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Table 10.7 Motor control deficits and corresponding physical therapy in Parkinson’s disease
Motor control deficits Corresponding physical therapy
Truncal stiffness Exercises involving trunk movements
Mis- scaling of movement amplitude Use large- amplitude movements
Respiratory complications and impairment Breathing exercises with relaxation techniques
Slowed gain, stepping cadence Gait exercises, especially varying walking cadence exercises
Stride length Rhythmic auditory stimulation
Balance instability, falling Self- initiated and external perturbations
Side- to- side rocking motion and facilitation of anterior/posterior motion
Pregait- type activities
Problems with simultaneous and sequential
movements
Impaired prediction of movements, inability to start
movements (‘freezing’)
Hastening Biofeedback and relaxation techniques
Dyskinesia and dystonia Slow stretching exercises
Tremor Upper- body karate training
Speech impairment Delayed auditory feedback device, prosodic exercises, rhythmic stimulation
Dysphagia Reclining neck at 60 degrees with head support
Psychological symptoms and problems Relaxation and cognitive restructuring, training in social skills specifically adapted to
Repetitive practice of functional activities, simultaneous sequencing of different motor
programmes, rising from seated position
Rhythmic activities with cueing signals, polysensory cueing
Selection of proper cueing frequencies
External damping device for the upper extremity
Parkinson’s disease, teaching programmes for relatives
10
MOTOR SYSTEMS II: THE BASAL GANGLIA
From Pohl M, Mrass GJ, Oertel WH, Rehabilitation in Parkinson’s disease (1999), In LeWitt PA, Oertel WH, eds. Parkinson’s Disease: The
Treatment Options, London, Martin Dunitz.
relatively spared. HD is an autosomal dominant disease
due to a mutation in a gene present on the short arm of
chromosome 4, which encodes the huntingtin protein.
A DNA test can identify the mutation. Individuals at
risk can be offered genetic testing after suitable counselling. Prenatal genetic testing can also be carried out. The
onset of the disease is in mid- life, and progression to
death takes place over 15–20 years. The disease occurs in
5–10/100,000 of the population. Transmission can occur
through parents of either sex and is fully penetrant.
The function of huntingtin is unknown. It is a large
protein that may act intracellularly as a scaffolding protein, thereby providing a platform to facilitate interactions between various proteins involved in multiple
cellular pathways. The protein is present in all tissues
and is essential for life, as homozygous knockout mice
are not viable. The mutation in exon 1 of the huntingtin
Fig. 10.16 Neurodegeneration in Huntington’s disease: brain sections
taken through the caudate putamen of a normal patient (left) and a
Huntington’s disease patient. The Huntington disease hemisphere
on the right shows degeneration of the caudate nucleus adjacent
to the lateral ventricle, which has enlarged in response to striatal
atrophy. (From Alexi T. et al. (2000). ‘Neuroprotective strategies for
basal ganglia degeneration: Parkinson’s and Huntington’s diseases.’
Progress in Neurobiology, 60:435.)
gene leads to an abnormal number of repeats of glutamine (encoded by the CAG codon) in the N- terminal
region of the protein. The mutated protein is expressed
early in life, but the disease becomes apparent in midlife. Interestingly, several other neurological diseases
are associated with the expansion of a CAG repeat in
the genome. Examples are spinobulbar muscular atrophy, dentatorubropallidoluysian atrophy (DRPLA) and
219THE NERVOUS SYSTEM
10
different types of spinocerebellar ataxias. Huntingtin
(as well as the other proteins containing polyglutamine
repeats) can directly interact with transcription factors and thus modify the expression of multiple genes.
Interestingly, only specific subsets of neurons are vulnerable in each of these diseases, although the affected proteins are present throughout the brain and other organs.
The length of the polyglutamine tract varies between
individuals. The number of repeats is inversely correlated with age at onset of the disease. Individuals with
more than 40 repeats will invariably develop adult- onset
disease, whereas the presence of 55 repeats or more leads
to onset at an age of less than 20 years. The disease has
several stages: the first stage is characterized by mood
changes, cognitive deficits and subtle motor changes.
