Stroke and TIA Flashcards
What is a stroke
Stroke – focal cerebral hypoperfusion resulting in reduced ATP and so sudden cessation of action potentials. This can either be due to haemorrhage (13%) or ischaemia (87%)
Describe the main causes of stroke
Large-artery atherosclerosis
Carotid artery Stenosis
Carotid Dissection most common cause in young adults
Cardio-embolic
Atrial fibrillation
Giant cell Arteritis
Small vessel disease
Hypertension causing haemorrhagic stroke and/or atherosclerosis
Amyloid Bleeds
What are the 5 stroke syndrome features
Sudden Onset Focal neurological signs Loss of function (i.e. not pain) also known as negative symptoms Attributable to a vascular territory Maximal at onset
Describe common stroke presentations
Most commonly present with unilateral limb weakness or loss of sensation, facial droop, dysphasia (left side), neglect (right side), visual field loss, loss of coordination.
Slurred speech, difficulty swallowing, and diplopia are not focal signs and must have other signs to be considered for a stroke.
Also note that symptoms that migrate are unlikely to be due to stroke and more likely stroke mimic especially with sensory or visual disturbances e.g. migraine and seizure. As well as this stereotyping of symptoms are extremely unlikely to be due to a stroke. There are 2 exceptions to these rules - capsular warning syndrome and intracranial stenosis
What is capsular warning syndrome
Capsular warning syndrome – hypoperfusion in the lenticulostriate end arteries can occur if blood flow through the MCA is reduced. This can cause intermittent and fluctuating impairments – can be confirmed as capsular warning syndrome on MRI.
What is intracranial stenosis
Intracranial stenosis – stereotyping can also be seen when intracranial stenosis interacts with another cause of generalised cerebral hypoperfusion e.g. palpitations, postural hypotension etc. Angiography can confirm stenosis.
Can you distinguish between hemorrhagic and ischaemic stroke by presentaiton?
It is impossible to distinguish between a haemorrhagic and ischaemic stroke clinically however haemorrhagic strokes are more like the present with • Loss of consciousness • Headache • Nausea and vomiting • Seizures
Describe the oxford community stroke project classification of TACS
TACS (total anterior circulation stroke)
All 3 of the following being present:
• Higher dysfunction – dysphasia, visuospatial disturbances
• Homonymous hemianopia
• Motor and/or sensory defects of face, arm or leg
Describe the oxford community stroke project classification of PACS
PACS (partial anterior circulation stroke)
Isolated higher cortical dysfunction or
2 out of
• Higher dysfunction – dysphasia or visuospatial disturbances
• Homonymous Hemianopia
• Motor and/or sensory defects of face, arm or leg
Note motor and/or sensory defect of only one somatic region i.e. face, arm or leg can only be a PACS due to vascular territories.
Describe the oxford community stroke project classification of LACS
LACS (Lacunar stroke) – perforating end arteries around the basal ganglia, internal capsule or thalamus presenting with one of
• Unilateral weakness and/or sensory deficit of 2/3 or more of face, arm or leg
• Ataxic hemiparesis
Describe the oxford community stroke project classification of POCS
POCS (Posterior circulation syndrome)
• Isolated homonymous hemianopia with macular sparing
• Cerebellar or brainstem stroke (bilateral signs or locked in syndrome)
• Ipsilateral cranial nerve palsies with contralateral motor and/or sensory deficit
What signs and symptoms do cerebellar strokes cause?
Cerebellar strokes – DANISH especially coordination, precision and timing. Can include the brainstem if blockage is proximal.
ISPILATERAL SIGNS
Describe the signs seen in brain-stem strokes?
Brainstem will illicit contralateral signs if tracts are affected, ipsilateral if cranial nerve nuclei are affected.
How does the location in a basilar artery stroke change its presentation?
Basilar artery – Distal occlusion causes bilateral occipital lobe infarction, bilateral thalamic infarction, bilateral midbrain involvement. Proximal occlusion causes ’locked-in-syndrome’.
How does a thalamic stroke present?
Thalamic Stroke – contralateral sensory signs only of all modalities that will be isolated to certain parts of the body (more commonly due to atherosclerosis than due to emboli).
What is Weber’s syndrome?
