Transient Ischemic Attack Flashcards
Definition of TIA
TIA is a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction. TIA has completely resolved within 24 hours of onset and cannot be explained by another condition such as hypoglycemia. Following the initial assessment, give a loading dose of aspirin to anyone with suspected TIA and refer the patient immediately for specialist assessment to be seen within 24H of onset of symptoms. Risk of recurrent stroke is high in the first 7 days following a TIA. Start secondary prevention therapy immediately once the diagnosis of TIA is confirmed.
Epidemiology of TIA
Stroke is a major health concern worldwide. Accounts for 11% of all deaths in England and Wales. Age-adjusted annual incidence rate for TIA in the UI has been estimated at 190 cases per 100,000 population
Risk factors for TIA
Risk factors: Strong: Atrial fibrillation Valvular disease Carotid stenosis Congestive heart failure Hypertension Diabetes mellitus Cigarette smoking Alcohol-use disorder Advanced age
Weak: Hyperlipidemia Patent foramen ovale Inactivity Obesity Hypercoagulability
Aetiology of TIA
Causes of TIA include:
- In situ thrombosis of an intracranial artery or artery-to-artery embolism of thrombus as a result of stenosis or unstable atherosclerotic plaque
- Cardioembolic events (intracardiac thrombus) due to stasis from impaired ejection fraction or AF. May be a precipitating factor within the heart such as infectious vegetation or artificial valve. Rarely, thrombus can pass from the venous system across a cardiac shunt to create paradoxical emboli.
- Small vessel occlusion: HTN and diabetes predispose to small ischaemic lesions.
- Occlusion due to hypercoagulability, dissection, vasculitis, vasospasm or sickle cell occlusive disease
- Uncertain mechanism
Pathophysiology of TIA
Severity depends on the complex interplay of between the degree of obstruction, area and function of tissue supplied by the vessel, the length of time the thrombus obstructed the vessel and the ability of collateral circulation to provide supplemental perfusion to the area at risk.
Cerebral blood flow is tightly autoregulated to maintain a blood flow of >50mL/100g/minute. If CBF falls to between 20 and 50 mL/100g/minute, the brain can compensate by increasing oxygen extraction, but below this threshold, neuronal quiescence occurs with neurological deficits. Below 15mL/100g/minute of CBF, neuronal death occurs. With partial blood flow, neuronal function is impaired, but cell death will be delayed by minutes to hours.
Early in the process, ischaemic neuronal injury, cytotoxic oedema causes influx of water to the intracellular space which is observable as hypersensitivity on MRI diffusion images.
Classification of TIA
- Total anterior circulation (carotid territory)
- Parietal anterior circulation
- Posterior circulation (vertebrobasilar territory)
- Lacunar
Hx and Exam of TIA
Hx and Exam:
Common:
Key diagnostic factors:
Sudden onset and brief duration of symptoms
Patient/witness report of focal neurological deficit
Other diagnostic factors: Unilateral weakness of paralysis Dysphasia Ataxia, vertigo or loss of balance Sudden transient loss of vision in one eye (amaurosis fugax) Homonymous hemianopia Dipolopia Risk factors
Investigations
- Blood glucose: to exclude hypoglycemia. Result: may be normal, may show hypoglycaemia
- Full blood count and platelet count: exclude other causes of sudden onset neurological symptoms e.g. infection. Result: usually normal
- Prothrombin time, INR, partial thromboplastin time: To exclude coagulopathy usually ordered in patients with TIA when the neurological deficits at the time of presentation, in case thrombolytic therapy is being considered. Result: normal unless the patient is anticoagulation or has liver disease or antiphospholipid antibodies
- Fasting lipid profile- as a baseline measure and to evaluate for treatable atherosclerotic risk factors. Result: may be normal; may show hyperlipidaemia
- Serum electrolytes: exclude electrolyte disturbance as a cause of sudden-onset neurological symptoms. Result: usually normal
- ECG:evaluate for atrial fibrillation and other arrhythmias and to rule out myocardial ischaemia. Result: may be normal, may show AF, other arrhythmias or myocardial ischaemia.
Consider: CT scan - may show haemorrhage
Mx of TIA
Initial: suspected transient ischemic attack
1st line: antiplatelet therapy
Primary options: aspirin; 300mg orally as a loading dose
Secondary options: clopidogrel: 300 mg orally as a loading dose
PLUS refer for special assessment
Acute: confirmed transient ischaemic attack
1st line: antiplatelet therapy
Primary options: Clopidogrel: 75 mg orally once daily
Secondary: Aspirin: 75mg orally once daily
PLUS high intensity statin
Primary option: atorvastatin 20-80mg orally once daily
Consider anticoagulation for AF. Low molecular weight heparin, direct thrombin inhibitor or factor Xa inhibitor (in people with non-valvular AF)