Subsequently, abrupt, involuntary movements (chorea)
become dominant, and swallowing, speech and gait
deteriorate. In the last stage of the disease there is significant weight loss, emerging bradykinesia and rigidity,
MOTOR SYSTEMS II: THE BASAL GANGLIA
and death becomes imminent.
The cortex of HD mutation carriers shows progressive
thinning up to 15 years before the onset of motor symptoms. Ultimately, the disconnection of corticostriatal afferents is likely to play a major role in the dysfunction that
occurs downstream in striatal projections. Initially, it is
likely that there is increased glutamate release and overexcitation of striatal spiny neurons, followed by silencing of the striatal neurons in the late stages of the disease.
The triplet expansion mutation in exon 1 of the huntingtin
gene leads to a toxic ‘gain of function’, which is ultimately
associated with a host of pathophysiological changes,
such as abnormal energy metabolism, disrupted neurogenesis, reduced axonal transport and protein trafficking
and disrupted production of brain- derived neurotrophic
factor (BDNF). Proteins with polyglutamine repeats can
aggregate and form fibrils similar to the amyloid β- fibrils
in Alzheimer’s disease. The mutant protein can be found
in the cytoplasm and is also present in large intranuclear
inclusions. Striatal projection neurons receive significant
glutamate input from the cortex; therefore, they may
be at an increased risk of excessive stimulation of glutamate receptors and subsequent uncontrolled rises in
cytoplasmic Ca2+, leading to cell death. Therefore, it has
been suggested that excitotoxicity is involved in striatal cell loss. The intrastriatal administration of excitatory
amino acids, such as kainic acid, ibotenic acid or quinolinic acid, leads to massive striatal neurodegeneration.
Agonists at the NMDA glutamate receptor such as quinolinic acid, injected intrastriatally in experimental models,
lead to a pattern of neuropathology that is very similar to
the pattern found in HD. Mitochondrial poisons such as
3- nitropropionic acid, which compromise energy metabolism, also lead to striatal degeneration. It cannot be ruled
out that metabolic compromise leads to secondary excitotoxicity through uncontrolled release of glutamate. It
is also known that in HD astrocytic glutamate transporters are deficient, and also that the ability of astrocytes to
buffer potassium is impaired, which leads to prolonged
depolarisations and underlies the increased neuronal
excitability. However, there are still missing links in the
pathophysiology cascade, between the production of the
protein with expanded CAG repeats and the triggering
of multiple deleterious effects including transcriptional
dysregulation, mitochondrial dysfunction, altered proteostasis, oxidative stress, disrupted axonal transport and
synaptic dysfunction.
As illustrated in Fig. 10.1C, the loss of striatal efferent pathways leads to disinhibition of the glutamatergic
thalamocortical input and the emergence of abnormal
movements that define a very characteristic hyperkinetic
syndrome. The patients affected present with chorea, that
is, an involuntary, jerking movement that affects the limbs
and axial muscle groups. Patients try to suppress these
movements and incorporate them into more purposeful ones. It is important to note that chorea can be due to a
variety of causes. It can be associated with a hereditary disease (e.g. HD) but can also be induced by drugs (e.g. antiparkinsonian drugs and oral contraceptives) or alcohol or
have an immunological or metabolic cause. Sydenham’s chorea is post-infectious and associated with rheumatic fever.
Chorea must be differentiated from hemiballismus, in
which movements are more violent and jerky and affect
only one side of the body as a result of damage to the subthalamic nucleus on the contralateral side. Writhing movements are also associated with athetosis, which is another
dyskinesia. In this case, movements are slower and reflect
gradual transitions from one dystonic posture to another.
Athetosis is typically encountered in cerebral palsy.
The cortical changes and loss of striatal efferent pathways are accompanied by dopaminergic hyperactivity,
especially in the earlier stages. Anti-dopaminergic medication, for example, dopaminergic antagonists such as
haloperidol, can alleviate the symptoms. Depletion of
vesicular amine stores in dopaminergic terminals, by
drugs such as tetrabenazine, may also help. Many patients
develop depression, which responds to antidepressant
medication (e.g. selective serotonin reuptake inhibitors or
serotonin- noradrenaline reuptake inhibitors). It has been
suggested that antidepressant drugs not only improve
mood but also may have some neuroprotective effects.
