What is a transient ischaemic attack (TIA)?
Transient episode of neurological dysfunction caused by temporary focal cerebral, spinal or retinal ischaemia without acute infarction i.e. weak limb, aphasia or loss of vision lasting seconds or minutes with complete recovery. Mostly unilateral
TIA is due to a vascular cause, typically lasts 1 hour
*<24h time limit no longer used
What is a distinguishing sign of TIA?
Signs specific to artery territory and presents similar to stroke
Amaurosis fugax
=> sudden transient loss in vision in one eye
=> due to emboli passing through retinal artery
=> often 1st clinical sign of internal carotid artery stenosis
*Global events i.e. syncope or dizziness not characteristic of TIA
What signs are present if TIA occurs in the anterior circulation (carotid system)?
Amaurosis fugax
Dysphasia
Hemiparesis
Hemisensory loss
Hemianopic visual loss
What signs are present if TIA occurs in the posterior circulation (verterbrobasilar system)?
Diplopia
Vertigo & vomiting
Choking & dysarthria
Ataxia
Hemisensory loss ; Hemianopic visual loss ; Bilateral visual loss
Tetraparesis
Loss of consciousness (rare)
What are the causes of TIA?
Atherothromboembolism from CAROTID = main cause
=> listen for bruits
Cardioembolism => mural thrombus post MI => AF, valve disease, prosthetic valve => Hyperviscosity i.e. polycythaemia, sickle cell anaemia => Vasculitis (rare)
Non-embolic cause of TIA: => Cranial arteritis => SLE => Syhillis => Polyarteritis nodosa
How do you diagnose TIA?
Clinical diagnosis
*Consciousness usually preserved
What are the differential diagnosis for TIA?
Which conditions mimic TIA?
Two most common stroke mimics:
Others:
=> Focal epilepsy / seizure => Bell's palsy => Mass lesions => Syncope => Sepsis => Seizure / epilepsy => Trauma => Overdose => Intoxication => Hepatic encephalopathy
Rare mimics of TIA: => Malignant hypertension => Intracranial tumours => Peripheral neuropathy => Phaeocromocytoma => Somatisation => MS (paroxysmal dysarthria)
How do you investigate for TIA?
What tests are carried out?
=> Carotid doppler ± angiography
Atherosclerosis in carotid artery may be source of emboli => all patients to have urgent carotid doppler unless they are not a candidate for carotid endarterectomy
=> Bloods: FBC, LFT, glucose, cholesterol, U&E, ESR, TFT if in AF
=> Chest Xray
=> ECG if AF
=> Echocardiogram (esp if crescendo TIA because likelihood of cardiac cause)
=> MRI is preferred to determine territory of ischaemia or to detect haemorrhage or alternative pathologies (done on the same day as specialist assessment if possible)
*CT or diffusion-weighted MRI only if clinical suspicion of an alternative diagnosis that can be detected by CT
How do you manage TIA?
You can only treat TIA after doing a full neurological exam and after symptoms have settled.
Prognostic score i.e. ABCD2 is no longer used.
UNLESS,
i) patient has bleeding disorder or is taking anti-coagulant (needs immediate admission for imaging to exclude a haemorrhage)
ii) patient already on low-dose aspirin => continue current dose until reviewed by specialist
iii) aspirin is contraindicated - discuss management urgently with specialist
What is the advice on driving with a single or multiple TIA?
Patient’s responsibility to notify DVLA after stroke / TIA
When do you refer patients for specialist review?
=> Discuss the need for admission or observation urgently with a stroke specialist
What is a stroke?
Stroke is a clinical syndrome of vascular origin characterized by rapidly developing signs of focal or global disturbance of cerebral functions over 24 hours or leads to death.
What are the 2 most common types of stroke?
=> Intracerebral haemorrhage occurs due to small cerebral vessel disease i.e. high BP and in the absence of vascular malformation, aneurysm and other structural causes.
=> Subarachnoid haemorrhage occurs due to rupture of saccular aneurysms = 80%
What is silent stroke?
