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11
Planes of section
Sagittal Coronal Axial
STROKE AND HEAD INJURY
E
E
D
C
B
A
M
L
K
J
F
G
H
I
A
D
C
B
F
G
H
I
M
L
K
J
Fig. 11.4 Distribution of the anterior cerebral artery in the sagittal (A–E), coronal (F–I) and horizontal (J–M) planes.
into the subclavian vein and returning to the heart via
the brachiocephalic vein and superior vena cava.
Functional anatomy of the cerebral vasculature
Any brain dysfunction of vascular origin will result in
specific clinical signs and symptoms. Thus it is essential
to have a clear understanding of how the blood supply
relates to the functional areas of the brain. This is shown
in Fig. 11.7 and Table 11.1. It is essential to be able to dis-
tinguish whether a vascular lesion is located within the
anterior or the posterior arterial systems.
Angiography
It is not possible to directly examine the cerebral blood
vessels in patients (unless it is at post-mortem!). Instead,
angiography is used (Fig. 11.8). This method of analysis is generally based on the principle of intravascular
injection of a contrast agent, for example, iodine- based,
followed by serial, time lapse imaging using X- rays or
computed tomography (CT) scans. The analysis can
detect three different types of abnormality: structural
abnormality due to stenosis or occlusion, alterations in
blood vessel position (due to displacement by a mass
lesion) and alterations in flow patterns such as those that
occur in arteriovenous malformations or during stenosis
or partial vessel occlusion (Figs 11.9, 11.14 and 11.15).
Stroke
Stroke is a generic term which defines neurological deficits associated with a vascular origin. Stroke is a heterogeneous condition that can be associated with a variety
of causes. Examples of risk factors for stroke are detailed
in Table 11.2. It is notable that many of these factors
are modifiable. The genetics of stroke are complex and
genetic predisposition is a non-modifiable risk factor.
The heritability of stroke is of approximately 30%–40%
and a substantial component of this is likely to be linked
to known risk factors for stroke. Some Mendelian conditions (e.g. small vessel vasculopathies, sickle cell disease,
Marfan syndrome, Fabry’s disease and cerebral amyloid angiopathy) have stroke as a primary manifestation. Genome- wide association studies have identified
229THE NERVOUS SYSTEM
11
Planes of section
Sagittal Coronal Axial
Cerebral
Internal
Superior
Inferior
Sigmoid sinus
petrosal sinuses
jugular vein
Confluence of sinuses
E
D
C
B
A
M
STROKE AND HEAD INJURY
L
K
J
F
G
H
I
A
E
D
C
B
F
G
H
I
M
L
K
J
Fig. 11.5 Distribution of the posterior cerebral artery in the sagittal (A–E), coronal (F–I) and horizontal (J–M) planes.
falx
Cavernous
Superior and inferior
Fig. 11.6 Schematic plane of the cerebral venous circulation.
sinus
cerebral
veins
sagittal
sinus
Internal
sagittal
sinus
Great cerebral vein
(of Galen)
Straight sinus
Basal vein
Transverse sinus
Tentorium cerebellum
Occipital sinus
many common genetic variants associated with stroke;
there are more than 35 loci associated with stroke risk.
Interestingly, most of these variants occur in non-proteincoding sequences of genes.
There are two main types of stroke: ischaemic and
haemorrhagic (Fig. 11.10). Each type has a different cause
and both can result in the death of brain tissue. Ischaemic
stroke occurs when a blood clot blocks an artery, disrupting the bloodborne supply of oxygen to the brain. It can
result from stenosis or thrombosis of large or small arteries or from the presence of thromboemboli in arteries
(cardioembolic events). Atrial fibrillation—a disorder of
cardiac rhythm associated with atrial cardiopathy—is the
leading cause of cardioembolism. Atherosclerosis is the
most important cause of ischaemic stroke (Box 11.3).
Stenosis is the narrowing of an artery due to build up of plaque material, so that blood flow becomes
restricted. If 50% of the normal blood pressure is not
maintained, then brain damage will occur. Very often,
an ischaemic stroke is the result of a build- up of
230 SYSTEMS OF THE BODY
11
Lateral view
Primary motor cortex
Medial view
artery distribution
artery distribution
artery distribution
Key
STROKE AND HEAD INJURY
Broca’s area
Anterior cerebral
Fig. 11.7 Distribution of the main cerebral arteries with respect to
major functional cortical areas.
