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Oxford Specialist
Handbooks in
Neurology
Stroke
Medicine
Second Edition

Hugh Markus
Professor of Stroke Medicine
University of Cambridge, and
Honorary Consultant Neurologist
Addenbrooke’s Hospital, Cambridge, UK

Anthony Pereira
Consultant Neurologist
Department of Neurology
St George’s Hospital, London, UK

Geoffrey Cloud
Consultant Stroke Physician
Department of Neurology
St George’s Hospital, London, UK

1
1
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Second Edition published in 2017
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 v

Preface to the
Second Edition
There have been major advances in the management of stroke since the last
edition in 2010. These culminated in a series of trials, led by the MR CLEAN
trial, showing that patients who had occlusion of the large cerebral vessels
had a better outcome if treated with thrombectomy compared with intra-
venous thrombolysis. The last 5 years have also provided more data show-
ing how organization of stroke care can have a major impact on outcome.
For example, centralizing care within London into eight hyperacute stroke
units with direct ambulance transfer to these units resulted in an approxi-
mately 30% reduction in mortality. These are exciting times for stroke.
In this Second Edition we have completely revised and updated the text
to take into account these and many other advances.
The First Edition received excellent feedback and we are grateful for all
the helpful comments we received. We are grateful to Hannah Cock for
contributing to the section on post-​stroke epilepsy in this edition.

Hugh Markus
Anthony Pereira
Geoffrey Cloud
vi

Preface to the
First Edition
Recent years have seen a revolution in the profile of stroke. Often thought
of as an untreatable disease we now realize that, not only can many
strokes be prevented, but acute treatment can have a major impact on
outcome. Organized care within stroke units markedly reduces mortality.
Thrombolysis is transforming the way in which acute stroke services are
organized. It is encouraging both the medical profession and the general
public to think of stroke as a potentially treatable “brain attack” requir-
ing urgent diagnosis, transfer to hospital, and treatment. Recent data has
shown that minor stroke and TIA is followed by a high risk of early recur-
rent stroke, much higher than previously appreciated. Preventing this early
recurrence prevents major challenges in how we reconfigure services, and
determine which early secondary prevention strategies are most effective.
These advances in stroke present many challenges in delivering services.
In many countries stroke has been a ‘Cinderella’ specialty and there have
been few senior doctors specifically trained in stroke care. Specialists from
geriatric medicine, neurology, and other disciplines are having to train them-
selves in hyperacute stroke management, and familiarize themselves with
the many other advances in management which are required to deliver
comprehensive stroke care. We will need many more stroke specialists in
the future and this has led to the establishment of dedicated stroke train-
ing programmes, such as the UK Stroke Specialty training programme, and
similar schemes in other countries.
Clinicians looking after stroke patients need rapid access to up to date
practical information on how to look after stroke patients. We hope this
text book of stroke medicine will provide such a source. It is written by two
neurologists and a stroke physician, who together run a busy district and
regional stroke service. It is aimed to provide a ready source of information
for both stroke trainees and consultants. It is written to cover the syllabus of
the UK stroke specialist training programme and other similar programmes
worldwide.

Hugh Markus
Anthony Pereira
Geoffrey Cloud
 vii

Contents

Symbols and abbreviations ix

1 Epidemiology and stroke risk factors   1

2 Neuroanatomy 47
3 Vascular anatomy and stroke syndromes 65
4 History-​taking in the stroke patient 97
5 Examination of the stroke patient 109
6 Investigation of the stroke patient 143
7 Imaging in stroke 151
8 Ischaemic stroke: common causes 203
9 Acute stroke treatment 227
10 Secondary prevention of stroke 281
11 Unusual causes of stroke and their treatment 329
12 Cerebral venous thrombosis 373
13 Cerebral haemorrhage 389
14 Recovery and rehabilitation 437
15 Vascular dementia 493
16 Organization of stroke services 515
17 Ethical issues in stroke care 527

