ACUTE NEUROLOGY

Stroke: causes and Key points

clinical features C Stroke is a clinically defined syndrome of acute, focal neuro-
logical deficit attributed to vascular injury (infarction, hae-
Stephen JX Murphy morrhage) of the central nervous system; in modern clinical
David J Werring practice, neuroimaging is increasingly used to confirm the
exact pattern of tissue injury

C Hypertension is the most important modifiable risk factor for

Abstract
stroke overall (though probably contributes to different ex-
Stroke is a clinically defined syndrome of acute, focal neurological
tents depending on the stroke mechanism)
deficit attributed to vascular injury (infarction, haemorrhage) of the
central nervous system. Stroke is the second leading cause of death
C Approximately 85% of strokes are ischaemic and are caused
and disability worldwide. Stroke is not a single disease but can be
by cerebral small vessel disease, cardioembolism and large
caused by a wide range of risk factors, disease processes and mech-
artery atherosclerosis-related thromboembolism
anisms. Hypertension is the most important modifiable risk factor for
stroke, although its contribution differs for different subtypes. Most
C About 15% of strokes are caused by intracerebral haemor-
(85%) strokes are ischaemic, predominantly caused by small vessel
rhage, which can be deep or lobar; 80% of these result from
arteriolosclerosis, cardioembolism and large artery athero-
cerebral small vessel diseases (deep perforator arteriopathy,
thromboembolism. Ischaemic strokes in younger patients can result
cerebral amyloid angiopathy)
from a different spectrum of causes such as extracranial dissection.
Approximately 15% of strokes worldwide are the result of intracerebral
C Stroke in adults <50 years old accounts for 15% of cases and
haemorrhage, which can be deep (basal ganglia, brainstem), cerebellar
can result from a different spectrum of diverse causes
or lobar. Deep haemorrhages usually result from deep perforator (hy-
compared with older individuals, including extracranial
pertensive) arteriopathy (arteriolosclerosis), while lobar haemorrhages
dissection
are mainly caused by cerebral amyloid angiopathy or arteriolosclero-
sis. A minority (about 20%) of intracerebral haemorrhages are caused
by macrovascular lesions (vascular malformations, aneurysms, caverno-
mas), venous sinus thrombosis or rarer causes; these are particularly of ischaemic and haemorrhagic stroke has risen over the last
important in young patients (<50 years). Knowledge of vascular and ce- decade to 85e94 per 100,000, but is much higher (1151e1216
rebral anatomy is important in localizing strokes and understanding their per 100,000) in people >75 years old. Moreover, 85% of all
mechanisms. This guides rational acute management, investigation, and stroke deaths occur in low-income countries, which also account
secondary prevention. for 87% of stroke-related disability-adjusted lifeeyears. In the
Keywords Cerebrovascular disease; intracerebral haemorrhage; UK, stroke treatment and productivity-loss result in societal costs
ischaemic stroke; MRCP; stroke pathogenesis; stroke risk factors;
of £8.9 billion a year, with care costs accounting for approxi-
transient ischaemic attack
mately 5% of total NHS costs. Cerebrovascular disease is the
leading cause of epilepsy in elderly individuals, and the second
most common cause of late-onset dementia.

Definitions
Epidemiology It is important to recognize that stroke and transient ischaemic
attack (TIA) are clinical syndromes and that the underlying
Stroke is a huge and increasing global health challenge. World-
vascular brain injury can have many different mechanisms
wide, stroke is the leading cause of acquired physical disability in
(associated with different risk factors and disease processes;
adults, and the second leading cause of mortality in middle-to
Figure 1). Thus ‘stroke’ and ‘TIA’ are not single or complete di-
high-income countries. In such countries, the overall incidence
agnoses, but a starting point for rational investigation and
treatment.

