Transient ischaemic attack Flashcards
what is the definition of TIA?
an acute loss of cerebral or ocular function with symptoms lasting less than 24 hours caused by an inadequate cerebral or ocular blood supply as a result of low blood flow, ischaemia, or embolism associated with disease of the blood vessels, heart or or blood, without infarction
Assess Risk Using ABCD2 Score
A — Age: 60 years of age or more (1 point)
B — BP (at presentation) 140/90 mm Hg or greater (1 point)
C — Clinical features, Unilateral weakness, 2 points, Speech disturbance without weakness, 1 point.
D — Duration (60 minutes or longer, 2 points, 10–59 minutes, 1 point)
D — presence of diabetes: 1 point.
High risk: ABCD2 score of 4 or more, Atrial fibrillation, More than one TIA in one week, A TIA whilst on an anticoagulant
Low risk: None of the above, Present more than a week after their last symptoms have resolved.
what is the epidemiology of TIA?
190/100000 population
what is the aetiology of TIA?
In situ thrombosis of an intracranial artery or artery-to-artery embolism of thrombus as a result of stenosis or unstable atherosclerotic plaque (16%). Cardioembolic events (29%). Intracardiac thrombus may form in response to some secondary risk factor such as stasis from impaired ejection fraction or atrial fibrillation. The precipitating factor may be a thrombogenic nidus within the heart such as an infectious vegetation or artificial valve. Rarely, thrombus can pass from the venous system across a cardiac shunt to create paradoxical emboli. Small-vessel occlusion (16%). Microatheromas, fibrinoid necrosis, and lipohyalinosis of small penetrating vessels are seen. Hypertension and diabetes predispose to small ischaemic lesions. Because these may occur in the brainstem and internal capsule, a small lesion can result in significant symptoms. Occlusion due to hypercoagulability, dissection, vasculitis, vasospasm, or sickle cell occlusive disease (3%). These are less common aetiologies. Uncertain mechanism (36%).
what are the risk factors for TIA?
Atrial fibrillation, valvular disease, carotid stenosis, congestive heart failure, hypertension, DM, smoking, alcoholism, advanced age
what is the pathophysiology of TIA?
Under normal circumstances, cerebral blood flow (CBF) is tightly autoregulated to maintain a blood flow of >50 mL/100 g/minute across a wide range of cerebral perfusion pressures by alteration in cerebrovascular resistance. If the CBF falls to between 20 and 50 mL/100 g/minute, the brain can compensate by increasing oxygen extraction, but below this threshold, neuronal quiescence occurs with neurological deficits. Below 15 mL/100 g/minute of CBF, neuronal death occurs. Thus, if there is complete loss of cerebral blood flow, then neuronal death will occur rapidly. With partial blood flow, neuronal function is impaired, but cell death will be delayed by minutes to hours. Restoration of flow, presumably via autolysis of the occluding thrombus, can arrest the progression to infarction.
what are the key presentations of TIA?
Suspect stroke in anyone presenting with an acute onset, ongoing focal neurological deficit that cannot be explained by hypoglycaemia or other stroke mimics.
Usually unilateral:
Facial weakness (MCA)
Unilateral weakness of the upper and/or lower limb (MCA/ACA)
Unilateral sensory loss of upper and/or lower limb (MCA/ACA)
Speech problems (MCA, dominant hemisphere)
Visual defects (PCA)
Disorders of perception (PCA)
Disorders of balance (posterior circulation)
Coordination disorders (posterior circulation)
what are the signs of TIA?
Sudden onset
Focal neurological deficit
what are the symptoms of TIA?
Facial weakness (MCA)
Unilateral weakness of the upper and/or lower limb (MCA/ACA)
Unilateral sensory loss of upper and/or lower limb (MCA/ACA)
Speech problems (MCA, dominant hemisphere)
Visual defects (PCA)
Disorders of perception (PCA)
Disorders of balance (posterior circulation)
Coordination disorders (posterior circulation)
what are the first line and gold standard investigations for TIA?
Blood glucose - may show hypoglycaemia
FBC - normal
Prothrombin time - normal unless the patient is already on anticoagulation, or has liver disease or antiphospholipid antibodies
Fasting lipid profile - may sow hyperlipidaemia
Serum electrolytes - normal
ECG - may be normal; may show atrial fibrillation or other arrhythmias or myocardial ischaemia
what are the differential diagnoses for TIA?
Stroke
Hypoglycaemia
Labyrinthine disorders (labyrinthitis, vestibular neuronitis, BPPV, Meniere’s disease)
Migraine (hemiplegic migraine, unilateral hemiparesis).
Mass lesions (subdural haematoma, cerebral abscess, tumours)
Postictal weakness (also known as Todd’s paralysis) , focal seizures, and generalised seizures
Functional hemiparesis
how are TIAs managed?
Low Risk:
Refer for specialist assessment within 7 days of the onset of symptoms, Start statin (e.g. simvastatin 40 mg), Antiplatelet drug (unless they are taking an anticoagulant) Clopidogrel 300mg (off-label use) or aspirin 300mg, Continue standard dose if already taking antiplatelet for secondary prevention), Treat BP (if raised), No driving until seen by a specialist (when definitive guidance will be given)
High risk TIA:
As above, But assessment within 24 hours
how are TIAs monitored?
Assess risk of stroke in next 7 days
Good quality evidence on which to base risk assessment of further stroke
High risk >4% over 7/7 (NICE) require urgent referral (seen within 24 hours)
what are the complications of TIAs?
stroke
MI
what is the prognosis for TIAs?
By definition, a patient with a TIA has no residual symptoms from the primary event. The most significant risk to the patient is a second ischaemic event causing permanent disability. For patients admitted for TIA, 8% will have a stroke during their hospitalisation and >10% of TIA patients seen in the accident and emergency department will have a stroke within 3 months.