Appendix 1 Glossary 543

Appendix 2 Useful stroke scales 557
Appendix 3 Useful websites 579
Index 583
 ix

Symbols and abbreviations

ACA anterior cerebral artery

ADC apparent diffusion coefficient
ADLs activities of daily living
AF atrial fibrillation
AHA American Heart Association
AICA anterior inferior cerebellar artery
aMTS abbreviated mental test score
ALD advanced life directive
ANCA antineutrophil cytoplasmic antibodies
ANH artificial nutrition and hydration
APTT activated partial thromboplastin time
ASA atrial septal aneurysm
ASPECTS Alberta Stroke Program Early CT score
BMET Brief Memory and Executive Test
BMI body mass index
BP blood pressure
CAA cerebral amyloid angiopathy
CADASIL cerebral autosomal dominant arteriopathy with subcortical
infarcts and leucoencephalopathy
CBF cerebral blood flow
CBV cerebral blood volume
CCD cognitive communication disorder
CEA carotid endarterectomy
CI confidence interval
CNS central nervous system
COC combined oral contraceptive
CPR cardiopulmonary resuscitation
CRP C-​reactive protein
CSF cerebrospinal fluid
CT computed tomography
CTA computed tomography angiography
CVD cardiovascular disease
CVP central venous pressure
CVT cerebral venous thrombosis
DNAR do not attempt resuscitation
DTI diffusion tensor imaging
x SYMBOLS AND ABBREVIATIONS

DVT deep venous thrombosis

DWI diffusion-​weighted imaging
ECG electrocardiogram
EC–​IC extracranial–​intracranial
EDH extradural haemorrhage
EDV end-​diastolic velocity
ESR erythrocyte sedimentation rate
FES functional electrical stimulation
FLAIR fluid-​attenuated inversion recovery
GCS Glasgow Coma Score
GDP gross domestic product
GI gastrointestinal
GOM granular osmiophilic material
GRE gradient spin echo
HbA1c haemoglobin A1c
HDL high-​density lipoprotein
HMPAO 99mTc-​hexamethyl propyleneamine oxime
HR hazard ratio
HRT hormone replacement therapy
hs-​CRP highly sensitive CRP
HSP hemiplegic shoulder pain
ICA internal carotid artery
ICH intracranial haemorrhage
ICP intracranial pressure
IEED involuntary emotional expression disorder
IMCA Independent Mental Capacity Advocate
IMT intima–​media thickness
INR international normalized ratio
IV intravenous
LACI lacunar anterior circulation infarct
LDL low-​density lipoprotein
LMWH low-​molecular-​weight heparin
LPA lasting power of attorney
LVH left ventricular hypertrophy
MCA middle cerebral artery
MCI mild cognitive impairment
MCS minimally conscious state
MDT multidisciplinary team
MELAS mitochondrial encephalopathy with lactic acidosis
and stroke-​like episodes
 SYMBOLS AND ABBREVIATIONS xi

MI myocardial infarction
MIT melodic intervention therapy
MMSE mini mental state examination
MRA magnetic resonance angiography
MRI magnetic resonance imaging
mRS modified Rankin Scale
MRS magnetic resonance spectroscopy
MTHFR methylene tetrahydrofolate reductase
MTT mean transit time
NG nasogastric
NHS National Health Service
NINDS National Institute of Neurological Disorders and Stroke
NNT number needed to treat
NOAC novel oral anticoagulant
NSAID non-​steroidal anti-​inflammatory drug
NSF nephrogenic systemic fibrosis
OCSP Oxfordshire Community Stroke Project Classification
OR odds ratio
OSA obstructive sleep apnoea
OT occupational therapist
PACI partial anterior circulation infarct
PCA posterior cerebral artery
Pcom posterior communicating artery
PCWP pulmonary capillary wedge pressure
PE pulmonary embolism
PEG percutaneous endoscopic gastrostomy
PET positron emission tomography
PFO patent foramen ovale
PICA posterior inferior cerebellar artery
POCI posterior circulation infarct
PSV peak systolic velocity
PVR post-​voiding residual volume
PWI perfusion-​weighted MRI
RCT randomized controlled trial
rtPA recombinant tissue plasminogen activator [generic name
alteplase]
SAH subarachnoid haemorrhage
SALT speech and language therapist
SBP systolic blood pressure
SCA superior cerebellar artery
xii SYMBOLS AND ABBREVIATIONS

