CEREBRO-VASCULAR

DISEASE & STROKE

RANDA AL-HARIZY
Professor of Internal
Medicine
BLOOD SUPPLY OF
BRAIN
 CEREBRO-VASCULAR
DISEASE & STROKE
Stroke is the second commonest
cause of death in developed countries.
Hypertension is the most treatable
risk factor.
Thromboembolic infarction (80%),
cerebral and cerebellar haemorrhage
(10%) and subarachnoid haemorrhage
(about 5%) are the major
cerebrovascular problems.
 DEFINITIONS
Stroke is defined as the clinical syndrome of rapid
onset of cerebral deficit (usually focal) lasting more
than 24 hours or leading to death, with no apparent
cause other than a vascular one.
Completed stroke means the deficit has become
maximal, usually within 6 hours.
Stroke-in-evolution describes progression during
the first 24 hours.
Minor stroke. Patients recover without significant
deficit, usually within a week.
Transient ischemic attack (TIA). This means a
focal deficit, such as a weak limb, aphasia or loss of
vision lasting from a few seconds to 24 hours. There
is complete recovery. The attack is usually sudden.
 PATHOPHYSIOLOGY
COMPLETE STROKE

One of three mechanisms is usual:

arterial embolism from a distant site
arterial thrombosis
haemorrhage into the brain (intracerebral or
subarachnoid).

Less commonly:
venous infarction
carotid or vertebral artery dissection
polycythaemia (hyperviscosity syndromes)
fat and air embolism
multiple sclerosis
mass lesions (e.g. brain tumour, abscess, subdural haematoma)
rarities: arteritis, neurosyphilis, systemic lupus erythematosus,
 PATHOPHYSIOLOGY OF
TRANSIENT ISCHEMIC
ATTACK
TIAs are usually the result of
microemboli.

Principal sources of emboli to the

brain are cardiac thrombi and
atheromatous plaques/thrombi
within the great vessels, and
carotid and vertebral systems.
 RISK FACTORS &
PREVENTION
Treatment of hypertension (of vital
importance)
Cessation of smoking; 50% reduction within
1 year reaching normal risk after 5 years
Active lifestyle
Moderate alcohol consumption
Statin therapy
Anticoagulation in atrial fibrillation
Weight reduction in obesity
Treating polycythaemia
 RISK FACTORS OF
CEREBRAL
HAEMORRHAGE

Hypertension
Bleeding disorders
Pre-existing cerebral aneurysm
Anticoagulant and antiplatelet drug
therapy
 TRANSIENT ISCHEMIC
ATTACKS (TIAs)