Stephen JX Murphy MRCPI MRCPUK PhD is a Stroke Fellow at Transient ischaemic attack and stroke: a TIA is traditionally
University College Hospital and The National Hospital, Queen defined as a brief episode of focal neurological dysfunction not
Square, London, UK. Competing interests: none declared.
associated with permanent cerebral infarction, and lasting less
David Werring FRCP PhD FESO is Professor of clinical neurology at than 24 hours. Stroke is defined as focal neurological deficit of
UCL Institute of Neurology, Queen Square, and Honorary Consultant sudden onset, with symptoms lasting more than 24 hours (or
Neurologist at University College Hospital and The National Hospital,
resulting in death before 24 hours). These definitions are no
Queen Square, London, UK. He trained in medicine at Guy’s
longer helpful in clinical practice for the following reasons:
Hospital, and in neurology in London including The Maudsley
Hospital, King’s College Hospital, St Thomas’ Hospital and the treatment of stroke is time sensitive and needs to be commenced
National Hospital. Competing interests: DJW reports honoraria from as soon as possible after diagnosis; the 24-hour time boundary is
Bayer, Alnylam and Portola. arbitrary; and 30e50% of patients with clinically-defined TIAs

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 ACUTE NEUROLOGY

have evidence of brain ischaemia or infarction on diffusion- causal arteriopathies would improve any future classification.
weighted magnetic resonance imaging (MRI). Atypical attacks, Other forms of intracranial bleeding (subdural, extradural, sub-
usually recurrent, stereotyped spreading paraesthesia and arachnoid) are not considered in this article.
numbness affecting the arm and face, are associated with con-
vexity subarachnoid haemorrhage, and therefore mandate brain Risk factors for stroke2
imaging, ideally with MRI. With the increasing availability of
MRI, it is likely that imaging-based definitions of TIA and stroke Non-modifiable risk factors
will take precedence in the future. The term ‘cerebrovascular Age: this is the most important contributor to stroke risk. The
accident’ or ‘CVA’ is outdated, inaccurate, encourages thera- incidence doubles for each decade after age 55 years.
peutic nihilism, and should no longer be used.
Sex: because of the risks of pregnancy and oral contraceptive
Classification of stroke use, premenopausal women have a stroke risk that is as high as
The Trial of Org 10172 in Acute Stroke Treatment (TOAST) or higher than the risk in men. At older ages stroke rates are
classification system is the most widely used mechanistic sub- slightly higher in men. Overall, more women than men have
classification system for patients with cerebral ischaemia, strokes in the UK.
defining five subtypes: (1) large artery atherosclerosis, (2) car-
dioembolic, (3) small vessel occlusion, (4) stroke of other Ethnicity: African Caribbean individuals in the UK and USA have
determined aetiology, and (5) stroke of undetermined aetiology.1 twice the risk of incident stroke compared with their white
In the more recent phenotype-based A-S-C-O system, every pa- counterparts. In younger black adults the risk of ICH is twice that
tient is classified according to the relative contribution of of age-matched white people. This may in part relate to the
Atherosclerosis, Small vessel disease, Cardiac source and Other increased prevalence of stroke risk factors, such as uncontrolled
causes. The value of this additional complexity has not been hypertension, obesity and diabetes, among African Caribbean
established in clinical practice. populations. Other ethnicity-related risks contributing to stroke
There is less consensus on classifying spontaneous (non- include carotid stenosis in white individuals, the metabolic
traumatic) intracerebral haemorrhage (ICH; bleeding into the syndrome in South Asians and Pacific islanders, and increased
brain substance). One system, SMASH-U, categorizes causes as rates of intracranial stenosis and ICH in East Asian populations.
Structural vascular lesions, Medication, Amyloid angiopathy,
Systemic disease, Hypertension or Undetermined. However, Genetics: in addition to the single-gene disorders that are asso-
these categories are a mixture of risk factors, mechanisms and ciated with stroke (CADASIL, CARASIL, Fabry’s disease, homo-
disease processes; improved neuro-imaging of the underlying cystinuria, sickle cell disease, connective tissue disorders; Table

Illustration of the differences between disease processes,

risk factors and mechanisms in stroke

Genetic factors
Ischaemic

Disease processes
Atherosclerosis
Small vessel disease
Cardiac disease

Risk factors Mechanisms

g
Haemorrhagic
• Hypertension • Large artery-to-artery
• Diabetes embolism
• Smoking • Small vessel occlusion
• Obesity or rupture
• Cardiac embolism
• Haematological • Haemodynamic
• Others • Other