HD is an irreversible neurodegenerative disease, and
in the last stages of the disease, cardiovascular and respiratory complications due to increased debility are a common cause of death. One of the possible strategies for
treating this disease is based on the principle of inhibition of expression of the mutant allele at the DNA or
RNA level. However, inhibition of the mutant allele
must not disrupt the parallel expression of the normal
allele, which is required for development. Antigene (i.e.
blockade of transcription) or antisense oligonucleotide
(blockade of translation) strategies have been extensively
explored. Encouraging observations suggest that an antisense oligonucleotide- based approach can be effective in
humans. The nature of the degenerative process in HD
has also led to much research on cell replacement strategies, as in PD. For recovery of normal movement, complete
restoration of striatal efferent circuits is required. Foetal
striatal cells have been commonly used for transplantation
220 SYSTEMS OF THE BODY
10
in animal models of HD. Encouraging results have led to
trials in patients using autografts or xenografts (porcine
donors). There is evidence that grafts of foetal striatal cells
implanted in the striatum of patients with HD may survive
and lead to long- lasting cognitive and motor improvement. The use of stem cells, including induced pluripotent
stem cells, is also under investigation and offers additional
hope for the treatment of this devastating disease.
Self- assessment case study
A 37- year- old shipyard welder was brought to the general practitioner by his wife. He had always been very
good- natured and of an even disposition. According to
her, his behaviour had altered a lot lately: he had become
irritable and aggressive, especially with his close family, and had memory lapses. He had also started moving his arms and hands in a strange, jerky, unpredictable
manner. His 82- year- old mother said that he reminded
her of his paternal grandfather, who had ‘turned funny’
at about the same age, and showed similar symptoms
before he died in a car accident.
On examination, the patient seemed slightly disoriented,
but speech, comprehension and memory appeared normal.
There were no abnormal eye movements, and pupils were
equal and reactive to light. Vision and hearing were normal. His facial expression was symmetrical. Deep tendon
reflexes were normal. His hands, legs and feet were affected
by jerky movement, which gave him a ‘dance- like’ appear-
ance. Superimposed on these jerky movements was a slow,
writhing movement of the arm. He was obviously trying to
hide the existence of these movements, pretending that they
were part of normal, purposeful ones.
After studying this chapter, you should be able to
answer the following questions:
1. What is the most likely cause of this patient’s
symptoms, and what is the diagnosis?
It is likely that this patient has Huntington’s disease,
judging by the specific type of abnormal movements displayed. There is a clear indication of an inherited aspect
of his condition.
2. What are the treatment options for this patient?
At present, treatment options are mostly symptomatic.
The loss of striatal efferent pathways is accompanied
by a hyperdopaminergic state, particularly in the earlier stages of the disease. Tetrabenazine, a synaptic vesicle monoamine transporter inhibitor, could be used to
decrease dopaminergic tone. Dopaminergic antagonists
could also be used to this effect. Antidepressant drugs
can be used throughout the disease.
3. What is the expected course and prognosis of this
disease?
This is a terminal neurodegenerative disease. The
patient will deteriorate gradually, and death will occur
approximately 15–20 years after diagnosis.
MOTOR SYSTEMS II: THE BASAL GANGLIA
221THE NERVOUS SYSTEM
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STROKE AND HEAD
INJURY
Chapter summary
1. Stroke is a generic term for a brain injury that has a vascular origin.
The majority of strokes are ischaemic and the consequence of a
loss of blood supply in various areas of the central nervous system
(CNS). A minority of stroke presentations are due to haemorrhage.
Both types of strokes are associated with significant and longlasting consequences for individuals. The neurological deficits are a
reflection of the functions associated with the brain areas where the
vascular supply is disrupted by ischaemia or haemorrhage. Temporary
disruptions in blood flow, such as in transient ischaemic attacks
(TIAs), lead to temporary deficits.
2. Blood is supplied to the brain via anterior and posterior arterial
circulations; the former supplies the supratentorial structures,
whereas the latter supplies the posterior fossa structures. Venous
drainage occurs through superficial and deep veins that drain into
the various venous sinuses and the internal jugular vein.
