Dr Dipankar Dutta explains why timely referrals to TIA clinics are important, how an accurate diagnosis can be made, and how national guidance can help

dutta dipankar

Independent content logo

mcq thumb

Read this article to learn more about:

  • how to diagnose a TIA
  • conditions that may mimic a TIA
  • the role of primary care in managing a person with a suspected TIA.

Key points

GP commissioning messages

After reading this article, ‘Test and reflect’ on your updated knowledge with our multiple-choice questions. Earn 0.5 CPD credits

P eople with transient ischaemic attack (TIA) have a very high early risk of stroke and are also at risk of myocardial infarction (MI) and vascular death. Transient ischaemic attacks can be difficult to diagnose as there is no specific diagnostic test, and there are pitfalls in their assessment, risk scoring, early management, and referral to specialist services.

While missing a TIA can have serious consequences for the patient, misdiagnosing a non-cerebrovascular condition as a TIA leads to unnecessary anxiety, inappropriate management, needless restrictions on driving, and adverse insurance implications. In addition, the real diagnosis can be missed and inappropriate referrals to TIA clinics cause delays for those patients who are likely to benefit most from clinic management.

This article focuses on:

  • the diagnosis of TIAs and the role of secondary care TIA clinics
  • common TIA 'mimics'
  • the ABCD2 scoring system1
  • immediate management of suspected TIA and long-term care
  • associated national guidance and recommendations.


The traditional definition of TIA is 'An acute loss of focal cerebral or monocular function with symptoms lasting less than 24 hours and which after adequate investigation was presumed to be due to embolic or thrombotic vascular disease'.2

A more recent tissue-based definition proposed by the American Heart Association is 'A transient episode of neurological dysfunction caused by a focal brain, spinal cord, or retinal ischaemia, without acute infarction'.3 This second definition relies on the use of early magnetic resonance (MRI) imaging,3 which is not always available in UK hospitals.

Risk of stroke after a transient ischaemic attack

The prevalence of prior TIA in patients who present with stroke has been reported to range from 7% to 40%3 and the risk of a stroke is highest in the first 24 hours after the TIA.4 The stroke risk after a TIA has been reported in studies to be 3.1% at 2 days, 5.2% at 7 days, and 9.2% at 90 days.5,6 In addition, patients who have a TIA are at risk of subsequent MI (1.7–2.7% per year7) and death (27% at 5 years in the Oxford Vascular Study 8).

Transient ischaemic attack is, therefore, a medical emergency and should be treated with the same kind of urgency as unstable angina.

Incidence of transient ischaemic attack

Between 2002 and 2004, the incidence of TIA in Oxfordshire was found to be about 0.66 per 1000 per year.3 So, taking these data into account, a practice with 5000 registered patients may expect to see about four people a year with TIA and many more individuals who have TIA mimics. Audit data from Gloucestershire show that about 50–60% of patients referred to a TIA clinic have seen their GP following symptom onset.9

Transient ischaemic attack clinics

Background and rationale

Evidence from two studies, EXPRESS10 and SOS-TIA,11 and the use of the ABCD2 scoring system1 have revolutionised the management of TIAs:

  • in the EXPRESS study, stroke risk after TIA was reduced by 80% by the process of early outpatient specialist assessment (median 1 day after TIA onset), early investigations (usually CT, Doppler and sometimes MRI), and immediate prescription of all secondary prevention (antiplatelets, statins, antihypertensives and anticoagulants as required)10
  • in the SOS-TIA study,11 TIA patients were admitted to a specialised hospital clinic with 53% of patients admitted within 24 hours of symptom onset, investigated, treated, and the majority discharged within 24 hours. The 90-day stroke rate of the treated patients was reduced from an expected rate of 5.96% to 1.24%.11

Need for rapid access and treatment

A TIA clinic is a one-stop specialist clinic where patients should, ideally, be seen on the same day as symptom onset if the ABCD2 score1 is ≥4 (see text under heading 'The ABCD2 score', and Table 1, below). As TIA and stroke are part of the same disease continuum, the TIA clinic is the ideal setting for management of minor/non-disabling strokes (strokes that do not need admission) in the most efficient manner.