SDH subdural haematoma

SIADH syndrome of inappropriate ADH secretion
SLE systemic lupus erythematosus
SNP single nucleotide polymorphism
SPECT single photon emission computed tomography
TACI total anterior circulation infarct
TCD transcranial Doppler
TED thromboembolus deterrent
TIA transient ischaemic attack
TOAST Trial of Organon in Acute STroke
TOE transoesophageal echocardiography
TTE transthoracic echocardiography
TTP time to peak
VCI vascular cognitive impairment
VTE venous thromboembolism
WHO World Health Organization
 Chapter 1 1

Epidemiology and stroke

risk factors

Introduction 2
Definitions for epidemiological studies 3
Stroke subtyping 4
Incidence and prevalence 8
Stroke mortality 10
Economic cost of stroke care 11
Determining risk 14
Stroke risk factors 18
Non-​modifiable stroke risk factors 20
Major modifiable stroke risk factors 24
Minor modifiable stroke risk factors 34
Relative contribution of different stroke risk factors 39
Framingham stroke risk 40
Further reading 44
2 Chapter 1 Epidemiology and stroke risk factors

Introduction
• Stroke is common. Someone suffers a stroke every 3.5 minutes in the
UK and every 40 seconds in the USA and every 2 seconds worldwide
• Every year over 17 million people throughout the world suffer a stroke
and 5 million are left significantly disabled with an estimated 34 million
people globally living with the effects of stroke
• In the UK and the USA, stroke is the third commonest cause of death
(more than 60 000 and 160 000 deaths per annum, respectively) and is
the leading cause of adult disability. There are nearly 5 million stroke
survivors in the USA today
• Stroke is thought to be the second biggest killer worldwide and is
responsible for over 5 million deaths per annum with wide variations
in mortality (e.g. low in western Europe compared to eastern, low in
Australia compared to SE Asia)
• A global increase in stroke prevalence is now being seen in low-​and
middle-​income countries
• A recent study funded by the Gates Foundation on global burden of
stroke between 1990 and 2010 reported a 25% increase in stroke in
those aged between 20 and 64 years, a 113% rise in prevalence of
stroke survivors, 70% increase in all strokes, and a 36% increase in
numbers of deaths due to stroke. Over 60% of global stroke occurs in
people aged under 75 years of age
• Over half of stroke deaths are in women
• The lifetime risk of suffering stroke is approximately 1 in 4 for men and
1 in 5 for women (the latter being 2–​3 times higher than the lifetime risk
of breast cancer)
• In developed countries, about 15% of all strokes are haemorrhagic and
85% ischaemic
• One-​quarter of strokes are recurrent events
• Because stroke is such a common disease, preventative interventions
which have only a small benefit to individual patients can have a large
population benefit
• Approximately 8 of 10 strokes are avoidable through a combination of
stopping smoking, increasing exercise, reducing obesity, reducing blood
pressure (BP) and improving diet. A person’s 5–​10-​year stroke risk can
be simply calculated using a Stroke Riskometer App that reflects these
• In the UK NHS in 2006, stroke patients had a typical hospital length of
stay of 28 days and occupied over 2.6 million acute hospital bed days
per year. The length of stay has decreased to a median of 17 days but
the total economic burden of stroke is of the order of £7 billion per
annum in England and Wales.
Further reading
Parmar P, Krishnamurthi R, Ikram MA, et al. (2015). The Stroke Riskometer(TM) App: validation of
a data collection tool and stroke risk predictor. Int J Stroke 10, 231–​44.
 Definitions for epidemiological studies 3

