Stroke & TIA

Question 1

What is a stroke?

Answer 1

An acute neurological defict lasting more than 24 hours and caused by cerebrovascular aetiology.

Question 2

What is the epidemiology of stroke?

Answer 2

100,000 new strokes occurring each year

Individuals who have experienced a stroke are at an increased risk of subsequent strokes.

9% of stroke survivors may experience another stroke within 10 years

Higher stroke risk in Black, South Asian, and Hispanic populations (linked to higher rates of hypertension, diabetes).

Question 3

What are the two type of strokes?

Answer 3

Ischaemic strokes, resulting from blood clots blocking blood flow to the brain, account for about 85% of all stroke cases.

Haemorrhagic strokes, caused by bleeding in or around the brain due to a rupture of a cerebral blood vessel, comprise the remaining 15%.

Question 4

What are the risk factors of stroke ?

Answer 4

Age>55
Men
Hypertension
Hyperlipidemia
DM
Atrial Fibrillation
ishemic heart disease
smoking
Hypercholesterolaemia
Sickle cell disease
Pro-thrombotic conditions .g anti-phospholipid syndrom
Alcohol
Higher stroke risk in Black, South Asian, and Hispanic populations (linked to higher rates of hypertension, diabetes).

Question 5

What is the classic presentation of stroke?

Answer 5

The classic presentation of a stroke involves the sudden onset of focal neurological symptoms. These symptoms can include numbness, weakness, slurred speech, or visual disturbances. ​ ​

To facilitate rapid recognition of these symptoms, NICE recommends using the FAST (Face Arm Speech Test) tool:

Face: Can the person smile? Has their mouth or eye drooped?​

Arm: Can the person raise both arms and keep them there?​

Speech: Is their speech slurred?​

Time: If any of these signs are present, it’s time to call emergency services.​

Question 6

What is the pathogenesis of an ischemic stroke?

Answer 6

Cause: Blockage of a blood vessel in the brain (clot or embolus).

Effect: Reduced blood flow → oxygen and nutrient deprivation (hypoxia/ischemia)→ brain cell death.

Key process:
Energy failure
Excitotoxicity (excess glutamate)
Inflammation and oxidative damage
Infarction (permanent damage) in the core area; surrounding penumbra may be saved if treated early.

Question 7

What is the pathogenesis of a hemorrhagic stroke?

Answer 7

Cause: Vacular Rupture with bleeding into the brain parenchyma, causing mechanical injury to brain tissue or into the subarachnoid space.

Effect: Direct brain tissue damage, increased pressure (ICP), swelling, and possible secondary ischemia.

Common triggers: High blood pressure, aneurysm rupture, arteriovenous malformation (AVM).

Question 8

What are the signs and symptoms of a stroke?

Answer 8

• Unilateral weakness or paralysis in the face, arm or leg
• Dysphasia
• Ataxia
• Visual disturbance

Question 9

What are the mechanisms of ischemia for an ischemic stroke?

Answer 9

Thrombotic: Blood clot forms locally in a cerebral artery (usually over a ruptured atherosclerotic plaque).

Embolic: A clot or debris travels from elsewhere (e.g., heart, carotids) and blocks a cerebral artery.

Lacunar: Small vessel occlusion, often related to chronic hypertension causing lipohyalinosis.

Hypoperfusion: Severe systemic hypotension causing watershed infarcts.

Question 10

What is the cascade of cellular injury in ischemic stroke?

Answer 10

Energy failure: Loss of ATP halts ion pumps.
Cell swelling and membrane depolarization

Excitotoxicity: Excessive glutamate release damages neurons.

Calcium influx: Activates enzymes that degrade cell structures.

Oxidative stress: Free radicals worsen cell injury.
Inflammation and apoptosis

Ischemic core and penumbra:
Core: Irreversible necrosis.
Penumbra: Potentially salvageable if reperfused early (target of thrombolysis).

Question 11

What are the mechanisms of bleeding in a hemorrhagic stroke and what are the consequences?

Answer 11

Mechanisms of Bleeding:
Intracerebral hemorrhage (ICH): Bleeding directly into brain tissue, often due to hypertension, arteriovenous malformations (AVMs), amyloid angiopathy, or anticoagulant use.

Subarachnoid hemorrhage (SAH): Bleeding into the subarachnoid space, commonly from a ruptured aneurysm.