Table 1: The ABCD2 scoring system
Risk factorCriteriaScore
A ge
  • ≥60 years
1 point
B lood pressure
  • systolic ≥140 mmHg and/or
  • diastolic ≥90 mmHg
1 point
C linical features
  • unilateral weakness
2 points
  • speech disturbance without weakness
1 point
  • any other symptom
0 points
D uration:
  • ≥60 minutes
2 points
  • 10–59 minutes
1 point
  • <10 minutes
0 point
D iabetes 1 point
Maximum 7 points
  • An ABCD2 score ≥4 is now considered to be high risk (patients expected to be seen and treated within 24 hours); a score of <4 is considered to be low risk (patients may be seen and treated within 7 days of onset).
  • In the original ABCD2 validation study, a score of:
    • <4 (low risk) gave a stroke risk of 1.0% at 2 days, 1.2% at 7 days, and 3.1% at 90 days
    • 4 or 5 (moderate risk) gave a stroke risk of 4.1% at 2 days, 5.9% at 7 days, and 9.8% at 90 days
    • 6 or 7 (high risk) gave a stroke risk of 8.1% at 2 days, 11.7% at 7 days, and 17.8% at 90 days

Rapid access TIA clinics have been widely established in the UK to manage TIA and minor ischaemic stroke, with a dramatic reduction in time to assessment.12 Data from a UK hospital TIA clinic confirm that, in keeping with clinical trial results, TIA clinic management leads to a substantial reduction in risk of stroke, both at 90 days and beyond, for treated patients. 13 The ABCD2 score1 is used to risk-stratify patients with TIA, and UK national guidelines require assessment and treatment in a TIA clinic within 24 hours of onset of symptoms in patients with an ABCD2 score of ≥4 and by 7 days or sooner in patients with a score of <4.14

After confirmation of the diagnosis and necessary investigations, all secondary prevention therapy is prescribed and started immediately. Typically, this includes antiplatelets, antihypertensives, and statins.14,15 Transient ischaemic attack clinic management also includes immediate anticoagulation for atrial fibrillation (AF) after brain imaging has been used to exclude haemorrhage or other pathology.14,15 The novel oral anticoagulants are often preferred in TIA clinics because of their immediate onset of action.

Transient ischaemic attack clinics have close links with vascular surgery and allow immediate referral for carotid endarterectomy if significant carotid stenosis is detected. Carotid endarterectomy has been shown to be most effective when carried out within 2 weeks after a TIA or a non-disabling stroke. 16 National guidelines recommend that endarterectomy is performed within 7 days of symptom onset.14

The TIA clinic should not be looked upon as a 'funny turn' clinic, a convenient way of getting a quick neurology opinion (most stroke physicians in the UK are not neurologists), nor an easy way of getting a CT head scan; careful assessment by the referring practitioner is important and a concise guide to diagnosis is given below.

Identification and diagnosis

Transient ischaemic attack is a clinical diagnosis almost always based on the history and its interpretation by the examining clinician. The symptoms can be very fleeting and the patient's recollection may be poor; terms such as 'heaviness', 'numbness', or 'dizziness' mean different things to different people.

About 50–60% of patients who are referred by non-specialists as having TIA are found to have non-cerebrovascular disorders or mimics.13,17 A whole host of conditions may mimic a TIA: migraines, seizures, syncope, sepsis, functional disorders, neuropathies, vestibular dysfunction, and metabolic problems are some of the common conditions reported in various studies.13,18,19

An accurate diagnosis of TIA involves taking a focused and critical history and working out the true significance of often very brief symptoms that patients find it difficult to explain. The clinical examination does not usually help because the symptoms have often resolved by the time the patient is seen. In fact, most TIAs last a few minutes and rarely more than 1 hour; the finding of clinical signs and ongoing symptoms a few hours after onset suggests that the patient may have had a stroke, rather than a TIA.

How to diagnose a transient ischaemic attack

A TIA is usually of abrupt onset and symptoms reach their full extent and severity very shortly after onset.18 The symptoms should be focal symptoms (i.e. those expected from ischaemia in a distinct arterial territory in the brain): for example, ischaemia in the (usually left) middle cerebral artery territory may cause dysphasia and right-sided weakness. Transient ischaemic attack involving the retina typically causes transient visual loss in one eye.

Certain common, non-focal symptoms are not accepted as being due to a TIA if they occur in isolation; these include: 19

  • loss of consciousness
  • falls
  • confusion
  • generalised weakness
  • dizziness
  • incontinence
  • amnesia
  • sensory symptoms confined to part of one limb or face.