Primary somatosensory cortex
Posterior cerebral
Posterior
parietal cortex
Wernicke’s area
Primary
auditory cortex
Primary visual
cortex
Primary motor
cortex
Primary
somatosensory
cortex
Primary
visual cortex
Middle cerebral
cholesterol and other debris in the arteries over many
years. Thrombosis refers to the total blockage of a
main brain artery by a blood clot (thrombus), plaque
or embolus. A thromboembolism is a piece of plaque
that has broken off from a thrombus elsewhere in the
body, for example, the heart, and travels through the
arterial system until it lodges in a brain artery, cutting off the supply beyond this point. If this occurs
in the small blood vessels deep within the brain, the
type of stroke is termed a lacunar stroke. The infarcts
produced by this type of stroke are small (0.5–10 mm).
Lacunar infarcts can also occur in the brainstem.
Classification of stroke
Stroke can be classified as stroke in evolution, where progression of neurological defects occurs over 24–48 hours,
suggesting an ongoing infarct, or completed stroke,
where infarction is complete and the patient’s neurological deficits do not increase further. The latter is the most
common type seen. The term stroke is apt because of its
distinct temporal profile; for most sufferers, the symptoms come on literally ‘at a stroke’. The key symptoms
include a sudden numbness, weakness or paralysis on
one side of the body. Signs of this may be a drooping
arm, leg or eyelid; a dribbling mouth; sudden slurred
speech; difficulty in finding words or understanding
speech; sudden blurring, disturbance or loss of vision,
Table 11.1 Functional areas associated with the main cerebral
arteries
Cerebral artery Cortical area
Anterior cerebral Paracentral lobule: primary motor cortex and
primary somatosensory cortex regions (hip
to feet)
Supplementary motor area (movement)
Prefrontal and orbitofrontal cortex (cognition
and emotion)
Corpus callosum
Septal nucleus (pleasure)
Middle cerebral Frontal lobe: primary motor cortex (hip to
head), premotor area, frontal eye field
Parietal cortex: primary somatosensory cortex
(hip to head), primary taste cortex
Temporal lobe: primary auditory cortex
(hearing), primary olfactory cortex (smell)
Basal ganglia (movement initiation)
Optic radiation (vision)
Uncus (emotion)
Dominant hemisphere: language centres –
Wernicke’s area (receptive speech) and
Broca’s area (expressive speech)
Non- dominant hemisphere: contralateral
awareness of self and surroundings
Posterior cerebral Visual cortex (primary and association)
Hippocampus (long- term memory)
Thalamus
Hypothalamus (autonomic function)
especially in one eye; dizziness; confusion; unsteadiness
and/or a severe headache.
The effects of a stroke vary enormously, depending
on which part of the brain is affected by the disrupted
blood supply and the extent of that disruption, which in
turn depends on which vessel is affected. Classification
of ischaemic stroke is based on artery territory, and there
are four main syndromes that correspond to different
vascular territories:
1. Total anterior circulation stroke that results from
occlusion of the MCA, with or without the ACA
2. Partial anterior circulation stroke that results from
occlusion of branches of the MCA or isolated ACA
occlusion
3. Posterior circulation stroke affecting the brainstem,
cerebellum or occipital lobe
4. Lacunar stroke produced by occlusion of the deep
brain (thalamostriate) arteries.
The symptoms associated with each type of stroke are
detailed in Table 11.3.
The second main type of stroke is haemorrhagic
stroke, when a blood vessel in or around the brain
bursts, causing a bleed or haemorrhage within the skull
cavity. Long- standing, untreated hypertension is the
231THE NERVOUS SYSTEM
11
1
2
3
4
5
6
1. Anterior cerebral artery.
2. Middle cerebral artery.
3. Internal carotid artery.
6. Vertebral arteries.
1
2
STROKE AND HEAD INJURY
3
4
5
6
Fig. 11.8 Normal angiogram of anterior (top pair) and posterior (bottom pair) circulations viewed in coronal (left) and sagittal (right) planes.