🧬 Consequences of Hemorrhage:
1. Direct tissue destruction by the hematoma.
2. Increased intracranial pressure (ICP)
3. Cerebral edema
4. Vasospasm (in SAH): Can cause secondary ischemia.
5. Neurotoxicity: From blood breakdown products (hemoglobin, iron).

Question 12

What is a transient Ischaemic attack (TIA)?

Answer 12

A Transient Ischaemic Attack (TIA) is a temporary interruption of blood flow to part of the brain, spinal cord, or retina, causing focal neurological symptoms that:

1. Last less than 24 hours (typically resolve within minutes to a few hours),
2. Do not cause permanent brain damage,
3. Act as a warning sign for future stroke risk.
4. Most patients with TIA usually have complete resolution of symptoms and signs within 1 hour.
5. Caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction

Often called a “mini-stroke” but should be treated as a medical emergency because it significantly increases the risk of a full stroke within days or weeks.

Question 13

What is the underlying pathophysiology of TIA?

Answer 13

1. Transient interruption of cerebral blood flow due to:

• Small thrombus (blood clot)
• Atheroembolism from a carotid plaque or heart (especially in atrial fibrillation)
• Small vessel disease
  Atheromas in small vessels
• Hypoperfusion from low systemic blood pressure

2. Temporary oxygen and glucose deprivation → neuron dysfunction without infarction
3. No permanent damage because perfusion restores before infarction occurs.
4. Rapid symptom resolution once blood flow normalizes.

Question 14

What is the management of acute stroke according to NICE?

Answer 14

1. Urgent assessment:
   -Use FAST (Face, Arm, Speech, Time) for rapid recognition.
   - Exclude hypoglycemia immediately (check blood glucose).
   - Refer urgently to a specialist stroke unit
2. Brain Imaging:
   - Immediate CT or MRI scan to differentiate ischemic vs. hemorrhagic stroke — ideally within 1 hour if:
   - Candidate for thrombolysis
   - Anticoagulated
   - Decreased consciousness
   - Papilledema or neck stiffness
3. Ischemic Stroke Management:
   Thrombolysis (Clot-busting treatment)

• Offer intravenous alteplase within 4.5 hours of symptom onset (if eligible).

Thrombectomy (Mechanical clot removal)

• Consider for patients with large artery occlusion, up to 24 hours in selected cases (based on imaging).

Antiplatelet Therapy

• Aspirin 300 mg immediately after hemorrhage is ruled out, continued for 2 weeks, then long-term secondary prevention.

Blood Pressure Management

• Do not lower blood pressure acutely unless >220/120 mmHg or indicated for thrombolysis.

Statin therapy

• Start high-intensity statin after the acute phase (usually 48 hours later).

Question 15

What is the Hemorrhagic Stroke management?

Answer 15

Specialist care in a neurosurgical or stroke unit

Manage blood pressure — lower to <140 mmHg systolic in acute intracerebral hemorrhage.

Reverse anticoagulation if appropriate.

Monitor for increased intracranial pressure.

Question 16

What is the primary prevention of stroke (NICE)?

Question 17

What is pharmacological intervention in the secondary prevention of stroke (NICE)?

Answer 17

A. Antiplatelet Therapy

Aspirin: Continue aspirin (300 mg) for 2 weeks post-stroke, unless contraindicated.

Clopidogrel: If aspirin alone is insufficient or if the patient has contraindications, offer clopidogrel (75 mg daily).

Combination Therapy: Consider aspirin plus dipyridamole for patients who are at high risk of recurrent stroke.

For patients who have experienced an embolism from atrial fibrillation, anticoagulation (e.g., warfarin, or direct oral anticoagulants) should be considered.

B. Statins

Start high-intensity statin therapy (e.g., atorvastatin 80 mg) within 48 hours post-stroke for all patients with a history of ischemic stroke or TIA, to reduce cholesterol and prevent further strokes.

Statins should be continued indefinitely.

C. Antihypertensive Therapy

Aim for target blood pressure <140/90 mmHg in patients with hypertension.
Consider ACE inhibitors, angiotensin II receptor blockers (ARBs), or calcium channel blockers.
Beta-blockers and diuretics can be used as alternative therapies.

D. Diabetes Management

Control blood glucose levels in patients with diabetes to reduce the risk of recurrent stroke.
Metformin should be used first-line, with insulin or other medications as needed.

