedure itself when it is. Intracranial stenting is performed by these neurologists personally at affiliated Sydney hospitals; patients are not referred outside the practice for the procedure.

Do I need stenting?

For most people with intracranial atherosclerosis, the answer is no. The 2011 SAMMPRIS trial showed that elective stenting was not better than aggressive medical management — and in that trial it was worse. Modern care therefore puts optimised medical therapy first: dual antiplatelet for 90 days then aspirin long-term, a high-intensity statin to a low LDL target (typically below 1.4 mmol/L), tight blood-pressure control (target below 130/80), glucose and weight management, and stopping smoking. Stenting is reserved for selected patients whose strokes recur despite that optimisation — supported by the more recent WEAVE/WOVEN registry data showing modern stenting is safer and more selective than the SAMMPRIS-era procedure.

What is wrong with stenting? Why is it not offered as a first move?

Nothing is wrong with stenting in the right patient — but in 2011 a randomised trial called SAMMPRIS showed that adding elective stenting on top of medical therapy was worse than medical therapy alone in patients with high-grade symptomatic intracranial stenosis. The peri-procedural stroke and death rate in the stenting arm was higher than expected, and the medical-therapy arm did better than expected because the trial used a particularly aggressive medical regimen. The conclusions: aggressive medical management is the right starting position for almost everyone, and stenting belongs further down the pathway, in selected patients whose strokes recur despite that optimisation. Subsequent registry data (WEAVE 2019, WOVEN 2021) suggests modern stenting under tighter selection is safer than the SAMMPRIS-era procedure.

I have just had a TIA or minor stroke and intracranial narrowing was found on my scan. How quickly will I be seen?

Recent TIA or minor stroke with imaging that shows intracranial atherosclerosis is triaged urgently at CURA. Routine new-referral wait times depend on current clinic load — for live availability, please call our reception or use the online booking page. If you currently have any FAST signs (face droop, arm weakness, slurred speech), do not wait for an appointment: call 000 or go to your nearest emergency department, where hyperacute stroke care including thrombolysis or clot retrieval is decided in the first hours.

Will I need to take antiplatelets and statins for the rest of my life?

Long-term antiplatelet (almost always aspirin) and a statin are the backbone of stroke prevention for intracranial atherosclerosis, and the working assumption is that both are continued indefinitely unless something changes. Dual antiplatelet (aspirin plus clopidogrel) is used for the first 90 days after a symptomatic event because that is the highest-risk window for early recurrent stroke; after 90 days the second agent is stopped because longer dual therapy increases bleeding risk without further reducing stroke. Statin therapy is titrated to a low LDL target — typically below 1.4 mmol/L — and is reviewed at each follow-up. Do not stop either medication on your own; if a side effect or planned procedure is in the way, ask your GP or call our reception so a coordinated decision can be made.

Where is the stenting procedure performed?

Intracranial stenting is performed at affiliated Sydney hospitals where Dr Hugh Stephen Winters, Dr Timothy Ang and Dr Emma Harrison hold neurointerventional appointments. The consultation, the decision to proceed, and all post-procedure follow-up sit with CURA in Drummoyne. You are not referred to a different specialist in a different city for the procedure — your CURA neurologist does the angiography, the pressure measurements, and (where appropriate) the stenting personally, then remains your specialist through long-term surveillance.

Do I need a GP referral?

Yes — a current GP referral is required to claim the Medicare rebate on a specialist consultation. A GP referral is valid for 12 months; a referral from another specialist for 3 months. If you have just had a TIA or stroke and are still in hospital or recently discharged, the discharging team can also refer directly.

What does the consultation cost?

Fees depend on consultation type and your Medicare and private-health eligibility. Current fees, expected Medicare rebate, and out-of-pocket gap are listed on our fees page (curaspecialists.com.au/fees). Vascular imaging (CTA, MRA), cardiac source workup (ECG, echocardiogram, Holter monitor), lipid panels, HbA1c and sleep studies are Medicare-rebatable when ordered for a clinical indication. The stenting procedure itself is performed in hospital and is covered through Medicare and private health insurance in the usual way for inpatient procedures; the inpatient cost question is best handled with the hospital admissions team and your health fund.