4. Posterior cerebral artery.
5. Basilar artery.
232
Fig. 11.9 Angiogram showing occlusion of the left common carotid artery (black arrows) and left vertebral artery (white arrows) caused by atheroma.
Table 11.2 Risk factors for stroke
Focal
Stroke type
brain tissue
Mass effect (EDH)
• Chronic hypertension
Focal
Risk Consequence
Untreated hypertension Damages arterial walls
Atrial fibrillation Increased risk of formation of clots in the heart that may dislodge and travel to the brain (irregular heartbeat)
Smoking Increases blood pressure and has adverse effects on arterial walls
Diabetes Increased risk of high blood pressure and atherosclerosis
Diet Diets high in saturated fat lead to arterial stenosis; high salt levels are associated with raised blood pressure
Heavy drinking Over time, excessive drinking raises blood pressure; alcohol binges can rapidly increase blood pressure, causing
blood vessels to burst
Age Strokes are more common in people older than 55 years of age, because of the gradual development of
atherosclerosis; arteries become less elastic with increasing age
Sex Men are at greater risk than women, especially if aged less than 65 years
Family history Having a close relative with a history of stroke increases the risk, as factors such as diabetes and high blood
pressure have a genetic component
Contraceptive pills Make blood more likely to clot and/or raise blood pressure
Genetic Numerous genetic variants associated with the main subtypes of stroke
Complex interactions between predisposing genes and environmental factors
Haematological disorders Thrombocytosis (platelet disorder that may predispose to cerebral ischaemia)
Polycythemia (increases number of blood cells, leading to blood thickening)
Haemophilia (blood thinning prevents it from coagulating)
Sickle cell disease (causes thrombosis in young black people)
Hyperuricaemia (gout; increased uric acid in the blood that may precipitate in blood and block the blood vessel)
Drug abuse Amphetamine or cocaine abuse induce changes in the vessel tone; this leads to a rapid rise in blood pressure
(minutes to hours); amphetamine is associated with haemorrhages (mostly in the subcortical white matter);
cocaine is associated with ischaemic and haemorrhagic stroke
Vascular inflammatory
disorders
Ethnic background Asians, Africans and Afro- Caribbeans have a higher risk; this is linked to other risk factors such as high blood
Previous transient
ischaemic attack (TIA)
Giant cell arteritis
Systemic lupus erythematosus (inflammatory changes stimulate platelet adhesion on damaged surfaces)
pressure (Africans) and diabetes (Asians)
20% of patients with TIA will go on to have a full- blown stroke
11
STROKE AND HEAD INJURY
Cause
Example
Effect on
Blood vessel
disease
• Atherosclerosis
• Hypertension
• Transient ischaemic
attack
Non-mass lesion
ischaemia
Cardiac
disease
• Atrial fibrillation
• Arrhythmia
• Mural thrombosis
• Endocarditis
• Valve disorders
Non-mass lesion
Fig. 11.10 Causes of ischaemic and haemorrhagic stroke.
Haematological
disorders
• Sickle cell disease
• Thrombocytosis
• Hypercoagulable
states
• Haemophilia
• Anti-coagulant
drugs
Non-mass lesion
Ischaemic
Haemorrhagic
haemorrhage
Extracerebral
• Subarachnoid
haemorrhage (SAH)
• Aneurysm
• Extradural
haemorrhage (EDH)
Non-mass lesion (SAH)
Intracerebral
• Arteriovenous
malformation
• Berry aneurysm
• Trauma
• Drug abuse
Mass effect
233THE NERVOUS SYSTEM
11
Anterior cerebral artery
A
Middle cerebral artery
Posterior communicating artery
Posterior cerebral artery
Internal carotid artery
Basilar artery
External
carotid artery
Ve
A
1. Tear in intima wall.
2. Formation of atheromatou
plaque by circulating platelets.
3. Emboli settle on the plaque
to form a mural thrombus.
m
Box
11.3
Atherosclerosis is the most important cause of ischaemic
stroke. It is a generalized vascular disease of unknown aetiology, that tends to primarily affect large- calibre blood vessels, such as the carotid arteries (at their bifurcation points),
and the circle of Willis at the junction of the internal carotid
artery and middle cerebral artery, and vertebral and basilar
arteries (Fig. 11.11).