Question 18

What are the lifestyle modifications of secondary prevention?

Answer 18

Smoking cessation
Dietary changes
Physical activity
Weight management

Question 19

What is the pathogenesis of strokes?

Answer 19

Depends on the underlying cause…
Occlusion:
Due to atherosclerosis, leading to thrombus formation
Due to an embolus e..g AF, endocarditis, arterial dissection
Thrombus formation in a hypercoagulable state e.g. antiphospholipid syndrome
Stenosis:
e.g. carotid artery or cerebral artery stenosis
Hypotension:
Reduced blood flow to perfuse brain tissue

Question 20

What is the difference between a territorial and lacunar infarct?

Answer 20

A territorial infarct is alarge area of tissue damagesecondary to obstruction of one of the majorarteries to the brain
A lacunar infarct is a smaller area oftissuedamage from obstruction of superficial ordeep penetrating arteries

Question 21

Name the different cerebral vascular territories and their functions and the stroke deficits for each territory.

Answer 21

1. Anterior Cerebral Artery (ACA)

Supplies: Medial frontal & parietal lobes, corpus callosum, motor & sensory cortex (lower limb).
Functions: Controls lower limb movement & sensation, higher cognitive functions, and bladder control.
Stroke Deficits: Leg weakness & numbness, frontal lobe dysfunction (apathy, personality changes), urinary incontinence and gait disturbance.

2. Middle Cerebral Artery (MCA)

Supplies: Lateral frontal, parietal, temporal lobes; motor & sensory cortex (face & upper limb), Broca’s & Wernicke’s areas.
Functions: Controls face, arm, speech, language, vision.
Stroke Deficits: Contralateral face/arm weakness, aphasia (dominant hemisphere), neglect (non-dominant hemisphere), visual field defects.

3. Posterior Cerebral Artery (PCA)

Supplies: Occipital lobe, inferior temporal lobe, thalamus, midbrain.
Functions: Vision, memory, sensory integration.
Stroke Deficits: Contralateral homonymous hemianopia, memory impairment, thalamic syndrome (sensory loss & pain).

Question 22

What is the difference in symptoms between a left MCA infarct and a right MCA infarct?

Answer 22

Right:
Left hemiparesis
Left sensory loss
Left inattention/neglect
Left homonymous hemianopia

Left:
Right sided weakness
Right sensory loss
Aphasia (expressive and receptive)
Right homonymous hemianopia

Question 23

What is the symptoms of a posterior circulation infarct?

Answer 23

Dizziness
Nausea and vomiting
Unsteadiness andataxia
Diplopia
Reduced GCS
Dysarthria
Nystagmus

Question 24

What are the symptoms of a cerebellar infarct?

Answer 24

Dizziness
Nausea and vomiting
Diplopia
Ataxia
Ipsilateral weakness

Question 25

What are the symptoms of a lacunar infarct?

Answer 25

Can be motor or sensory or mixed sensorimotor Clumsy hand Dysarthria Ataxic hemiparesis Usually cognitively intact Affects basal ganglia, thalamus, internal capsule, corona radiata, and pons Commonly caused by hypertension, hypercholesterolaemia, diabetes mellitus May be asymptomatic so in practice, commonly found incidentally on head imaging Increase risk of vascular dementia – acute or subacute cognitive impairment after a neurological event with a stepwise progression is suggestive of vascular dementia

Question 26

What is the management of an ischemic stroke?

Answer 26

Ischaemic stroke is a medical emergency "Time is brain" Aim of treatment is to restore blood flow (reperfuse) brain tissue Treatment for acute ischaemic stroke is Thrombolysis  Onset of symptoms must be within 4.5 hours Ensure no contraindications  Ischaemic stroke must be ruled out on imaging  OR Thrombectomy with thrombolysis Pre-stroke functional status <3 on the modified Rankin Scale Score >5 on the National Institutes of Health Stroke Scale (NIHSS) Potential to salvage brain tissue, as shown by perfusion imaging

Question 27

What are the NICE recommendations of thrombolysis?

