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Stroke

Table of contents
Key points ⚡
Succinct notes to superpower your revision
Stroke\: acute neurological de
haemorrhage.
Aetiology\:
Ischaemic stroke\:
Large vessel atherosclerosis\: common site is the internal carotid artery.
Small vessel occlusion\: lacunar strokes due to lipohyalinosis or atheroma.
Cardioembolic\: atrial
Other causes\: arterial dissection, vasculitis, vasoconstriction, genetic conditions, haematological disorders, cryptogenic.
Haemorrhagic stroke\:
Hypertension\: most common cause, typically basal ganglia or thalamic haemorrhages.
Cerebral amyloid angiopathy\: causes lobar haemorrhages.
Other causes\: bleeding disorders, anticoagulants, vascular malformations, sympathomimetic drugs.
Risk factors\: high BMI, high fasting plasma glucose, high systolic BP, high LDL cholesterol, kidney dysfunction, smoking,
low physical activity, poor diet, alcohol consumption, environmental factors.
History\: establish likelihood of stroke by focal, persistent, acute de
thrombolysis and rule out stroke mimics (seizure, migraine, tumour, etc.).
Clinical examination\: look for facial droop, arm drift, abnormal speech (FAST), and use NIHSS scoring to assess severity
and vascular territory.
Di
functional neurological disorder, CNS infection, Wernicke’s encephalopathy.
Investigations\: blood sugar, CT head, CT angiogram and perfusion, chest X-ray, ECG, blood tests (U&Es, LFTs, pregnancy),
24-hour ECG, carotid dopplers, MRI, lumbar puncture, echocardiogram.
Management\:
Immediate\:
Ischaemic stroke\: thrombolysis, thrombectomy, aspirin, decompressive hemicraniectomy.
Haemorrhagic stroke\: anticoagulant reversal, BP control, neurosurgical intervention.
Initial ward care\: admit to ASU or HASU, manage aspiration risk, blood sugar, VTE risk, fever, seizures, BP control, cardiac
rhythm monitoring.
Long-term care\: multidisciplinary rehabilitation, risk factor modi
Complications\: aspiration pneumonia, long-term neurological de
hydrocephalus, haemorrhagic transformation, further strokes.
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Introduction

A stroke is an acute neurological de
vascular occlusion (ischaemia) or haemorrhage.
Stroke is the second most common cause of death globally and is one of the leading causes of disability.
1

Aetiology

The aetiology of a stroke is either ischaemic or haemorrhagic, with ischaemic stroke being the more common (being
responsible for 71% of stroke globally).
1

Ischaemic stroke

Large vessel atherosclerosis
Large vessel atherosclerosis is a common cause of ischaemic stroke. 1
The buildup and subsequent rupture of
atherosclerotic plaques leads to the occlusion of the blood supply. In Western populations, the most common site of
atherosclerosis is the internal carotid artery, but the circle of Willis (a common source in Asian patients), vertebral arteries,
and the aortic arch may also be sources.
2
Small vessel occlusion
Small vessels are penetrating arteries that branch o
1
and brainstem structures. These are responsible for lacunar strokes. These vessels lose blood supply due to a process
called lipohyalinosis (narrowing due to exposure to high blood pressure), or an atheroma at the origin of the vessel may
occlude blood
3
Cardioembolic ischaemic stroke
Cardioembolic ischaemic strokes occur when a piece of debris from the heart shoots o
most common cause is atrial . 4
Other possible emboli are from endocarditis, venous clots that bypass
pulmonary circulation through a patent foramen ovale (PFO), another septal defect, or a thrombus forming in an akinetic
segment of a ventricle.
5,6,7
Other rarer causes are as follows\:
Arterial dissection may cause a thrombus to form because tearing the intimal layer exposes the subintimal vessel
surface that allows a clot to form. 1
This is the most common cause in younger patients.
Non-atherosclerotic arterial wall disease\: vasculitis (in
vasoconstriction (drugs/cocaine, or reversible cerebral vasoconstriction syndrome).
1,8,9
Non-in

10, 11
Haematological disorders can make people more likely to have blood clots form. These may be inherited conditions
such as sickle cell or homocystinuria, or acquired conditions such as leukaemias.
12
13
Cryptogenic\: in over 25% of cases of ischaemic stroke, no cause of the stroke is found .