Symptoms:
TIAs cause sudden loss of function,
usually within seconds, and last for
minutes or hours (but by definition
<24 hours). The site is often
suggested by the type of attack.
 TRANSIENT ISCHEMIC
ATTACKS (TIAs)
Features of transient ischemic attacks
Anterior circulation Posterior circulation
Carotid system Vertebrobasilar system
Amaurosis fugax Diplopia, vertigo, vomiting
Aphasia Choking and dysarthria
Hemiparesis Ataxia
Hemisensory loss Hemisensory loss
Hemianopic visual loss Hemianopic visual loss
Transient global amnesia
Tetraparesis
Loss of consciousness
(rare)
 Clinical findings in TIA
It is unusual to witness an attack.
Consciousness is usually preserved in TIA.
There may be clinical evidence of a source
of embolus, such as: carotid arterial bruit
(stenosis), atrial fibrillation or other
dysrhythmia, valvular heart
disease/endocarditis, recent myocardial
infarction or difference between right and
left brachial BP.
 Un underlying condition
may be evident
atheroma
hypertension
postural hypotension
bradycardia or low cardiac output
diabetes mellitus
rarely, arteritis, polycythaemia
antiphospholipid syndrome
 Differential diagnosis
Mass lesion
Focal epilepsy
A focal prodrome of migraine
Prognosis: Prospective studies show that 5
years after a single thromboembolic TIA:
30% have had a stroke, a third in the first
year
15% have suffered a myocardial infarct.
TIA in the anterior cerebral circulation
carries a more serious prognosis than one
in the posterior circulation
 TYPICAL STROKE
SYNDROMES Cerebral
Clinical features:
infarction
The most common stroke is caused by infarction in the
internal capsule following thromboembolism in a middle
cerebral artery branch. A similar picture is caused by
internal carotid occlusion.
Limb weakness on the opposite side to the infarct develops
over seconds, minutes or hours.
There is a contralateral hemiplegia or hemiparesis with
facial weakness.
Aphasia is usual when the dominant hemisphere is
affected.
Weak limbs are at first flaccid and areflexic.
Headache is unusual. Consciousness is usually preserved.
After a variable interval, usually several days, reflexes
return, becoming exaggerated. An extensor plantar
response appears.
 BRAIN STEM
INFARCTION
CLINICAL PICTURE STRUCTURE INVOLVED
Hemiparesis or tetraparesis Corticospinal tracts
Sensory loss Medial lemniscus and spinothalamic
tracts
Diplopia Oculomotor system
Facial numbness Fifth nerve nuclei
Facial weakness (LMN) Seventh nerve nucleus
Nystagmus, vertigo Vestibular connections
Dysphagia, dysarthria Ninth and tenth nerve nuclei
Dysarthria, ataxia, hiccups Brainstem and cerebellar connections
Horner's syndrome Sympathetic fibres
Altered consciousness Reticular formation
This causes complex signs depending on the
relationship of the infarct to cranial nerve
nuclei, long tracts and brainstem connections
 The lateral medullary
syndrome
The lateral medullary syndrome, also called
posterior inferior cerebellar artery (PICA)
thrombosis, or Wallenberg's syndrome, is a
common example of brain-stem infarction
presenting as acute vertigo with cerebellar
and other signs. It follows thrombo-
embolism in the PICA or its branches,
vertebral artery thrombo-embolism or
dissection. The clinical picture depends on
the precise structure damaged.
 Clinical picture of PICA
occlusion
Ipsilateral
Facial numbness 5th
Diplopia 6th
Nystagmus
Ataxia (cerebellar)
Horners syndrome
9th and 10th nerve lesion
Contralateral
Spinothalamic sensory loss
Hemiplegia (mild, unusual)
 Lacunar infarction
Lacunes are small (<1.5 cm3) infarcts
seen on MRI or at autopsy. Hypertension
is commonly present. Minor strokes
(e.g. pure motor stroke, pure sensory
stroke, sudden unilateral ataxia and
sudden dysarthria with a clumsy hand)
are syndromes caused typically by
single lacunar infarcts. Lacunar
infarction is also often symptomless.
 Hypertensive
encephalopathy
This describes the neurological
sequelae of malignant hypertension.
Severe headaches, TIA, stroke, and
rarely subarachnoid haemorrhage
occur. Papilloedema may develop,
either as part of an ischaemic optic
neuropathy or following brain
swelling due to multiple acute
infarcts.
 Multi-infarct dementia
(vascular dementia)
Multiple lacunes or larger infarcts cause
generalized intellectual loss seen with advanced
cerebrovascular disease. The condition tends to
occur with a stepwise progression over months
or years with each subsequent infarct. There is
eventually dementia, pseudobulbar palsy and a
shuffling gait with small steps (parkinsonism).
Binswanger's disease is an imaging term
describing low attenuation in cerebral white
matter, with dementia, TIAs and stroke episodes
in hypertensive patients.
 Acute stroke: immediate care,
and thrombolysis
Paramedics and members of the public are
encouraged to make the diagnosis of stroke on a
simple history and examination
FAST:

Face sudden weakness of the face

Arm sudden weakness of one or both arms
Speech difficulty speaking, slurred speech
Time the sooner treatment can be started, the
better.
Dedicated units with multidisciplinary, organized

teams deliver higher standards of care than a general

hospital ward
 Investigations
The purpose of investigations in both
stroke and
TIA is:
to confirm clinical diagnosis