STROKE AND HEAD INJURY
Damage to the intima layer of the arterial cell wall produces
focal desquamation, exposing the underlying connective tissue to circulating platelets. These aggregate and stick to the
arterial wall. Aggregation causes platelets to secrete substances that, in conjunction with certain lipids, react to form
a fibrous plaque that projects into the arterial lumen. With
further arterial damage, this process is repeated, and the
plaque enlarges, causing stenosis of the vessel (Fig. 11.12).
quence of this process is a thrombus that may form on the
plaque. A thrombus is formed by platelets and fibrin sticking
Atherosclerosis
The basic pathological lesion is the atherosclerotic plaque.
Because the plaque slows blood flow, a secondary conse-
nterior communicating artery
together via interactions with clotting factors that convert
soluble fibrinogen to insoluble fibrin. Thrombus formation
is particularly likely in veins, where blood flow rate is slower
and blood pressure is lower; in addition, the presence of
valves provides pockets of stagnant flow. Anything that
causes hypercoagulation of the blood, such as inherited protein C or S deficiency or increased amounts of clotting factor
VII or fibrinogen (as occurs in pregnancy or after surgery),
increases the risk of thrombosis. If an embolus then breaks
off a thrombus, it can become lodged in a distal vessel.
The combination of changes in the vascular wall, reduced
blood flow and increased blood coagulability are known as
Virchow’s triad.
Drugs such as aspirin or drugs that selectively inhibit the
enzyme thromboxane synthase (which converts prostaglandin
H2 to thromboxane A2, a potent platelet aggregator and vasoconstrictor) or stimulate the production of endothelial prostacyclins (which dilate blood vessels), are useful in preventing
thromboembolism complications in atherosclerotic stroke.
Fig. 11.11 Locations of severe atherosclerotic blockage of the
anterior and posterior circulations.
rtebral artery
orta
1
4
3
2
4. Blood dams up behind the
s
occlusive thrombus to for
a stagnant thrombus.
Fig. 11.12 Formation of an atherosclerotic plaque.
234 SYSTEMS OF THE BODY
Table 11.3 Neurological signs associated with stroke in the anterior arterial circulation or posterior arterial circulation
Stroke type Symptoms
11
STROKE AND HEAD INJURY
Total anterior circulation
(high mortality longterm morbidity rates)
Partial anterior
circulation
Posterior circulation Cortical: contralateral homonymous hemianopsia, cortical blindness (visual agnosia), alexia (inability to read),
Lacunar Pure motor hemiparesis (face, arm and leg weakness on one side; no other symptoms except dysarthria; lesion in
ACA, Anterior cerebral artery; MCA, middle cerebral artery.
Contralateral flaccid hemiplegia (MCA + ACA)
Contralateral hemisensory loss (MCA + ACA)
Homonymous hemianopsia (MCA – anterior choroidal)
Global aphasia (dominant hemisphere, MCA)
Sensory neglect (non-dominant hemisphere, MCA)
Dysarthria and dysphagia (MCA)
Incontinence (ACA)
Gait apraxia (ACA)
Perception difficulties such as prosopagnosia (recognizing familiar objects or knowing how to use them). There may
also be problems with abstract concepts such as telling the time
Although vision may not be affected directly, it may be difficult for the brain to interpret what the eyes see
Cerebral dementia involving cognitive problems such as thinking, learning, concentrating, remembering, decision-
making, reasoning and planning (frontal lobes)
Different combinations of the above deficits, depending on which area is affected. Some of the more common
ones: MCA inferior branches – receptive aphasia, constructional apraxia, expressive aphasia, neglect, perception
difficulties; ACA branches – split- brain syndrome (pericallosal artery), dyspraxia
amnesia, disturbances of higher mental function
Brainstem: dissociated hemiparesis (ipsilateral face, contralateral body), dissociated hemisensory loss (ipsilateral face,
contralateral body), diplopia, dysphagia, dysarthria, vertigo, ataxia
internal capsule)
Pure hemisensory stroke (loss of superficial sensation and paraesthesia of one side of the body; thalamic lesion)
Ataxic hemiparesis (distal leg weakness, arm–leg incoordination; Babinski sign and inability to walk unaided; lesion
in internal capsule, cerebellum or pons)
Dysarthria and clumsy hand syndrome (moderate to severe dysarthria and clumsiness of hand movement and facial
weakness on one side; lesion in internal capsule or pons)
most common cause of this type of stroke. Intracranial
arteries differ from those found elsewhere in the body,
in that they are thin- walled and susceptible to blockage
or rupture. Thus, untreated hypertension increases the
strain on the artery walls, increasing the risk of bursting and bleeding. Onset is sudden, without warning,
usually while the patient is awake. Headache is often
present but is not a diagnostic feature. Loss of consciousness is also common.