Radiological or pathological evidence of an infarction or haemorrhage not caused by trauma without an attributable history of acute neurological dysfunction attributable to the lesion.
What are the risk factors for stroke?
1. Lifestyle factors: => Smoking => Alcohol misuse and drug abuse => Physical inactivity => Poor diet
3. Non-modifiable factors: => Older age => Male => Previous TIA/stroke => Family hx => Genetic / hereditary factors
4. Other medical conditions: => Migraine => Hyperlipidaemia => Diabetes => Sickle cell disease => CKD => Ehler's-Danlos syndrome => Marfan's syndrome
What is the most common cause of stroke?
Atrial fibrillation => thrombosis in a dilated left atrium => emboli = the most common cause of stroke
What are the causes of stroke?
=> infective endocarditis ; rheumatic & degenerative calcific valve changes
=> congenital valve disorders
=> left ventricular mural thrombus
=> severe hypoperfusion due to MI = infarction in watershed areas especially if there is severe stenosis of proximal carotid vessel
Consider in younger patients:
=> sudden BP drop >40mmHg
=> carotid artery dissection (spontaneous or from neck trauma)
=> Vasculitis
=> Subarachnoid haemorrhage
=> venous sinus thrombus
=> Anti-phospholipid syndrome
=> Thrombophilia
What are the modifiable risk factors for stroke?
Smoking
Diabetes
Hypertension
Dyslipidaemia
Obesity
Alcohol
What are the non-modifiable risk factors of stroke?
Age
Men under 65 and Women over 65 years more likely to have stroke (due to loss of E2)
South asian and Afro-carribean
Heart disease (valvular, ischaemic, AF)
Peripheral vascular disease
Carotid bruit
Pregnancy
Combined oral contraceptive pill
Increased clotting i.e. high plasma fibrinogen, low antithrombin III
Polycythaemia vera
Family history
Which main arteries make up the circle of willis to supply the anterior cerebral circulation and the posterior cerebral circulation?
Anterior cerebral circulation => two internal carotid arteries
Posterior cerebral circulation => vertebrobasilar arteries
Cerebral infarction
Vessel occlusion => brain ischaemia => neuronal failure => infarction + cell death
The ‘CORE’ is the centre of the stroke - the ischaemic area where hypoxia leads to neuronal damage.
=> Fall in ATM results in release of glutamate => opens calcium channel, releasing free radicals => inflammation, necrosis and apoptotic cell death
The ischemic ‘PENUMBRA’ surrounds the ischemic region which is not functioning but is structurally intact.
=> timely revascularisation can help regain function in this area
Cerebral infarction
Vessel occlusion => brain ischaemia => neuronal failure => infarction + cell death
The ‘CORE’ is the centre of the stroke - the ischaemic area where hypoxia leads to neuronal damage.
=> Fall in ATM results in release of glutamate => opens calcium channel, releasing free radicals => inflammation, necrosis and apoptotic cell death
The ischemic ‘PENUMBRA’ surrounds the ischemic region which is not functioning but is structurally intact.
=> timely revascularisation can help regain function in this area
Where does anterior circulation infarcts take place?
What are the associated symptoms?
Infarcts in territory of: => internal carotid => middle cerebral (MCA) => anterior cerebral (ACA) => ophthalmic arteries
Complete MCA infarct = devastating stroke
=> contralateral hemiplegia
=> contralateral hemisensory loss
=> facial weakness - forehead spared in stroke because of bilateral innervation (if whole face affected = bell’s palsy)
=> neglect syndrome
=> aphagia / dysphagia
=> hemianopia
=> initially flaccid limbs (floppy limbs like dead weight) then becomes spastic
Internal carotid strokes = similar picture as MCA strokes
What is lacunar infarction?
What area is affect?
What are the symptoms?
Lacunes = small infarcts in basal ganglia, internal capsule, thalamus and pons
Hypertension is the major risk factor
Lacunar infarcts often symptomless or: => Ataxia hemiparesis => Pure motor => Pure sensory => Sensorimotor => Dysarthia/clumsy hand
*cognition/consciousness intact