to distinguish between haemorrhage

and thromboembolic infarction

to look for underlying causes of disease

and to direct therapy, either medical or

surgical
 Imaging TIA & stroke
patients
Imaging TIA and stroke patients CT and MRI.
CT imaging will demonstrate haemorrhage
immediately while a patient with an infarct may
have a normal scan. Infarctions are usually
detectable at 1 weeK although 50% are never
detected on CT. CT or MRI should be carried
out urgently in the majority of cases. Diffusion-
weighted imaging (DWI) MR can identify
infarcted areas within a few minutes of onset.
Conventional T2 weighting is no better than CT.
Imaging will also show the unexpected, e.g.
subdural haematoma, tumour or abscess.
 Further investigations
Routine bloods (for polycythaemia,
infection, vasculitis, thrombophilia,
syphilitic serology, clotting studies,
autoantibodies, lipids)
Chest X-ray
ECG
Carotid Dopplers
Angiography
 Management of cerebral
infarction
The possible sources of embolus should be
sought (e.g. carotid bruit, atrial fibrillation,
valve lesion, evidence of endocarditis, previous
emboli or TIA)
Assess hypertension and postural hypotension
The brachial blood pressure should be
measured in each arm; a difference of more
than 20 mmHg is suggestive of subclavian
artery stenosis.
The neurological deficit should be carefully
documented.
 Immediate management
Admit to multidisciplinary hospital stroke unit if
possible.
General medical measures
Care of the unconscious patient, Oxygen by mask,
Assessment of swallowing, Check BP and look for source of
emboli.
Immediate brain imaging is essential.
Cerebral infarction : If CT shows infarction, give aspirin
(300 mg/day initially) antiplatelet therapy if no
contraindications, give alteplase thrombolysis, which must
be started within 3 hours (aim for 90 min) of stroke;
informed consent is essential.
Cerebral haemorrhage: If CT shows haemorrhage, do not
give any therapy that may interfere with clotting.
Neurosurgery may be required.
 Further management
Appropriate drugs for hypertension, heart
disease, diabetes, other medical conditions
Other antiplatelet agents, e.g. dipyridamole
Question of endarterectomy
Question of anticoagulation
Speech therapy, dysphagia care,
physiotherapy, occupational therapy
Specific neurological issues, e.g. epilepsy,
pain, incontinence
Preparations for future care
 Long term management
Medical management
Treatment of all risk factors
Antihypertensive treatment
Antiplatelets: Combined aspirin 75 mg
daily and dipyridamole 200 mg twice
daily is probably the best prophylaxis
against further thromboembolic stroke
or TIA.
Anticoagulants: in AF, prosthetic valves,
cardiomyopathy
 Surgical treatment
Internal carotid endarterectomy:
Surgery is recommended in TIA or
stroke patients shown to have internal
carotid artery stenosis greater than 70%.
Successful surgery reduces the risk of
further TIA/stroke by approximately
75%. Endarterectomy has a mortality
around 3%, and a similar risk of stroke.
Percutaneous transluminal angioplasty
(stenting) is an alternative procedure.
 Rehabilitation (speech
therapy & physiotherapy)
Skilled physiotherapy in the first few weeks
after stroke, relieves spasticity, prevents
contractures and teaches patients to use
walking aids.
In aphasia: It is possible that spontaneous
return of speech is hastened as much by
normal conversation with a relative as by a
therapist.
If the patient cannot swallow safely without
the risk of aspiration, either nasogastric
feeding or percutaneous gastrostomy will be
needed.
 Prognosis
Twenty-five per cent of patients die within
2 years of a stroke. Around 30% of this
group die in the first month
Gradual improvement usually follows
stroke, although the late residual deficit
may be severe. Of those who survive,
about one-third return to independent
mobility and one-third have serious
disability requiring permanent
institutional care.
 Intracerebral
hemorrhage
This comprises:
intracerebral and cerebellar
haemorrhage
subarachnoid haemorrhage

subdural and extradural

haemorrhage/haematoma.
 Intracerebral
hemorrhage
Etiology
Intracerebral haemorrhage causes

around 10% of strokes.

Haemorrhage is usually massive,

often fatal and occurs in chronic

hypertension and at well-defined sites
- basal ganglia, pons, cerebellum and
subcortical white matter.
 Recognition
At the bedside, there is no entirely reliable way
of distinguishing between intracerebral
haemorrhage and thromboembolic infarction.
Both produce stroke. Intracerebral haemorrhage,
however, tends to be dramatic with severe
headache. It is more likely to lead to coma than
thromboembolic stroke.
Brain haemorrhage is seen on CT imaging
immediately - as intracerebral, intraventricular,
or subarachnoid blood. MR imaging may not
identify an acute haemorrhage correctly in the
first few hours. Thereafter T2 weighted MR is
very reliable.
 Managing hemorrhagic
stroke
The principles are those for cerebral infarction.
The immediate prognosis is less good.
Antiplatelet drugs and, of course,
anticoagulants are contraindicated.
Control of hypertension is vital.
Urgent neurosurgical clot evacuation is
sometimes considered when there is deepening
coma and coning (particularly in cerebellar
haemorrhage).
The outlook is usually poor.
 Cerebellar hemorrhage
There is headache and rapid reduction of
consciousness with signs of brainstem
origin (e.g. nystagmus, ocular palsies).
Gaze deviates towards the haemorrhage.
There are unilateral or bilateral
cerebellar signs, if the patient is awake.
Cerebellar haemorrhage sometimes
causes acute hydrocephalus. Emergency
surgical clot evacuation is often
necessary after imaging.
 Subarachnoid
hemorrhage (SAH)
Causes
Saccular aneurysms

