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The brain derives its blood supply from four large trunks, the two internal carotids & the two
vertebral arteries. Each internal carotid divides into middle & anterior cerebral arteries. The
two vertebral arteries unite to form the basilar artery which in turn divide into two posterior
cerebral artery.

An unbroken arterial circle (circle of Willis) is formed at the base of the brain connecting all the
four large trunks. It is formed by the two communicating arteries
OY Anterior communicating: which unites two ACA
OY Posterior communicating: which unites the internal carotid with posterior cerebral
artery

The three major cerebral arteries (ACA, MCA, PSA) give off two types of branches:
1.Y c : which are given off at the arterial circle & perforate the base of the
brain & ramify to supply its central part consisting of the white matter & basal ganglia.
2.Y  c: which are given off in the pia matter & ramify to supply the
cortex.

 
A clinical syndrome characterized by the acute onset of a neurological deficit that persists for at
least 24 hours, reflects focal involvement of the central nervous system, and is the result of a
disturbances of the cerebral circulation.

 
The underlying pathologic process in stroke can be either
OY Ischemia (infraction)
OY ºemorrhage

G 
 
Ñ Interruption of the blood flow to the brain deprives neurons from oxygen & lead to cell death.
Ñ If the blood flow to ischemic brain is restored before neurons are irreversibly injured, the
clinical symptoms & signs are transient (TIA).
Ñ Prolonged interruption of blood flow lead to irreversible ischemic injury (infarction) &
persistent neurological deficits.
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In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of
the brain tissue in that area. There are four reasons why this might happen:
OY Thrombosis: obstruction of a blood vessel by a blood clot forming locally.
OY Embolism: obstruction due to an embolus from elsewhere in the body.
OY Systemic hypoperfusion: general decrease in blood supply e.g. shock.
OY penous thrombosis

Ischemic stroke is classified as being due to:

1.Y Thrombosis due to atherosclerosis of a large artery in the neck.
2.Y Embolism of a cardiac origin or carotid arteries.
3.Y Occlusion of a small blood vessel (lacunar).
4.Y Undetermined cause.

^   
Ñ Interfere with cerebral function by: destruction/compression of brain tissue & compression of
vascular structures leading to secondary ischemia and edema.
Ñ Intracranial hemorrhage is classified by its location as intracranial ºge, subarachnoid, subdural
or epidural. All of which except subdural are usually caused by arterial bleeding.

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OY Transient ischemic attack
OY Cerebral ischemia: Thrombosis, Embolism
OY Cerebral hemorrhage
OY Cerebral aneurysm & subarachnoid hemorrhage
OY Thrombosis of intracranial venous sinuses
OY ºypertensive encephalopathy
 @ 
 "@
 

A transient ischemic attack (TIA) or ͞mini stroke͟ is a neurologic episode resembling a stroke
but resolving completely within a short period of time. By definition, symptoms of TIA resolve
within 24 hours and symptoms lasting longer than that are termed a stroke. A TIA is caused by
brief interruption of the blood supply to a specific brain region, and it may warn of impending
stroke.

When the brain loses blood supply, its tries to restore blood flow. If the blood supply is
restored, function may return to the affected brain cells, permitting return of function to the
affected body part. This is what happens with a TIA.

TIAs are often warning signs of the future stroke. The risk of a stroke increases dramatically in
the days after a TIA and the TIA may offer an opportunity to find a cause or minimize the risk to
prevent the permanent neurologic damage that results because of a stroke.

c @

Brain cells require oxygen and glucose to function. If the blood supply is lost, then nutrient
supply is lost, and the brain cells stop working. The blood supply to brain cells can be lost in a
different ways.

The underlying causes of the arterial blockage are the same for both TIAs and strokes. The most
common causes is a buildup of atherosclerotic plaques, or fatty deposits containing cholesterol
in the wall of the artery.

1) Atherosclerosis: ThromboÑembolic
Damage to the arterial lining may cause platelets to stick together around the injured area as a
normal part of the clotting and healing process. When cholesterol and other fats are deposited
in this area, a plaque forms within the lining of the artery and narrows the channel through
which blood passes. This causes blood flow to slow down & increases the natural tendency of
blood to clot.