There are several types of haemorrhagic stroke (see
Fig. 11.10):
1. A haemorrhagic stroke may be due to an
intracerebral haemorrhage, in which a blood vessel
bursts within the brain itself. The blood may form
a haematoma (a pool of collected blood) within the
brain parenchyma (tissue), resulting in a focal mass
effect (Fig. 11.13), or in existing spaces such as the
subdural or subarachnoid spaces (non-mass effects).
Parenchymal haemorrhages occur most frequently in
the basal ganglia (50%), thalamus (10%), hindbrain
(pons or cerebellum, 20%) or lobular white matter
(20%). White matter strokes are often severe and
cause extensive neurological deficits by disrupting
the passage of axon tracts, such as the internal
capsule.
2. A subarachnoid haemorrhage occurs when a blood
vessel on the surface of the brain bleeds into the
subarachnoid space – the area between the brain and
the meninges. The most common cause is head injury
(see later).
3. An aneurysm is due to a weakness of the thin- walled
intima layer of arteries, that causes a localized
dilatation of the artery lumen. Blood collects in
these ‘berry- like’ swellings, called Berry aneurysms.
They often occur in the circle of Willis (Fig. 11.14).
Eventually, as the pressure builds, the aneurysm
bursts and bleeds into the subarachnoid space, causing
an increase in intracranial pressure, which can be fatal
if not treated. In addition, the filling of the aneurysm
balloon can lead to raised intracranial pressure by a
mass effect that may cause brain damage. Normally,
aneurysms go undetected and they are akin to ticking
time- bombs. They may be fortuitously detected in
angiograms that are performed for other reasons. If
detected, they may be clipped during a neurosurgical
235THE NERVOUS SYSTEM
11
STROKE AND HEAD INJURY
Fig. 11.13 Examples of fatal intracerebral haemorrhage. Left: infarct of the lenticulostriate arteries of the middle cerebral artery. Right: anterior
cerebral artery. Both cause death through the consequences of mass effect (see text for details).
Fig. 11.14 Angiogram revealing an aneurysm (arrow) affecting the
posterior cerebral artery.
operation. The classic presentation of a burst
aneurysm is a sudden, severe headache, neck stiffness,
vomiting and loss of consciousness. Often, there are
focal neurological signs.
4. Arteriovenous malformations are congenital
abnormalities that result from defective developmental
communications between arteries and veins, without
the intervening capillaries. They appear in angiograms
as a Medusa- like tangle of distorted and contorted
blood vessels (Fig. 11.15) that may be atrophied and
therefore prone to rupture, or hypertrophic. Often,
rapid shunting of blood occurs, producing ischaemia
in neighbouring parts of the brain, which may result in
tissue infarction or seizure activity.
5. Intraventricular haemorrhage is the most common
neurological complication in approximately 40%
Arteriovenous
malformation
ACA
MCA
ICA
Fig. 11.15 Angiogram showing an arteriovenous malformation
located in the anterior cerebral artery (ACA). ICA, Internal carotid
artery; MCA, middle cerebral artery.
of premature babies (<1.5 kg body weight). The
hypoxic pressure exerted on the baby’s head during
delivery can cause haemorrhage. The prognosis for
large haemorrhages is poor, but for smaller ones it is
good. Children may be left with variable degrees of
neurological deficit.
