Transient Ischaemic Attacks
- Defining a TIA and how to diagnose clinically
- Role of TIA clinic
- Familiarity of all differentials and avoiding TIA over diagnosis
- Appropriate investigations
- Long term management
- Also see <a href="transientmonocularblindness.php" title="transient monocular blindness">Transient monocular blindness</a>
Transient ischaemic attacks are harbingers for developing a possibly disabling or lethal stroke. The risk is greatest in the first 24-48 hours for those with certain clinical features as seen below. Their occurrence should be considered as a medical emergency and a warning sign that patients need rapid and expert assessment, diagnosis confirmed or refuted, risk factors identified and treatments initiated that can significantly reduce the likelihood of future stroke. The expert opinion is firstly to confirm the diagnosis. If the symptoms are not coming from a TIA then the stroke risks obviously do not apply. In the last 5-10 years much work has been done to both identify those at risk of stroke and setting up effective clinical pathways to see, assess and manage patients quickly.
- Clinical: Neurological deficit of presumed neurovascular origin lasting less than 24 hours. However many episodes with less than 24 hrs of clinical evidence of deficit had MRI findings of tissue infarction.
- Imaging based (MRI): An episode of Ischaemia affecting eye, brain or spinal cord without infarction. Difficult if patient cannot have MRI.
The definition of TIA is identical to stroke except that either symptoms which may be brain or affecting <a href="transientmonocularblindness.php" title="transient monocular blindness">Monocular vision </a> last less than 24 hours or that imaging shows no evidence of brain infarction. All of the symptomatic episode must be explicable by the expected neurology caused by the transient occlusion of a cerebral vessel. If you cannot say precisely which artery was occluded and this must account for the entire symptom complex then you need to reflect and reconsider the diagnosis. Without some diagnostic rigour it is easy to overdiagnose TIA which can have serious implications for patients. All of those who see patients with TIA need to be well versed in the differentials and particularly in all the different clinical manifestations of migrainous symptomatology.
The clinical symptoms associated with TIA are pretty much identical to stroke except for the transient nature. However transient neurology over minutes or hours has a very different differential diagnosis to that of more persisting neurology and stroke. The table below shows a list of very common TIA mimics. The diagnosis of TIA is beset by the fact that there is no blood or imaging tests for it - in fact it is the lack of imaging changes that aids one in diagnosing it so there is always a degree of subjectivity in the more grey cases. The TIA clinic is one of the places where history which is 90% of the diagnosis in neurology becomes almost 99% of the diagnosis for diagnosing TIA. Great care and attention must be taken to extract exactly what happened, in what setting and get as much history from witnesses. Diagnosis must be based on the history plus a priori risk factors.
The examination (neurology will be resolved) will be looking for persisting risks e.g. hypertension, AF will help and this will be assessed together with the presumed a priori risk of TIA in this patient. An identical presentation in an 80 year old hypertensive diagnosed as TIA may be diagnosed as non TIA or even unknown in an 18 year old. It is often better to say cause unknown than to assign a wrong diagnostic label. TIA should never be a diagnosis simply because there is no other explanation.
