Cerebrovascular Attack

Dr Dinesh Parmar
Professor & Unit Head
Unit A
 Introduction
• 17 million strokes per yr
• 1 stroke every 2 seconds
• 6.5 million deaths per yr
• 26million stroke survivors
Stroke : Arterial stroke (95%),
Venous (1-5%)
Ischemic is 85% &
Hemorrhagic is 15%
• In stroke pt do CT (to rule out bleed )
• Diffusion weighted MRI (look for infarction )
 Defination

• A Stroke / CVA, It is an abrupt onset of focal

neurologic deficit due to a focal hypoperfusion
i.e. Vascular cause which can be due to
• Thrombus or
• Thromboembolism
1. Artery to Artery Thromboembolism
2. Cardioembolism
• TIA : It is transient episode of neurologic dysfunction
caused by
Focal brain ischemia
Spinal cord ischemia or
Retinal ischemia with no evidence of acute infarction.
• All neurologic signs & symptoms resolve within 24 hr
• No evidence of brain infarction on brain imaging as
blood flow is quickly restored, brain tissue can
recover fully and the pt’s symptoms are only
transient
• Stroke has occurred if the neurologic signs & symptoms
last for >24 hr or brain infarction is demonstrated on
brain imaging.
 Etiology of stroke
• Cardio Embolic :
• Hyperacute onset ,
• LOC / Saeizures ,
• Full weakness at onset,
• Hemorrhagic transformation,
• Red clot pressent .
• Thrombotic thromboembolic :
• Stroke in evolution ,
• Increasing headache ,
• Fully evolved weakness in 48-72hrs ,
• Fibrin clot present
 TIA
• TIA is predictor of MI and Stroke
• Usually last several mins to hrs (<10min)
• Several attacks (1 to 100 attacks ) may occur before final
stroke (classical of ICA involvement )
• Final stroke may follow TIA in matter of hrs or less
frequently wks to months (max.risk in next 48hrs)
• DW-MRI Normal
• Anterior circulation TIA : Amaurosis fugax
C/L weakness
C/L homonymous hemianopia
Aphasia
• Posterior circulation TIA : Crossed hemiplegia
Lower cranial nerve palsy
 ABCD2 Scoring
• To measure risk of stroke following TIA
ABCD 2 Score Points
Age > 60yrs 1
BP > 140/90 mmHg at initial evaluation 1
Clinical features of TIA
Speech disturbance without weakness ,or 1
U/L weakness 2
Duration of symptoms
10-59 min ,or 1
> 60 min 2
DM in pt’s history 1
• Low risk : Score 0-3
• Moderate risk : Score 4-5
• High risk : Score 6-7
 CHADS2-VASc score
• To determine risk of stroke in pt with Atrial fibrillation
Risk factor Points
C – CHF 1
H- Hypertension 1
A2- Age ≥75yrs 2
D- Diabetes 1
S2- Prior stroke or TIA 2
V- Vascular disease 1
A – Age 65-74yrs 1
Sc - female sex 1
CHA2DS2-VASc Stroke rate/ 100 pts
score yr
0 0
1 1.3
2 2.2
3 3.2
4 4.0
5 6.7
6 9.8
7 9.6
8 6.7
9 15.2
Recommendations on use of Anti-thrombotics based on
CHADS2 score

CHADS2 Score Antithrombotics

0 Aspirin or no antithrombotics

1 Aspirin or oral anticoagulant

>1 Oral anticoagulant

 Classification of Stroke
• Arterial stroke Cerebral Venous thrombosis
(95-99%) (1-5%)

Ischemic Haemorrhagic Hypercoaguable state Pregnancy

Stroke stroke
(85%) (15%) Inherited Acquired

Cardioembolic stroke (AF) ICH,SAH

Artery to artery embolic stroke Factor V leiden APLA
Thrombotic stroke mutation syndrome
Infarct Haemorrhagic stroke
Proximal Hyperdense MCA MCA dot sign in distal part
sign (arrow) in the M1 of MCA in the sylvian fissure
segment of MCA (arrow)
 Causes of Thrombosis of large vessels
• Atherosclerosis (DM,HTN)
• Dissection
• Takayasu Arteritis
• Fibromuscular Dysplasia
• APLA syndrome
Causes of Cardio Embolism
• AF
• MS/AS
• Prosthetic valve
• Sick sinus syndrome
• Dilated cardiomyopathy
• Recent MI
 Common risk factors of stroke
Factor Population attributable risk Risk reduction with
treatment
Lifestyle
Cigarette smoking 12-14% 50% within 1yr of quitting
Physical inactivity 30%
Excess alcohol consumption 7%

Medical
Hypertension >90% 38%
Diabetes 5-27% No proven effect
Atrial fibrillation 2-24% 68% Warfarin,21% Aspirin
Carotid stenosis 2-7% 65% at 2 yrs
Sickle cell ds - 91% with transfusion
therapy in children
Stroke syndromes are divided into
• (1) large-vessel stroke within the anterior
circulation,
• (2) large-vessel stroke within the posterior
circulation, and
• (3) Small-vessel disease of either vascular
bed.
 Blood supply of Brain
• Anterior circulation
• Posterior circulation
Major supplying artery Area supplied

