CEREBROVASCULAR DISEASES

Kopchak O.O.

Head of the Department of Neurology, Psychiatry and

Physical Rehabilitation of
Kyiv Medical University
 Mission, Vision and Values
of the University
Mission
To teach, research, treat and serve
humanity, constantly striving for
perfection
Vision
Transform the health care system for the benefit of
people and communities and become a national leader
in the training of health professionals

Values
Perfection, innovation, devotion, integrity,
respect, responsibility
 CEREBROVASCULAR DISEASES
• Vascular diseases of the nervous system are amongst the most frequent
causes of admission to hospital.
• Better control of hypertension, reduced incidence of heart disease and a
greater awareness of all risk factors have combined to reduce mortality
from stroke. Despite this, stroke still ranks third behind heart disease
and cancer as a cause of death in affluent societies

• Prevention of cerebrovascular disease is more likely to reduce death and

disability than any medical or surgical advance in management.
Prevention depends upon the identification of risk factors and their
correction. Increasing age is the strongest risk factor (but is not
amenable to correction).
 Anterior cerebral
Anterior communicating
Middle cerebral

Posterior communicating Internal carotid

Posterior cerebral
Basilar

Vertebral

Circle of Wills
 The anatomy of the
blood vessels supplying Posterior
circulation
the brain can be
subdivided according to Basilar
vessel size Vertebral

(large or small)
and vessel site
(anterior or posterior)
(Fig. 1): Posterior
anterior and posterior cerebral

circulation. Basilar

Vertebral

Fig. 1 Anterior and posterior arterial circulation.

■
Anterior circulation:

large vessels: the
internal carotid artery Posterior
(ICA) and its main circulation
branches, the middle
(MCA) and anterior Basilar
(ACA) cerebral arteries

small vessels: branches Vertebral
from the MCA and
ACA.

■
Posterior circulation:

large vessels: the
vertebral arteries, Posterior
which join to form the cerebral
basilar artery and its
Basilar
main branches, the
posterior cerebral
arteries Vertebral

small vessels: branches
from all these vessels. Fig. 1 Anterior and posterior arterial circulation.
 Posterior
The anterior circulation circulation

supplies the anterior Basilar

two-thirds of the Vertebral
cerebrum, while the
posterior circulation
provides the supply for
the occipital lobes of the Posterior
cerebral
cerebrum and the brain
Basilar
stem and cerebellum
(Fig. 1). Vertebral

Fig. 1 Anterior and posterior arterial circulation.

 RISK FACTORS

Hypertension
Hypertension is a major factor in the development of thrombotic cerebral
infarction and intracranial haemorrhage.
A 6 mmHg fall in diastolic blood pressure is associated in relative terms with a
40% fall in the fatal and non-fatal stroke rate.
Systolic hypertension (frequent in the elderly) is also a significant factor and
not as harmless as previously thought.
Cardiac disease
Cardiac enlargement, failure and arrhythmias, as well as rheumatic heart
disease, patent foramen ovale and, rarely, cardiac myxoma are all associated
with an increased risk of stroke.
Diabetes
The risk of cerebral infarction is increased twofold in diabetes. More effective
treatment of diabetes has not reduced the frequency of atherosclerotic
sequel.
 RISK
Heredity FACTORS
Close relatives are at only slightly greater risk than non-genetically related family
members of stroke patient. Diabetes and hypertension show familial propensity thus
clouding the significance of pure hereditary factors.
Blood lipids, cholesterol, smoking, diet/obesity
These factors are much less significant than in the genesis of coronary artery disease.
Haematocrit
A high blood haemoglobin concentration (or haematocrit level) is associated with an
increased incidence of cerebral infarction. Other haematological factors, such as
decreased fibrinolysis, are important also.
Oral contraceptives
Combined oral contraception (COC) containing high dose of estrogen increased the risk
of thrombosis, including stroke. The effect of low dose of estrogen COC is less clear.
 Transient ischaemic attacks and prevention of strokes

A transient ischaemic attack (TIA) is an acute loss of

neurological function or monocular vision caused by ischaemia
(temporary blockage of blood flow to the brain) with symptoms
lasting few minutes (less than hour).
This occurs in 10% of patients prior to the development of a
stroke. The annual incidence is 30 per 100 000.
A TIA is caused by artery-to-artery emboli or cardiac emboli.
The pathogenesis is the same as for embolic stroke. The
investigation and management of TIAs and small strokes from
which a good recovery has been made is the same because both
provide a potential opportunity to prevent a more major stroke.
 Clinical features
Anterior circulation TIAs include:
■
amaurosis fugax (fleeting blindness) - loss of vision in one eye, like a shutter
coming down’
■
aphasia, or other language problems such as dyslexia or dysgraphia.
Amaurosis fugax (Latin fugax meaning fleeting,
Greek amaurosis meaning darkening, dark, or
Posterior circulation TIAs include: obscure) is a painless transient
monocular or binocular visual loss (i.e., loss of vision
■
homonymous visual field loss in one or both eyes that is not permanent).
■
dysarthria
■
combined brain stem symptoms: vertigo, diplopia, dysphagia; these are rarely
TIAs if they occur in isolation
■
bilateral weakness or sensory loss.