If a thrombus or clot forms at the site of the plaque, it may block the blood vessel at the
location. Pieces of the plaque or thrombus may break off and travel downÑstream to
progressively narrower arteries forming an embolus that can temporarily block these arteries
and cause a TIA until it dissolves or it is dislodged.
2) Cardioembolic
In a similar fashion, an embolus moving to the brain from the heart or elsewhere on the body
can also cause a TIA.

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A) Non modifiable risk factors
OY  amily history
OY Being 55 years old or older
OY Sex: Men have slightly higher likelihood of TIA and stroke than women do, but more
than half of deaths from stroke occur in women.
OY aces; Blacks are at greater risk of dying of a stroke than people of other races, partly
because of the higher prevalence of high blood pressure and diabetes among blacks.

B) Modifiable risk factors

OY Elevated blood pressure
OY Cardiovascular disease
OY Carotid artery disease
OY Peripheral artery disease (PAD)
OY Cigarette smoking
OY Physical inactivity
OY Diabetes mellitus
OY Poor nutrition
OY ºigh cholesterol
OY ºigh level of homocysteine
OY Obesity
OY ºeavy drinking
OY Use of illicit drugs
OY Use of birth control pills

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The symptoms of TIA vary depending on what part of the brain is affected.
üY Carotid (anterior) circulation TIAs
Interrupt the blood supply to most of the frontal part of the brain (cerebrum, including the
frontal, parietal and temporal lobes)
üY pertebrobasilar (posterior) circulation TIAs
Involve the blood supply to the back part of the brain, including the occipital lobe,
cerebellum, and brainstem.
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OY Transient monocular blindness or amaurosis fugax: sudden painless darkness or blurring
on the same side (ophthalmic artery)
OY Transient contralateral mono or hemiparesis
OY Transient contralateral sensory deficit
OY Transient dysphasia (dominant hemisphere)

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1.Y Ischemia of the brain stem
a.Y Cranial nerve nuclei on one or both sides
i.Y Ocular nuclei: ophthalmoplegia & diplopia
ii.Y pestibular nuclei: vertigo & dizziness
iii.Y Bulbar nuclei: dysphagia & dysarthria
b.Y Tracts
i.Y Pyramidal: alternating/bilateral + cranial NS
ii.Y Sensory: alternating or bilateral
iii.Y Central reticular formation: confusion/drop attack
2.Y Ischemia of the cerebellum
Cerebellar ataxia on one or both side
3.Y Ischemia of visual cortex
Temporal hemianopia ʹ posterior cerebral artery
Blindness on both eyes with preservation of light reflex ʹ basilar artery

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1.Y ºysteria: young female & hysterical personality
2.Y  ocal epilepsy: slow march motor fits or sensory fits
3.Y Migraine: frequently accompanied or followed by considerable headache

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OY The characteristic history of a TIA with sudden onset, rapid resolution.
OY ºistory of risk factors for atherosclerosis
OY  amily history of heart disease or stroke
OY The specific symptoms associated with TIA will help the physician determine which
portion of the brain & which blood vessels were involved.
OY Neurological examination is usually normal (may be subtle signs related to previous
strokes)
OY eneral exam may reveal evidence or atherosclerotic plaques (a bruit or abnormal
sound heard with stethoscope placed over the carotid artery in the neck)
 OY Ophthalmoscopic exam: cholesterol emboli in the tiny arteries of the retina
OY Carotid ultrasonography: determine if there is narrowing (stenosis, or plaque formation)
in the carotid arteries. In this painless and harmless test, a transducer sends highÑ
frequency sound waves into the neck, and deflections of these waves are analyzed as
images on a screen.
OY Computed tomography (CT) scanning images of the brain. The CT may show strokes, but
often fail to give sufficiently detailed views of the blood vessels.
OY Computerized tomography angiography (CTA) scanning: to improve blood vessel
visualization, uses injection of a contrast dye into a blood vessel.
OY Magnetic resonance imaging (MI) that are very good at detecting small strokes.
OY Magnetic resonance angiography (MA) uses similar technology to study the arteries in
the neck and brain
OY Electrocardiogram: if the heart is thought to be the source of emboli to detect any
changes in heart rhythm
OY Transesophageal echocardiography (TEE)
OY Other tests may determine if there are any underlying conditions causing TIA, including
blood tests for arteritis, sickle cell anemia, diabetes and hyperviscosity syndromes.