Nature and duration of symptoms

The nature of the symptoms in a TIA is usually negative (i.e. loss of function such as loss of muscle power, loss of speech, loss of sensation, or loss of vision).18

Positive symptoms (i.e. symptoms suggesting central nervous system neuronal hyperactivity, such as limb jerking, tingling/pins and needles, scintillations, and fortification spectra) usually suggest an alternative diagnosis, for example seizures or migraine.18 It is important to note, however, that both seizures and migraine may begin with positive symptoms and then proceed to some negative symptoms as well; for example, a focal seizure may begin with a few jerking movements (positive) followed by weakness (negative).18

Transient difficulty with speech can be due to dysarthria (i.e. slurring of speech) and, in isolation, is not always due to cerebrovascular disease. Dysphasia, on the other hand, is a more specific symptom of cerebrovascular disease and is a disorder of language, i.e. altered word content, jumbled and ungrammatical speech, word substitution, and the use of 'nonsense' words.18 This is often associated with difficulty reading. Seizures can sometimes cause 'speech arrest' where there is brief loss of speech, which can often be recurrent and stereotyped. 18

Attacks that happen again and again, particularly over a number of years, are more likely to be due to seizures, migraine, or syncope, particularly if they are stereotypical.18 Some TIAs, however, may recur over hours, days or a week or two and are referred to as 'crescendo TIAs'. Symptoms of recurrent TIAs, although sometimes stereotyped, may be different if different parts of the brain are affected. 18

Table 2 (see below) lists some of the distinguishing characteristics of TIAs and mimics.

Table 2: Transient ischaemic attack—guide to diagnosis
Features that make diagnosis of a TIA more likelyFeatures that make diagnosis of a 'mimic' more likely
Higher a priori probability—older patient, presence of hypertension, diabetes, and other vascular risk factors Lower a priori probability—younger patient, no vascular risk factors, previous diagnosis of migraine or epilepsy
Focal (stroke-like) symptoms that can be explained by ischaemia in a specific vascular territory Non-focal symptoms in isolation (e.g. confusion, amnesia, falls, incontinence, light-headedness, loss of consciousness, sensory symptoms confined to part of face or limb)
Negative symptoms, e.g. loss of power, speech, and sensation Positive symptoms, e.g. tingling/numbness/pins and needles, jerking of limbs, flashing lights
Abrupt onset with all symptoms coming on at roughly the same time Symptoms may build up over a few minutes and may 'march' from one part to another (e.g. tingling starting in the face and spreading down to the arm and hand). One symptom may improve before another starts (e.g. visual aura ceases and dysphasia begins)
Recurrent TIAs may be different in character Recurrent, stereotyped symptoms occurring several times a day or over years
Vertigo, dysarthria, diplopia, or dysphagia in combination with each other or with other focal symptoms suggest a posterior circulation TIA Vertigo, dysarthria, diplopia, dysphagia in isolation can have other causes
Very brief attacks lasting seconds are unusual except for amaurosis fugax. Many TIAs last for around 10 minutes and most less than 1 hour The duration can be variable; typically <5 min for seizures and 30 min for migraine aura
  • TIA=transient ischaemic attack

Conditions commonly mistaken for a transient ischaemic attack

Migraine aura

Migraine aura is the most common mimic and typically presents with visual symptoms, including spreading scotoma, flashing lights, geometric patterns, or other visual symptoms often described as like 'looking through a heat haze, waterfall, or kaleidoscope'. Other modalities affected include speech disturbances, sensory symptoms (usually positive and typically with a march of symptoms, i.e. starting with one symptom and developing others, with resolution of the original symptom). The headache usually follows soon after onset but migraine auras can occur without headache or there may be a delayed headache. Negative (motor) symptoms can also occur.18,20


When assessing for seizures, eye-witness history is useful and it may be necessary to ask about jerking, involuntary movements as these can be very brief and subtle. Postictal confusion, incontinence, and tongue-biting may be useful clues. Focal weakness (Todd's paresis) can occur after seizures and mimic stroke or TIA. Speech problems in seizures include complete speech arrest and postictal dysphasia in dominant hemisphere seizures. There may be a previous history of epilepsy and the attacks may be recurrent and stereotyped.18