Arteriovenous malformation (AVM)

No lesion found

Rare associations: bleeding

disorders, mycotic aneurysms
Internal carotid artery
aneurysm
A-V malformation
 Clinical picture of SAH
There is a sudden devastating headache,
often occipital. This is usually followed by
vomiting and often by coma.
The patient remains comatose or drowsy for
several hours to several days, or longer.
After major SAH there is neck stiffness and a
positive Kernig's sign.
Papilloedema is sometimes present.
Minor bleeds cause few signs, but almost
invariably headache.
 Investigations
CT imaging is the initial investigation of choice.
Subarachnoid or intraventricular blood is usually seen.
Lumbar puncture is not necessary if SAH is confirmed
by CT, but should be performed if doubt remains. The
CSF becomes yellow (xanthochromic) several hours
after SAH. Visual inspection of the supernatant CSF is
usually sufficiently reliable for diagnosis, but there is a
move to use spectrophotometry to estimate bilirubin
released from lysed cells to define with certainty SAH
in doubtful cases.
MR angiography is usually performed in all potentially
fit for surgery, i.e. generally below 65 years and not in
coma. In some cases, no aneurysm is found despite a
definite SAH.
 Complications
Blood in the subarachnoid space can lead
to obstruction of CSF flow and
hydrocephalus. This can be asymptomatic
but may cause deteriorating
consciousness after SAH. Diagnosis is by
CT. Shunting may be required.
Severe arterial spasm (visible on cerebral
angiography and a cause of coma or
stroke) sometimes complicates SAH. It is
a poor prognostic sign.
 Management
Immediate treatment of SAH is bed rest and
supportive measures.
Hypertension should be controlled.
Dexamethasone to reduce cerebral oedema and to
stabilize the blood-brain barrier.
Nimodipine, a calcium-channel blocking agent,
reduces mortality.
When angiography demonstrates aneurysm, a direct
neurosurgical approach to clip the neck of the
aneurysm is carried out.
Invasive radiological techniques, such as inserting a
fine wire coil into an aneurysm are also used.
Direct surgery, microembolism and focal
radiotherapy ('gamma knife') are used in AVM.
 Subdural hematoma
SDH means accumulation of blood in the
subdural space following rupture of a vein. It
usually follows a head injury, which may be
trivial. The interval between injury and
symptoms may be days, weeks or months.
Chronic, unsuspected or spontaneous SDH is
common in the elderly and in alcohol abuse.
Headache, drowsiness and confusion are
common; symptoms are indolent and often
fluctuate. Focal deficits such as hemiparesis or
sensory loss develop. Epilepsy occasionally
occurs. Stupor, coma and coning may follow, but
there is a tendency for SDH to resolve
spontaneously.
 Extradural hemorrhage
This follows a linear skull vault fracture tearing
a branch of the middle meningeal artery. Blood
accumulates rapidly over minutes/hours in the
extradural space. The most characteristic
picture is of a head injury with a brief duration
of unconsciousness followed by a lucid interval
of recovery. The patient then develops a
progressive hemiparesis and stupor, and rapid
transtentorial coning, with first an ipsilateral
dilated pupil, followed by bilateral fixed dilated
pupils, tetraplegia and respiratory arrest.
An acute subdural haemorrhage presents in a
similar way.
 Management
Suspected extradural or subdural
haemorrhage needs immediate imaging.
Extradural bleeding requires urgent
neurosurgery. If performed early, the outlook
is excellent.
Subdural bleeding may allow; more
conservative management - even large
subdural collections can resolve. Progress is
assessed with serial imaging, but close liaison
with a neurosurgeon remains essential.