Definitions for epidemiological studies

Stroke
• A standardized definition of stroke is vital for epidemiological studies
• The World Health Organization (WHO) definition of stroke has been
used for most studies and defines stroke as:
Rapidly developing clinical signs of focal (or global) disturbance of cerebral
function, with symptoms lasting 24 hours or longer, or leading to death, with
no apparent cause other than of vascular origin
• This definition includes ischaemic stroke, intracerebral haemorrhage,
and subarachnoid haemorrhage. It excludes transient ischaemic attack
(TIA), subdural haematoma and haemorrhage or infarction secondary
to tumour or infection
• It has been suggested by some authorities that TIA with acute brain
infarction on imaging should be classified as equivalent to a stroke.
Transient ischaemic attack
• Stroke symptoms which last less than 24 hours are termed transient
ischaemic attack (TIA)
• One should not think of TIA as an independent entity but rather a very
short-​lived stroke
• About 15% of strokes are preceded by a TIA
• Magnetic resonance imaging (MRI) of patients who have suffered a TIA
lasting longer than 1 hour shows that over 50% have visible areas of
infarction. Technically, they have not suffered a ‘stroke’ but they have
suffered cerebral infarction. This emphasizes that TIA and stroke are a
continuum
• A revised definition of TIA has been proposed which excludes patients
with cerebral infarction on imaging but it has not yet been widely
adopted:
A brief episode of neurological dysfunction caused by focal brain or retinal
ischaemia, with clinical symptoms typically lasting less than 1 hour, and
without evidence of acute infarction.
Reversible ischaemic neurological deficit (RIND)
• This term is now rarely used and is not terribly useful
• It defines a type of minor stroke caused by cerebral infarction whose
clinical course lasts between 24 and 72 hours
• RIND is used in some countries to describe a minor stroke with
complete recovery
• It is probably better to think of RIND as ‘minor stroke’.
Most stroke physicians now accept that the terms TIA and RIND are arti-
ficial and think of these clinical syndromes as merely identifying different
durations of symptoms from the same underlying disease process.
4 Chapter 1 Epidemiology and stroke risk factors

Stroke subtyping
• The definition of stroke does not differentiate between haemorrhagic
and ischaemic stroke or between subtypes of ischaemic stroke
• Stroke subtyping attempts to address this
• Stroke subtyping has been attempted using the following classifications.
Clinical classifications
These rely on clinical features and were introduced before the widespread
availability of brain and cerebral vascular imaging. The most used is the
Oxfordshire Community Stroke Project Classification (OCSP, Table 1.1).
The OCSP:
• is simple and easy to apply
• relates to prognosis and is useful to look at case-​mix between
populations
• does not differentiate pathophysiological subtypes well, for example, the
OCSP stroke syndrome may not match the identified infarct
(e.g. a lacunar infarct (LACI) frequently turns out to be caused by a non-​
lacunar infarct, such as a small cortical infarct or a striatocapsular infarct)
• is less suited to look at the pathological process causing the stroke, and
the risk factor profiles for different stroke subtypes.
Pathophysiological classifications
Here the results of additional investigations are taken into account before
identifying a pathophysiological subtype of stroke. For example, brain imag-
ing may show a cortical infarct, the Doppler may show 80% stenosis due to
atherosclerotic plaque, and the echocardiogram (echo) and electrocardio-
gram (ECG) may be normal. This stroke is then classified as a large artery
atherosclerotic infarct.
Pathophysiological classifications:
• are aimed at identifying the causes of individual subtypes
• need intensive investigation (e.g. extracranial and ideally intracranial
cerebral artery imaging, echo, etc. if they are to provide useful data)
• may not identify a mechanism even if the patient is fully investigated
(approximately 25% of strokes remain of unknown cause).
The most used is the Trial of Org 10172 in Acute Stroke Treatment
(TOAST) study, which was a 7-​year, randomized, double-​blind, placebo-​
controlled, multicentre study of 1281 acute stroke patients in 36 centres
across the USA, sponsored by the National Institute of Neurological
Disorders and Stroke (NINDS).
 Stroke subtyping 5

Table 1.1 Oxfordshire Community Stroke Project Classification

Stroke type Symptoms/​presentation
LACI (lacunar infarct) Pure motor or pure sensory stroke or
Outcome = sometimes good a combination of motor and sensory
(sensorimotor) or ataxic hemiparesis
TACI (total anterior Motor and/​or sensory deficits which affect
circulation infarct) the arm, leg and face in at least two areas
Outcome = usually poor and hemianopia (visual problems) and higher
cerebral dysfunction such as dysphasia
PACI (partial anterior Any two components of a TACI or isolated
circulation infarct) cerebral dysfunction, which are more restrictive
Outcome = varied than in a LACI classification
POCI (posterior circulation Symptoms of brainstem dysfunction or
infarct) Outcome = varied hemianopia (isolated)
Reproduced from Lancet, 337(8756), Bamford J, Sandercock P et al., Classification and natural
history of clinically identifiable subtypes of cerebral infarction, pp. 1521, Copyright (1991), with
permission from Elsevier.