Patients with syncope are referred to TIA clinics surprisingly often. Syncope is usually a non-focal symptom and leads to transient loss of consciousness with loss of postural tone and rapid recovery. Patients sometimes have pre-syncopal symptoms (e.g. feeling faint and light-headed, with dimness of vision). Vasovagal syncope can sometimes occur after a meal, in a hot room, and may be associated with sweating and pallor. Postural hypotension and cardiac arrhythmias are other common causes.18

Transient global amnesia

In this condition, patients present with a temporary inability to form new memories. Patients appear confused, unsure and there is often repetitive questioning. Personal identity and procedural memory are intact. Attacks typically last several hours and can recur in a small proportion of people. Most patients are aged over 50 years. This condition does not have the same connotation as a TIA and does not lead to increased stroke risk.18,21

Peripheral vestibular disturbance

Isolated dizziness is much more likely to be due to peripheral vestibular disturbance than a TIA. Dizziness has a broader differential diagnosis, including presyncope, and has to be distinguished from true vertigo. The diagnosis of a posterior circulation TIA or stroke is more likely where more than one symptom occurs (e.g. vertigo with diplopia, dysarthria, and ataxia) but the diagnosis may be difficult in older patients with multiple risk factors and requires careful analysis and often brain imaging (i.e. MRI with diffusion-weighted sequences). 18,19

The ABCD2 score

The ABCD2 score (see Table 1, above) is a clinical prediction tool used to identify those patients with suspected TIA who are at high risk of early ischaemic stroke.1 In the original ABCD2 validation cohort, the score was applied to patients presenting in the previous 7 days with transient symptoms suggestive of a TIA, 1 and in most validation studies, the underlying diagnosis has been assumed to be TIA.22 Transient ischaemic attack clinic studies, however, show that a very high proportion of patients referred with suspected TIA are found to have mimics. 13,17 The validity of the ABCD2 score when applied by non-specialist doctors therefore seems to be limited.23,24 This is most likely due to:

  • inappropriate application of the score
  • misinterpretation of clinical features23 (e.g. tingling and numbness is given the same weight as weakness)
  • applying the score to obvious TIA mimics (e.g. seizure or syncope)
  • applying the score to completed strokes
  • applying the score to delayed presentations (i.e. beyond 7 days).

A low ABCD2 score (if accurately applied) may help in screening out mimics, although with limited sensitivity and specificity.22 The ABCD 2 score, however, has been criticised for not taking into account other important prognostic features, including carotid disease, recurrent TIAs, AF and evidence of tissue damage on MRI. Also, the score does not prompt urgent assessment in patients on anticoagulants with suspected TIA, where urgent CT scanning to exclude a brain haemorrhage is advocated.14 It is possible that the ABCD2 score will assume less importance in the future as stroke services strive to see more patients who have a high probability of a genuine TIA on the day of referral, regardless of ABCD 2 score.



Brain imaging in a TIA that affects the brain (but not the eye) is usually considered helpful, although often shows no abnormality. Magnetic resonance imaging with diffusion-weighted sequences is the recommended scanning modality, but is not yet universally available in all UK hospitals, where CT scanning is often used instead.3,14

Imaging can reveal new and old brain strokes, exclude alternative non-cerebrovascular diagnoses, give clues as to the underlying vascular mechanism (e.g. small vessel disease or cardiac embolism) and provide prognostic information.3

Carotid duplex ultrasound is the most commonly used imaging method to detect extra-cranial carotid artery stenosis. This test is undertaken in patients with symptoms of carotid territory TIAs to select those suitable for carotid endarterectomy.3,14 Imaging of the vertebro-basilar system is more difficult and performed more selectively.

The cardiac evaluation of TIAs is usually done using echocardiography and Holter monitoring in selected cases. The evidence base underpinning these tests is not very strong and clinical judgement has to be used in test selection. 3 If there is no cardiac history and if the cardiovascular examination and ECG are normal, the yield of transthoracic echocardiogram is lower than 3%.3 There is very little evidence to guide the timing of echocardiography after a TIA.

Blood tests

Routine blood tests, including a full blood count, glucose, lipid profile, and biochemistry, are useful in suggesting an underlying cause (e.g. previously unsuspected diabetes, hyperlipidaemia, or polycythaemia vera) and in guiding management. 3

The role of primary care

See Figure 1 (below) for a pragmatic approach to managing a person with a suspected TIA. Primary care physicians should have a good knowledge of local TIA referral pathways. Various TIA referral systems are in place (e.g. telephone, faxed forms, online). 'Choose and book' is clearly not an option for TIA. Because the diagnosis of TIA can be uncertain, many stroke and TIA services have formal or informal systems to give advice. Neurologists or geriatricians may also advise, as appropriate.

