They have to be asymptomatic now for it to be considered a TIA, otherwise if they still have symptoms it is a stroke or something else. TIA is a difficult diagnosis. By definition you are 100% reliant on the history and patients will vary in how well they can articulate that history. There are a lot of transient neurological episodes that are not transient ischaemic episodes.
Transient global amnesia is one example, which presents with isolated amnesia, repetitive questioning, and no focal neurological deficits. Patients can continue to drive and all the usual activities, they just cannot remember what they did. That is a very recognisable clinical syndrome that has nothing to do with ischaemia.
Migrainous phenomena with visual changes are probably one of the more common things we see. Again, symptoms of TIA are classically “negative”, i.e. involving loss of function, whereas with migraine you often get some positive visual phenomena and parasthesia rather than just loss of sensation.
We used to say if it starts in the hand and migrates up the arm to the face over 15 minutes, that is the cortical spreading depression of migraine. Unfortunately, occasionally stroke can precipitate that cortical spreading depression, so we have to be a little careful about attributing spreading symptoms to migraine.
I think the question has hit the nail on the head. The timing is what matters, so it really depends on your local system and resources. If you are able to access CT brain, carotid imaging and ECG to look for atrial fibrillation, and start the medications rapidly then there’s no problem with managing the patient through your clinic. Otherwise send them to ED.
At our hospital, we have a rapid assessment pathway for people who present to ED.
Importantly, if the patient still has any symptoms when you see them, that is not a TIA, that is probably a stroke, and they should definitely go to ED.
If it is fully resolved and you are seeing them a day or two down the track, it is acceptable to get a quick CT and carotid imaging, ECG and start aspirin. You would probably give clopidogrel as well for the first three weeks, as most minor stroke and TIA patients now get dual antiplatelets for three weeks, then revert to a single antiplatelet.
You would start a high-dose statin, and address their blood pressure. Blood pressure should not be drastically reduced within 24 hours, but aiming for less than 140mmHg systolic over the next 1-2 weeks is beneficial.
Lifestyle advice is important. We recommend a “Mediterranean diet plus nuts” rich in vegetables and fruit, low in saturated fat and processed foods. Many people’s blood pressure is sensitive to salt intake, so they should be advised to reduce dietary salt, and to get active, for example a 30-minute brisk walk a day.
The answer is no. There are not enough stroke physicians in Australia to handle that, even if seeing TIAs was all we did. TIA management is very much bread-and-butter cardiovascular risk management and GPs do that very well.
I think the ones to refer are where there is a question about diagnosis. If people are having recurrent events and they are all the same, that is a red flag that this probably is not a TIA. If you imagine most TIAs are embolic, for an embolus to find its way to exactly the same part of the brain to cause exactly the same symptoms multiple times starts to stretch credibility. It can happen if you have got an intracranial stenosis but that is rare. So recurrent events, diagnostic dilemmas, that is where the neurologist might add value.
If it is pretty clear-cut that they have had transient hemiparesis, they have got traditional vascular risk factors, and you are going to manage those, that is perfectly okay to keep within the general practice sphere.
For TIAs, it is about getting the diagnosis right. Not everything transient and neurological is ischaemic. Think broadly about the migraines, the seizures, the functional disorders and things like cerebral amyloid angiopathy that can cause transient neurological events.
Management is time critical. Either get them to an emergency department or get carotid imaging, ECG, a CT brain and start aspirin, clopidogrel, statin and think about blood pressure management. Whether that happens with you or in the ED is up to your local system and resources.
I think with antithrombotics, we are still under-doing anticoagulation for AF. We are not looking hard enough to find it in the first place and when we find it, there are too many patients who do not receive anticoagulation, or who do not receive the appropriate dose of anticoagulation. By that act of omission we are causing strokes and disability, which can be worse than what we tend to worry about, which is causing bleeding.
The standard management with antiplatelets for minor stroke and TIA is aspirin and clopidogrel for three weeks. Just be aware some people have reasons to be on it for longer – cardiac stents, carotid stents and sometimes intracranial atherosclerosis.