Establishing the diagnosis
|Symptoms suggesting not TIA|
Role of GP and Emergency Department: If there is any residual neurology then treat as stroke and 999 patient to the Emergency Department. If seen by GP or ED and all neurology has definitely resolved then start Aspirin 300 mg od, advise patient not to drive and do immediate referral via fax or phone to local TIA clinic
|TIA differential Diagnosis and comments|
|Stroke||Brain scan may show new Infarct or Haemorrhage despite resolution of symptoms|
|Migraine with aura (3%)||Headache and positive symptoms useful. Often younger, female. Symptoms cross vascular territories including the midline. Progression is over minutes. Headache can be missing. Some symptoms and progression not explicable by single vessel obstruction.|
|Acephalgic Migraine with aura||More difficult to diagnose when there is no headache|
|Dementia (4%)||Possibly a step wise progress in deteriorating neurology in an patient with known Dementia|
|Space occupying lesion (9%)||Metastatic or Primary tumour may be seen on CT or many need contrast.|
|Focal (partial) Seizure (21%)||Positive symptoms spread quickly over seconds. Sensory or motor or both. Speech can be affected with transient inability to speak 'speech arrest' which can be misdiagnosed as dysphasia. Seizure may suggest underlying structural brain lesions (tumour, abscess) and may need MRI/EEG if CT normal.|
|Transient Global Amnesia||Classical history very easy to differentiate from TIA|
|Multiple Sclerosis||Symptoms usually more than 24 hours. Young. Known MS. Optic neuritis|
|Mononeuropathy/Nerve palsy (6%)||Pressure palsies can cause transient weakness. Be aware - radial, ulnar, common peroneal|
|Subdural Haematoma||Are they on warfarin. CT head diagnostic|
|Anxiety/Normal experience||Mild tingling and many transient neurological symptoms may be ascribed as within the normal experience|
|Subarachnoid haemorrhage||Headache should be expected. Focal TIA neurology should infer significant bleed/vasospasm|
|Syncope (9%)||Often referred but syncope and/or loss of consciousness not typically due to TIA|
|Sepsis (13%)e.g UTI in older person||Can cause slurred speech, confusion, ataxia and may be labelled primary neurological|
|Delirium (9%)||Usually of the hypoactive type. Multiple causes possible.|
|Vestibular disease (7%)||Isolated vertigo - BPPV, Labyrinthitis, Vestibular migraine|
|Toxic/Metabolic upset (11% )||Hypoglycaemia, Hyponatraemia, Hypocalcaemia (tingling), Hyperglycaemia. All Can cause slurred speech, confusion, ataxia and may be labelled primary neurological|
|Temporal arteritis||Must be considered in all with transient ocular symptoms - headache ? Raised ESR ?|
Much of the time the patients seen in the TIA clinic do not have TIAs. Many have had symptoms greater than 24 hours and made recovery and really have the diagnostic label of stroke. Others have syncope etc. Much depends on whether you screen referrals, the information given to the referrer on the form. We make our form as simple as possible and include an ABCD2 score but if the history on the form is clearly not TIA we decline the referral. If we have any doubt we see the patient.
Risk Assessment - ABCD2 scoring [Johnston SC et al. 2007]
A substantial risk of stroke exists in the early period after TIA. The magnitude of risk is greater and the time to event shorter than previously recognised. A recent systematic review reported an overall 7 day stroke risk of 5.2% after TIA. The most commonly used (and best validated) tool is the ABCD2 score12 (table 1). The ABCD2 algorithm(1) predicts a patient's very early risk of stroke following a TIA. The score is calculated according to 5 important clinical features:
|B||Blood pressure||>= 140/90 mmHg||+1|
|C||Clinical features of the TIA||unilateral weakness||+2|
|speech disturbance without weakness||+1|
|D1||Duration of symptoms||>= 60 min||+2|
|D2||Diabetes||diagnosed with diabetes?||+1|
The corresponding 2 day risks for a subsequent stroke are:
Risk of stoke at 2 days</th>
ABCD2 estimates risk of recurrence at two days from 1% for patients with a low risk of up to 8.1% for those patients with a high risk. ABCD2 scoring is recommended in UK national guidelines and many centres offer same day assessment of patients at highest risk of stroke. ABCD2 may also be useful in diagnosis. Single centre registry data (3646 patients) showed that few referrals with an ABCD2 score of 0 were subsequently found to have a cerebrovascular diagnosis. Traditionally those with an ABCD2 score of 4 or more were considered high risk and current metrics insist should be seen=, assessed and imaged within 24 hours of initial presentation. The remainder should have the same within 7 days. The new guidance from <a href="http://guideline.ssnap.org/2016StrokeGuideline/index.html">Royal College Physicians</A> suggests that all should be seen within 24 hours with no differentiation. It may be appropriate to perform some form of telephone triage to help separate TIA from all the other non TIA referrals.