3. The pathophysiology cascade of stroke includes a wide
range of different mechanisms, for example, excitotoxicity,
increased oxidation, disruption of cerebral metabolism and
neuroinflammation, which compound the initial cell loss and expand
the area which is initially compromised by the vascular accident.
11
4. Several factors can modify the risk of stroke. They include atrial
fibrillation, hypertension, smoking, a diet rich in saturated fat, age,
sex, ethnicity and previous strokes or TIAs.
5. Head injury can present with various levels of severity. One of the
immediate consequences of traumatic injury to brain tissue incurred
during a head injury is the swelling of brain tissue. Cerebral oedema
can be vasogenic or cytotoxic. The increased cranial pressure
associated with oedema can lead to herniation and ultimately death,
because of compression of the brainstem and the compromise of
11
vital functions. The pathophysiology of traumatic brain injury shares
many similarities with the pathophysiology of stroke.
6. Traumatic brain injury, even as a single occurrence, can enhance
the risk of neurodegenerative disease later in life. Repetitive mild
concussion, such as that incurred during sports or in a military
context, for example, upon repeated exposure to blast waves linked
to explosions, can lead to chronic traumatic encephalopathy, a
distinct form of neurodegeneration which is accompanied by major
STROKE AND HEAD INJURY
changes in mood, behaviour and cognition.
7. The acute period following a stroke or traumatic brain injury offers
a window of opportunity for intervention with neuroprotective
agents. However, various compounds that have shown efficacy in
experimental studies have failed to show efficacy in clinical trials.
Specialist rehabilitation regimes, which harness brain plasticity
and compensatory mechanisms, can support the recovery of some
neurological function after stroke or traumatic brain injury.
Introduction
The blood supply to the brain provides it with oxygen,
nutrients and a means to excrete metabolic waste. If the
blood supply is interrupted in any way, devastating
consequences can ensue. The brain has high metabolic
demands and the capacity for anaerobic metabolism is
minimal; interruption of the oxygen supply for a few
minutes can cause irreversible damage. The vascular
system is a supporting system, and diseases of vascular
origin will cause secondary alterations in other systems
such as the central nervous system (CNS). Vascular disease is often identified by its characteristic temporal
profile of sudden onset, with the rapid appearance of
specific combinations of neurological symptoms.
A stroke, or cerebrovascular accident, is characterized
by a temporary, or permanent, loss of function of brain
tissue caused by disruption of the vascular supply. Brain
infarctions (ischaemic stroke) account for approximately
85% of strokes, and cerebrovascular haemorrhagic accidents, such as subarachnoid or intracerebral haemorrhages, account for the remaining 15%.
Stroke is the second largest cause of death worldwide
and the fourth in the UK. Approximately one third of
stroke patients die within a year after stroke. In the UK,
someone has a stroke every 5 min, and approximately
100,000 people have a stroke each year, 38,000 of whom
will die. In the USA there are approximately 750,000
strokes per year, with 160,000 deaths. The incidence
and mortality rate are higher in older patients and the
mortality rate increases with subsequent strokes. There
Box
11.1
Mr Arthur Attack is a 71- year- old who arrives at Accident
and Emergency accompanied by his wife. Mrs Attack says
that he had just finished his fried breakfast 2 hours ago
and was doing nothing in particular when suddenly, midconversation, he became unable to speak. Arthur appears
perfectly aware of his surroundings but is unable to understand anything that his wife or the doctor say to him or
write down for him. Arthur has difficulty in speaking and
when he does speak the speech is unintelligible. On examination, he weighs 108 kg and is hypertensive. Neurological
examination reveals increased reflexes and some weakness
of his right arm and face; somatosensation on the right
side of his face and arm is also absent. His doctor tells his
wife that he has just had a stroke and he is immediately
prescribed a drug called alteplase (t- PA). Ten days later,
there has been some improvement in his condition. All sensation has returned and he is now able to understand verbal and written commands. However, he is still unable to
speak properly, and the motor symptoms remain.
1. What are the main causes of stroke?
2. What is the blood supply to the brain?
3. How does the main arterial blood supply relate to the
4. What are the mechanisms underlying cell injury in
5. What is the prognosis for this patient?
Case history
This case gives rise to the following questions:
main functional areas of the cerebral cortex?
stroke and how does this influence treatment?