Anterior or posterior circulation TIAs include:

■
unilateral weakness affecting the face, arm or leg in isolation or combination
• a unilateral sensory loss affecting the face, arm or leg in isolation or
combination.

The onset is usually rapid over seconds or minutes. The resolution is more variable,
with complete recovery in minutes to the full 24 h.
 Differential diagnosis
Most TIAs are sufficiently clear-cut for a confident clinical diagnosis to be
made. The conditions that produce similar presentations include the
following:
■
Migraine: there is usually a slower progression of the
neurological deficit, taking 15-30 min to develop; there are usually
positive symptoms such as flashing lights or marked tingling
associated with this. There is usually an associated migrainous
headache.
• Partial seizures: these are usually much shorter lived, lasting
seconds to a few minutes; when they recur they are very
stereotyped.
■
Transient global amnesia: this causes profound anterograde
amnesia, lasting hours, with normal physical function.
■
Intracranial lesions: these usually produce progressive deficits;
occasionally they may produce intermittent symptoms.
■
Metabolic changes: hypoglycaemia can produce transient
neurological deficits.
■
Peripheral nerve lesions: for example, carpal tunnel syndrome
produces intermittent sensory loss in the hands.
 Diagnostics and differential diagnosis
Most TIAs are sufficiently clear-cut for a confident
clinical diagnosis to be made.
Diagnosis of TIAs depends on the history.
Examination of a patient following a TIA usually
reveals no neurological abnormalities
Fundoscopy (Occasionally a cholesterol embolus
is seen on fundoscopy)
 Blood analysis (blood lipids, cholesterol, glucose
level, haemoglobin concentration, haematocrit level
and so on)
 Ultrasound Doppler of the head and neck ateries
Transient ischaemic attacks and prevention of strokes

■ Diagnosis of TIAs depends on the history.

■ 10% of patients have a TIA prior to having a stroke.

■ Management relies on understanding the pathophysiology of

the TIA.

■ Management includes control of vascular risk factors and use of

aspirin, and in selected patients, anticoagulation or carotid
endarterectomy.
 Stroke
Stroke refers to damage to the brain caused by abnormalities of blood supply.
This presents with a rapidly developing focal neurological deficit, which may lead to
coma or death.
If this deficit lasts less than 24 h it is referred to as a transient ischaemic attack .

•Stroke is the third most common cause of death in developed countries.

•The incidence of first stroke is 2 per 1000 per year. The incidence increases with
age. It is rare below 45 years of age and increases from 2 per 1000 per year for
people aged 45-54 years to 10 per 1000 per year for those aged 65-74 years and to
about 30 per 1000 per year in those aged over 80 years.
•About a quarter of these patients will be dead within 6 months (the majority of
these within 1 month). Stroke is a major cause of disability; after their first stroke,
40% of surviving patients will be dependent at 6 months.
 Factors that increase the risk of stroke include the following:
o Advanced age.
o Positive family history with early onset of atherosclerotic disease (< 55
years).
o History of cardio- or cerebrovascular disease or peripheral arterial
occlusive disease.
o Arterial hypertension.
o Sedentary habits.
o Obesity.
o Hypercholesterolemia.
o Diabetes mellitus.
o Sleep apnea syndrome.
o Cigarette smoking.
o Alcoholism.
o Estrogen use (estradiol, mainly in combination with cigarette smoking).
o Migraine with aura.
o Heart disease, especially atrial fibrillation or flutter.
Stenosis of the cerebral vesseles, especially the internal carotid artery
 Cerebral ischemia can be classified according to:
Etiology, Course, Severity, Based on the caliber of the vessels involved.
Etiology:

A system for categorization of subtypes of ischemic stroke mainly based on

etiology has been developed for the Trial of Org 10172 in Acute Stroke Treatment
(TOAST).
The TOAST classification denotes five subtypes of ischemic stroke:
•large-artery atherosclerosis,
•cardioembolism,
•small-vessel occlusion,
•stroke of other determined etiology
 
Cerebral infarction results from an interruption in blood supply to an
area of the brain.
This can be due to :
emboli (30% of all strokes)
thrombosis (30%)
small vessel disease (20%).
 
 Thrombotic
Thrombosis
strokes arises in three main circumstances.

Abnormality in the vessel wall. Thrombosis usually occurs in the context of atheroma, which
produces stenosis and irregularities in the vessel wall from which thrombosis can propagate.
More rarely, thrombosis can occur in inflammatory arterial diseases, such as temporal arteritis,
systemic lupus erythematosus, rheumatoid arthritis and other rarer diseases.