Answer 27

NICE recommendations: - Give intravenous alteplase to eligible patients if not contraindicated  AND - Treatment is started as soon as possible within 4.5 hours of onset of stroke symptoms  AND - Intracranial haemorrhage has been excluded using appropriate imaging techniques Do not delay treatment  while waiting for results or waiting to perform tests, unless there are suspected contraindications that must be ruled out first (e.g. hypoglycaemia, coagulopathy) Alteplase should only be administered within a well-organised stroke service by staff trained in delivering thrombolysis and in monitoring for complications

Question 28

What are the contraindications of thrombolysis?

Answer 28

Major surgery or trauma in previous 14 days Serum glucose <2.8 mmol/L History of GI or GU bleeding Seizure at onset of stroke with post-ictal neurological impairment Pregnancy Untreated intracranial vascular malformation  Large unruptured, untreated intracranial aneurysm  Caution: Age  >80 years Oral anticoagulant use regardless of INR Severe stroke (NIHSS >25) Only minor isolated neurological signs or rapidly improving symptoms Combination of both previous ischaemic stroke and diabetes mellitus

Question 29

What are the NICE recommendations of a Thrombectomy?

Answer 29

NICE recommendations: As soon as possible and within 6 hours of symptom onset (together with intravenous thrombolysis) for patients with confirmed occlusion of the proximal anterior circulation. As soon as possible to patients who were last known to be well between 6 and 24 hours previously (including wake-up strokes) with confirmed occlusion of the proximal anterior circulation demonstrated As soon as possible for patients known to be well up to 24 hours previously (including wake-up strokes) with confirmed occlusion of the proximal posterior circulation  Candidates for thrombectomy alone include those who cannot receive thrombolysis, however the efficacy of thrombectomy alone without intravenous thrombolysis has not yet been ascertained Decision to treat should be made by clinicians experienced in the use of thrombolysis for stroke and in interpretation of relevant imaging

Question 30

What is Anti-platelet therapy?

Answer 30

Anti-platelets may be started as first line treatment for: Patients with minor ischaemic stroke (NIHSS <3) and no persistent disabling neurological deficit Patients who are not candidates for hyperacute treatment with thrombolysis and/or mechanical thrombectomy NICE recommendations: Give aspirin 300mg within 24 hours to patients with acute ischaemic stroke  Intracerebral haemorrhage must be excluded by brain imaging Administration of aspirin is usually delayed 24 hours after alteplase, once a further CT scan has excluded significant bleeding Continue aspirin 300mg daily until 2 weeks after the onset of stroke symptoms, then start definitive long-term antithrombotic treatment Clopidogrel 75mg OD is recommended  If a patient has been started on aspirin during the acute stage, it should be switched to clopidogrel after 2 weeks

Question 31

What is the primary prevention of stroke?

Answer 31

NICE recommendations: Assess cardiovascular disease risk using QRISK score Lifestyle modifications for those with high cardiovascular risk: Exercise regularly Maintain a healthy diet Manage weight Reduce alcohol consumption Stop smoking Reduce caffeine intake in people with hypertension Manage underlying conditions that predispose a patient to stroke such as: Atrial fibrillation Hypertension Hypercholesterolaemia Type 1 and type 2 diabetes Transient ischaemic attacks

Question 32

What is the secondary prevention of stroke?

Answer 32

Anti-platelet therapy: Clopidogrel treatment is recommended lifelong Statin therapy: High dose e.g. atorvastatin 80mg OD for cardiovascular risk reduction Anti-hyptensives: Monitor blood pressure lowering treatment frequently and adjust treatment as tolerated to achieve a target systolic blood pressure <130 mmHg Anticoagulants: Started in people with stroke and paroxysmal, persistent, or permanent atrial fibrillation or atrial flutter once intracranial bleeding and other contraindications (such as uncontrolled hypertension) are excluded

Question 33

What is the definition of a hemorrhagic stroke?

Answer 33

Vascular rupture with bleeding into the brain parenchyma, causing mechanical injury to brain tissue or into the subarachnoid space (SAH)

Question 34

What are the risk factors of haemorrhagic strokes?

Answer 34

Hypertension Haemophilia  Cerebral amyloid angiopathy Anticoagulation  Use of illicit sympathomimetic drugs Vascular malformations e.g. aneurysm, arteriovenous malformation (AVM)

Question 35

What is the pathogenesis of hemorrhagic strokes?