224
SYSTEMS OF THE BODY
11
are approximately 1.2 million stroke survivors in the
UK. The cost of stroke to the National Health Service
in the UK is estimated to be over £3.4 billion and this
is expected to rise over the next 20 years. Stroke is the
single largest cause of disability, and a third of people
suffering from a stroke have a long- term disability. The
proportion of care home residents who have had a stroke
is between 25% and 45%.
Head (or traumatic brain) injury accounts for approximately 1% of deaths in developed countries, one third
of all trauma deaths and up to one half of road traffic
accident- related deaths. Traumatic brain injury is the
leading cause of death in young people and it increasingly affects the older population, because of the current
demographic shifts that show that the world population
is ageing. US studies suggest that the age- adjusted rate
of hospitalization for non-fatal traumatic brain injury
in the general population is 61/100,000, whereas for
those aged 65 years and older this rate is 156/100,000,
with falls being responsible for over 50% of cases. In
the USA alone, in the 21st century, the elderly population will double to 70 million by 2030, and the costs of
caring for older adults with traumatic brain injury, in
monetary and human terms will be staggering, as it
costs approximately 2.2 billion dollars a year to treat this
population. Approximately 50 million people experience
traumatic brain injury worldwide in a year and the estimated economic cost of this is approximately US$400
billion. Traumatic brain injury is, like stroke, a common
cause of death and disability. The sequelae can be very
long- lasting and, in many cases, permanent and life
changing. In the USA there were approximately 61,000
traumatic brain injury- related deaths in 2019. In the UK,
for every 100 survivors, 60% make a good recovery, 20%
have minor psychiatric/psychological problems, 15% are
severely disabled and 5% remain in a persistent vegetative state. The mortality rate is approximately 30 people
per 100,000. There is considerable overlap in the neurological symptoms presented by patients with head injury
and those with cerebrovascular disease.
This chapter describes the vascular supply to the brain
and how it is visualized using angiography. Following
stroke, it is important to identify the type of stroke,
minimize its size and evaluate what treatment options
are available to prevent the problem from reoccurring,
and to maximize recovery of function after the event.
Similarly, acute head injury management aims to control
secondary mechanisms of injury: hypoxia, haemorrhage
and raised intracranial pressure.
Physiological control of cerebral blood flow
Brain cells are dependent on aerobic metabolism for their
survival; if the brain tissue is deprived of oxygen for
20 s (anoxia), an individual lapses into unconsciousness,
as the affected neurons cease electrical activity. This can
become irreversible if anoxia extends beyond 5 min. It
takes longer for this process to occur in the brainstem
and spinal cord. The brain represents approximately 2%
of body weight but uses 20% of the available oxygen and
15% of the cardiac output. Blood flow is approximately
750 mL/min and this remains constant throughout the
day, whether we are asleep, awake, lying down or standing up. The average blood flow is 50–55 mL/100 g of
brain tissue/min. If this falls to less than 30 mL/100 g/
min, ischaemia (lack of bloodborne oxygen) ensues and
infarction (tissue cell death) occurs below 20 mL/100 g/
min.
The factors that determine constant blood flow are
blood perfusion pressure and the vascular resistance.
The cerebral perfusion pressure is defined as the mean
arterial pressure minus the intracranial pressure, rather
than cerebral venous pressure. This is because the brain
is enclosed within the skull; it is the pressure within
this ‘closed box’ that is effectively acting on the arteries and thus is the one that opposes arterial pressure.
The cerebral perfusion pressure does not always remain
constant, and as mean arterial pressure is closely regulated within a narrow range, changes must occur in the
cerebral vascular resistance to compensate for changes
in perfusion pressure. This occurs through mechanisms intrinsic to the brain: when perfusion pressure
decreases, vascular pressure decreases; if perfusion pressure increases, so does the resistance. Cerebral blood
flow is kept relatively constant by several processes.