Figure 1

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 ACUTE NEUROLOGY

1), the MEGASTROKE consortium identified 32 genome-wide

significant loci, 22 of which were novel.3 Some loci were Potential mechanisms of stroke in younger patients
strongly linked to particular stroke mechanisms (e.g. large artery (selected more common or important ones are in bold)
disease, small artery disease, cardiac embolism), while half the Haematological conditions Protein C/S/antithrombin III deficiency
loci showed a shared genetic association with other vascular (venous risk only)
pathologies, the largest correlation being for blood pressure. Prothrombin/factor V Leiden mutations
(venous risk only)
Modifiable risk factors
Acquired prothrombotic states
Hypertension: this is the most important modifiable risk factor
(pregnancy, oral contraceptive use,
overall for stroke. Approximately half of all stroke patients, and an
cancer, nephrotic syndrome, anabolic
even greater proportion of those with ICH, have a history of hy-
steroid use, antiphospholipid syndrome)
pertension. Even among those not defined as hypertensive, the
Myeloproliferative disorders
higher the blood pressure, the higher the risk of stroke. This
Inflammatory Primary central nervous angiitis,
makes the diagnosis and control of hypertension paramount for
granulomatosis with polyangiitis,
primary and secondary prevention of strokes. The attributable risk
€gren’s syndrome, Takayasu’s arteritis
Sjo
from hypertension declines after age 60 years, where it confers
Genetic CADASIL, CARASIL, Fabry’s disease,
relative risk of 3.5, to a non-significant contribution at age 80.
MELAS, homocystinuria, sickle cell
disease, connective tissue/collagen
Diabetes mellitus: this is an independent risk factor for stroke,
vascular disorders
associated with a 2-fold increased risk. Stroke accounts for 20%
Vascular (non- Extracranial arterial dissection, Susac’s
of all deaths in people with diabetes.
arteriosclerotic) syndrome, reversible cerebral
vasoconstriction syndrome, Sneddon’s
Cardiac factors: cardioembolic infarction (mainly from atrial
syndrome, migrainous infarction,
fibrillation (AF)) is the most severe ischaemic stroke subtype,
fibromuscular dysplasia, moyamoya
with high disability and mortality. The presence of AF increases
disease
with age, causing 20e25% of strokes in patients >80 years old.
Cardiac AF, infective endocarditis, paradoxical
Anticoagulation is extremely effective in preventing stroke in
embolization through patent foramen
people with AF (relative risk reduction about two-thirds).
ovale, atrial tumours
Infective diseases Syphilis, varicella zoster vasculopathy,
Smoking: this doubles the risk of stroke. Smoking cessation
tuberculous meningitis, HIV, possibly
rapidly reduces the risk, with excess risk nearly disappearing 2
coronaviruses
e4 years after stopping.
Recreational drugs Cannabis, cocaine, opiates,
amphetamines, MDMA,
Hyperlipidaemia: the relationship between dyslipidaemia and
g-hydroxybutyrate (GHB)
stroke is complex. There is an increased risk of ischaemic stroke
with increased total cholesterol, and a decreased risk of ischae- CADASIL, Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts
mic stroke with elevated high-density lipoprotein-cholesterol. In and Leukoencephalopathy; CARASIL, Cerebral Autosomal Recessive Arteriopa-
thy with Subcortical Infarcts and Leukoencephalopathy; MELAS, Mitochondrial
contrast, total cholesterol is inversely associated with risk of ICH. Encephalopathy, Lactic acidosis, and Stroke-like episodes. Note that MELAS
The use of statins in secondary prevention appears to reduce the causes stroke-like attacks rather than conventional ischaemic stroke.
risk of ischaemic stroke (as well as functional outcome and
mortality) with no definite increase in the risk of intracerebral Table 1
haemorrhage. Current evidence and expert opinion favours of-
fering statins to survivors of ICH who have a strong indication for
their use (e.g. clinically relevant ischaemic heart disease). Inflammation: raised inflammatory biomarkers have a modest
association with increased risk of arteriosclerosis and stroke.
Alcohol consumption and substance abuse: light and moderate Infection can trigger stroke, and there is evidence that stroke
alcohol consumption (<4 units/day) has been reported to be rates are lower in individuals vaccinated against influenza.
associated with a lower risk of ischaemic stroke, whereas higher Coronavirus disease (COVID-19) has been linked to large vessel
quantities are clearly associated with increased stroke risk. occlusions in association with a hyperinflammatory and hyper-
Alcohol consumption has a linear relationship with ICH risk. coagulable state.
Recreational drugs including cocaine, heroin, amphetamines,
cannabis and ecstasy are associated with an increased risk of Pathogenesis of stroke
stroke (both ischaemic stroke and ICH). Stroke in the young: about 10e15% of all strokes occur in
adults aged 25e49 years. Table 1 contains a list of stroke aeti-
Obesity and sedentary behaviour: most of the effect of body ologies to consider in this population. Extracranial carotid or
mass index on stroke risk is mediated by blood pressure, vertebral dissection is common and important to consider but
cholesterol and glucose concentrations. People who are physi- should be actively sought through the history, examination and
cally active have a lower risk of stroke and overall stroke mor- neuro-imaging. Cardiac causes (e.g. patent foramen ovale,
tality than those who are inactive. rhythm disturbances, endocarditis), recreational drugs and