Answer 35

Depends on the underlying cause... Hypertension   Damage to blood vessel walls Rupture of an aneurysm or arteriovenous malformation (AVM) Auto-regulatory dysfunction  Causing excessive cerebral blood flow e.g. reperfusion injury, haemhorrhagic transformation Arteriopathy (disease of the blood vessels) e.g. cerebral amyloid angiopathy – deposition of amyloid results in fragile vessels Altered haemostasis e.g. following thrombolysis, anticoagulation, bleeding diathesis Haemorrhagic necrosis e.g. tumour Venous outflow obstruction e.g. cerebral venous thrombosis – blood clot blocks a vein draining blood from the brain, leading to leakage of blood into the brain parenchyma

Question 36

What are the signs and symptoms of a hemorrhagic stroke?

Answer 36

Hypertension Nausea and vomiting Seizures  Reduced GCS Headache

Question 37

What are the specific brain sites and associated deficits that are caused by haemorrhagic strokes?

Answer 37

Putamen Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or apraxia Thalamus Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion Lobar Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia Caudate nucleus Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion Brainstem Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability Cerebellum Ipsilateral ataxia, facial weakness, sensory loss; gaze paresis, skew deviation, miosis, or decreased level of consciousness

Question 38

What is the management of hemorrhagic strokes?

Answer 38

Haemhorragic stroke is an emergency "Time is brain" - Patients with intracranial haemhorrage can deteriorate rapidly  - Urgently refer to neurosurgical team for immediate review - Stop statin, aspirin and other anti-platelets  - Reverse anticoagulation  - Review need for rapid reduction in blood pressure - Consider referral to critical care if reduced GCS and risk of airway compromise - Do not start statin treatment in patients with primary ICH unless required for other indications

Question 39

What is the primary prevention of haemorrhagic strokes according to NICE?

Answer 39

NICE recommendations: Assess cardiovascular disease risk using QRISK score Lifestyle modifications for those with high cardiovascular risk: Exercise regularly Maintain a healthy diet Manage weight Reduce alcohol consumption Stop smoking Reduce caffeine intake in people with hypertension Manage underlying conditions that predispose a patient to stroke such as: Atrial fibrillation Hypertension Hypercholesterolaemia Type 1 and type 2 diabetes Transient ischaemic attacks

Question 39

What is the secondary prevention of hemorrhagic strokes according to NICE?

Answer 39

Monitor blood pressure lowering treatment frequently and adjust treatment as tolerated  - Aim to achieve and maintain target systolic blood pressure below 130 mmHg Optimise management of other comorbidities and risk factors such as:  Diabetes mellitus Cerebral amyloid angiopathy Heavy alcohol Amphetamine drugs or cocaine use Antiplatelet, anticoagulant, and statin use

Question 40

What should you do on admission if stroke is suspected?

Answer 40

- Exclude hypoglycaemia as a cause of symptoms - Use the ROSIER scale (Recognition of Stroke in the Emergency Room) to establish the diagnosis rapidly - Complete a neurological examination  - Use NIHSS to determine severity of stroke - Admit everyone with suspected stroke directly to a hyperacute (or acute) stroke unit as soon as possible UK guidelines recommend doing this within 4 hours of presentation - Determine the time of symptom onset If the onset was unwitnessed, the definition of symptom onset is the time when the patient was last seen well - Request an immediate non-contrast CT scan of the head

Question 41

What is the differential diagnosis of stroke?

Answer 41

Neurological: Todd's paresis Complicated migraine Non-convulsive status epilepticus Bell's palsy Multiple sclerosis Metabolic: Hypo/hyperglycaemia Hypo/hypernatraemia Hepatic encephalopathy  Infectious: Meningitis Encephalitis Toxic: Drug overdose Vascular: Vasculitis  Vertebral/cerebral artery dissection Neoplastic: Space occupying lesion

Question 42

When should a non-contrast CT scan be requested?

Answer 42

- CT scan is used to rule out haemorrhagic stroke - Request an immediate non-contrast CT scan of the head to exclude intracerebral haemorrhage (within 1 hour of arrival at hospital, whichever is sooner) if any of the following apply: Indications for thrombolysis or thrombectomy On anticoagulant treatment A known bleeding tendency A depressed level of consciousness (Glasgow Coma Scale score <13) Unexplained progressive or fluctuating symptoms Papilloedema, neck stiffness, or fever Severe headache at onset of stroke symptoms Uncertain diagnosis In people without indications for immediate CT head, request scan as soon as possible and definitely within 24 hours of symptom onset. Consider diffusion-weighted magnetic resonance imaging (MRI) of the head if the diagnosis remains uncertain despite radiology

Question 43

What are the microbiology investigations for hemorrhagic strokes?