Weber’s Syndrome – branch of the posterior cerebral artery that supplies the midbrain causing ipsilateral CN III palsy and contralateral weakness of the upper and lower limbs.
What is lateral meduallary syndrome/Wallenberg Syndrome?
Lateral medullary syndrome or Wallenberg syndrome – posterior inferior cerebellar infarct causing ipsilateral facial pain and temperature loss, ataxia, nystagmus, dysphagia and CN palsies, contralateral limb/torso pain and temperature loss.
What immediate investigations is required for a suspected stroke?
NIHSS score is very important for stroke management
CT scan (non-contrast) to rule out haemorrhagic stroke allowing thrombolysis if eligible MRI later on to look for stroke if CT showed nothing (CT will only show large ischaemic stroke acutely)
On the CT you’ll see Hyperattenuation, effacement of sulci and obscuration – loss of grey-white matter border.
What general investigations should be ordered in a suspected stroke?
Blood glucose ECG and BP Carotid artery doppler GCA (giant cell arteritis) investigation if warranted Thrombophilia screen if necessary Lipid level
What is the management pathway for an ischaemic stroke?
Thrombolysis
Given if less than 4.5 (ideally <3) hours since onset and no absolute contraindications
Thrombolysis is done using a fibrinolytic drug such as alteplase, this is most effective on smaller vessel disease.
Thrombectomy Revascularisation therapy (thrombectomy) for selected patients with large vessel occlusion. Guidance from CT angiogram, 6-hour window, if NIHSS score > 5 usually thrombolyse first. Also done within 24 hours if proximal posterior/anterior infarct and CT/MRI shows small infarct so chance to save large volume of tissue.
Pharmacological – Give aspirin 300mg for 2 weeks directly after stroke (or 24 hours after thrombolysis). After this give anticoagulation therapy (warfarin or apixaban) indefinitely if caused by AF – check AF notes for CHADVASc and HASBLAD scoring. If not, then after the 2 weeks continue on Clopidogrel indefinitely (or aspirin and dipyridamole if clopidogrel is contraindicated).
What are the absolute contraindications for thrombolysis
- Previous intracranial bleed
- Intracranial neoplasm
- Stroke or traumatic brain injury in previous 3 months
- Lumbar puncture in previous 7 days
- Active bleeding or GI bleed in last 3 days
- Pregnancy
- Seizure at onset of stroke
- Uncontrolled hypertension >200/120
- Liver disease – platelets <100m INR > 1.7
What is the management pathway for a hemorrhagic stroke?
Typically, a hypertensive bleed will occur in the basal ganglia
Control of BP to a target of 140 SBP
Stop anticoagulant or antiplatelet therapy and reverse if necessary
Refer for neurosurgical review – clot reduction or decompression craniotomy if required
Intraventricular shunting if required
What general management options are important in stroke patients?
Referral to occupational therapy and physiotherapy where needed. Peak neurological recovery time is from 1-3 months post stroke.
Nil by mouth if swallow is unsafe or any concerns until swallow is assessed. Should be assessed by speech and language therapist within 72 hours of admission and considered for nasogastric tube if not safe. Referral to dietician is important. If NG feeding isn’t tolerated, then can be considered for gastrostomy (PEG) or nasal bridle tube.
Commence a statin if cholesterol >3.5 – usually wait until 48hours after onset.
Can stroke patients drive?
Patients must not drive for 1 month
How can you prevent strokes?
Smoking cessation Weight <25BMI Avoid Alcohol intake (heavy) Low fat, salt and sugar and high fibre 5 x 30mins aerobic exercise sessions per week
Anticoagulation therapy for AF
BP control < 130/80
Controls of lipid levels – TC <4 and LDL < 2
Good glycaemic control
If carotid atherosclerosis > 50% of symptomatic side, then surgery
Do strokes directly cause death?
Not often, complications are important as few stroke patient die from strokes but rather from the complications of stroke or from being in hospital.
Describe some common complications of stroke
Complications include recurrent stroke, immobility, RIC, infections, mood or cognitive change, post stroke fatigue, post stroke pain and spasticity, contractures and secondary epilepsy.
What is malignant MCA syndrome and how is it managed?
Malignant MCA infarct – very large proximal MCA infarct which causes raised ICP and midline shift due to extensive oedema – treat with decompressive hemi-craniotomy.