Abnormal tendency of the blood to thrombose. Thrombosis can also occur when there is a
predisposition to clotting, for example polycythaemia, thrombocythaemia, sickle cell disease
and coagulation disorders that result in thrombophilia (e.g. protein C and S deficiencies and
antiphospholipid syndrome).

Stasis of the blood flow. Stasis usually occurs in association with severe atheromatous
stenosis. An arterial dissection can arise if the intimai lining of an artery is torn, then blood can
track beneath this layer in the wall. This produces a stenosis of the vessel and potential stasis
and may lead to thrombosis. This is the commonest identifiable cause of stroke in young
adults.
 Stenosis can develop and proceed to occlusion of a vessel without resulting in cerebral ischaemia.
The atheromatous plaque can lead to cerebral ischaemia in several ways:
■ It can produce a stenosis that is not compensated for by anastomoses.
■ The plaque may ulcerate and fragments can act as emboli.
■ The base of an ulcerated plaque is irregular and may act as a focus for propagation of thrombus.

■ Haemorrhage into an ulcerated plaque can produce a rapidly developing stenosis or

occlusion.

Embolic strokes
An embolus is an abnormal particle within the bloodstream that can lodge in, and block,
blood vessels. Emboli commonly arise from either the heart or the proximal arteries in the
neck. The most common sources of emboli from the heart include thrombus from atrial
fibrillation, mural thrombus following myocardial infarction and left ventricular dilatation.
Rare embolic sources include bacterial vegetations in subacute bacterial endocarditis,
calcium from heart valves or fragments from an atrial myxoma.
Emboli from the heart account for about 10% of all strokes.
 Severity:
The severity of cerebral ischemia is correlated with its clinical course
if untreated.
The National Institutes of Health Stroke Scale is used to assess the
severity of stroke:
• mild stroke - NIHSS score ≤5;
• moderate stroke - NIHSS score 5-14;
• severe stroke - the NIHSS score 15-24
• very severe ≥ 25.
The NIHSS is a 42-point scale.
Patients with minor strokes usually have a score of less than 5. 
 Based on the caliber of the vessels involved:
 Territorial Infarction:
• mainly produced by occlusions of the main trunks or major branches of cerebral arteries
(cerebral macroangiopathy) due to thrombosis, embolism, or other cause
• includes both cortex and subcortical white matter and sometimes the basal ganglia and
thalamus
 
 Watershed Infarction (border zone infarction)

 is of hemodynamic origin due to macroangiopathic processes;

 perfusion is impaired in the vulnerable regions at the borders between the territories of
two or more arteries.
 Lacunar Infarction

 caused by microangiopathy due to hypertension;

 less than 1.5 cm in diameter and often multiple;
 found mainly in the basal ganglia, thalamus, and brainstem, and sometimes in the
cerebral cortex and subcortical white matter;
 the clinical presentation depends on their number and localization.
 Pathologic Consequences of Cerebral Ischemia
Signs and symptoms of ischemia begin to appear when the perfusion falls
below 20 mL per 100 g per minute.
The functional metabolism of the a ffected brain tissue is impaired, but it can
regain its normal function as soon as the perfusion renormalizes, because the
infarction threshold has not yet been crossed.
The longer this ischemia lasts, the lower is likelihood of the regaining of the
normal function.
The ischemic penumbra is the zone of tissue in which the local cerebral
perfusion lies between the functional threshold and the infarction threshold.
Brain perfusion within the penumbra is linearly related to the arterial blood
pressure.
The penumbra is of great importance in the diagnostic evaluation of stroke,
in therapeutic decision-making and prognosis.
Within the penumbra there is perfusion–diffusion mismatch: perfusion is
decreased, but diffusion is still normal, which can be recognized on the MRI. There
is a high correlation between the extent of spontaneous neurological recovery and
the volume of penumbra that escapes infarction; therefore, saving the penumbra
should improve the clinical outcome.
Prolonged ischemia leads to irreversible structural damage of the a ffected
brain’s region.
Cellular metabolism collapse starts, the water—flows into the cells due to
the sodium/potassium pump impaired function, that in turn causes cytotoxic
cerebral edema.
 Clinical features

A common feature of all strokes is the onset.

The neurological deficit comes on over a short time, from seconds to a
progression over hours.
The clinical manifestations of stroke depend on the area of the brain affected,
which in turn depends on which blood vessel is affected.
A simple syndromic classification divides strokes into the following
categories, which have important differences in terms of pathogenesis,
treatment and prognosis:
Total anterior circulation stroke.
Partial anterior circulation stroke.
Posterior circulation stroke.
Lacunar stroke.
 Anterior circulation large vessel strokes