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Ideally
OY Patient with symptoms suggesting TIA or acute stroke should be evaluated within 60
minutes.
OY Prompt evaluation is needed to identify the specific cause of the TIA
OY Begin appropriate treatment

A) Antiplatelet agents
Drugs that reduce the tendency of platelets to clump together, may reduce the risk of the
future TIA or stroke
1.Y Aspirin: least expansive and safest
2.Y Dipyridamole: in combination with lowÑdose aspirin
3.Y Clopidogrel: alone or with aspirin
4.Y Ticlopidine

B) Anticoagulants
Indicated for patient with TIA caused by cardiac embolus
1.Y ºeparin: is given only for a limited period, while the patient is still in the hospital
2.Y Warfarin: for longÑterm use
Drug level must be monitored with blood test
ºeparin: partial thromboplastin time (PTT) daily
Warfarin: prothrombin time (PT) & international normalized ratio (IN) weekly

C) Surgery
If carotid artery testing reveals moderate or severe narrowing or stenosis (more than 70%) to
improve blood flow and prevent future stroke or TIA
1.Y Carotid endartectomy: involves opening the artery through a neck incision, removing
atherosclerotic plaques, then closing the artery.
2.Y Carotid angioplasty or stenting: using a balloonÑlike device, surgeon open the clogged
artery & places a stent, or small wire tube within the artery to keep it open

D) educe treatable risk factors for stroke including

1.Y ºigh blood pressure, heart diseases, diabetes and high cholesterol levels may require
treatment with specific drugs or may be controlled by lifestyle changes alone.
2.Y Stopping smoking, weight control
3.Y Eating a balanced diet low in saturated fats, salts and sugar, high in vegetables fruits and
fibers.
4.Y Structured exercise programs may help patients achieve these goals
  

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1.Y Ischemic
The most common type of stroke (83%). It occurs when clots block an artery. The
underlying condition for this type of obstruction is the development of fatty deposits
lining the vessel walls called atherosclerosis. These fatty deposits can cause two
types of obstruction.
OY Cerebral thrombosis
A thrombus (blood clot) that develops at the clogged part of the vessel
OY Cerebral embolism
Blood clot that forms at another location in the circulatory system (heart &
large arteries of the neck). A portion of the blood clot breaks loose, enter the
bloodstream & travels through the brain͛s blood vessels until it reaches
vessels too small to let it pass. A second important cause of embolism is an
irregular heartbeat, known as atrial fibrillation. It creates condition where
clots can be form in the heart, dislodge and travel to the brain.
2.Y ºemorrhagic
ºemorrhagic stroke is the least common, but can be fatal. ºemorrhagic strokes
happen when a weakened vessel in the brain ruptures and bleeds into the
surrounding brain tissue. The two types of hemorrhagic strokes are
OY Intracerebral hemorrhage
OY Subarachnoid hemorrhage
Two types of weakened blood vessels usually cause hemorrhagic stroke are
aneurysms and arteriovenous malformations (ApMs)

  

1.Y Deterioration in the conscious level
2.Y Ipsilateral blindness (ophthalmic artery)
3.Y Contralateral hemiplegia
4.Y Contralateral hemisensory disturbances
5.Y Contralateral homonymous hemianopia
6.Y aze palsy (eye deviate to the side of lesion)
7.Y ºorner syndrome (oculosympathetic)
8.Y lobal aphasia (dominant hemisphere)