Trial of Org 10172 in Acute Stroke (TOAST) classification

The TOAST classification denotes five subtypes of ischaemic stroke
(Table 1.2):
1. Large-​artery atherosclerosis
2. Cardioembolism
3. Small-​vessel occlusion
4. Stroke of other determined aetiology
5. Stroke of undetermined aetiology
6. Stroke caused by more than one potential cause
The original TOAST classification:
• Divided most causes into probable and possible. However, many
clinicians use only one category for both probable and possible when
using it clinically or for research
• Used risk factors in the definition of subtype: e.g. hypertension for
lacunar stroke. This is often not applied, particularly in studies looking
at risk factor profiles as it will, of course, exaggerate the role of
hypertension as a risk factor for lacunar stroke.
6 Chapter 1 Epidemiology and stroke risk factors

Table 1.2 TOAST diagnostic classification

Diagnostic Case Collapsed
group description group
1 Atherosclerosis, Atherosclerosis New-​onset left hemiparesis with sensory
probable deficit affecting face and arm more than leg.
Left homonymous hemianopia. Left hemispatial
neglect. CT shows loss area of ill-​defined loss
of grey–​white junction in right parietotemporal
region. Doppler shows >95% stenosis in right
ICA. Angiogram shows 80% stenosis right
ICA with branch occlusion in right MCA.
Patient in normal sinus rhythm. ECG normal.
Echocardiogram normal. No coagulopathy
2 Atherosclerosis, New-​onset left hemiparesis with sensory
possible deficit affecting face and arm more than leg.
Left homonymous hemianopia. Left hemispatial
neglect. CT shows loss area of ill-​defined loss
of grey–​white junction in right parietotemporal
region. Doppler shows >60% stenosis in right
ICA. Angiogram shows <50% stenosis right
ICA with branch occlusion in right MCA.
Patient in normal sinus rhythm. ECG normal.
Echocardiogram normal. No coagulopathy
3 Cardioembolic, Cardioembolic New-​onset left hemiparesis with sensory
probable deficit affecting face and arm more than
leg. Left homonymous hemianopia. Left
hemispatial neglect. CT shows loss area of
ill-​defined loss of grey–​white junction in right
parietotemporal region. Doppler shows <50%
stenosis in ICAs. Patient in atrial fibrillation.
Echocardiogram dilated left atrium without clot.
No coagulopathy
4 Cardioembolic, New-​onset left hemiparesis with sensory
possible deficit affecting face and arm more than leg.
Left homonymous hemianopia. Left hemispatial
neglect. CT shows loss area of ill-​defined loss
of grey–​white junction in right parietotemporal
region. Patient in atrial fibrillation.
Echocardiogram dilated left atrium without clot.
No coagulopathy
5 Lacunar, Lacunar History of hypertension. New-​onset left
probable hemiparesis affecting face, arm, and leg to same
extent. No cognitive, visual, or sensory deficits.
CT shows loss area of ill-​defined decreased
attenuation in right internal capsule. Doppler
shows <50% stenosis in ICAs. Patient in normal
sinus rhythm. ECG normal. Echocardiogram
normal. No coagulopathy
6 Lacunar, History of hypertension. New-​onset left
possible hemiparesis affecting face, arm, and leg to same
extent. No cognitive, visual, or sensory deficits.
CT shows loss area of ill-​defined decreased
attenuation in right internal capsule. Doppler
shows <50% stenosis in ICAs. Patient in normal
sinus rhythm. ECG normal. Echocardiogram
patent foramen ovale. No coagulopathy
 Stroke subtyping 7