The middle cerebral artery (MCA)supplies most of the motor and sensory cortex,
including that controlling the contralateral arm and face, both Wernicke’s and Broca’s
areas in the dominant hemisphere, the internal capsule and optic radiation.
The anterior cerebral artery (ACA) supplies the motor cortex controlling the leg, the
frontal lobe and the corpus callosum.
Total anterior circulation stroke: can arise from a complete (MCA) infarct, from
internal carotid disease or massive intracerebral haemorrhage.
These strokes carry a high mortality and severe long-term morbidity.
Complete infarction of the area produces a devastating deficit:
•hemiparesis, affecting the arm, face and leg and a homonymous hemianopia;
•possible drowsiness initially with eyes averted away from the hemiparetic side;
•complete aphasia if the dominant hemisphere is affected;
•marked inattention or neglect if the non-dominant side is involved;
•transient dysarthria and swallowing may be impaired; incontinence.
Middle cerebral artery.
About half of all strokes affect the territory of the MCA.
The site of occlusion (main trunk vs. branch of the MCA) determines the clinical manifestations:
• mainly brachiofacial hemiparesis and hemisensory deficit
•homonymous hemi- or quadrantanopsia
•horizontal gaze palsy toward the side of the hemiparesis
•aphasia and apraxia (dominant hemisphere)
•impairment of spatial orientation (while one on the nondominant side).
An infarct involving a large percentage (or all) of the MCA territory can give rise to massive
cerebral edema and intracranial hypertension; this is called “malignant MCA infarction.”
In the aftermath of the stroke, if the hemiparesis fails to improve over time, or does so only
partially, a typical, permanent impairment of gait results: circumduction of the spastically
extended lower limb, flexion of the paretic upper limb at the wrist and elbow, and absence of arm
swing on the affected side (Wernicke–Mann gait).
Anterior choroidal artery:
•homonymous visual field defect;
• a hemisensory deficit;
•less commonly, hemiparesis.
•There may also be extrapyramidal motor signs, such as hemiballism.
Anterior cerebral artery.
•contralateral hemiparesis mainly affecting the lower limb,
•contralateral ataxia and,
•if the lesion is left-sided, by apraxia.
•there may be apathy, abulia (pathologic lack of drive and motivation)
•
Ophthalmic artery:
•amaurosis fugax (transient monocular blindness due to transient
ischemia),
•longer-lasting ischemia causes retinal infarction.
Retinal ischemia is often due to embolism of cholesterol crystals from
ulcerating plaques in the internal carotid artery into the ophthalmic
artery. Embolized crystals within the arteries of the retina can
occasionally be seen by ophthalmoscopy.
Internal carotid artery.
Stenosis or occlusion of the internal carotid artery can simultaneously
cause ischemia of the eye with monocular visual loss (as in ophthalmic
artery occlusion) and a large infarct in the territory of the middle cerebral
artery.
Ischemia in the territory of the internal carotid artery usually presents
with:
• monocular visual loss
•or variably severe hemiparesis
• neuropsychological deficits.
Partial anterior circulation stroke

Infarction in the territory of

one of the branches of the
middle cerebral artery (MCA)
produces different
combinations of deficits
depending on the affected
hemisphere.
 Territory of the Vertebral Arteries and Basilar Artery

Posterior cerebral artery. This artery is involved in 10% of all

ischemic strokes, often bilaterally (embolism). Proximal occlusion can
lead to infarction in the cerebral peduncle, the thalamus, mediobasal
portions of the temporal lobe, and the occipital lobe, with a similar
constellation of clinical findings to MCA occlusion.
Clinical signs:
•contralateral homonymous hemianopsia,
•neuropsychological deficits.
Thalamic infarction (results from occlusion of one of the perforating
arteries supplying the thalamus):
•contralateral hemisensory deficit
•mild paresis and hemiataxia.
• memory impairment.
Basilar artery (occlusion of the main stem or of a branch of the basilar
artery causes brainstem, cerebellar, and thalamic signs):
Main stem thrombosis generally causes tetraparesis and is often fatal.
Ventral pontine infarction can present clinically with locked-in
syndrome .
The basilar tip syndrome reflects a bilateral midbrain and thalamic
infarct, usually due to an embolus that becomes lodged in the distal
portion of the basilar artery proximal to its bifurcation into the posterior
cerebral arteries:
•impaired consciousness
• upward gaze palsy,
• uni- or bilateral hemisensory deficit,
•ataxia,
• uni- or bilateral hemianopsia,
•neuropsychological deficits such as amnesia and cortical blindness.
Nystagmus, dysarthria and diplopia are features that point to a brain
stem lesion.
Brainstem infarction (are usually lacunar).
They arise in the territory of one or more small perforating arteries that branch off the
basilar trunk and can be seen by MRI. Their clinical presentation depends on the
particular nuclei and fiber tracts that they affect
Brainstem stroke causes ipsilateral cranial nerve deficits and a contralateral
hemisensory defect and/or hemiparesis.
The most clinically relevant brainstem syndrome is Wallenberg syndrome, which is due
to occlusion of the posterior inferior cerebellar artery.
Territory of the Cerebellar Arteries
Occlusion of the superior, anterior inferior, or posterior cerebellar artery
presents with:
• vertigo
• nausea
• unsteady gait
• dysarthria
• acute headache.
The neurologic examination reveals ataxia, dysmetria, and nystagmus.
Not uncommonly, edema in and around the infarcted area rapidly leads to a life-
threatening elevation of pressure in the posterior fossa, with progressive impairment of
consciousness (with or without accompanying occlusive hydrocephalus).
 The diagnosis of stroke can be confirmed by CT or MRI scanning, which will
indicate whether the stroke is haemorrhagic.
Early CT scans can be normal, indicating that the stroke is ischaemic and not
haemorrhagic. MRI diffusion weighted images (DWI) can be used to
distinguish new from old ischaemic lesions.