Do not tolerate a blood pressure of 145mmHg systolic. If you think it is genuine and not just whitecoat hypertension, that does need to be addressed and will lower their risk of stroke if you can get it closer to 120mmHg.
Let us start with when you would use anticoagulation. Anticoagulation is predominantly for atrial fibrillation, and also mechanical heart valves and other things not stroke-related. Occasionally we use it for people with a hypokinetic left ventricular segment with a possible mural thrombus but that is often a more time-limited form of anticoagulation.
So, predominantly we are looking to see if the patient has atrial fibrillation. Paroxysmal AF is hard to find so you need to look for it, and then keep looking for it. Every time you see the patient, feel their pulse and make sure they have not slipped into atrial fibrillation.
If the patient does not have atrial fibrillation, or another unusual cardiac condition mentioned above, then we use antiplatelets, mainly aspirin and clopidogrel. In minor stroke and TIA, the evidence is for three weeks of aspirin and clopidogrel, and then to continue on single antiplatelet therapy. There are circumstances where we use dual antiplatelet therapy longer term, particularly for patients who have had a stent inserted in their carotid or intracranially. Those patients will often have six months or more of dual antiplatelets and moving to single antiplatelet therapy in that instance is a specialist decision.
Ticagrelor has some evidence in stroke but it is not PBS listed for that at the moment. Possibly when it becomes generic it will become a more affordable option but, for the moment, we use predominantly aspirin and clopidogrel.
Aspirin and clopidogrel have similar efficacy. Studies that compare them head-to-head had a 0.5% per annum absolute risk reduction for clopidogrel versus aspirin, a number needed to treat of 200 per year, so there is a slight benefit of clopidogrel.”
One downside of clopidogrel is that surgeons are much more concerned about it than about aspirin. Some will request that the patient be converted perioperatively to aspirin.
There is also, with clopidogrel, an issue of resistance. Clopidogrel is a prodrug, requiring an enzyme to convert it to the active form. Particularly in Han Chinese ethnicity, but also in the broader population, there is quite a prevalence of people who are clopidogrel-resistant. Many stroke specialists will switch to ticagrelor in future when it is available at an economical price because it is not a pro-drug.
Generally, in minor stroke or TIA, we give three weeks of aspirin plus clopidogrel and then drop one of them. If they were taking aspirin before the event we would usually drop the aspirin and continue clopidogrel but there is no particular evidence for that.
If the stroke is attributed to intracranial atherosclerosis, we would often keep dual antiplatelets going a little longer. The Stenting versus Aggressive Medical Therapy for Intracranial Arterial Stenosis trial (SAMMPRIS) used dual antiplatelets for three months, and was a very positive trial for medical management. GPs may see patients who have intracranial atherosclerosis put on dual antiplatelet therapy for three months.
In general, long-term aspirin plus clopidogrel just causes more bleeding and does not have a significant impact on ischemic stroke so we do not generally prescribe long-term dual antiplatelets for stroke prevention.
The reality is that all the evidence is for daily administration. People do complain about easy bruising and I understand that that is annoying but I think it is probably better to educate the patient in how important it is to prevent stroke and disability compared to the cosmetic and inconvenient nature of cutaneous bruising.
Antiplatelets, particularly aspirin, are irreversible. They have a seven day action on platelets, but new platelets are made every day, so taking an antiplatelet daily will have a greater effect.
We see quite a lot of under-dosing of anticoagulants as well. People fear causing bleeding but they do not quite understand that the act of omission of causing a stroke by not adequately dosing the anticoagulant is at least as bad.
We need to be careful that the reduced doses of 110 mg of dabigatran, 2.5 mg of apixaban and 15 mg of rivaroxaban are not used inappropriately. For apixaban, 2.5 mg BD is only the recommended dose if there are at least 2 of the following features: the patient is aged over 80, weighs 133. For everyone else the dose is 5mg bd and it is critically important not to underdose.
We see far too many people coming in with under-dosed anticoagulation and strokes.
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