Answer 43

Serum glucose  Exclude hypoglycaemia and hyperglycaemia Serum electrolytes  Exclude electrolyte disturbance as a cause for sudden onset neurological signs Serum urea and creatinine  Exclude renal failure - may be a potential contraindication to some stroke interventions Cardiac enzymes  Exclude concomitant myocardial infarction. Full blood count  Exclude anaemia or thrombocytopenia prior to possible initiation of thrombolysis, anticoagulants, or antithrombotics May reveal a cause for arterial occlusion (e.g. polycythaemia, thrombocytosis) or haemorrhage (e.g. thrombocytopenia) Coagulation screen  Exclude coagulopathy as cause for stroke Abnormally high INR may be causative of haemorrhagic stroke Subtherapeutic INR if on warfarin may indicate suboptimal anticoagulation in AF Fasting cholesterol and glucose

Question 44

What are the imaging investigations for stroke?

Answer 44

ECG to exclude cardiac arrhythmia (AF) or ischaemia 24/48/72 hour Holter monitor if high suspicion but ECG normal Echocardiogram Assess for valvular abnormalities, patent foramen ovale, vegetations (cardioembolic), LV thrombus Carotid doppler  Assess for carotid artery stenosis (ischaemic stroke) Extracranial CTA Assess for vertebral artery dissection (ischaemic stroke)  Intracranial CTA  Assess for intracranial artery stenosis Intracranial aneurysm (haemorrhagic stroke) Space occupying lesion (haemorrhagic stroke) MRI/MRA Assess for cerebral amyloid angiopathy CXR  Assess for aspiration pneumonia

Question 45

What are the considerations for all patients with acute stroke?

Answer 45

Supportive Measures in Stroke Management: Protect brain tissue with supportive care. Consider intubation if GCS is low. Oxygen only if SpO₂ < 93% (not routine if not hypoxic). Monitor & control blood glucose (target 4–11 mmol/L). Continue pre-existing antihypertensives, but avoid new ones for 7 days post-ischemic stroke. Delay statins for 72 hours post-ischemic stroke; hold statins in hemorrhagic stroke. Maintain euvolaemia & normal body temperature. Regularly monitor GCS & NEWS score.

Question 46

What are the complications associated with stroke?

Answer 46

Oedema accompanying an ischaemic stroke or an intracranial bleed can compress adjacent brain structures and cause raised intracranial pressure (ICP). High tone (UMN lesion) and contractures Infection - Avoid urinary catheterisation due to high risk of sepsis and death Aspiration pneumonia Pressure ulcers Seizures Delirium  VTE

Question 47

When should an urgent CT scan be repeated?

Answer 47

An urgent CT head must be repeated urgently if: New or worsening severe headache  Clearly deteriorating consciousness  Clinical signs of mass effect  Sustained (>1 hr) significant increase in BP  Clearly worsening stroke signs Specific to ischaemic stroke: Haemorrhagic transformation Specific to haemorrhagic stroke: Re-bleeding

Question 48

What is the psychosocial impact of stroke?

Answer 48

Depression Dependency / lack of independence Need for carers Financial impact

Question 49

How is driving effected with TIA and stroke patients?

Answer 49

All TIA and stroke patients must not drive for 1 month after single event Patients with >1 event in 1 month should not drive for 3 months and should contact the DVLA All patients may resume driving after this time if clinical recovery is complete (focal neurological deficit resolved)  All patients must notify DVLA if there is a residual  focal neurological deficit after 1 month Vocational license / Group 2 (e.g. HGV) drivers should contact DVLA and not drive for 12 months

Question 50

Summarise the stroke rehabilitation pathway in the UK.

Answer 50

Early Mobilisation – Start within 24–48 hours if stable; physiotherapy aids mobility, and occupational therapy restores daily activities. Speech & Language Therapy (SLT) – Helps with swallowing (dysphagia) and speech/language (aphasia) recovery. Cognitive & Psychological Support – Assesses memory, attention, and provides emotional support for depression/anxiety. Nutritional Support – Dietitian input; enteral feeding if needed. Continence Management – Retraining for bladder/bowel control. Social Reintegration – Assistance with returning to work, driving, and home adaptations. Long-term Follow-up – Ongoing rehab through stroke units, community services, and outpatient care. Multidisciplinary Team (MDT) – Coordinated care by physios, OTs, SLTs, psychologists, nurses, and social workers.