Anterior cerebral
artery

Anterior
. circulation

Middle cerebral
artery

Posteri Posterior
or
circulation
Vascular supply of the brain in the projection commonly used for scanning. cerebral
 Posterior circulation strokes

Posterior circulation infarct: left cerebellar.

 Small vessel lacunar stroke

Intracerebral small vessel disease refers to the process of

lipohyalinosis (or microatheroma) that occurs in
penetrating and branch arteries, resulting in their
occlusion.

Lacunar strokes arise from occlusion of small branches of

both the anterior and posterior circulation vessels.
The lacunar syndromes are as follows:
Pure motor hemiparesis: face, arm and leg weakness with no other
•

deficits. Usually an internal capsule lesion.

Ataxic hemiparesis: motor hemiparesis with cerebellar type ataxia on
•

that side. Lesion site is variable: posterior internal capsule, midbrain or

pons.
Dysarthria/clumsy hand syndrome: marked dysarthria with tongue
•

and face weakness with hand clumsiness on the same side.

Pure sensory stroke: hemisensory loss of superficial sensation. Usually
•

thalamic lesions.
Sensorimotor stroke is a combination of sensory and motor strokes.
•
 Differential diagnosis

Space- occupying lesions (SOLs) are

usually more insidious in onset than Differential diagnosis of stroke
stroke, though some tumours can
present with a Vascular’ onset,
■
Intracranial space-occupying lesion
particularly if there is bleeding into
a tumour.

tumour
Cerebral abscesses have a more 
bleed into tumour
rapid progression than most SOLs
but the patient is usually unwell 
Abscess
and septic.
Chronic subdural haematoma is a • Subdural haematoma
very important diagnosis to
consider because of the need for ■
Multiple sclerosis
neurosurgical intervention. The
onset is usually slower and very ■
Flead injury
often the patient is mentally slower,
as well as exhibiting focal deficits, ■
Hypoglycaemia
and there may be signs of raised
intracranial pressure.
■
Seizures with Todd's paralysis
 Differential diagnosis
In younger patients, the onset of
multiple sclerosis can be mistaken
for a stroke and vice versa.
Differential diagnosis of stroke
Head injury is usually easily
diagnosed but sometimes it can be ■
Intracranial space-occupying lesion
difficult to tell whether the stroke
caused the fall or the head injury tumour


resulted in the neurological deficit,

particularly in elderly patients. bleed into tumour


Hypoglycaemia can produce focal Abscess



deficits and needs to be considered

early in the assessment of diabetics • Subdural haematoma
with neurological deficits.
A Todd’s paralysis, weakness in a ■
Multiple sclerosis
limb after seizure, may mimic a ■
Head injury
stroke. In addition, patients with
critical ischaemia, for example due to ■
Hypoglycaemia
severe carotid stenosis, can present
with focal seizures. ■
Seizures with Todd's paralysis

Haemorrhagic and ischaemic strokes cannot be reliably distinguished clinically.

 Treatment and prognosis

The treatment of patients with strokes aims to:

• give general medical support of the patient
■
minimize stroke size
■
prevent complications of stroke
■
optimize recovery
■
prevent recurrence of stroke.
Much of the advice is based on clinical trial data.
General medical support of the patient

Initially the patient with a large stroke may need to be

resuscitated with protection of the airway, giving
nasogastric or parenteral fluids.
Most patients will need assessment of their swallowing
to determine whether it is safe for them to have oral
fluids.
In managing the fluid balance, it is best to keep the
patient slightly underhydrated for the first week to
minimize cerebral edema.
 General medical support of the patient
The blood pressure is elevated in over 80% of patients with
strokes.
Most should be managed conservatively as a reduction in
blood pressure can further compromise the cerebral circulation.

If there is more severe hypertension (diastolic >120), a gentle

introduction of antihypertensive therapy is appropriate.

More severe hypertension associated with hypertensive

encephalopathy needs aggressive management.