Haemorrhagic stroke

Haemorrhagic stroke refers to bleeding into the brain substance itself rather than the extra-parenchymal bleeds such as
extradural and subdural haemorrhages.
The most common causes of intracerebral haemorrhage (ICH) are\:
Hypertension\: hypertensive damage to small penetrating blood vessels branching o
cause of intracerebral haemorrhage. 14 15
This stereotypically leads to basal ganglia or thalamic haemorrhages (Figure 1).
Cerebral amyloid angiopathy\: Amyloid deposition around blood vessels weakens blood vessel walls, making them
liable to rupture. 16
This tends to cause bleeding into the lobes rather than the deep matter of the brain (Figure 2).
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Figure 1. Basal ganglia haemorrhage
Figure 2. Lobar intracerebral haemorrhage
Other causes of ICH are\:
Bleeding disorders\: patients may have spontaneous bleeds due to an underlying bleeding disorder.
14
Drugs\: anticoagulants increase the risk of spontaneous as well as traumatic bleeding. 17
as cocaine may also cause ICH.
14
Sympathomimetic agents such
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Vascular malformations\: various blood vessel problems such as cavernous angiomas and arteriovenous malformations
may predispose to ICH.
14
A subarachnoid haemorrhage is a further form of haemorrhagic stroke but with very di
patients are normally cared for in neurosurgical units.

Risk factors

Physiological risk factors for stroke include\:
18
High BMI
High fasting plasma glucose
High systolic blood pressure
High LDL cholesterol
Kidney dysfunction
Other risk factors include\:
18
Tobacco smoking\: including second-hand smoking
Low physical activity
Diet\: high in sodium and red meat, low in fruit/ vegetable/ whole grains
Alcohol consumption
Environmental\: air pollution, low ambient temperatures, lead exposure

Clinical features

History and examination are crucial in the identi
stroke and TIA history taking.
In emergency settings, among patients presenting with nontraumatic, noncomatose neurological de
transient ischaemic attack (TIA) are frequently diagnosed conditions, accounting for approximately 10% of such
cases.
19

History

The history should aim to establish the likelihood of a stroke through the following features\:
1. A focal neurologic de
2. A persistent neurologic de
3. A de
4. No history of head trauma.
If all 4 of these factors are present, there is a 4 in 5 chance that the patient has had a stroke.
If 1-3 of these factors are present, the probability of stroke is increased above the baseline 10%, but it’s uncertain. If none of
these 4 factors are present, the probability of a stroke is about 3 in 200.
Eligibility for thrombolysis
Key features to establish when considering eligibility for thrombolysis include\:
Time from onset of symptoms
The time the patient was last known to be una
If the patient was asleep, whether they woke up with a de
Do they have any conditions that might preclude thrombolysis, such as malignancy, recent surgery, or medical
problems that mean they are usually on anticoagulants?
Stroke mimics
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Assess for features which may suggest a stroke mimic (see the section on di
Is there any evidence that there was any seizure activity?
Is there any headache indicating this could be a migraine or giant cell arteritis?
Have they had longstanding issues to indicate that this could be a space-occupying lesion?
Is there evidence or a history of malnutrition that could indicate Wernicke’s encephalopathy as a possibility?
Is there a possibility there may be underlying endocarditis or an acute aortic syndrome which has precipitated the
neurological symptoms?

Clinical examination

The most sensitive signs of a stroke outside of a hospital are facial droop, arm drift, and abnormal speech. 19
This explains
why we have public awareness campaigns for FAST. These are good red
are not de
Examination within a hospital aims to identify a pattern of normal and abnormal a
vascular territory in ischaemia, as well as deNIHSS scoring system guides the examination.
Bamford stroke classi

Di

Anything which disturbs neuronal function is a potential di
in its response to insults, and so a global insult may cause focal neurology.
Di
Todd’s Paresis\: neuronal hypofunctioning following a seizure
Hypoglycaemia\: neurons need glucose to function, so lack of glucose will cause lack of function
Old stroke\: a new physiological insult can cause reappearance of old stroke symptoms
Hemiplegic migraine/migraine aura\: migraine is a brain disorder that changes the way neurons function
Brain tumours or other space-occupying lesions\: Local compression from lesions may cause focal neurology
Hypertensive encephalopathy\: a rare condition where chronically high blood pressure can cause cerebral blood vessel
damage
Functional neurological disorder\: can present with stroke-like symptoms
Central nervous system infection\: either a cerebral abscess or encephalitis
Wernicke’s encephalopathy\: ataxia from Wernicke’s may be mistaken for a posterior circulation stroke