236 SYSTEMS OF THE BODY
Table 11.4 Clinical features of hypertensive haemorrhage
Location Coma Pupil reaction (to light) Sensorimotor disturbance Hemianopsia
Basal ganglia (putamen) Common Normal Hemiparesis Common
Thalamus Common Small, sluggish Hemisensory loss Transient
Subcortical white
matter
Cerebellum Delayed (12–24 h) Small, reactive Gait ataxia No
Pons (often fatal) Immediate Pinpoint, non-reactive Quadriplegia No
Massive haemorrhages may rupture brain tissue and
leak into the ventricles, resulting in blood in the CSF.
A fatal outcome occurs when brain herniation occurs,
due to the mass effect of the oedema and haematoma.
Clinical presentation depends on the site of the haemorrhage. The most common site for hypertensive haemorrhage is in the basal ganglia. The clinical features of
hypertensive intracerebral haemorrhage in various brain
regions are detailed in Table 11.4.
In the case history presented in Box.11.1, it is likely
that Arthur is suffering from atherosclerosis. He has
several risk factors that predispose him towards ischaemic stroke: his age, high blood pressure and the
fact that he is overweight. His hypertension accelerates the atherosclerotic process and increases the risk
of blood vessel damage. Additionally, in older people,
the blood vessels have less elasticity, predisposing
them to stenosis. The doctor is able to make the diagnosis based on the history (sudden onset) and neurological examination (in this case, it is a partial anterior
circulation stroke). Whether the stroke is ischaemic or
haemorrhagic cannot be reliably distinguished clinically but, as Arthur did not lose consciousness, it is
more likely to be ischaemic. However, several tests
and investigations can be performed to confirm the
diagnosis. These are detailed in Box 11.4. Neurological
impairment can be assessed using the NIH Stroke
Scale (NIHSS) (Table 11.5). As a patient gradually
recovers some function, the improvement can be
assessed using the Barthel Index, which consists of
10 activities that specifically measure a person’s daily
living and mobility. These include feeding, bathing,
moving from wheelchair to bed and return, grooming, transferring to and from a toilet, walking on a
level surface, going up and down stairs, dressing and
continence of bowels and bladder. They are weighted
according to whether the person has received help
while doing the task, using scores of 0 (unable), 5, 10
or 15 (independent). Middle scores imply that over
50% of the effort comes from the patient. The scores
Rare Normal Hemiparesis and/or hemisensory loss Common
Box
11.4
The major signs of stroke can be recognized using the FAST
system:
F for facial weakness (assessed by asking the person to
A for arm weakness (assessed by asking the person to raise
S for speech; is the person’s speech clear and can they
T time to call the emergency services.
identify the type of stroke that has occurred and the best
treatment options. The precise tests will differ from person
to person, but common tests performed in every stroke
patient include:
• Brain scans or angiograms to determine the type and
location of the stroke and to look for signs of damage.
These are the most definitive diagnostic procedures
currently available.
• Doppler ultrasound scans of the carotid arteries to check
blood flow to the brain.
• Cerebrospinal fluid examination for diagnosing
subarachnoid haemorrhage.
• Blood pressure measurement.
• Blood tests to check blood glucose, blood clotting,
cholesterol levels, thyroid function, erythrocyte
sedimentation rate, plasma viscosity and the presence of
haematological disease.
• Chest X- ray to check for cardiac or respiratory problems.
• An electrocardiogram to measure the rhythm and
activity of the heart, or an echocardiogram.
Recognizing and diagnosing stroke
smile or by observation of a drooping face or eyelid)
both arms)
understand what you say?