Metabolic mechanisms involve the action of vasodilating agents such as adenosine, K+, H+ and nitric oxide
(NO), which regulate arteriole size. Autoregulation is a
major homeostatic mechanism whose function is to keep
blood flow constant over the pressure range 60–150
mmHg. It is closely related to local metabolic processes,
and uses chemical and neurogenic mechanisms to control pressure, the most important being the levels of
carbon dioxide and oxygen. Hypoxia or hypercarbia
cause an increase in cerebral blood flow, whereas hypocarbia causes a decrease in blood flow, by relaxing or
constricting the arteriole smooth muscle. These changes
are brought about by alterations in the H+ concentration in the extracellular fluid compartment surrounding
the blood vessels. Another source of autoregulation is
the level of intraluminal pressure within the arterioles.
Any increase in pressure produces a direct, myogenic
response that is sufficient to maintain a steady state of
perfusion. These processes are not controlled by the
sympathetic nervous system, as drugs that affect blood
pressure do not, in general, have any effect on cerebral
blood flow.
Too much oxygen can also have deleterious effects on
brain cells. Increased levels of extracellular oxygen can
lead to the formation of free radical ions, such as superoxide (O
of excitotoxicity (see later). Free radicals also destabilize
neurotransmission by changing tissue pH and this can
increase auto- oxidation, which can further exacerbate the
toxicity. In the case of glutamate, increased extracellular
accumulation of glutamate depletes antioxidant defences
and thus causes oxidative glutamate toxicity.
–
), which can damage brain cells by the process
2
STROKE AND HEAD INJURY
THE NERVOUS SYSTEM
225
11
circulation
circulation
Anterior
communicating artery
communicating artery
communicating
communicating
Brachiocephalic
= Anterior circulation
Not all areas of the brain are equally active at the same
time. Oxygen is shunted around to areas (and cells) that
need it most for a particular task at a particular time,
because they are more metabolically active. For example,
there is relatively more blood flow to the motor cortex
when someone is performing a motor task. This suggests that blood is shunted around to whichever area
needs it. A consequence of this is that areas that are not
actively processing information have a decreased blood
flow. This observation has led to the development of
brain scan techniques that measure regional cerebral
blood flow to functionally active areas, following injec-
STROKE AND HEAD INJURY
tion of a radioactive isotope of the inert gas xenon (
into an artery. This was the first method used to provide
detailed insight into how various brain areas function in
normal and pathological conditions, because of the direct
relationship between blood flow and cellular metabolic
activity.
Blood supply to the brain
133
Xe)
= Posterior circulation
= Central nervous
system
Posterior
cerebral artery
Basilar artery
Vertebral artery
Middle
cerebral artery
Anterior
artery
Posterior
artery
Carotid siphon
Internal
carotid artery
External
carotid artery
Common
carotid artery
Blood circulation to the brain is via the anterior and
posterior circulations. The anterior circulation supplies
supratentorial structures (the cortex and diencephalon),
whereas the posterior circulation supplies the structures in the posterior fossa (cerebellum and brainstem).
Both arterial circulations initially arise from the aortic
arch, but the posterior circulation enters the skull cavity
through the foramen magnum, while the anterior circulation enters through the foramen lacerum (Fig. 11.1).
The anterior circulation carries 80% of the blood supply to the brain. It is derived from the internal carotid
arteries (ICAs), which branch off from the common
carotid arteries and enter the brain cavity through the
carotid canal (in the skull vault) to emerge on its interior
surface via the foramen lacerum (which is only visible
in a dried skull, as in life it is filled with cartilage). The
arteries make a series of stepwise turns, passing through
the cavernous sinus, before emerging, on each side, next
to the optic chiasm, where they divide into their major
branches, the middle cerebral artery (MCA) and anterior cerebral artery (ACA). The anterior communicating
artery connects the two anterior cerebral arteries. The
posterior circulation comprises the vertebral, basilar
and posterior cerebral arteries (PCAs) and they convey
the remaining 20% of the arterial supply to the posterior
fossa brain structures and inferior surface of the posterior aspects of the cortex.
The anterior and posterior circulations are connected
at the base of the midbrain around the optic chiasm
by a network of arteries called the circle of Willis, first
described by Thomas Willis, doctor to King James II, in
1664. The arteries that form the circle of Willis are a single anterior communicating artery, a pair of ACAs, ICAs,
PCAs and a pair of posterior communicating arteries
(Fig. 11.2). There is a substantial amount of anatomical
variation between individuals in the arrangement of this
circle, due to developmental changes. During embryonic
artery
Fig. 11.1 Anterior and posterior circulation to the head. (Adapted
from McNeill EM. (1997) Neuroanatomy Primer, Colour to Learn.