Directory

For referring GPs

Triage at CURA

  • Same-day / ED first: any active stroke symptoms, crescendo TIA pattern (multiple events in 48 hours), new neurological deficit lasting more than a few minutes, sudden severe headache.
  • Urgent CURA slot: recent TIA or minor stroke (within the last 4–6 weeks) with imaging showing intracranial atherosclerotic stenosis; recurrent TIAs in a patient already on antiplatelet therapy.
  • Routine new referral: incidental imaging finding of intracranial atherosclerosis in an asymptomatic patient; established ICAD on stable medical therapy seeking specialist review or second opinion.

Worked example: 50-year-old with a recent transient right-arm weakness, CTA showing a 70% left middle cerebral artery stenosis, currently on aspirin = urgent slot; please flag on the referral.

What to include in the referral

  • Symptoms, dates, and current neurological status
  • Vascular imaging reports (CTA, MRA, carotid ultrasound) and ideally the imaging on disc or via secure link
  • Cardiac workup if done: ECG, echocardiogram, Holter or other ambulatory monitoring
  • Recent lipid profile, HbA1c, renal function and full blood count
  • Current medications, with particular attention to antiplatelet or anticoagulant therapy already started post-event
  • Risk-factor profile: blood pressure trend, smoking status, BMI, family history of premature stroke

How to refer

Referrals are accepted via secure messaging, fax, and email. For current HealthLink EDI, fax, and email details, please contact our reception or visit the Refer a Patient page. To flag urgency on a specific referral, call our reception directly.

What we send back

A written consultation letter to the referring GP with the confirmed or provisional diagnosis, imaging interpretation, medication started or adjusted (antiplatelet, statin, BP and glucose targets), the follow-up cadence we’re proposing, the trigger points that would move us toward stenting, and a clear plan for shared care with your practice on titration.

XII.

Patient resources

  • Stroke Foundation Australia — strokefoundation.org.au. The leading Australian patient charity, with plain-English stroke-prevention guides, recovery resources, and StrokeLine (1800 787 653).
  • Brain Foundation Australia — brainfoundation.org.au
  • Healthdirect Australia — healthdirect.gov.au (Healthdirect helpline 1800 022 222)
  • Quitline (smoking cessation) — 13 7848 (13 QUIT)
  • NSW Ambulance — 000 for any stroke emergency

References cited in this guide

  • Chimowitz MI, Lynn MJ, Derdeyn CP, et al. Stenting versus aggressive medical therapy for intracranial arterial stenosis. New England Journal of Medicine. 2011;365(11):993–1003.
  • Alexander MJ, Zauner A, Chaloupka JC, et al. WEAVE Trial: Final Results in 152 On-Label Patients. Stroke. 2019;50(4):889–894.
  • Alexander MJ, Zauner A, Gupta R, et al. The WOVEN trial: Wingspan One-year Vascular Events and Neurologic Outcomes. Journal of NeuroInterventional Surgery. 2021;13(4):307–310.
  • Kleindorfer DO, Towfighi A, Chaturvedi S, et al. 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke Association. Stroke. 2021;52(7):e364–e467.
  • Wang Y, Wang Y, Zhao X, et al. Clopidogrel with aspirin in acute minor stroke or transient ischemic attack (CHANCE). New England Journal of Medicine. 2013;369(1):11–19.
  • Johnston SC, Easton JD, Farrant M, et al. Clopidogrel and aspirin in acute ischemic stroke and high-risk TIA (POINT). New England Journal of Medicine. 2018;379(3):215–225.

CURA Medical Specialists — intracranial atherosclerosis and stenting care in Drummoyne, Sydney’s Inner West. Book a consultation · For referring GPs