Investigations

Initial ('front door') investigations

Relevant initial investigations in the context of stroke include\:
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Blood sugar\: hypoglycaemia can be a very convincing stroke mimic.
CT head\: All patients with a suspected stroke should have an urgent CT-head; its purpose is mainly to rule out an
intracerebral haemorrhage (in early ischaemic strokes, the CT-head appearances are usually normal).
CT Angiogram and CT Perfusion\: CT angiography and CT perfusion are further modalities which can establish eligibility
for thrombolysis and thrombectomy. Patients eligible for thrombectomy should have CT-A immediately. 20
However, not
all hospitals in the UK have access to CT perfusion studies.
Chest X-ray\: a baseline chest x-ray is very important as the patients are at high risk of aspiration.
ECG\: catching an episode of AF or future episodes of AF may alter the patient’s long-term management. There may also
be demand-induced myocardial ischaemia or centrally-mediated changes.
Blood tests\: U&E, LFTs, and pregnancy testing
A basic swallow assessment should be done at the front door.

Subacute investigations

Further relevant investigations include\:
24-hour ECG recording ('24-hour tape')\: to identify any episodes of atrial , the duration of the tape (24h – 7
days) may vary
Carotid dopplers\: to identify carotid stenosis, patients with greater than 50% occlusion on the side of the stroke may be
eligible for carotid endarterectomy.
MRI\: if an overt infarct cannot be identi
from new strokes using di
Lumbar puncture\: for suspected subarachnoid haemorrhage (if CT normal) or CNS infection
Echocardiogram\: to identify a cardiac source of emboli
Stroke in younger people
Young stroke bloods are done in people under 50 who may have a rarer cause of stroke\:
Vasculitis screen (ANAs and ANCAs)
Haematological causes of stroke\: sickle cell, PCV, HIIT, homocysteine, antithrombotic de
HIV and syphilis

Diagnosis

The diagnosis of a stroke relies on the history of symptom onset (i.e. is the history of an acute de
vascular event) and the neurological deBamford
classi).
This information is hopefully backed up by radiological data (i.e. proof of ischaemia or haemorrhage on MRI or CT).
However, imaging doesn’t always provide all the answers, so it is important to still take a good history and know the
neuroanatomy of the various stroke syndromes!

Management

The key to initial stroke management is identifying whether there is a bleed or ischaemia. After managing this in an acute
setting, the priority is to identify why the bleeding or blockage happened in the
the underlying risk factors to ensure the patient does not have another stroke.

Immediate management

For more information, see the Geeky Medics guide to the acute management (ABCDE approach) of a suspected stroke.
Ischaemic stroke
Immediate management for ischaemic stroke includes\:
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Thrombolysis\: thrombolysis involves the administration of a tissue plasminogen activator (tPA), such as alteplase or
tenecteplase, to break down a clot. This is given within 4.5 hours or may be given up to 9 hours after stroke (see Royal
College of Physicians criteria)
Thrombectomy\: thrombectomy involves using interventional radiology techniques to retrieve the clot and can be
performed up to 24 hours after the stroke.
Aspirin\: 300mg aspirin can be started immediately or after 24 hours if thrombolysis has been given. Patients can
continue on this for up to 2 weeks but sometimes may stop earlier (for example, if the stroke is due to atrial
patients may start anticoagulants before the 2 weeks have elapsed)
Decompressive hemicraniectomy\: in some circumstances where there is a large area of the MCA territory infarction,
resulting oedema in the infarcted tissue can cause raised intracranial pressure and require hemicraniectomy.
Haemorrhagic stroke
Immediate management for haemorrhagic stroke includes\:
Anticoagulant reversal\: this can be achieved with vitamin K, prothrombin complex concentrate, or speci
agents, depending on the anticoagulant being taken
Blood pressure control\: if elevated, patients’ systolic blood pressure should be lowered to 130 and 140mmHg for up to a
week after a bleed to prevent haematoma expansion
Neurosurgical intervention\: to evacuate a haematoma

Initial ward care

All patients with acute stroke should be admitted to an acute or hyperacute stroke unit (often called ASU or HASU). The
multidisciplinary care provided in these units is associated with a signi
21
Medical issues in this phase are primarily aspiration risk and blood sugar control in diabetic patients, as well as managing
VTE risk. Fever may occur following a stroke due to hypothalamic dysfunction. This can be managed with paracetamol,
but infectious causes of fevers should also be ruled out.
Some patients may develop seizures and require antiseizure medications.
Blood pressure control doesn’t tend to be a huge issue in ischaemic stroke as there is very limited evidence of
improvement in long-term prognosis after the 22
However, in ICH, patients should have strict BP control to have
a blood pressure of \<150 systolic for 7 days 23
. BP should be maintained \<185/110 for 24 hours in patients who have
received intravenous thrombolysis.
Intermittent pneumatic compression is used for VTE prophylaxis for patients with reduced mobility after stroke.
In patients not known to have atrial
hours, ideally as an inpatient