Hypoxia, hyperglycaemia and hypoglycaemia should be

treated.
Minimize stroke size
Thrombolysis with recombinant tissue
plasminogen activator (rTPA) decreases
ischaemic stroke size and improves
outcome if given within 3 h of stroke
onset.
Prior to treatment, a CT scan needs to
be performed to exclude haemorrhage
or significant cerebral damage, which
could be transformed into fatal
haemorrhage by rTPA.
This is currently only possible for a
minority of patients with stroke who are
present very early and who have no
other contraindication.
Aspirin also reduces 30-day stroke
mortality.
Major contraindications to IV
thrombolysis in acute ischaemic stroke
No motor deficit
Symptom onset >3 h
Impaired consciousness
Recent epileptic seizure
History of intracranial
haemorrhage
Pregnancy
Lumbar puncture or arterial
puncture within 7 days
Surgery or delivery within 15 days
BP: systolic >185; diastolic >110
mmHg
Coagulopathy (INR >1.5)
 Complications of stroke
Prevent complications
Acute complications
Raised intracranial pressure may Raised intracranial pressure and herniation
lead to fatal brain herniation and, Aspiration and pneumonia
when it occurs after a large anterior
Complications of immobility
circulation infarct, it is usually
unresponsive to treatment, though Pneumonia
in selected patients a decompressive Contractures
hemicraniectomy may be used. Deep vein thrombosis
Bed sores
However, a large intracranial
haematoma can be surgically Urinary tract infections
drained and large cerebellar strokes Constipation
can cause brain stem compression
and hydrocephalus and may need Later complications
posterior fossa decompression to Depression
control intracranial pressure. Epilepsy
Thalmic pain
Social problems

Prevent complications
The complications of
immobility are not unique to
stroke. These require active
nursing care with 2-hourly turns
and appropriate positioning to
prevent bed sores.
Complications of stroke
Acute complications
Raised intracranial pressure and herniation
Aspiration and pneumonia
Complications of immobility
Pneumonia
Contractures

Appropriate feeding, which Deep vein thrombosis

may include using a nasogastric Bed sores
tube or percutaneous Urinary tract infections
gastrostomy if more long term,
Constipation
positioning and physiotherapy
to prevent pneumonia are Later complications
required. Physiotherapy is Depression
initially used to maintain passive
Epilepsy
movements and prevent
contractures. Thalmic pain
Social problems
 Complications of stroke
Prevent complications
Acute complications
Graded pressure stockings can Raised intracranial pressure and herniation
be used as prophylaxis for deep Aspiration and pneumonia
vein thrombosis. Heparin should
Complications of immobility
probably be avoided in the early
phase of recovery from a Pneumonia
haemorrhagic stroke and its use Contractures
in ischaemic stroke is being Deep vein thrombosis
evaluated.
Bed sores
Urinary catheterization should Urinary tract infections
be avoided, if possible, as it
Constipation
increases the risk of infection.
Laxatives, suppositories and Later complications
enemas may be needed for Depression
bowel control.
Epilepsy
Thalmic pain
Social problems

Prevent complications
The later complications are
more difficult to prevent.
Psychological support for the
patient and the family from the
doctors, nurses and therapists
concerned can help a patient
come to terms with the stroke.
Social difficulties may
sometimes be anticipated and
minimized. However, it is
important to recognize when a
patient becomes depressed
because this is treatable.
Depression affects up to 50%
of patients after stroke.
Complications of stroke
Acute complications
Raised intracranial pressure and herniation
Aspiration and pneumonia
Complications of immobility
Pneumonia
Contractures
Deep vein thrombosis
Bed sores
Urinary tract infections
Constipation
Later complications
Depression
Epilepsy
Thalmic pain
Social problems
 Complications of stroke
Prevent complications
Acute complications
About 5% of patients will have Raised intracranial pressure and herniation
a seizure within 1 year of their Aspiration and pneumonia
stroke. Anticonvulsants may be
Complications of immobility
required.
Pneumonia
Thalamic pain is a deep Contractures
gnawing pain that can follow Deep vein thrombosis
stroke, typically with some
Bed sores
sensory involvement. This may
respond to pain-modulating Urinary tract infections
drugs such as amitriptyline and Constipation
carbamazepine and can be
difficult to treat. Later complications
Depression
Epilepsy
Thalmic pain
Social problems
Optimize recovery

The treatment of a patient with a stroke depends on a

multidisciplinary team of nurses, physiotherapists, occupational
therapists, speech therapists, dietician, psychologists and social
worker.
This team aims to assist the patient in functional recovery and to
help adapt the patient’s environment to minimize the impact of
the physical disability. The patient’s family needs to be closely
involved. After the patient leaves hospital there may be other
agencies that can provide assistance, for example district nurses,
day hospital or day centres.
There is evidence that care of stroke patients within a stroke unit,
where there is a closely integrated team of therapists, reduces
mortality by about 25% and improves functional recovery.
Secondary prevention of stroke and transient ischaemic attacks
Control of risk factors
Treatment of hypertension, control of diabetes, cessation of
smoking and moderation in alcohol intake, and control of
hypercholesterolaemia all combine to reduce the progression of
atheroma.
Most patients end up on a cocktail of a diuretic, an angiotensin
converting enzyme inhibitor and a statin. These measures also
reduce the risk of ischaemic heart disease, the commonest cause
of death following TIA.
Postmenopausal oestrogen therapy (hormone replacement
therapy) increases the risk of stroke and should be avoided.
 Secondary prevention of stroke and transient ischaemic attacks
Aspirin
Aspirin reduces the recurrence of ischaemic stroke or TIA from 10%
to 8% per year. The adverse effects are directly related to dosage.
A typical dose is 75-300 mg per day. This is also useful in the
prevention of other vascular complications.