Anterior cerebral artery Medial surface of brain

Middle cerebral artery Superolateral surface of

brain

Posterior cerebral artery Brainstem

Diagram of a cerebral hemisphere in coronal section showing the
territories of the major cerebral vessels that branch from the
internal carotid arteries.
Circle of Willis
 Anterior circulation
• It starts with internal carotid artery
• Major arteries of anterior circulation :
1. Anterior cerebral artery
2. Middle cerebral artery
3. Intracranial branches of Internal Carotid artery
Ophthalmic artery
Posterior communicating artery
Anterior choroidal artery
Anterior cerebral artery
Middle cerebral artery
Diagram of a cerebral hemisphere, lateral aspect, showing the branches
and distribution of the MCA and the principal regions of cerebral
localization. Note the bifurcation of the MCA into a superior and inferior
division.
 Middle Cerebral Artery
Branches :
• M1 segment (extends from origin of MCA from ICA)
• M2 segment (MCA in Sylvian fissure) :
1. Superior &
2. Inferior divisions
 Middle Cerebral Artery
• The proximal MCA (M1 segment) gives rise to
Penetrating branches (lenticulostriate
arteries) :
• Putamen,
• Outer GP,
• Posterior limb of the IC
• Adjacent Corona Radiata, &
• Most of the caudate nucleus .
• In the Sylvian fissure, the MCA divides into
• Superior :
• Frontal &
• Superior Parietal cortex
• Inferior divisions (M2 branches).
• Inferior Parietal &
• Temporal cortex,
 Proximal MCA occlusion /
M1 segment occlusion
• Causes Cortical stroke in Superolateral cortex (so
weakness predominantly involve face and upper limb in
MCA occlusion)
• Clinical features : 3H
1. Contralateral Weakness/ Hemiplegia
2. Contralateral Hemisensory loss
3. Contralateral Homonymous Hemianopia
4. Global Aphasia (if dominant lobe involved )
5. Frontal eye field(FEF) involvement / gaze palsy
6. Significant Cerebral edema
7. LOC / Seizures due to cerebral edema
M2 segment Oclusion:
• Similar features as M1 segment occlusion (3H’s)
+ Transcortical aphasia
• Cerebral edema is less
M2 Superior division occlusion:
• Broca’s aphasia + Weakness + FEF involved
M2 Inferior division occlusion:
• Wernicke’s aphasia (as supply temporal lobe ) +
no weakness
• Jargon speech and an inability to comprehend
written and spoken language are prominent
features, often accompanied by a contralateral,
homonymous superior quadrantanopia
Lenticulostriate artery occlusion:
• Supplies internal capsule
• C/F:
1. Dense contralateral Hemiplegia
( both UL& LL involve )
2. Homonymous hemianopia
3. Hemisensory loss
4. Facial nerve palsy
5. No cerebral edema
 Specific lobar findings
• Frontal lobe : Prefrontal cortex
Personality changes
Antisocial behaviour
Lack of initiative
Impaired memory
Incontinence
Grasp reflexs
Anosmia
• Temporal lobe :
Medial : supplied by PCA
Lateral : supplied by MCA & also supplies auditory
area so wernicke’s aphasia occur without weakness
 Features of dominant Parietal lobe lesions
• Apraxia – Inability to perform learned skilled
movements
• Acalculia – Difficulty performing simple mathematical
tasks
• Alexia – Inability to recognize or read written words or
letters
• Agnosia – Inabilty to recognize & identify
objects,persons or sounds
• Dysphasia – Language disorder marked by deficiency in
generation of speech and its comprehension
• Contralateral inferior homonymous quadrantnopia
• Gerstmann syndrome ( Acalculia ,Dysgraphia ,Finger
agnosia, Right- Left confusion)
 Anterior cerebral artery
• Supplies medial surface of brain
• The ACA is divided into two segments:
• Precommunal (A1) circle of Willis, or stem, which connects the internal carotid artery
to the anterior communicating artery, and
• The A1 segment gives several deep penetrating branches that supply
Anterior limb of the internal capsule
Anterior perforate substance
Amygdala,
Anterior hypothalamus, &
Inferior part of the head of the caudate nucleus.
• Occlusion of the proximal ACA is well tolerated & do not produce stroke because of
collateral flow through the anterior communicating artery and collaterals through
the MCA and PCA
• Postcommunal (A2) segment distal to the anterior communicating artery .
• A2 segment supplies
Frontal pole ,
Entire medial part of frontal & parietal lobe
• A2 syndrome / ACA stroke:
1. Contralateral LL weakness
2. Urinary incontinence ( due to paracentral
lobule involvement)
3. Gait Apraxia : inability to lift foot but no
motor weakness
4. Primitive reflexes + ( contralateral grasp,
Sucking reflex)
5. Cortical sensory loss
Diagram of a cerebral hemisphere, medial aspect, showing the
branches and distribution of the ACA and the principal regions
of cerebral localization.
 Posterior Circulation
• Major artery : Posterior Cerebral Artery (PCA)
• In 75% of cases, both PCAs arise from the
bifurcation of the Basilar artery
• In 20%, one has its origin from the ipsilateral
internal carotid artery via the posterior
communicating artery
• In 5%, both originate from the respective
ipsilateral internal carotid arteries
• PCA branches: P1 segment , P2 segment
 Area of brain Supplied by