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a)Y Main artery occlusion
i.Y Deterioration in the conscious level
ii.Y Contralateral hemiplegia
iii.Y Contralateral hemisensory disturbances
iv.Y Contralateral homonymous hemianopia
v.Y aze palsy (eye deviate to the side of lesion)
vi.Y lobal aphasia (dominant hemisphere)
vii.Y ºemineglect ( nonÑdominant hemisphere)
b)Y If upper division of MCA is occluded
i.Y ºemiparesis usually affect the face & arm more than leg
ii.Y Brocas aphasia (dominant hemisphere)
c)Y If lower division is occluded
i.Y Wernicks aphasia
ii.Y Contralateral homonymous hemianopia
iii.Y Contralateral cortical sensory loss
d)Y LenticuloÑstriate branch occlusion
May cause lacunar infarction in the involved internal capsule producing syndrome of
pure motor hemiparesis

    
1.Y Weakness and sensory loss affecting mainly contralateral legs and urinary incontinence,
impaired memory, speech disturbances (aphasia0
2.Y Infarction in the territory of medial lenticulostriate artery (artery of ºeubner) causes
weakness of the face and arms (faciobrachial monoplegia) without sensory loss due to
affection of anterior limb of IC.

    

1.Y Cortical branch
Contralateral homonymous hemianopia with macular sparing, visual hallucination and
visual agnosia
2.Y Thalamic branch
Pure sensory stroke: contralateral hemianaesthesia to all modalities of sensation &
thalamic pain (persistant pain & hyperalgesia)
3.Y Subthalamic nucleus
Chorea or hemiballismus
4.Y Midbrain
Third nerve palsy with contralateral hemiplegia
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Infarct involves posterior fossa structures are suggested by:
1.Y Bilateral long tracts (motor or sensory) signs
2.Y Croessed (e.g left face & right limb)
3.Y Cerebellar signs
4.Y Stupor or coma
5.Y Involvement of the cranial nerves (ipsilateral cranial nerve lesions & contralateral
hemiplegia, this is called crossed hemiplegia)

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 irst: confirm the patient͛s impairment are due to ischemic stroke not hemorrhagic
Second: the evaluation helps determine advisability for acute treatment with thrombolytic
agents.
Third: diagnostic studies are carried out to screen for acute medical or neurological
complications of stroke
 inally: the evaluation provides historical data or other information that can be used to
establish the vascular distribution of the stroke and to provide clues about its likely
pathophysiology and etiology.

1.Y ºistory and physical examination

ºistory of sudden or rapid onset of focal neurological symptoms. Some patients may
have a stepwise or gradual worsening or waxing and waning of
2.Y Differentiation of ischemic from hemorrhagic stroke
Because of the marked difference in the management of these conditions. ºistory &
examination can help: coma on arrival, vomiting, severe headache, current warfarin
therapy, systolic blood pressure > 220mm ºg are common with hemorrhagic stroke.
3.Y NonÑcontrast enhanced computed tomographic scan of the brain (CT brain)
4.Y The standard MI sequences
5.Y Cardiac tests: cardiovascular examination & 12 lead EC & electrocardiography
6.Y Blood tests: include blood glucose, electrolytes, complete blood count with platelet
count, prothrombin time, activated partial thromboplastin time and hepatic & renal
function tests.
7.Y pascular studies
a.Y Transcranial Doppler ultrasonography
b.Y Magnetic resonance angiography
c.Y CT angiography
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1.Y People who have had a stroke are admitted to a stroke unit
2.Y Definitive therapy is aimed at removing the blockage by breaking the clot down by
thrombolysis by
a.Y Intravenous tissue plaminogen activator (tpA)
Ñ tpA is used to dissolve the clot and unblock the artery
Ñ clinical benefit if it administered within 3Ñ4.5 hours from stroke onset
Ñ complication: 6% of patients with large brain strokes developed brain
hemorrhage so it is contraindicated if it is hemorrhage in CT
b.Y IntraÑarterial thrombolysis: a catheter is passed up an artery into the brain and
medications injected at the site of thrombosis
3.Y Antiplatelet therapy
To minimize clot enlargement or prevent new clots formation such as Acetylsalicylic acid
(aspirin), clopidogrel and dipyridamole may be given to prevent platelets aggregating.
4.Y Dehydrating measures
If there is brain edema on CT scan such as diuretics
5.Y Anticoagulant
Are prescribed to patients with recent stroke to prevent early recurrence:
a.Y CardioÑembolic stroke
b.Y Progressive stroke (stroke in evolution)
c.Y ºistory of TIAs
d.Y Carotid artery diseases (stenosis)
Ñ parenteral heparin: monitored by PT &PTT
Ñ oral anticoagulant: monitored by IN
6.Y eneral supportive care and treatment of acute complications
a.Y Airway, ventilator support and oxygen
b.Y  ever: lowering an acutely elevated body temperature
c.Y Treatment of cardiac arrhythmia
d.Y Optimal control of blood pressure
e.Y Control glucose level