Other antiplatelet agents

Dipyridamole has recently been demonstrated to be helpful when
used in combination with aspirin. Clopidogrel, another antiplatelet
agent, has been assessed in large trial and has similar benefit to
aspirin. They are useful in aspirin- intolerant patients.
 Secondary prevention of stroke and transient ischaemic attacks
Anticoagulation
In patients with TIA or stroke in atrial fibrillation, the risk of
stroke is reduced from 12% per year to 4% by anticoagulation
to an international normalized ratio (INR) of 2-3, and the
vascular mortality is reduced from 17% to 8%.

The risk of recurrent stroke needs to be estimated in each

patient and balanced against the risk of anticoagulation,
including the risk of falls, difficulties taking the tablets or in
monitoring treatment, etc.
 Secondary prevention of stroke and
Both studies found a reduced transient ischaemic attacks
risk of recurrent stroke in Carotid stenosis
patients with a greater than
70% stenosis in the surgical
group and especially those
with stenosis greater than
80%.

The risk of stroke is greater

with a tighter stenosis and if
the plaque is ulcerated, so the
benefit is greater for these
patients.
Initial studies have found
angioplasty to have similar 0 1 2 3 4 5 678

effectiveness to Time since randomization (years)

endarterectomy, though
further studies are ongoing.
Kaplan-Maier survival curves to show survival time free of stroke in patients
with 80-99% carotid stenosis following endarterectomy (surgery) and in
controls. (By kind permission of the Lancet: European carotid
surgery trialists' collaborative group 1998. Randomised trial of
endarterectomy for recently symptomatic carotid stenosis; final
results of the MRC European carotid surgery trial (ECST). Lancet
351: 1379-87.)
 Primary prevention of stroke

Control of risk factors for atheroma in the general population, in

particular the control of hypertension.
Control of hypertension reduces the stroke rate by 40%,
regardless of age.

There is dispute about the best management of asymptomatic

carotid stenosis. Trials found that the stroke risk was about 2%
per year in unoperated patients compared with 1% in the
operated group, suggesting a very small benefit compared with a
2% operative risk.
86 patients need to have the operation to prevent one stroke.
 Intracerebral haemorrhage
Intracerebral haemorrhage is usually due to hypertension (primary intracerebral
haemorrhage 15% of all the hemorrhagic strokes ). This occurs when small penetrating
arteries within the brain rupture at sites of weakness, as a result of lipohyalinosis and
microaneurysms (Charcot- Bouchard aneurysms]. Intracerebral haemorrhages occur
most frequently in the basal ganglia (50%), lobar white matter (20%], pons (10%] and
cerebellum (10%].
Risk Factors :
1.Hypertension
2.Amyloid vasculopathy
3.Aneurysm
4. Arteriovenous malformation
5. Neoplasm
6. Coagulation disorder e.g. haemophilia
7. Anticoagulant therapy
8. Vasculitis
9. Drug abuse e.g. cocaine
10. Trauma

CT scan showing intracerebral haemorrhages

Ruptured saccular aneurysms produce subarachnoid haemorrhage
Arteriovenous malformations can rupture and produce intracerebral
haemorrhage.

Clinical criteria of diagnostics of hemorrhagic stroke

 young and middle age of a patient, hypertonic cerebral crises in anamnesis

 sudden onset on the background of physical or emotional over tension
 consciousness disturbances, marked meningeal symptoms
 hyperemia of face, midriasis on the lesion side
 breath is hoarse, irregular, body temperature is increased
 blood pressure is extremely high, pulse is tensed
 there are focal and dislocation brainstem symptoms
 blood formula of peripheral blood is moved to the left
 cerebral spinal fluid is bloody, with presence of changed erythrocytes
 on eye ground – hemorrhages in retina
 M-echo is moved on 6-7 mm by data of Echo-ES
 brain MRI shows hemorrhage lesion
 
 Treatment of hemorrhagic stroke

1.Basic treatment:
•Maintenance of the breathing function
•Regulation of the arterial blood pressure
•Correction of the water and electrolyte balance
•Correction of the glucose level
•Maintenance of the normal body temperature
•Treatment of dysphagia
•Treatment of seizure attacks
2. Special therapy
•Correction of the hemostasis
•Treatment of the intracranial hypertension
Surgical treatment
In the case of intracranial hematoma (especially this treatment is
effective in the case of lateral hematoma within cerebral
hemisphere; hematomas in the cerebellum; operation is ineffective
in case of deep brain hematomas)
Rehabilitation treatment
 Subarachnoid haemorrhage