Question 51

Describe the management of acute management of TIA according to NICE

Answer 51

1️⃣ Immediate Assessment & Risk Stratification Use the ABCD² score to assess stroke risk (although some services now prioritize urgent specialist review over scoring). Emergency referral: High-risk patients should be assessed by a stroke specialist within 24 hours. 2️⃣ Antiplatelet Therapy Aspirin 300 mg immediately (unless contraindicated). If aspirin is not suitable, clopidogrel 300 mg or dipyridamole + aspirin may be used. Continue long-term secondary prevention with clopidogrel 75 mg daily. 3️⃣ Specialist Review & Imaging Urgent brain imaging (MRI with diffusion-weighted imaging or CT scan) if symptoms are atypical or there’s diagnostic uncertainty. Carotid ultrasound or CTA/MRA for carotid artery stenosis assessment. 4️⃣ Blood Pressure & Cardiovascular Management Start antihypertensive therapy if BP is persistently high. Consider statins (e.g., atorvastatin 20–80 mg) to lower cholesterol. Assess for atrial fibrillation (AF) and start anticoagulation (e.g., DOACs or warfarin) if present. 5️⃣ Lifestyle & Secondary Prevention Smoking cessation, diet changes, weight management, and exercise. Address diabetes, AF, and other vascular risk factors. 6️⃣ Driving Restrictions Stop driving for at least 1 month after a TIA (longer if multiple TIAs).

Question 52

What are the risk factors of a TIA?

Answer 52

AF Valvular disease Congestive heart failure Carotid artery stenosis Hypertension Smoking Diabetes mellitus

Question 53

What is the urgent management of patients with suspected TIA?

Answer 53

All patients with suspected TIA to be at high risk of having a stroke Give a loading dose 300mg aspirin immediately to any patient with a suspected TIA Refer patient immediately to TIA clinic for specialist assessment and investigation Aim is  to be seen within 24 hours of onset of symptoms Do not use CT head scanning in patients with suspected TIA unless there is suspicion of an alternative diagnosis that CT could detect Send bloods for: Full blood count Coagulation  Fasting lipid profile Serum electrolytes

Question 54

When should TIA patients be admitted?

Answer 54

Arrange immediate emergency admission to an hyperacute (or acute, depending on availability) stroke unit for anyone with:  Persisting neurological symptoms who is suspected of having acute stroke Resolved neurological symptoms who has a bleeding disorder or is taking an anticoagulant

Question 55

What is the primary prevention of TIA?

Answer 55

Same as Ischemic stroke

Question 56

What is the secondary prevention of a TIA?

Answer 56

Anti-platelet therapy Once TIA is confirmed (after specialist assessment): Stop aspirin Start clopidogrel 75mg OD immediately for long-term secondary prevention Statin therapy High dose e.g. atorvastatin 80mg OD for long-term secondary prevention Anti-hyptensives Monitor blood pressure lowering treatment frequently and adjust treatment as tolerated to achieve a target systolic blood pressure <130 mmHg Anticoagulants Started in patients with confirmed atrial fibrillation Carotid endarterectomy  Patients with 50-99% stenosis of the carotid arteries on carotid doppler should be referred for urgent carotid endarterectomy

Question 57

What are the considerations that should be taken with patients with TIAs?

Answer 57

Patients should not drive for 4 weeks due to high risk of having a subsequent stroke  Safety netting – patients should seek urgent medical attention if they develop any new neurological symptoms In the community, monitor and review medications and strategies used in long-term secondary prevention aimed at: Risk factor modification (including blood pressure control and smoking cessation) Managing comorbidities that predispose patients to stroke 

Question 58

What are the possible complications of TIA?

Answer 58

Following TIA, the patient has no residual symptoms from the primary event The most significant risk to the patient is a second ischaemic event causing permanent disability The period following TIA is most high risk due to unstable atherosclerotic plaque, thrombus, or exposed thrombogenic surfaces TIA is also often indicative of cardiac atherosclerotic disease, which carries its own complications