Figure 1: TIA management algorithm
Transient ischaemic attack (TIA) management algorithm
  • TIA=transient ischaemic attack; OD=once daily; BP=blood pressure

NICE Clinical Knowledge Summary

Suspected transient ischaemic attack

The NICE Clinical Knowledge Summary series on Stroke and TIA is a highly recommended source of essential information for primary care practitioners dealing with suspected TIA. 25 The 'Scenario: Suspected TIA' includes the recommendation to assess the ABCD2 score to identify patients at high risk (≥4), but to be aware that people with a suspected TIA who have AF, more than one TIA in 1 week, or who are on anticoagulants are at high risk too. See the full Clinical Knowledge Summary and Box 1 (below) for further details on managing people assessed as being at high and low risk of stroke.

Box 1: Managing TIA with high or low risk of stroke25

How should I manage someone at high or low risk of stroke following a TIA?

  • Refer for specialist assessment with the expectation of assessment within 24 hours of onset of symptoms if at high risk of stroke or within 7 days if at low risk of stroke
  • Give a statin such as simvastatin 40 mg*
  • Give an antiplatelet drug unless they are taking an anticoagulant drug, when they should be assessed as high risk in TIA clinic
    • if they are not taking an anticoagulant or an antiplatelet drug, immediately give either aspirin 300 mg or clopidogrel 300 mg (off-label use )
      • do not delay treatment in people with uncontrolled blood pressure
      • consider prescribing a proton pump inhibitor if the person is at high risk of gatrointestinal adverse effects
      • for further information on antiplatelet therapy (including managing adverse effects), see the CKS topic on antiplatelet treatment
    • if they are taking low-dose aspirin regularly, continue the current dose of aspirin until reviewed by a specialist. In people already on an antiplatelet, there is no evidence supporting an in-crease in the dose, a change to an alternative antiplatelet, or combining two antiplatelets.
      • if non-compliance is suspected, give either aspirin 300 mg or clopidogrel 300 mg
  • Consider assessing and managing cardiovascular disease risk factors for patients with low risk TIA while awaiting specialist review. For further information see the CKS topic on CVD risk assessment and management
  • Advise them not to drive until they have been seen by a specialist (when definitive guidance will be given).
  • * NB NICE CG181 recommends atorvastatin.26
  • NB at the current time, clopidogrel does not have marketing authorisation for the management of TIA. The prescriber should follow relevant professional guidance, taking full responsibility for the decision. In-formed consent should be obtained and documented. See the General Medical Council's Good practice in prescribing and managing medicines and devices27 for further information.
  • TIA=transient ischaemic attack; CKS=clinical knowledge summary; CVD=cardiovascular disease
  • Adapted from NICE Clinical Knowledge Summaries on Stroke and TIA.

Long-term care

Primary care physicians have a pivotal role in the long-term care and support of people with confirmed TIA. The NICE Clinical Knowledge Summary on Stroke and TIA,25'Scenario: Confirmed TIA—long-term care and support' highlights the importance of:

  • an annual review in primary care for lifestyle measures (smoking cessation, cardio-protective diet, regular exercise, satisfactory body weight, and alcohol advice) and to check and optimise drug treatments for the secondary prevention of cardiovascular disease. These include treatments relating to:
    • AF and diabetes
    • hypertension
    • long-term lipid modification
    • long-term antiplatelets— clopidogrel 75 mg is first line; aspirin plus modified-release dypiridamole 200 mg twice daily, or aspirin 75 mg alone, can be used if clopidogrel is contraindicated or not tolerated. NB at the current time, clopidogrel does not have marketing authorisation for the management of TIA. The prescriber should follow relevant professional guidance, taking full responsibility for the decision. Informed consent should be obtained and documented. See the General Medical Council's Good practice in prescribing and managing medicines and devices26 for further information.)
  • annual blood pressure and lipid profile checks; 140/90 mmHg is acceptable as a target but 130/80 mmHg is preferable. For statins, it is recommended that cholesterol is checked 1–3 months after starting treatment and that the medication dose is increased if cholesterol is >4 mmol/L or low-density lipoprotein cholesterol is >2 mmol/L
  • annual pre-winter influenza immunisation.