7 Other Other History of DVT and spontaneous abortion.

determined determined New-​onset left hemiparesis affecting face, arm,
aetiology, aetiology and leg to same extent. No cognitive, visual,
possible or sensory deficits. CT shows loss area of ill-​
defined decreased attenuation in right internal
capsule. Doppler shows <50% stenosis in ICAs.
Patient in normal sinus rhythm. ECG normal.
Echocardiogram normal. PTT prolonged
without anticoagulants
8 Other History of DVT and spontaneous abortion.
determined Prior workup showed protein C deficiency.
aetiology, New-​onset left hemiparesis affecting face, arm,
probable and leg to same extent. No cognitive, visual,
or sensory deficits. CT shows loss area of ill-​
defined decreased attenuation in right internal
capsule. Doppler shows <50% stenosis in ICAs.
Patient in normal sinus rhythm. ECG normal.
Echocardiogram normal
9 Undetermined Undetermined New-​onset left hemiparesis with sensory
aetiology, aetiology deficit affecting face and arm more than leg.
complete Left homonymous hemianopia. Left hemispatial
evaluation neglect. CT shows loss area of ill-​defined loss
of grey–​white junction in right parietotemporal
region. Doppler shows <50% stenosis in ICAs.
Angiogram normal. Patient in normal sinus
rhythm. ECG normal. Echocardiogram normal.
No coagulopathy
10 Undetermined New-​onset left hemiparesis with sensory
aetiology, deficit affecting face and arm more than leg.
incomplete Left homonymous hemianopia. Left hemispatial
evaluation neglect. CT shows loss area of ill-​defined loss
of grey–​white junction in right parietotemporal
region. Patient in normal sinus rhythm. No
coagulopathy
11 Multiple New-​onset left hemiparesis with sensory
possible deficit affecting face and arm more than
aetiologies leg. Left homonymous hemianopia. Left
hemispatial neglect. CT shows loss area of
ill-​defined loss of grey–​white junction in right
parietotemporal region. Doppler shows >70%
stenosis in right ICA. Angiogram shows 80%
stenosis in right ICA with branch occlusion
in right MCA. Patient in atrial fibrillation.
Echocardiogram dilated left atrium without clot.
No coagulopathy
CT, computed tomography; DVT, deep vein thrombosis; ICA, internal carotid artery; MCA,
middle cerebral artery; PTT, partial thromboplastin time. Adapted from Stroke, 24(1), Adams
HP, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh E, Classification of subtype
of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org
10172 in Acute Stroke Treatment, pp. 35–​41, Copyright (1993), with permission from Wolters
Kluwer Health, Inc.; Stroke, 32(5), Goldstein LB, Jones MR, Matchar DB, Edwards LJ, Hoff J,
Chilukuri V, Armstrong SB, Horner RD, Improving the reliability of stroke subgroup classification
using the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria, pp. 1091–​8,
Copyright (2001), with permission from Wolters Kluwer Health, Inc.
8 Chapter 1 Epidemiology and stroke risk factors