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 ACUTE NEUROLOGY

Figure 2 (a) Axial diffusion-weighted MRI showing an acute small subcortical infarction in the right centrum semiovale white matter consistent with
a small vessel occlusion (red arrow). (b) Extracranial computed tomography (CT) angiography demonstrating
95% carotid stenosis (red arrow). (c)
Non-contrast axial CT of the brain showing acute thrombus in the right middle cerebral artery (the ‘hyperdense MCA sign’, red arrow). (d) Resulting
acute infarction showing high signal indicating restricted diffusion on axial diffusion-weighted MRI of the brain.

thrombophilias are also important to seek in unexplained strokes lacunes on computed tomography (CT). Its prevalence increases
in younger people. with age with no differences between sexes, and can be higher in
Asian populations. The most important risk factor for CSVD is
Ischaemic stroke: approximately 85% of strokes are ischaemic, hypertension. More rarely, genetic disorders (Table 1), radiation
predominantly the result of cerebral small vessel disease (CSVD), exposure and immune-mediated vasculitides can cause CSVD.
cardioembolism and large artery disease (atheroscleroisis).
Cardioembolic stroke: a further 25% of ischaemic strokes are
Cerebral small vessel disease: CSVD includes deep perforator caused by cardioembolic disease (mainly AF), the risk increasing
arteriopathy (also termed arteriolosclerosis or hypertensive with age. In stroke patients, paroxysmal AF is more prevalent
arteriopathy) and cerebral amyloid angiopathy (CAA). Deep than persistent AF. Post-stroke AF is found in approximately 8%
perforator arteriopathy affects the structure and function of small of individuals presenting to A&E with a stroke, 11% of those
vessels (usually in the range of hundreds of microns) supplying using 24e72-hour Holter monitoring and 17% of those using
the basal ganglia and brainstem; it causes approximately 25% of external or implanted loop recording; however, the clinical sig-
ischaemic strokes, 80% of nontraumatic intracerebral haemor- nificance of short runs (<30 seconds) of AF is uncertain. Other
rhage, and contributes to about 45% of dementia (Figure 2a). rarer causes of cardiac embolism are detailed in Table 1.
CAA affects small vessels but is considered separately as a more
important cause of ICH than ischaemic stroke (see below). CSVD Large artery disease: stenosis or occlusion of the large cerebral
is diagnosed on the basis of radiological markers, including: arteries (predominantly the extracranial carotid) is the cause of
recent small subcortical infarcts, white matter hyperintensities, about 20% of ischaemic strokes (see Figure 2b). Rupture of
lacunes, cerebral microbleeds, enlarged perivascular spaces and arteriosclerotic plaques leads to in situ thrombus formation and
cerebral atrophy on MRI; or white matter hypodensities and distal embolization. In addition, ruptured carotid plaques lead to

Figure 3 (a) Non-contrast axial computed tomography (CT) scan showing a deep intracerebral haemorrhage in the basal ganglia. (b) Non-contrast
axial CT scan showing venous haemorrhagic infarction of the right temporoparietal region due to right transverse sinus thrombosis. (c)
Susceptibility-weighted imaging showing lobar haemorrhage, superficial haemosiderin staining within and around cerebral sulci (cortical superficial
siderosis, blue arrow), and strictly lobar parenchymal microbleeds (red arrow) consistent with CAA.

