Stroke

By Dr. Salwa Essam

Introduction
• Its a heterogenous group of disorders involving sudden,
focal interruption of cerebral blood flow that causes
neurological deficit.
• Stroke result from ischemic infarction or bleeding into part
of the brain, manifest by rapid onset( eg. seconds-
minutes) of focal CNS sign and symptoms(focal
neurological defect_ almost always some sort of
hemiplegia with /without other neurological signs).
• Its the major neurological disease of our time.
• Mortality after 1st stroke : 12% by day56
 Classification:
• Haemorrhage -10_20% resulti from vascular rupture(SAH)
• Brain Ischemia (Infarct) 80_90%:
1. Thrombus
2. Other type of embolism
3. Systemic hypoperfusion
• TIA _Transient Ischaemic Attack;
This is a minor stroke , it may present with stroke like
symptoms ( limb weakness, dysphagia, visual defects)
but the clinical effect will completely resolve within
24hrs.They are usu tlt of micro emboli (80%) but not
always.Sometimes a mass lesion may mimic a TIA and
other times, they are result of a temporary reduce
blood flow eg;with massive postural hypotension,
decreased bld flow through stenosed artery
• Complated stroke :
the clinical effects have reached their maximum - usu
within 6hrs of the onset.
Prognosis:
• Mortality-20% in 1st 2 months, then roughly 10% year.
• <40% of stroke ( not TIA) Pts make a full recovery.
• Drowsyness at presentation has a poor prognosis.
Mechanism of Stroke:
• Arterial embolism;
From distant site;eg. carotids, vertebral or basilar arteries.
The embolus will occlude an artery of the brain resulting in
infraction. May also come from Heart valves in endocarditis.
• Haemorrhage:
Can be in the cerebrum it self , or also a SAH may cause
a similer effect.
• Damage will occur when the blood flow to the brain tissue
drops below 50% of normal value.
Uncommon causes:
• Venous infract
• Carotid/vertebral arteries dissection
• polycythemia
• Fat/air embolism -eg.in dilvers
• MS - a demyelinating plaque may act as an embolus.
• Mass lesion ( tumour).
• Migraine
• Thrombophilia
• Vasculitis
• Drugs - cocaine.
Epidemiology:
• 10/1000 per yr at age 75 _ the 3rd most common cause
of death in the devloped world .
• More common in black Africans than in caucasians.
• More common in men.
• Uncommon before the age of 40
• 25% of stroke Pts will die of the condition.
• Most stroke occur in the morning - the blood pressure is
lowered during the night whilst asleep, but on waking the
BP rises, and is now more likely to dislodge any
embolism.
 Aetiology
• Hypertension ;Damages the arterial wall - increase risk of
thrombus formation and haemorrhage.
• Smoking ; increase BP, effects arterial wall, ( stopping
reduces risk by 50% in the 1st year and is indistinguishable
from non smoker after 5 yrs)
• Lifestyle ; recommended 30_60mins exercise 4_6x per wk)
• AF; increasethe chance of thrombus formation.
• DM ; increase risk of high BP and atherosclerosis.
• Alcohol ;
• Hyperlipidaemia
• Age ; >65 the biggest risk factor.
• Gender ; men> women
• Carotid artery stenosis
• Family history
• Cerebral aneurysm ( Haemorrhage)
• Valvular heart diseases.
Risk factors:

Modifiable :
• HTN, cigarette smoking, Dyslipidemia, DM, insuline resistance,
abdominal obesity, excess alcohol cosumption,lack of physical actinity,
high risk diet, heart disorders,intracranial aneurysms, use of certain
drugs, vasculitis
Unmodifiable:
• prior stoke,older age, family history of stoke, genetic factors.
 TIA
• comletely resolve within 24 hrs.
• 80% due to thromboembolus.
• site of damage can roughly located from clinical signs:
• Anterior circulation; likly thrombus from CA most likly
affecting cerebral function( aphasia/dysphasia ,
hemiparesis, Amaurosis fugax,hemi sensory loss,
hemianopic visual loss
*Amaurosi fugax; sudden loss of vision in 1 eye, caused
by an infract in the retinal artery
• Posterior Circulation ; likely thrombus from
vertbrobasilar system, most likely affecting cerbellar /
brainstem function( diplopia, vertigo, vomiting,
chocking, dysartheria, hemianopic visual loss , sensory
loss ,Transient global amnesia,tetraparesis ,LOC)
* Transient global amnesia; episod of emnesia - >65yrs
age- compLetely resolve within 24hrs .
Diagnosis of TIA:
• Usually clinical
check the following:
• carotid bruit
• ECG; for any arrhythmia -AF
• Valvular HD
• Recent MI
• Radial pulse / radial delay
• Check for the underline cause/RFs:
• Atheroma
• Hypertension
• Postural hypotension
• DM
• Polycythemia
• Antiphospholipid syndrome.
DD for TIA:
• Mass lesion
• Epilepsy
• Migraine
PROGNOSIS:
• 5yrs after TIA _30% of Pts have a stroke( of these 30%
occure within 1st year), 15% have MI.
Investigation and management:

• Resolve after 24 hrs , if not or we suspect something

serious, then follow the protocolas for stroke.
• Otherwise, patients are often admitted to hospital on
the basis of their ABCD2 score. This score preddicts
the likelihood of further CVA event.
• A patient with score of >4 should be admitted to the
hospital and investigation within 24 hrs .
• A patient with score of <3 can be investigated as an
outpatient, but should be investigated within 1 wk.
• Follow up investigations include:
• Carotid doppler US: level of 70% stenosis, for
endarterectomy .
• ECG
• Blood test
• Echocardiogram to check cardic source of emboli
• Brain imaging
Immediate Management:

• High dose aspirin( 300mg) should be given once

diagnosis is confirmed ( CT scan)
• continue 100mg dialy thereafter.
 Stroke
Cerebral Infraction

• The clinical impact is vary,and depends on both the

size of the infract,and the location.They can vary from
infracts that lead to death , to ones that are completely
silent.
Causes:
• 60% Atherosclerosis of the carotid arteries and aortic arch
.
• 20% Valvular heart disease.
• 20% Diseaes of the vessels in the brain itself.
 Clinical features:
• The most common stroke presentation is in the a branch of the MCA -
affecting the internal capsule.
• A similar set of signs will be caused by internal carotid occlusion.In these
cases there is:
Contralateral;
• Hemiparesis, Hemiplegia,
• Numbness
• Limbs usu floppy and reflexes reduced /absent.
• Facial weakness( not always).
• Hemianopia and other visual disterbances
• Aphasia ( dominant hemisphere)
• Confusion
• Dizziness
• loss of balance and coordination
• Headache.
• other manifestations, rather than neurologic deficits often
suggest the type of stroke for example,
– sudden sever headache _SAH
– impaired consciousness or coma often accompanied by
headache , nausea, and vomiting suggests ICP which can occur
48 to 72 hrs after large ischemic strokes and earlier in many
hemorrhagic strokes ,fatal brain herniation may result
• Very rare epileptic seizure at the time of onset.

Recovery:
• The symptoms are maximal just after the time of onset.
• Recovery will occur gradually over days , weeks, and
even months.
• Reflex will return early on , often become exaggerated.
• there is headach and /or impaird consciousness
(haemorrhage)
 Examining for stroke:

• start with general examination to check for cluse as to the origin

of the lesion:
Eyes
• Diabetic changes.
• Retinal emboli.
• Hypertensive changes.
• Arcus senils( corneal arcus)
Cardiovascular system
• BP
• Arrythemias.
• Murmurs
• JVP- HF
• Peripheral bruses and bruits
Respiratory System
• Pulmonary oedema
• Infection
Abdomen - feel bladder for urinary retention
 Pathology:
• Sudden cessation of blood supply to neurons, lead to
quickly to hypoxic cells- oedema of the cell( penumbera)-
increas ICP(further affect the blood supply - release of free
radicals -necrosis in the area .
– Anterior Cerebral artery: typically causes unilateral
symptoms.Contralateral hemiparesis(maximal in the leg),urinary
incontenence, apathy, confusion,grasp reflex,gaite apraxia.
– Middle Cerebral Artery : contralateral hemiparesis( worse in the
arm and face than leg)dysarthria, hemianesthesia,contralateral
hoomnymous hemianopia, aphasia(dominant)apraxia, sensory
neglect(nondominant).
• Posterior Cerebral Artery:
Contralateral homonymous hemianopia,unilateral
cortical blindness,memory loss, unilateral 3rd CN palsy,
hemiballismus
• Carotid and Vertebral Artery Dissection:
Account for just under 20% of the stroke in those under
40 , and is often the result of trauma .Symptoms resmbl
the stroke , TIA or migraine, with pain at the sit of the
dissection.
• Brainstem Infract:

Clinical depend on which the nuclei are involved and if the

involvement is bi or unilateral;eg:
1. Hemi/tetraparesis_ corticospinal tract
2. Sensory loss _Medial lemniscus/spinothalamic tract
3. Diplopia_ occulomotor nuclei
4. Facial numbness_ 5th nerve nuclei
5. Facial weakness_ 7th nerve nuclei
6. Nystagmus and vertigo_ vestibular connections
7. Dysphagia/Dysartheria_ 9th/10th nuclei
8. Horner syndrome_ sympathetic fibres
9. Altered consciousness_ reticular formation
• Lateral medullary syndrome/posterior inferior cerebellar artery
thrombosis(PICA);
present with acute vertigoand other cerebellar signs:
• Contralateral :
Spinothalamic sensory loss
Hemiparesis( usually mild, rare)
• Ipsilateral:
1. facial numbness(V)
2. Diplopia(VI)
3. Nystagmus
4. Ataxia
5. Horner syndrome
6. 9th and 10th nerve lesion
• Locked in syndrome :
The patient is aware and awake , but virually all motor
neurons are paralysed , patient can not move , usu the
eyes are the only move . Caused by an upper brainstem
infract.
• Pseudo bulber palsy :
The result of a lower brainstem infract , result in bilateral
impirment of the 9_12th cranial nerve .
Lacunar Infraction:
• Deep artery infract may account for up to 25%of
ischemic strokes. Often is symptomless , may present
with very localised symptoms( purely sensory / purely
motor)
1. Aphasia
2. Hemiparesis
3. Hemisensory loss
4. Unilateral ataxia
Weber syndrom:
• infract on one side of the midbrain( ipsilateral 3rd nerve
palsy, contralateral hemiplagia)
Hypertensive Encephalopathy:
• In malignant hypertension , result in ; TIA , stroke , and
rarely SAH .
• there is commonly papilloedema, which can be due to:
1. Direct infract affecting the optic nerve
2. Infract of other part of the brain , resulting in oedema -
increas ICPand then pressure of the optic disc.
• other syndroms like:
1. Anton syndrome_ infraction of the visual cortex .
2. Multi-infract dementia.
Investigations:
CT and MRI:
• Infraction will always show up as a wedge shape on both CT or MRI.
• Haemorrhage ; blood appears bright white(dense) on CT -but longer
it become darker, 1_2wks it may be indistinguishable from brain
tissue.
• new stroke(<2hrs old) may not show up at all , but 2_6 hrs will be
clearly visible
• Diffusion MRI scans_earlier diagnosis.
MR angiography:
• look at the blood vessels in the head, and neck( stenosis and aneurysms).
Carotid doppler US.
OTHER:ECG, CXR,Blood test( ESR,plateletes, glucose,lipid profil
 Cerberal Haemorrhage:
• LOC , headache
• Neurological defects are usu sudden , and more progressive
• most common cause is uncontrol hypertension ,other:
aneurysm, AV malformation, clotting disorders,tumours ,and
cocaine.
• large hage can cause increase ICP and can lead to
herniationof the brainstem, or the blood can leak into the
ventricular system , causing acute hydrocephalus
investigations:
• CT or MRI
• Any dense abnormality in the brain is blood until proven
otherwise.
Treatment;
• stabilization
• reperfusion for some ischemic strokes
• supportive measures and treatment of complications
• strategies to prevent future strokes
Management:
• General emergency measures _ABCs.
• For Ischemic stoke: for thrombolysis unless there are
contra indications
• for those have contraindication shoul offered for them:
1. Aspirin 300mg/day for 2wks then100mg/day
2. dipyridamole
3. warfarin ( AF)_INR2-3
• Carotid endarterctomy
• For Haemorrhagic stroke:
• supportive treatment
• control BP
• surgery
• Stroke rehabilitation
• Occupational therapy
• Primary Prevention:
• control risk factors( HTN, obsity, hyperlipidemia, DM ,
smoking)
• Anticoagulation; lifelong therapy for those with
rheumatic heart disease , prosthetic valves, or AF.
• Secondary Prevention:
• combining aspirin with cloidogrel or another
antiplatelet.
Complications:
• sleep problems, confusion
• depression
• incotinence
• atelctasis and pneumonia,swallowing dysfunction
(aspiration)
• dyhdartion or undernutrition
• immoblity can lead to thromboembolic diseases
• UTI
• pressure ulcers and contractures
Subarachnoid Hemorrhage
(SAH)
• SAH is bleeding between the arachanoid and pia mater. head truma
is the most common cause of SAH.Spontaneous (primary) SAH
usually result from ruptured aneurysms
• A comgenital berry aneurysm is the cause in about 85% of Pts.
• Bleeding may stop spontaneously.
• Aneurysmal hag may occur at any age but is most common from 40
to 65
• Less common causes are ; AV malformations , and bleeding
disorders.
Pathophysiology:
• Blood in the subarachnoid space causes a chemical
meningitis that commonly increases ICP for days or a few
weeks. Secandary vasospasm may cause focal brain
ischemia and about 25% of pts develop signs of TIA or
ischemic stroke. Brain edema is maximal and risk of
vasospasm and subsequent infraction is highest between
72 hrs and 10 days
• Secandery acute hydrocephalus is also common
• A 2nd rupture sometimes occurs most often within 7 days.
symptoms and signs:
• Headache; is usually sever peaking within seconds
• LOC immediately or sometimes not for several hrs
• Sever neurologic deficit may develop and become irreversable.
• Restless and seizures are possible.
• witin 24 hrs chemical meningitis causes modrate to marked
meningismus, vomiting,and sometimes bilateral extensor planter
• Heart and respiratory rate is often abnormal
• Fever, continued headache and confusion are common during the
first 5 to 10 days
Diagnosis:

• Noncontrast CT or MRI
• LP( RBCs, Xanthochromia, increased pressure)
Prognosis:

• About 35% of pts die after the 1st aneurysmal SAH;

another 15% die within a few weeks because of
subsequent rupture.
• In general prognosis is better with an AV malformation,
and best when 4 vessel angiography dose not detect a
lesion.
Treatment:

• Treatment in comperehensive stroke center

• Nicardipine if mean arterial pressure is >130 mmHg
• Nimodipine to prevent vasospasm
• Occlusion of causative aneurysms
Finally
Salwa