Incidence and prevalence

Incidence is the number of new cases of stroke per annum in a population.
Prevalence is the total number of patients who have had stroke at any time
within a population.
Stroke incidence
Stroke incidence is probably under-​reported for several reasons:
• Owing to the limitations of epidemiological studies using the WHO
clinical definition alone
• The fact that not all stroke patients go to hospital
• Stroke diagnosis may not be recorded in those individuals who die
shortly after stroke onset (brain imaging is required to confirm a
diagnosis of stroke)
• There are no reliable estimates of incidence in developing countries.
The incidence of stroke varies geographically but in the UK is typically 2–​3/​
1000 per annum.
This would mean a family doctor (general practitioner) in a practice
of 5000 would have more than 10 patients a year with new stroke and
a typical general hospital serving a population of 250 000 may admit over
500 stroke cases a year.
Stroke incidence has been falling in many westernized countries. For
example, over 20 years or more of prospective study in Oxford (UK),
incorporating both OCSP and OXVASC, incidence seems to have fallen by
about a third (other estimates have UK stroke incidence falling by 19% from
1990 to 2010). This is thought to be due principally to a reduction in levels
of hypertension and smoking within the population, and the introduction of
statin and antiplatelet therapy for primary prevention of those with vascular
risk factors. However, there are at least 110 000 new strokes per annum in
England and 780 000 in the USA.
Interestingly, although stroke incidence has fallen in Oxfordshire, case
fatality has remained at about 17%, emphasizing the importance of preven-
tion rather than cure.
The Global Burden of Disease Study 2010 identified studies published
between 1990 and 2010. It concluded that although age-​standardized rates
of stroke mortality have decreased worldwide in the past two decades, the
absolute number of people who have a stroke every year, stroke survivors,
related deaths, and the overall global burden of stroke (disability-​adjusted
life-​years (DALYs) lost) are great and increasing.
Stroke prevalence
• In the UK, there are over 1 million stroke survivors and over half are
dependent on others for everyday activities, with 300 000 living with
significant disability from their stroke
• In the USA, there are over 5 million survivors (approximately 2.6% of
the total population). Fig. 1.1 shows stroke prevalence in the USA by
age and gender.
 Incidence and prevalence 9

14.8
80+

12.4

6.5
60–79

6.2
Ages

1.2
40–59

2.3

Men
0.5
20–39

Women
0.5

0 3 6 9 12 15
Percent of population

Fig. 1.1 Stroke prevalence in the USA by age and gender.

Source data from the National Health and Nutrition Examination Survey (NHANES) 1999–​2005.
10 Chapter 1 Epidemiology and stroke risk factors

Stroke mortality
• Estimates of stroke mortality are more robust than those of incidence
as minor (almost all non-​fatal) strokes are more easily missed than
major ones
• Within Europe, there is a fivefold gradient of increased stroke mortality,
from France and Switzerland with the lowest mortality rates to Russia
and the former Soviet bloc with the highest. This difference is mainly
determined by socioeconomic factors. About 66% of the variance
can be ascribed to the amount of gross domestic product (GDP)
countries spend on stroke care. GDP is not the whole story, however,
as countries such as Norway with high GDP spent on stroke care still
have relative increased stroke mortality rates in comparison to other
countries such as France
• Overall, rates of stroke mortality are:
• decreasing in western Europe
• increasing in eastern Europe
• seem to have ‘bottomed out’ in both the USA and Japan
• Stroke mortality is falling in the UK but still 25% of people die within a
year of stroke—​with case fatality twice as high in patients aged over 85
as those below 65 years
• Early stroke mortality is frequently reported at 30 days and should
always be adjusted for case mix especially age, stroke severity (e.g.
NIHSS) and stroke sub-​type (e.g. haemorrhagic vs ischaemic). Atrial
fibrillation-​related stroke is also associated with increased 30-​day
mortality
• In the UK, 30-​day mortality has fallen from approximately 1 in 4 to 1
in 8—​presumed to be primarily due to increased access to stroke
unit care.

Table 1.3 Thirty-​day case-​fatality rates for stroke in the USA in 1999.
Figures are for first-​ever stroke, by ethnicity and stroke subtype
% Case-​fatality rates (95% CI)
All† Black* White*
All stroke subtypes 14.7 12.8 16.9
Ischaemic 10.2 9.1 11.5
Intracerebral haemorrhage 37.6 36.2 39.0
Subarachnoid haemorrhage 31.3 28.2 34.7
†
 Adjusted for age, gender and race.
*
 Adjusted for age and gender.
Adapted from Stroke, 37, Kleindorfer D, Broderick J, Khoury J et al., The unchanging incidence
and case-​fatality of stroke in the 1990s: a population-​based study, pp. 2473–​8, Copyright (2006),
with permission from Wolters Kluwer Health, Inc.
 Economic cost of stroke care 11