What is a hemorrhagic transformation
Conversion of a ‘dry’ ischaemic infarct into a ‘wet’ hemorrhagic one as dead and dying tissue begins to bleed. This is the reason why thrombolysis has an effective window
Describe some stroke mimics
Group 1 – identifiable on brain imagine
SOL e.g. tumour, haemorrhage and abscess
Multiple Sclerosis
Group 2 – syndromically distinguishable
Postictal paresis
Hypoglycaemia
Sepsis
Group 3 – requires specialist input to distinguish
Functional weakness
Migraine with aura
Focal Seizures
What does HEMI stands for?
Common stroke mimics - Hypoglycaemia, Epilepsy, Migraines aura/MS and Intracranial tumours
What is transient global amnesia?
Transient Global amnesia – can be following trauma, slowly regains ability to form new memories and rarely happens again.
What is Todd’s paresis?
Todd’s paresis – tonic clonic seizure followed by unilateral weakness which may involve, face, arm or leg weakness, aphasia, or gaze palsy lasting from 30mins to 36hours.
Describe common stroke chameleons
Venous infarcts, small cortical strokes (appear as peripheral nerve lesions), limb shaking TIA, occipital stroke (confused and delirious), stroke amnestic syndrome and a stroke mimicking vestibular dysfunction.
What is a TIA?
A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia, without evidence of acute infarction. Often called a mini stroke by patients.
Give some statistics that describe the relationship between TIA and strokes
A quarter (23%) of all strokes are preceded by a TIA. In very high-risk TIA groups, a quarter have a stroke by 3 months and a quarter are dead by 5 years (20-25%).
What are the clinical features of a TIA?
Amaurosis Fugax – retinal artery Sensory loss Weakness Facial drooping Dysphasia Multiple stereotyped TIAs indicates crescendo TIAs and suggests critical intracranial stenosis
What are the causes of a TIA?
Cardioembolic from carotid atherosclerosis
Cardio-embolus
Hyperviscosity
How should you examine and investigate a suspected TIA?
Listen for Bruits
MRI
Carotid US doppler
Check BP, lipids and HbA1c
How is a TIA managed?
If the patient has had a suspected TIA in the last 7 days or more arrange urgent assessment (within 24 hours) by a specialist stroke physician.
STAT 300mg Aspirin and continue for 2 weeks, unless contraindicated e.g. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage).
If the patient has had more than 1 TIA (‘crescendo TIA’) or has a suspected cardioembolic source or severe carotid stenosis: discuss the need for admission or observation urgently with a stroke specialist.
After 2 weeks clopidogrel is recommended first-line (as for patients who’ve had a stroke).
aspirin + dipyridamole should be given to patients who cannot tolerate clopidogrel.
When is a carotid endarterectomy indiciated?
Recommend if patient has suffered stroke or TIA in the carotid territory and are not severely disabled but should only be considered if carotid stenosis is >70% ECST criteria or 50% NASCET criteria and on the affected side.
Can patients who have had a TIA drive?
Patients must not drive for 1 month
What is the Barthel index?
Barthel Index measure disability or dependence in activities of daily living in stroke patients. Can be used to monitor their improvement over time.
How should hydration be managed in an acute stroke?
Hydration – very important to maintain euvolaemic status post stroke. Being hypervolaemic will cause cerebral oedema, cardiac failure and hyponatraemia whilst being hypovolaemic may worsen the ischaemic penumbra. Oral hydration is preferable but if IV hydration is to be used then normal saline without dextrose is recommended.
How should glycaemic control be managed in an acute stroke?
Glycaemic control – also important to maintain this as post stroke hyperglycaemia increases mortality due to increased tissue acidosis. Maintain blood glucose between 4 and 11. Diabetics should be managed in a sliding insulin scale and glucose infusions.
How should blood pressure be managed in an acute stroke?
Blood pressure – Using anti-hypertensive medications in stroke patients should only be done in hypertensive emergencies – hypertensive encephalopathy, hypertensive nephropathy, hypertensive MI/cardiac failure, aortic dissection, or pre-eclampsia/eclampsia. As lowering blood pressure can compromise collateral blood flow to the affected region. If treatment is required use IV labetalol, nicardipine and clevidipine.