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Intracerebral hemorrhage occurs when a diseased blood vessel within the brain bursts, allowing
blood to leak inside the brain. The sudden increase in pressure within the brain can cause
damage to the brain cells surrounding the blood. If the amount of blood increases rapidly, the
sudden buildup in the pressure can lead to unconsciousness or death.
Intracranial hemorrhages are classified according to location into:
1.Y Intra parenchymal or intracerebral hemorrhage
2.Y Subrachnoid hemorrhage
3.Y Extradural hemorrhage
4.Y Subdural hemorrhage
5.Y Intraventricular hemorrhage


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OY Sustained hypertension
OY Cerebral amyloid angiopathy
OY pascular malformations & ruptured aneurysms
OY Coagulation disorders
OY Excessive anticoagulants & thrombolytic agents
OY ºemorrhage into a cerebral infarct
OY Bleeding into brain tumors
OY Drug abuse


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ºemorrhagic strokes result in tissue injury by causing compression of the adjacent brain tissue
from an expanding hematoma or hematomas. This can distort and injure tissue causing
neuronal dysfunction. In addition, the pressure may lead to a loss of the blood supply to
affected tissue with resulting infarction and the blood released by brain hemorrhage appears to
have direct toxic effects on the brain tissue and vasculature.


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Most intracerebral hemorrhages occur in:
1.Y Basal ganglia: thalamus & lenticular nucleus then extend to involve the internal capsuke
2.Y Cerebral lobes
3.Y Internal capsule
4.Y Cerebellum
5.Y Pons or occur in the other parts of the brain stem (mid brain)

OY Sudden headache, often during activity.
OY Disturbed consciousness is often within seconds or a few minutes,
OY Nausea, vomiting
OY  ocal or generalized seizures.
OY Neurological deficits are usually sudden and progressive
OY Large hemorrhages, when located in the hemisphere: hemiparesis
OY When located in the posterior fossa, they cause cerebellar or brain stem deficits (e.g.
conjugate eye deviation or ophthalmoplegia, stertorous breathing, pinpoint pupils,
coma)

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Ñ Large hemorrhages are fatal within a few days in about half of the patients
Ñ In survivors, consciousness returns and neurologic deficits gradually diminish to various
degrees as the extravasated blood is resorbed. Some patients have surprisingly few neurologic
deficits because hemorrhage is less destructive to brain tissue than infarction.
Ñ Small hemorrhage may cause focal deficits without impairment of consciousness and with
minimal or no headache and nausea (mimic ischemic stroke)


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1.Y Immediate non contrast CT brain
2.Y Magnetic resonance imaging
3.Y CT or MI angiography
4.Y Contrast cerebral angiography should be considered for all patients without a clear
cause of hemorrhage who are surgical candidates.
5.Y ºemoglobin analysis ʹ blood loss
6.Y Prothrombin time and PTT ʹ coagulation problem
7.Y Blood glucose level

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Initial management in emergency unit
OY Airways and oxygenation
OY Blood pressure management
OY Intracranial pressure management
OY  luid management
OY Prevention of seizures
OY Management of body temperature
OY Treatment of agitation
  
Patient with surgically large accessible hematoma e.g patient with cerebellar hemorrhage >3cm
in diameter who are neurologically deteriorating or who have brain stem complication and
hydrocephalus from ventricular obstruction.

 or the patient with small hemorrhage or minimal neurological deficit, they should be given
medical treatment as they respond well to medical treatment alone.

Patient with CS score ч4 should be treated medically because they uniformly die or have
extremely poor functional outcome and their condition not improve with the surgery.