Lippincott, Williams and Wilkins.)
Anterior
Optic
chiasm
Posterior
Fig. 11.2 Schematic view of the circle of Willis.
Subclavian
artery
Aorta
cerebral artery
Anterior
Internal carotid artery
Middle
cerebral artery
Posterior
Posterior
cerebral artery
Basilar artery
Vertebral artery
development the ICA supplies the ACA, MCA and PCA,
but as the brain develops, the PCA develops from the
basilar artery, as the posterior communicating artery
atrophies. However, in approximately 20% of people, the
embryonic pattern remains and the PCA branches off the
226 SYSTEMS OF THE BODY
11
anterior circulation. Common variations in the circle of
Willis include absence of one or both posterior communicating arteries, origination of the PCAs from an enlarged
posterior communicating artery or multiple small anterior communicating arteries. These anastomoses allow
for a certain amount of shunting of blood from the anterior to posterior circulation, or from one side to the other
in the event of arterial occlusion, but generally the anastomoses are not effective against total occlusion of one of
the major supply arteries.
Main terminal branches of the anterior system
The ICA gives rise to several small branches at its proximal portion before dividing into its two main terminal
branches—the MCA and ACA. The hypophysial artery
forms a plexus around the pituitary stalk. The ophthalmic
artery is the most proximal branch of the ICA. It supplies
the orbit, the eye muscles and the retina and eventually
connects to the external carotid (facial and superficial
temporal) arteries through anastomoses with arteries of
the forehead and nose (ethmoidal, nasal, supraorbital and
supratrochlear). Occlusion of the ophthalmic artery is an
important diagnostic sign in transient ischaemic attacks
(TIAs) (Box 11.2). Another artery that is important in providing anastomoses between different arterial systems
is the posterior communicating artery, which links the
carotid and vertebral systems. Clinically, this is one of the
most frequent sites for aneurysm formation, at the junction where it leaves the ICA (see later).
The MCA is the largest and most important branch of
the ICA and receives 80% of the carotid blood flow (Fig.
11.3). Its proximal part gives off three deep branches. The
lateral and medial striate arteries supply the striatum
and the internal capsule regions of the brain. Occlusion
of these deep arteries is the chief cause of classic stroke,
and the most common location is the putamen and internal capsule. The anterior choroidal artery supplies parts
of the limbic system, the hippocampus and amygdala in
the medial temporal lobe, the posterior part of the internal capsule and the optic radiation and choroid plexus
of the inferior horn of the lateral ventricle, which is
important in the formation of cerebrospinal fluid (CSF).
Occlusion of this artery may cause hemiparesis, hemianaesthesia, hemianopsia and loss of short- term memory.
The more distal part of the MCA travels laterally
through the lateral fissure and then separates into superior and inferior branches that supply most of the lateral
side of the brain (frontal, parietal, temporal and occipital
regions). This ramification is known as the middle cerebral
candelabra (from angiographic studies). The branches are
named with respect to the cortical region that they supply
(see Fig. 11.3).
The ACA supplies the medial side of the frontal and
parietal lobes as far back as the parieto- occipital sulcus
and overlaps onto the orbital and lateral surfaces of the
brain. It winds around the genu of the corpus callosum
before dividing into two main terminal branches. The
callosomarginal artery supplies the cingulate and fron-
Box
11.2
There are temporary disturbances of blood flow to localized brain areas that can spontaneously resolve and leave
no neurological deficits. It is important to recognize these,
as they serve notice of impending major illness. Without
treatment, one in four people suffer a heart attack within
5 years, and one in six suffer a stroke.
brain function, lasting less than 30 min, with total recovery
within 24 h; there is rarely loss of consciousness. It is possible to have several attacks in one day. Reversible ischaemic neurological defects are lengthy TIAs that continue for
more than 12 h before symptoms resolve. It is thought that
the majority of these are caused by emboli that break off
atherosclerotic plaques. The diagnosis is based on symptoms alone. The symptoms mimic those of true strokes,
and severe TIAs cannot be distinguished from real strokes
until recovery occurs. They can occur in both the anterior
and the posterior circulation. A TIA of the posterior circulation produces symptoms of vertigo, diplopia, ataxia and
amnesia, whereas a TIA in the anterior circulation produces
symptoms of motor weakness, hemisensory loss, dysphasia,
difficulty in reading and writing, and transient monocular
blindness (amaurosis fugax). This last symptom is due to
occlusion of the ophthalmic artery. It is an important neurological sign, as it reflects proximal blockage of the internal carotid artery.