Economic cost of stroke care

• Acute stroke care in England is responsible for 6% of all NHS
expenditure and in 2010 was estimated to cost the NHS around £3
billion per year (see Table 1.4). Stroke patients have historically a typical
hospital length of stay of 28 days and occupy over 2.6 million acute
hospital bed days per year
• With the cost of lost productivity and disability estimated at £1.8
billion and the cost of informal carers at £2.4 billion, the total annual
societal cost of UK stroke care is estimated at £9 billion, comparable to
coronary heart disease
• The cost of stroke (indirect and direct) in the USA was estimated
in 2004 to be $53.6 billion, with a mean lifetime cost of $140 048
per stroke
• Over one-​quarter of strokes occur in people of working age
• Cerebrovascular disease is also the second commonest cause of dementia,
is the commonest cause of late-​onset epilepsy, and a major cause of
depression, compounding the healthcare economic burden of stroke.
Costs (in pounds sterling) of stroke in England (total
population of 50 million) from the 2010 National
Audit Office report
• In an ageing population, the incidence, prevalence, and cost are all set
to rise
• The number of people in England aged 65 years and over increased
by nearly 4 million between 1952 and 2002. The proportion of older
people is predicted to rise from 16% in 2003 to 23% in 2031. The total
cost of stroke care is predicted to rise in real terms by 30% between
1991 and 2010 (see Table 1.5).

Table 1.4 Total cost of stroke in England (in pounds sterling)

Cost items Cost £ million Percentage
Diagnosis costs 45,604 0.51
Inpatient care costs 865,872 9.64
Outpatient costs 109,679 1.22
Outpatient drug costs 505,588 5.63
Community care costs 2,857,113 31.82
Annual care cost total 4,383,858 48.82
Informal care costs total 2,420,921 26.96
Income lost due to mortality 592,733 6.6
Income lost due to morbidity 740,158 8.24
Productivity loss total 1,332,892 14.85
Benefit payments 841,254 9.37
Total 8,978,926
 12
Table 1.5 Interim life table for England. This shows the main number of years of remaining life at different ages
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Age now
Male 76.52 75.95 74.98 74.00 73.02 72.03 71.04 70.05 69.05 68.06 67.07 66.0 65.08 64.09 63.10 62.12 61.13 60.15 59.19 58.23 57.26 Life
added
Chapter 1

years
Female 80.93 80.30 79.33 78.35 77.36 76.37 75.38 74.39 73.39 72.40 71.40 70.41 69.42 68.43 67.44 66.44 65.45 64.47 63.49 62.50 61.52
21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 Age
now
Male 56.31 55.35 54.39 53.44 52.48 51.52 50.56 49.60 48.65 47.69 46.74 45.78 44.83 43.88 42.93 41.98 41.04 40.09 39.15 38.21 37.27 Life
added
years
Female 60.54 59.56 58.58 57.59 56.61 55.63 54.65 53.67 52.69 51.71 50.73 49.75 48.78 47.80 46.83 45.86 44.89 43.93 42.96 42.00 41.04
42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 Age
now
Male 36.33 35.40 34.48 33.55 32.63 31.72 30.81 29.91 29.02 28.13 27.25 26.38 25.51 24.65 23.80 22.95 22.11 21.28 20.47 19.67 18.88 Life
added
years
Female 40.08 39.13 38.18 37.23 36.29 35.35 34.42 33.50 32.57 31.66 30.75 29.84 28.93 28.04 27.14 26.26 25.38 24.50 23.64 22.78 21.93
63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 Age
now
Male 18.12 17.35 16.61 15.87 15.15 14.44 13.75 13.07 12.40 11.76 11.14 10.54 9.96 9.40 8.86 8.35 7.85 7.38 6.93 6.51 6.11 Life
added
Epidemiology and stroke risk factors

years
Female 21.09 20.26 19.44 18.63 17.84 17.05 16.27 15.51 14.75 14.02 13.30 12.60 11.92 11.26 10.63 10.01 9.41 8.83 8.28 7.75 7.24
84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 Age
now
Male 5.72 5.33 4.96 4.62 4.33 4.06 3.82 3.56 3.32 3.10 2.91 2.70 2.53 2.37 2.22 2.10 1.96 Life
added
years
Female 6.75 6.28 5.83 5.40 5.03 4.67 4.34 4.02 3.73 3.46 3.22 3.01 2.81 2.62 2.46 2.31 2.15
Economic cost of stroke care
13
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