Management of underlying cause

The following should be considered for people who are inpatients with an ischaemic stroke\:
Endarterectomy if a carotid vessel is occluded by >50% on the side where a stroke has happened. 24, 25
Endarterectomy
should be done “as soon as possible”
, ideally within a week.
20, 26
Cardiological or surgical intervention if there’s evidence that a cardiac lesion (such as endocarditis) is the cause of the
stroke

Long term care

Long-term care for stroke focuses on rehabilitation from the neurological de
input. Physiotherapists tend to manage weakness, occupational therapists will manage cognitive issues and any changes
needed at home, and speech and language therapists will manage swallowing and speech issues.
Long-term medical care focuses on reducing the risk of subsequent strokes by modifying the risk factors. The underlying
aetiology of the bleeding or ischaemia will drive the ongoing management. Given the numerous causes of stroke, the
following is not exhaustive, but it encapsulates an overview of the management of the most common risk factors
recommended in the 2023 RCP national stroke guideline\:
20
Blood pressure\: people with stroke or TIA should aim to have a clinic systolic blood pressure \< 130mmHg
Lipids\: high-intensity statins (e.g. 80mg atorvastatin) should be started for atherosclerotic strokes
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Antiplatelets\: after two weeks of 300mg aspirin, ischaemic stroke without evidence of AF should have 75mg clopidogrel
OD long term. 75mg aspirin OD can be used if the patient cannot tolerate clopidogrel
Anticoagulation\: oral anticoagulation with a DOAC can be used after the initial aspirin if the cause of an ischaemic stroke
is suspected to be AF
Lifestyle factors\: smoking, diet, and alcohol intake should also be addressed

Complications

Complications of stroke include\:
Aspiration events\: due to swallowing dysfunction, it is common for stroke patients to aspirate, which increases their risk
of pneumonia
Long-term neurological de
Seizures may occur in the acute phase, or some patients may go on to develop post-stroke epilepsy
Cerebral oedema can occur if an acute ischaemic infarct is large enough. This may require neurosurgical intervention (a
decompressive hemicraniectomy)
Obstructive hydrocephalus can occur after haemorrhagic strokes, particularly in the posterior fossa, as the 4 th
ventricle
can be compressed
Ischaemic stroke can undergo haemorrhagic transformation
Further stroke\: once patients have had one stroke, they are vulnerable to having another, especially in the
after an event

References

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Holmstedt CA, Turan TN, Chimowitz MI. Atherosclerotic intracranial arterial stenosis\: risk factors, diagnosis, and treatment.
Lancet Neurol. 2013;12(11)\:1106-14.
Nah HW, Kang DW, Kwon SU, Kim JS. Diversity of single small subcortical infarctions according to infarct location and
parent artery disease\: analysis of indicators for small vessel disease and atherosclerosis. Stroke. 2010;41(12)\:2822-7.
Link MS, Giugliano RP, Ru
From the ENGAGE AF-TIMI 48 Trial (E
Thrombolysis in Myocardial Infarction 48). Circ Arrhythm Electrophysiol. 2017;10(1).
Pruitt AA. Neurologic complications of infective endocarditis. Curr Treat Options Neurol. 2013;15(4)\:465-76.
Mas JL, Derumeaux G, Guillon B, et al. Patent Foramen Ovale Closure or Anticoagulation vs. Antiplatelets after Stroke. N
Engl J Med. 2017;377(11)\:1011-21.
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Rodrigues MA, Samarasekera N, Lerpiniere C, et al. The Edinburgh CT and genetic diagnostic criteria for lobar intracerebral
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Related notes

Image references

Figure 1. Case courtesy of Frank Gaillard, Radiopaedia.org, rID\: 10598
Aphasia
Figure 2. Case courtesy of Jeremy Jones, Radiopaedia.org, rID\: 6153
Benign Paroxysmal Positional Vertigo (BPPV)
Cervical Radiculopathy

Reviewer

Chiari Malformations
Down's Syndrome
Dr Jacob Day
Neurology SpR

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Contents

Introduction
Aetiology
Risk factors
Clinical features
Di
Investigations
Diagnosis
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