in the morning on waking up, as blood pressure is lowered
during sleep. When a person gets out of bed, the sudden
change in pressure can dislodge an embolism into the arterial circulation.
Reversible strokes
Transient ischaemic attacks (TIAs) cause temporary loss of
Ischaemic strokes and TIAs are more likely to occur early
tal gyri and the paracentral lobule (Fig. 11.4). The pericallosal artery supplies the corpus callosum. On the
lateral surface of the brain, its branches anastomose
with terminal branches of the MCA. The ACA gives off
one proximal branch, the recurrent artery of Heubner,
which supplies the ventral part of the basal ganglia and
the anterior limb of the internal capsule. It anastomoses
with the lateral striate arteries of the MCA. Occlusion of
this artery is rare but can cause ‘clumsy hand’ syndrome,
with contralateral weakness of the arm and face.
Main terminal branches of the posterior system
The vertebral arteries originate from the subclavian and
brachiocephalic arteries and pass through the transverse
foraminae of the C1–C6 vertebrae, before entering the
skull cavity via the foramen magnum, to travel along the
ventral surface of the brainstem. The main branches are
the anterior and posterior spinal arteries, which supply
the spinal cord (see Chapter 4), and the posterior inferior cerebellar artery, which supplies the medulla and
cerebellum. The two vertebral arteries join to form the
STROKE AND HEAD INJURY
227THE NERVOUS SYSTEM
11
Planes of section
Sagittal Coronal Axial
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. 11.3 Distribution of the middle cerebral artery in the sagittal (A–E), coronal (F–I) and horizontal (J–M) planes.
basilar artery at the pontomedullary junction. The basilar
artery runs in the basilar sulcus on the ventral surface of
the pons and ends at the midbrain, where it divides to
form the PCA, which travels along the ventral surface of
the midbrain, passing around cranial nerve III, to anastomose with the posterior communicating artery. Details
of the blood supply to the brainstem are described in
Chapter 6. The deep cortical branches of the PCA sup-
ply the thalamus and posterior limb of the internal capsule (via the thalamogeniculate and posterior choroidal
arteries). Other branches supply the inferior and medial
surfaces of the temporal lobe (limbic region) and the
occipital lobe. The main terminal branches are the calcarine and parieto- occipital arteries. Terminal branches
of the PCA extend onto the lateral surface of the brain
to anastomose with terminal branches of the MCA (Fig.
11.5).
Venous system
Cerebral drainage is through valveless superficial and
deep veins (Fig. 11.6). The superficial veins are located
in the subarachnoid space above each hemisphere; they
collect blood from the neocortex and subcortical white
matter and empty into the cranial venous sinuses. The
upper part of the hemisphere drains via the superior
cerebral vein into the superior sagittal sinus, the middle
part (via the inferior cerebral veins) into the cavernous
sinus and the lower part into the transverse sinus. The
deep cerebral veins that drain blood from the caudate
nucleus and thalamus (thalamostriate and choroidal
veins) join to form the internal cerebral vein on each side
and these unite to form the great cerebral vein of Galen.
The anterior and deep cerebral veins unite to form the
basal vein, which also empties into the great cerebral
vein. This pierces the tentorium cerebelli to join with
the inferior sagittal sinus, which drains the falx cerebri and then joins with the straight sinus that connects
to the transverse sinus. The cavernous sinus drains into
the transverse sinuses via the petrosal sinuses. The two
transverse, the straight and the superior sagittal sinuses,
meet at the confluence of sinuses. Blood drains away
‘downhill’ through the transverse sinuses to the sigmoid
sinus and into the internal jugular vein (at the jugular foramen). The internal jugular vein receives venous
drainage from the face, scalp and neck, before draining
228 SYSTEMS OF THE BODY