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 ACUTE NEUROLOGY

intracerebral haemorrhage’ is unhelpful because hypertension is

Clinical localization of stroke by vascular territory neither necessary nor sufficient to cause most ICH. Detection of
the neuro-imaging markers of CSVD mentioned above (including
Anterior cerebral artery cerebral microbleeds) can help increase confidence that an ICH is
C Leg more than arm involvement with hand sparing due to CSVD.
C Urinary incontinence CAA e a CSVD characterized by the presence of amyloid-b
C Gait apraxia protein within the cortical and leptomeningeal blood vessel
C Akinetic mutism walls e is an important cause of lobar (but not deep) ICH in
Middle cerebral artery
older people.4 CAA is also associated with cognitive impair-
C Homonymous hemianopia/quadrantanopia (involvement of infe-
ment, transient focal neurological episodes (usually recurrent
rior division)
stereotyped attacks of spreading paraesthesias affecting the
C Faceearmeleg involvement
arm and face, often related to small convexity subarachnoid
C Aphasia (Broca’s ¼ superior division; Wernicke’s ¼ inferior
haemorrhages). CAA can be diagnosed by brain imaging
division)
showing haemorrhage restricted to the lobar brain regions
C Inattention
(Figure 3c).
C Gaze paralysis (usually indicates a large area of frontal damage)
After CSVD (which causes about 80% of all ICH), the next
Vertebrobasilar
most common cause of ICH is macrovascular abnormalities
C Occipital lobe e homonymous hemianopia, cortical blindness,
(arteriovenous malformation, dural arteriovenous fistula); these
other cortical visual deficits
are more common in (but are not limited to) younger people and
C Cerebellum e ataxia, nystagmus
can only be identified by imaging of the brain vessels (e.g. using
C Brainstem cranial nerve palsies e diplopia, facial numbness/
CT angiography, MR angiography or digital-subtraction intra-
weakness, vertigo, dysphagia, dysphonia
arterial angiography). Rarer causes of ICH include haemorrhagic
C Spinal tracts e hemiparesis and hemisensory loss
Lacunar stroke syndromes (due to occlusion of deep perforating transformation of ischaemic infarcts, venous sinus thrombosis,
small arteries) brain tumours, reversible cerebral vasoconstriction syndrome
C Pure motor hemiparesis and endocarditis (see Figure 3). Recreational drug use (especially
C Pure sensory stroke cocaine) increasingly contributes to ICH in younger people.
C Sensorimotor stroke
C Ataxic hemiparesis Stroke localization
Knowledge of intracranial vascular territories and neuroana-
Table 2 tomical pathways allows the localization of lesions with rele-
vance for interpreting brain imaging and understanding the
widespread platelet activation, and recurrent events are very functional deficit, prognosis and mechanism of stroke (Table 2).
common, particularly in the first few weeks. Less commonly, ICH cannot be reliably differentiated from ischaemic stroke
stenosis of the vertebrobasilar or intracranial arteries causes without imaging.
ischaemic strokes. Haemodynamic strokes can occur when sys-
temic blood pressure drops in the context of arterial stenosis, Anterior circulation: this comprises territories supplied by the
leading to infarction of border zone territories. Extracranial dis- anterior and middle cerebral arteries, which are branches of the
sections of cervico-cephalic arteries (sometimes traumatic) ac- internal carotid artery. The first branch of the internal carotid is
count for about 1 in 5 ischaemic strokes in patients <50 years the ophthalmic artery. Carotid thrombo-embolic disease due to
old. carotid atherosclerosis can thus lead to ‘amaurosis fugax’ (tran-
sient monocular loss of vision) in the affected eye. A full prox-
Cryptogenic stroke: in 20e30% of patients with ischaemic imal occlusion of the middle cerebral artery (often from a cardiac
stroke, no cause is found. These strokes may relate to undiag- embolus) typically causes contralateral hemiparesis and hemi-
nosed cardioembolic disease, hypercoagulable states, paradoxi- sensory loss (see Figure 2c), visual field defect, hemineglect and
cal emboli via a patent foramen ovale, sub-stenotic atheromatous (if in the dominant hemisphere) aphasia. Involvement of the
disease, non-atherosclerotic arteriopathies, occult recreational superior division of the middle cerebral artery produces contra-
drug use or undiagnosed genetic conditions or risks. lateral hemiplegia, hemisensory loss and, on the dominant side, a
non-fluent (Broca’s) aphasia. Involvement of the inferior division
Intracerebral haemorrhage: spontaneous (non-traumatic) ICH often produces a contralateral hemianopia and, if left-sided, a
can be anatomically divided into deep and lobar (Figure 3). Deep fluent (Wernicke’s) aphasia. If more distal branches are involved
haemorrhages account for approximately two-thirds of ICH the territory of neurological deficit becomes more limited (the
cases, and occur in the basal ganglia and internal capsule (35 extreme of this being a ‘cortical hand’ syndrome due to infarction
e70%) or brainstem (5e10%). About 5e10% of ICHs are in the of primary sensorimotor cortex).
cerebellum. The remainder are lobar haemorrhages located in
cortico-subcortical areas in the cerebral lobes, often near or Vertebrobasilar circulation: the right and left vertebral arteries
reaching the cerebral convexities. Hypertensive (deep perforator) join to form the basilar artery, which divides to form the poste-
arteriopathy (CSVD) is the most important cause of deep ICH, rior cerebral arteries. These supply the occipital cortex, so that
although it also contributes to lobar ICH. The term ‘hypertensive infarction leads to hemianopia. Strokes in the vertebrobasilar