If the person has failed any of these, then it is:
At the hospital, a number of investigations can help
for each activity are summed to create a total score of
up to 100. This is used as a record of what the patient
can do independently, without help, but using aids if
necessary. The assessment is used to monitor improvement in activities of daily living over time. The higher
the score, the more ‘independent’ the person. In the
UK, often the 5, 10 and 15 scores are substituted by 1,
2 and 3. This gives a potential maximum of 20 rather
than 100. The modified Rankin scale (mRS) is another
11
STROKE AND HEAD INJURY
237THE NERVOUS SYSTEM
11
Table 11.5 The NIH Stroke Scale (each examination is assessed independently from previous examinations)
Category Score
1. Level of consciousness
General response 0 = alert, 1 = drowsy, 2 = stupor, 3 = coma
Response to two questions 0 = both correct, 1 = one correct, 2 = none correct
Response to two commands 0 = both correct, 1 = one correct, 2 = none correct
2. Gaze 0 = normal, 1 = partial gaze palsy, 2 = forced eye deviation
3. Visual fields 0 = normal, 1 = bilateral quadrantonopia, 2 = homonymous hemianopsia, 3 = cortical blindness
STROKE AND HEAD INJURY
4. Facial movement 0 = normal, 1 = minor paresis, 2 = partial paresis, 3 = complete palsy
5. Motor function: arms, legs 0 = no drift, 1 = minor drift, 2 = some effort against gravity, 3 = no effort against gravity, 4 = no movement
6. Limb ataxia 0 = absent, 1 = unilateral presence in arm or leg, 2 = unilateral presence in arm and leg or bilateral,
7. Sensory 0 = normal, 1 = mild loss, 2 = severe loss (unilateral)
8. Language (aphasia) 0 = none, 1 = expressive or receptive aphasia (mild–moderate), 2 = global aphasia (severe), 3 = mute
9. Dysarthria 0 = normal articulation, 1 = mild–moderate, 2= unintelligible, 9 = untestable
10. Neglect 0 = none, 1 = partial (can recognize stimuli on right or left but not both), 2 = complete (bilateral neglect)
9 = untestable (no motor function or coma)
example of a scoring tool that can also be used to measure disability and functional impairment, and their
evolution in time after a stroke.
Mechanisms of cell injury in ischaemic stroke
The brain has a very high rate of oxidative metabolism. Anaerobic metabolism in the brain is negligible
and, consequently, the brain is extremely vulnerable to
hypoxic damage. Cell death occurs in stroke because of
anoxia and the resultant loss of ability of cells to maintain the integrity of the cell membrane and ion gradients,
through the activity of the energy- dependent ATPase
pumps. The pathophysiological consequences of stroke
involve a complex sequence of events. The main mechanisms involved include excitotoxicity, oxidation, inflammation and programmed cell death, and the molecular
pathways for these have been extensively studied (Fig.
11.16). These processes evolve over time (Fig. 11.17) and
set up several vicious circles that ultimately lead to brain
tissue loss. The mechanisms involved are different in different areas of the stroke region: at the site of infarct—the
core region—hypoxia is most severe and brain tissue rapidly dies. Surrounding the core is an area called the ischaemic penumbra, where there is residual blood flow and
where brain cells undergo potentially reversible injury
associated with metabolic failure. These cells have not
yet entered signal cascades that lead to cell death. The
size of the penumbra is variable. The importance of this
penumbra where cell damage may be reversible, is that
drugs that target the key players of the pathophysiological cascade may be able to protect the penumbra and so
limit the extent of functional deficit. This is the general
principle underlying the concept of neuroprotection.
When the brain becomes hypoxic, ATP levels start to
fall and the ATP- dependent Na+ pumps in the neuronal
and glial cell membranes become dysfunctional. The
Na+ that enters the cells, either during action potentials
or because of the ongoing leaks in the membrane, cannot
be pumped out, causing membrane depolarization. This
creates an inward osmotic force, as the influx of Na+ (and
Cl–) is much greater than the efflux of K+ and the cells
swell due to the passive influx of water, causing oedema.
Cells eventually burst, as the cell membrane fails; this
is necrotic cell death. The brain is encased in a rigid
box—the skull—so if the neurons start to swell, this will
increase intracranial pressure, leading to compression of
the cerebral blood vessels. Compression of the vessels,
especially the veins, reduces the blood flow and hence
further decreases the oxygen supply. A vicious circle is
set up, that leads to a rapid decline in cerebral perfusion.
Brain oedema is one of the earliest events in stroke (or
head injury, as discussed later) and its magnitude is one
of the major factors that determine whether the patient
will survive beyond the first few hours.
The reuptake process that removes glutamate from
the synaptic cleft and stabilizes glutamatergic transmission is also energy- intensive and requires ATP. As soon
as oxygen levels fall and ATP levels decline, the reuptake
process slows down. Consequently, glutamate begins to
accumulate in the synaptic cleft and, with the associated
rise in extracellular K+, further depolarization of cells
may occur. This leads to more hyperexcitability and more
glutamate release, and yet another vicious circle.
238 SYSTEMS OF THE BODY