TIA Flashcards
TIA
Transient ischaemic attack is a cerebrovascular event that is caused by abnormal perfusion of cerebral tissue.
TIA overview
TIA is defined as transient neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without evidence of acute infarction. It is a medical emergency, within the first week following a TIA, the risk of stroke is up to 10%. The estimated incidence of TIA within the UK is 50 per 100,000 people per year.
Traditionally, transient neurological dysfunction with resolution within 24 hours was diagnostic of TIA. However, up to a third of patients whose symptoms have resolved within 24 hours have evidence of infarction on imaging. Consequently, the definition is now ‘tissue-based’ rather than ‘time-based’ with the incoporation of the phrase ‘without evidence of acute infarction’. Thus, the end-point is biological tissue damage, not an arbitrary time cut-off.
TIA is caused by temporary blockage to blood flow, which leads to ischaemia.
Ischaemia refers to the absence of blood flow to an organ, which deprives it of oxygen. Cerebral ischaemia may be due to in situ thrombosis, emboli, or rarely, dissection.
Thrombosis: local blockage of a vessel due to atherosclerosis. Precipitated by cardiovascular risk factors (e.g. hypertension, smoking) or small vessel disease (e.g. vasculitis, sickle cell).
Emboli: propagation of a blood clot that leads to acute obstruction and ischaemia. Typically due to atrial fibrillation or carotid artery disease.
Dissection: a rare cause of cerebral ischaemia from tearing of the intimal layer of an artery (typically carotid). This leads to an intramural haematoma that compromises cerebral blood flow. May be spontaneous or secondary to trauma.
Risk factors for TIA are due to conditions that affect the integrity of vessels or increase the risk of embolisation.
TIA is a cardiovascular disease, and as such, it shares many common risk factors with conditions such as ischaemic heart disease and peripheral vascular disease.
Smoking Diabetes mellitus Hypertension Hypercholesterolaemia Obesity Atrial fibrillation Carotid artery disease Age Thrombophilic disorders (e.g. antiphospholipid syndrome) Sickle cell disease
Clinical features TIA
A TIA presents with sudden, focal neurological deficit that reflects the area of the brain devoid of blood flow.
A variety of neurological deficits can present in TIA, but the majority of symptoms will resolve within 1-2 hours.
TIA
Neurological deficit
Unilateral weakness or sensory loss
Dysphasia
Ataxia, vertigo, or incoordination
Amaurosis fugax: see below
Homonymous hemianopia: visual field loss on the same side of both eyes
Cranial nerve defects: particularly if associated with contralateral sensory/motor deficits
Amaurosis fugax
This is a classical syndrome of short-lived monocular blindness, which is often described as a black curtain coming across the vision. It is a term usually reserved for transient visual loss of ischaemic origin.
The principle cause of amaurosis fugax is transient obstruction of the ophthalmic artery, which is a branch of the internal carotid artery. However, other ischaemic causes to consider include giant cell arteritis (i.e. temporal arteritis) and central retinal artery occlusion. An important differential of transient visual loss, particularly in young patients, is migraine.
Any patient with ongoing symptoms requires urgent referral to a stroke unit.
TIA is a clinical diagnosis based on the history as the majority of patients will have complete resolution of symptoms. Any patient with ongoing symptoms needs to be treated as an acute stroke and urgently referred to a stroke unit.
Key aspects to making the diagnosis of TIA include:
Onset & duration of symptoms: collateral history may be needed
Associated symptoms (suggest alternative diagnosis): headache, vomiting, syncope, seizures
Neurological deficit: see clinical features
Cardiovascular risk factors: hypertension, diabetes, smoking, high cholesterol, family history
Co-morbidities: heart disease, atrial fibrillation, carotid disease, previous stroke/TIA
Anticoagulation history
Clinical examination: cardiovascular exam including BP, neurological examination, fundoscopy
The Face Arm Speech Time Test (FAST test)
A rapid diagnostic screen to assess for features of TIA/stroke used in the community. Anyone with a positive screen should be assessed urgently at a stroke unit. The test is positive if any of the following are met:
New facial weakness
New arm weakness
New speech difficulty
Numerous conditions can present similarly to TIA, which are collectively referred to as ‘stroke mimics’.
Toxic/metabolic: hypoglycaemia, drug and alcohol consumption
Neurological: seizure, migraine, Bell’s palsy
Space occupying lesion: tumour, haematoma
Infection: meningitis/encephalitis, systemic infection with ‘decompensation’ of old stroke
Syncope: extremely uncommon presentation of TIA, many causes
All patients with a suspected TIA should be referred to a specialist TIA clinic and be seen within 24 hours.
At the TIA clinic, patients should have a comprehensive medical assessment including blood tests, electrocardiogram (ECG) and imaging. If the episode occurred > 1 week ago, the assessment should be within 7 days.
The ABCD2 is a prognostic score that was traditionally used to identify people at high risk of stroke after a TIA score. It was originally used to triage the urgency of TIA referrals and treatment with aspirin. NICE no longer recommend its use.
… is the key investigation in a patient with suspected TIA.
MRI is the key investigation in a patient with suspected TIA.
Bloods - TIA
Haematology: full blood count (FBC), HbA1c +/- haemoglobin electrophoresis
Routine biochemistry: Urea & electrolytes (U&Es), bone profile, liver function tests (LFTs), lipid profile
Coagulation: routine clotting
Special (as indicated): ‘young stroke screen’ (e.g. thrombophilia screen, Fabry’s)
Cardiac investigations - TIA
ECG: assessment for arrhythmias, especially atrial fibrillation
Echo: not routinely offered unless suspicion of heart disease or confirmed stroke
Imaging - TIA
MRI head with diffusion-weighted imaging (DWI): preferred to CT unless alternative diagnosis suspected that CT could detect. Enables detection of small infarcts.
Carotid dopplers: all patients who are candidates for carotid endarterectomy.