See the full Clinical Knowledge Summary25 for further details.


A TIA is a medical emergency and a diagnostic challenge for both primary and secondary care physicians. It is imperative to identify TIAs promptly because of the very high early risk of ischaemic stroke and this requires urgent assessment and preventive treatment in specialist TIA clinics.

Most patients with TIA-like symptoms tend to present to their GPs. Guidelines do not deal with the difficulty in making the diagnosis of TIA; awareness of mimics and a careful analysis of the history are important to establish the diagnosis.

There is no definite diagnostic test but investigations are useful to guide management and exclude other pathology. A higher a priori probability of TIA among patients referred by primary care and accurate ABCD 2 scoring should aid optimum management of this condition. In addition, primary care physicians have a very important role in the ongoing management and secondary prevention of TIA.


Key points

  • A TIA is a medical emergency with a very high risk of early stroke and ongoing risk of myocardial infarction and death
  • Early assessment and management in TIA clinics has been shown to reduce the incidence of subsequent stroke
  • The diagnosis of TIA is difficult and a large proportion of patients referred to TIA clinics turn out to have other diagnoses
  • Although it would be tragic to miss a TIA, the misdiagnosis of non-cerebrovascular conditions as a TIA is not without consequences
  • A focused history along with awareness of common mimics will enable primary care physicians to refer patients more appropriately to TIA clinics
  • The ABCD2 score is sometimes used inaccurately and can lead to inappropriate triage and adverse consequences for patients
  • A large proportion of patients with TIA present to primary care and primary care physicians have a major role to play in initial assessment and referral
  • Primary care physicians have a crucial role in the ongoing management of patients with TIA.

Back to top

GP commissioning messages

It should be a priority for CCGs to commission effective services for TIA as prompt investigation and management can prevent serious stroke-related debility for patients and considerable health and social care costs for commissioners.

  • CCGs with local providers should define clear local diagnostic and referral pathways for suspected TIA and stroke:
    • these pathways should be built as specifications into contracts with local emergency providers including Out of Hours GP services, ambulance providers, and local acute trusts.
  • CCGs should aim to commission 7-day rapid assessment services for TIAs using the Best Practice Tariffs for Stroke and TIA to incentivise this.
  • The ABCD2 tool is of some use in prioritising high-risk TIAs but is not completely robust and the emphasis should be on rapid assessment for all TIAs within 24 hours.
  • CCGs should monitor practice achievement against the QOF stroke indicators to identify any potential deficits in secondary preventative activity and also achievement against the atrial fibrillation and hypertension indicators, which can act as markers for good preventative care
  • PbR tariff prices for:a
    • TIA (non admitted) £302, best practice additional tariff adjustment for care within 24 hours £101
    • TIA (admitted) with complications £1256, without complications £552.

CCG=clinical commissioning groups; TIA=transient ischaemic attack; QOF=quality outcomes framework; PbR=payment by results