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 ACUTE NEUROLOGY

territory are a diagnostic challenge because of the large number KEY REFERENCES
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example, brainstem ischaemia can lead to ‘crossed’ signs, while subtype of acute ischemic stroke. Definitions for use in a multi-
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2 O’Donnell MJ, Chin SL, Rangarajan S, et al. Global and regional
Small vessel occlusions (small subcortical infarcts): Small effects of potentially modifiable risk factors associated with acute
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arteries are probably often asymptomatic but when they occur 2016; 388: 761e75.
in eloquent brain areas produce ‘lacunar syndromes’. The most 3 Malik R, Chauhan G, Traylor M, et al. Multiancestry genome-wide
common lacunar syndromes (and corresponding infarct loca- association study of 520,000 subjects identifies 32 loci associ-
tions) are pure motor stroke (posterior limb of the internal ated with stroke and stroke subtypes. Nat Genet 2018; 50:
capsule), pure sensory stroke (lateral thalamus), sensorimotor 524e37.
stroke (thalamo-capsular region), dysarthriaeclumsy hand 4 Banerjee G, Carare R, Cordonnier C, et al. The increasing impact of
syndrome (usually pons) and ataxic hemiparesis (posterior in- cerebral amyloid angiopathy: essential new insights for clinical
ternal capsule, pons, centrum semiovale). The progression of practice. J Neurol Neurosurg Psychiatry 2017; 88: 982e94.
CSVD with accumulation of small subcortical infarcts and pro- 5 Banerjee G, Stone SP, Werring DJ. Posterior circulation ischaemic
gressive white matter damage causes a typical clinical syn- stroke. Br Med J 2018; 361: k1185.
drome of progressive cognitive impairment (typically executive
dysfunction) and gait disturbance with reduced stride length
and falls. A

TEST YOURSELF
To test your knowledge based on the article you have just read, please complete the questions below. The answers can be found at the
end of the issue or online here.

Question 1 What is the most likely finding on the MR scan?

A public health programme was being planned to reduce the A Cerebral microbleeds, white matter hyperintensities and
incidence of stroke in a population by identifying modifiable risk lacunes
factors. B Localized cerebral infarction in the left middle cerebral
artery territory
What risk factor modification is most likely to succeed in C Frontal lobe space-occupying lesion
reducing future stroke risk? D Deep intracerebral haemorrhage
A Reduction in body mass index E Reduction in perivascular spaces
B Treatment of hypertension
C Stopping smoking Question 3
D Good control of diabetes A 63-year-old woman presented with sudden-onset right leg
E Lowering of raised low-density lipoprotein cholesterol level weakness sparing the upper limb and face. She also had new
onset urinary incontinence and reduced verbal output.
Question 2
A 78-year-old man presented with a 6-month history of pro- What artery is most likely to have been affected?
gressive cognitive difficulties, including problems with recent A Posterior cerebral artery
memory and planning domestic tasks. He had had several epi- B Middle cerebral artery
sodes of slurred speech each lasting for about 10 minutes. Over C Anterior cerebral artery
the last year or so he had also become more unsteady with D Vertebral artery
shortening stride length, and had fallen on two occasions. E Perforating arteries
Clinical examination, apart from memory loss was normal. A
magnetic resonance (MR) scan of the brain was performed.

MEDICINE 48:9 566 Ó 2020 Published by Elsevier Ltd.