• Subarachnoid haemorrhage (SAH) is an important and potentially

preventable cause of death and neurological disability.
• SAH is uncommon, with an incidence of 6-20 per 100 000 per year.
It is rare below the age of 20 years and most frequent between 40
and 60 years of age.
• SAH usually results from rupture of an intracranial aneurysm into
the subarachnoid space
 Subarachnoid haemorrhage
Clinical features:
■
a sudden severe headache - ‘as if hit by a baf’
■
transient loss of consciousness
■
vomiting
• neck stiffness and sometimes focal neurological signs
A 3rd (oculomotor) nerve palsy with pupillary involvement is occasionally seen and is
of particular significance, indicating enlargement or rupture of a posterior
communicating artery aneurysm. In an unconscious patient, a 3rd nerve palsy can
also occur with uncal herniation due to raised intracranial pressure. A 6th
(abducens) nerve palsy can occur as a false localizing sign due to hydrocephalus.
Ophthalmoscopy can occasionally reveal subhyaloid haemorrhage.
On arrival to hospital, about a third are drowsy and 20% are stuporous or in coma. In
those who can give a history, almost all have had sudden severe headaches. Fifty
per cent of patients have had some loss of consciousness.
 Subarachnoid haemorrhage
Investigations
Investigations are in two phases:
To prove that the patient has had an SAH. A
CT brain scan is positive (Fig.1) in 95% of
cases within the first 24 h after onset of
headache but in only 67% by 3 days.
If this is negative then a lumbar puncture
should be performed, at least 6 h after the
onset, when diffuselyblood-stained CSF with
xanthochromic (yellow) supernatant (Fig. 3)
is found.

Fig. 1CT scan showing subarachnoid

haemorrhage. The subarachnoid blood
appears white and fills the space around
the brain that would normally contain CSF
Fig. 3 Xanthochromic CSF. and would appear dark.
 Subarachnoid haemorrhage
nvestigations
2. To discover the source of the bleed.
A four-vessel cerebral angiogram locates the aneurysm (Fig. 4a].
About 1 in 10 patients with definite SAH will have no source of bleeding found and
have a low risk of recurrence. Magnetic resonance and CT angiography are increasingly
used to locate aneurysms without the risks of angiography (Fig. 4b).

Fig. 4 Discovering the source of the bleed, (a) Digital subtraction angiogram showing a large multiloculated
aneurysm arising from the middle cerebral artery (arrow), (b) CT angiogram showing an aneurysm on the
middle cerebral artery (arrow).
 Subarachnoid haemorrhage
Complications
The main complications are:

■ rebleeding from the ruptured aneurysm

■ cerebral ischaemia because of vasospasm of the cerebral arteries; it is not clear
how SAH causes vasospasm
■ hydrocephalus.

These present with a deterioration in the level of consciousness or development of

focal signs. They can only reliably be distinguished on repeat CT scanning.

Occasionally patients may develop hyponatraemia, neurogenic pulmonary oedema

and cardiac arrhythmias. Patients may also develop complications from bed rest
and impaired consciousness: deep vein thromboses and aspiration and basal
pneumonia.
 Subarachnoid haemorrhage

Treatment and prognosis

• Rebleeding can be prevented either by endovascular occlusion of the

aneurysm with a coil or by surgically clipping the aneurysm.
• The risk of ischaemic complications, thought to be due to vasospasm, can be
reduced by sustained hypervolaemia (3 litres of normal saline per day) and a
calcium antagonist (nimodipine).
• Aggressive control of blood pressure increases ischaemic complications, and
antihypertensives should be avoided.
• Fludrocortisone or hypertonic saline can be used to treat hyponatraemia.
• Hydrocephalus should be treated with an appropriate drainage procedure.
 Subarachnoid haemorrhage

Treatment and prognosis

Patients who are alert on arrival at hospital have the

best prognosis; three- quarters make a full recovery
and there is a 10% mortality rate.

In patients who are comatose on arrival, three-

quarters die, 10% are severely disabled or in a
persistent vegetative state and only 10% make a good
recovery.
 Take-home message

•Stroke is the third most common cause of death in developed

countries.

•The treatment of a patient with a stroke depends on a

multidisciplinary team of nurses, physiotherapists, occupational
therapists, speech therapists, dietician, psychologists and social
worker.

•Treatment of hypertension, control of diabetes, cessation of

smoking and moderation in alcohol intake, and control of
hypercholesterolaemia all combine to reduce the progression of
atheroma.
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THANKS FOR YOUR ATTENTION !!!!!
References:
Geraint Fuller, Mark Manford: Neurology, 2010
Kenneth W Lindsay, Ian Bone, Geraint Fuller:
Nerology and Neurosurgery Illustrated, 2010 et al.