A transient ischaemic attack (TIA) is a brief neurological functional impairment caused by local ischaemia in the brain or retina. The associated clinical symptoms usually last for less than one hour, typically 2-15 minutes and imaging studies do not reveal any signs of cerebral infarction that would explain the symptoms.
Cerebral imaging is the only way to differentiate between a TIA and a cerebral infarction with transient symptoms. If the ischaemic symptoms last for several hours the patient has more probably suffered a cerebral infarction than a TIA.
Its aetiology is the same as that of a cerebral infarction, i.e. atherosclerosis of large vessels, microangiopathy, or cardiogenic embolism. Other, more rare aetiologies should be considered especially in young (below 50 years) patients.
After the first TIA, up to almost 10% of the patients will suffer cerebral infarction within a week and 10-20% within 3 months. One in four patients with cerebral infarction has a history of preceding TIA.
Emergency investigations snould be carried out in independent patients with a TIA or a cerebral infarction that has occurred within the last 2 weeks and, as required, their follow-up should take place at a hospital ward. The aim is to detect significant stenosis of the carotid vessels and atrial fibrillation as soon as possible and to start secondary prevention by pharmacotherapy at the right time.
Studies have shown that investigations performed and secondary prevention initiated on an emergency basis decrease the risk of cerebral infarction within 3 months by 80%.
A TIA ABCD2 risk scoring system is used primarily to support the planning of the timing of different investigations in patients with TIA, and consequently routine hospital treatment may be avoided.
With carotid artery involvement, the symptoms generally consist of hemiparesis or hemiparaesthesia predominantly in the upper extremity with associated weakness in the lower branch of the facial nerve.
Ischaemia of the dominant hemisphere causes dysphasia, which may sometimes be the only sign of a TIA.
Loss of vision in one eye (amaurosis fugax) is indicative of ipsilateral retinal ischaemia. It is usually associated with an embolus originating from the carotid artery or from further away in the circulation.
A typical symptom of posterior circulation, i.e. vertebrobasilar system involvement is vertigo, which is accompanied with brainstem or cerebellar symptoms (diplopia, dysphagia, dysarthria as well as numbness and paresis, involving one or both sides of the body). Vertigo alone is not suggestive of disturbed cerebral circulation.
In differential diagnostics, binocular blurring of vision is most often associated with precollapse, and scintillating visual disturbance is typically a migraine aura.
Isolated unilateral visual field defect may be the only symptom.
The type of TIA and its circulatory area may give clues about its aetiology, which is necessary to identify in order to implement successful prophylactic treatment.
Clinical examination and signs indicating TIA
Investigations concerning the aetiology of TIA are usually carried out in an emergency setting within a hospital with adequate expertise.
Risk factors for disturbances of cerebral circulation are carefully found out.
A TIA usually warrants imaging of the head (CT or MRI) http://www.dynamed.com/condition/transient-ischemic-attack-tia#TOPIC_JYB_DYP_L3B. CT scan of the head is in most hospitals the primary investigation due to its availability, price and quickness. Diffusion weighted MRI imaging of the brain is more reliable in discerning an early ischaemic signal change which is associated with a higher risk of recurrence. An ischaemic finding warrants hospitalization. MRI scan is used during pregnancy.
If in the ultrasonography a significant stenosis is detected or the visibility is suboptimal, a CT or MRI scan of the carotid vessels should be perfomed during the same hospital stay.
Atrial fibrillation is the most important cardiac aetiology, but also valvular disease, artificial valves, fresh myocardial infarction, dilated cardiomyopathy, endocarditis and aortic atheromatosis may be involved.
The ABCD2 risk scoring system does not take into account carotid stenosis or atrial fibrillation, which both are associated with a high risk of cerebral infarction, and consequently, when the system is used, the aforementioned emergency investigations should be performed before the patient is discharged.
If the hospital has an efficiently organized TIA outpatient department it is possible that maybe only one in four TIA patients is hospitalized, and preventive treatment is initiated in low-risk patients on an emergency basis.
The following routine laboratory tests http://www.dynamed.com/condition/transient-ischemic-attack-tia#BLOOD_TESTS should be taken in all patients: basic blood count with platelets, CRP, blood glucose, potassium, sodium, creatinine, prothrombin time or INR [warfarin therapy], APTT, and, using an early morning sample: fasting blood glucose, HbA1c and lipid profile.
A self-caring patient who warrants active treatment must be sent immediately to an emergency department of an appropriate hospital or to a neurological unit, if no more than 2 weeks have elapsed since the occurrence of TIA symptoms.
If the patient presents later than this, the investigations may be carried out at an outpatient clinic. Should the patient suffer a new TIA, immediate investigations are required.
If the aetiology of the TIA is known and the treatment has already been instigated, a neurological unit should be consulted before referring the patient.
Antithrombotic medication
Aspirin should be administered even if a TIA is only suspected, unless there are contraindications, or a need for anticoagulation due to cardiac aetiology.
Should a new vascular event occur during antithrombotic therapy, the aetiology and the management of risk factors should be assessed anew. A change in antithrombotic therapy is not a sufficient measure as such.
Surgical management should be carried out within 2 weeks from the occurrence of a TIA provided that there are no contraindications and that the total risk of complications (stroke and death) associated with carotid surgery is lower than 6%.
A carotid artery stenosis is sought by ultrasonography, and if the finding suggests stenosis, it is confirmed by CT angiography.
In symptomless women, the benefit of surgery is smaller than in men.
Asymptomatic carotid stenosis denotes in any case an increased risk of stroke and is indicative for the introduction of effective primary and secondary prevention which is required independent of possible surgical management.
A patient's eligibility for surgery should always be judged by a neurologist, who will also consult a vascular surgeon.
Lavallée PC, Meseguer E, Abboud H et al. A transient ischaemic attack clinic with round-the-clock access (SOS-TIA): feasibility and effects. Lancet Neurol 2007;6(11):953-60. [PubMed]
Amarenco P, Lavallée PC, Labreuche J et al. One-Year Risk of Stroke after Transient Ischemic Attack or Minor Stroke. N Engl J Med 2016;374(16):1533-42. [PubMed]
Lemmens R, Smet S, Thijs VN. Clinical scores for predicting recurrence after transient ischemic attack or stroke: how good are they? Stroke 2013;44(4):1198-203. [PubMed]