Back to top

Now Test and reflect: view our multiple choice questions


  1. Johnston S, Rothwell P, Nguyen-Huynh M et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet 2007; 369 (9558): 283–292.
  2. Hankey G, Slattery J, Warlow C. The prognosis of hospital-referred transient ischaemic attacks.J Neurol Neurosurg Psychiatry 1991; 54: 793–802.
  3. Easton J, Saver J, Albers G et al. Definition and evaluation of transient ischemic attack. Stroke 2009; 40: 2276–2293.
  4. Chandratheva A, Mehta Z, Geraghty O et al. Population-based study of risk and predictors of stroke in the first few hours after a TIA.Neurology 2009; 72 (22): 1941–1947.
  5. Giles M, Rothwell P. Risk of stroke early after transient ischaemic attack: a systematic review and meta-analysis. Lancet Neurol 2007; 6 (12): 1063–1072.
  6. Wu C, McLaughlin K Lorenzetti D et al. Early risk of stroke after transient ischaemic attack: a systematic review and meta-analysis. Arch Intern Med 2007; 167 (22): 2417–2422.
  7. Touzé E, Varenne O, Chatellier G et al. Risk of myocardial infarction and vascular death after transient ischemic attack and ischemic stroke: a systematic review and meta-analysis. Stroke 2005; 36 (12): 2748–2755.
  8. Luengo-Fernandez R, Paul N, Gray A et al, on behalf of the Oxford Vascular Study. Population-based study of disability and institutionalization after transient ischemic attack and stroke: 10-year results of the Oxford Vascular Study. Stroke 2013; 44 (10): 2854–2861.
  9. Dutta D,Price M, Kumar A, Deering A, Hellier K. The effect of FAST awareness on patient response to TIA like symptoms. Cerebrovascular Diseases 2013; 35 (suppl 3): 737
  10. Rothwell P, Giles M, Chandratheva A et al. Effect of urgent treatment of transient ischaemic attack and minor stroke on early recurrent stroke (EXPRESS study): a prospective population-based sequential comparison. Lancet 2007; 370 (9596): 1432–1442.
  11. Lavallée P, Meseguer E, Abboud H et al. A transient ischaemic attack clinic with roundthe- clock access (SOS-TIA): feasibility and effects. Lancet Neurol 2007; 6 (11): 953–960.
  12. Royal College of Physicians, Clinical Effectiveness and Evaluation Unit, on behalf of the Intercollegiate Stroke Working Party.Sentinel stroke national audit programme (SSNAP) acute organisational audit report. 2014. London: Royal College of Physicians. Available at: www.rcplondon.ac.uk/projects/ ssnap-clinical-audit
  13. Dutta D, Bowen E, Foy C. Four year follow up of transient ischemic attacks, strokes, and mimics: a retrospective transient ischemic attack clinic cohort study. Stroke 2015;46:1227-1232.
  14. Intercollegiate Stroke Working Party. National clinical guideline for stroke. 4th edition. London: Royal College of Physicians, 2012. Available at: www.rcplondon.ac.uk/sites/default/files/national-clinical-guidelines-forstroke-fourth-edition.pdf
  15. Rothwell P, Algra A, Amarenco P. Medical treatment in acute and long-term secondary prevention after transient ischaemic attack and ischaemic stroke. Lancet 2011; 377 (9778): 1681–1692.
  16. Rothwell P, Eliasziw M, Gutnikov S et al. Endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery. Lancet 2004; 363 (9413): 915–924.
  17. Dennis M, Bamford J, Sandercock P, Warlow C. Incidence of transient ischemic attacks in Oxfordshire, England. Stroke 1989; 20 (3): 333–339.
  18. Nadarajan V, Perry R, Johnson J, Werring D. Transient ischaemic attacks: mimics and chameleons. Pract Neurol 2014; 14 (1): 23–31.
  19. Special report from the National Institute of Neurological Disorders and Stroke. Classification of cerebrovascular diseases III.Stroke 1990; 21 (4): 637–676.
  20. Angus-Leppan H. Migraine: mimics, borderlands and chameleons. Pract Neurol 2013; 13: 308–318.
  21. Owen D, Paranandi B, Sivakumar R, Seevaratnam M. Classical diseases revisited: transient global amnesia. PostgradMed J 2007;83: 236–239.
  22. Quinn T, Cameron A, Dawson J et al. ABCD2 scores and prediction of noncerebrovascular diagnoses in an outpatient population: a casecontrol study. Stroke 2009; 40 (3): 749–753.
  23. Wong J, Fotherby M, Eveson D. Comparison of ABCD2 scoring between first healthcarecontact and stroke-specialist physicians for transient ischaemic attack in a rapid-access clinic. Age Ageing. 2012; 41 (1): 115–118.
  24. Edwards D, Cohn S, Mavaddat N et al. Varying uses of the ABCD2 scoring system in primary and secondary care: a qualitative study. BMJ Open 2012; 2: 1–7.
  25. NICE website. Clinical Knowledge Summaries. Stroke and TIA. cks.nice.org.uk/stroke-andtia#!topicsummary (accessed 16 April 2015).
  26. NICE. Lipid modification: cardiovascular risk assessment and the modification of blood lipids for the primary and secondary prevention of cardiovascular disease. Clinical Guideline 181. NICE, 2014. Available at: www.nice.org.uk/ guidance/cg181 (accessed 13 May 2015).
  27. General Medical Council. Good practice in prescribing and managing medicines and devices. London: GMC, 2013. Available at: www.gmcuk. org/guidance/ethical_guidance/14316.asp (accessed 16 April 2015).