Midbrain, Subthalamus , P1 segment ( proximal to

Thalamus Post.Communicating artery)

Medial Temporal lobe , P2 segment ( distal to

Occipital lobe Post.Communicating artery)
• Diagram of the posterior circulation, showing the intracranial vertebral
arteries forming the basilar artery that gives off the anterior inferior
cerebellar, superior cerebellar, and posterior cerebral arteries. The posterior
inferior cerebellar artery arises from each of the vertebral segments. The
majority of brainstem blood flow arises from numerous deep branches of the
basilar artery that penetrate directly into the brainstem
 P1 Syndrome
• Infarction usually occurs in the
• Ipsilateral Subthalamus &
• Medial Thalamus and in the
• Ipsilateral Cerebral Peduncle and midbrain.
• Weber’s syndrome: Crus Cerebri is site of lesion
I/L LMN 3rd nerve palsy +
C/L hemiplegia
• Claude’s syndrome : Tegmentum is site of lesion
I/L LMN 3rd nerve palsy +
Contralateral Ataxia/ Tremors
The Ataxia indicates involvement of the Red nucleus /
Dentato Rubrothalamic tract;
• If the Subthalamic nucleus is involved:
Contralateral hemiballismus may occur.
• Artery of Percheron involvement :
1. Drowsiness & confusion
2. Vertical gaze palsy
3. Memory disturbance
• Extensive infarction in Midbrain & Subthalamus
occurring with bilateral proximal PCA occlusion
presents as
• Coma,
• Unreactive pupils,
• Bilateral Pyramidal signs, &
• Decerebrate rigidity.
• Occlusion of the penetrating branches of Thalamic
and Thalamogeniculate arteries produces less
extensive Thalamic and Thalamocapsular lacunar
syndromes.
Thalamic Déjérine - Roussy syndrome :
1. Contralateral hemisensory loss followed
later by an agonizing, searing, or burning
pain in the affected areas.
2. It is persistent and responds poorly to
analgesics.
3. Anticonvulsants
Carbamazepine /
Gabapentin /
TCA may be beneficial.
 P2 Syndromes
Unilateral P2 syndromes :
1. Splenium of Corpus callosum : Alexia without
Agraphia
2. Medial temporal lobe: Memory loss
3. Visual association area : Visual agnosia
4. Occipital lobe : Contralateral Incongruent
Homonymous Hemianopia with macular
involvement & pupillary sparing
 Bilateral P2 Syndromes
• Anton syndrome : Cortical blindness (awareness of
blindness is absent & pt denies of having blindness )
• Balint syndrome : Watershed infarct of B/L PCA
• Optic ataxia ( can touch the object with eyes closed but
not with eyes open due to development of ataxia as a
result of loss of scanning of visual field )
• Occulomotar Apraxia
• Palinopsia ( Persistence of an image inspite of changing
gaze)
• Simultanagnosia (Inability to synthesize whole image)
 Vertebral Artery
• Vertebral artery arises from the Innominate Artery on the right
and the subclavian artery on the left, consists of four segments.
• The first (V1) extends from its origin to its entrance into the
sixth or fifth transverse vertebral foramen.
• The second segment (V2) traverses the vertebral foramina
from C6 to C2.
• The third (V3) passes through the transverse foramen and
circles around the arch of the atlas to pierce the dura at the
foramen magnum.
• The fourth (V4) segment courses upward to join the other
vertebral artery to form the basilar artery
• Disease of the distal 4th segment of the vertebral artery
can promote thrombus formation manifest as embolism
or with propagation as basilar artery thrombosis.
• Stenosis proximal to the origin of the PICA can threaten
the lateral medulla and posterior inferior surface of the
cerebellum.
• If the subclavian artery is occluded proximal to the
origin of the vertebral artery, there is a reversal in the
direction of blood flow in the ipsilateral vertebral artery.
• Embolic occlusion or thrombosis of a V4 segment causes
ischemia of the lateral medulla.
Lateral medullary (Wallenberg’s) syndrome
• Vertigo+ numbness of the ipsilateral face and
contralateral limbs + diplopia + hoarseness +
dysarthria + dysphagiam+ ipsilateral Horner’s
syndrome + Ipsilateral upper motor neuron facial
weakness can also occur.
• Due to ipsilateral vertebral artery occlusion i.e. PICA
occlusion is responsible mainly .
• Hemiparesis is not a typical feature of vertebral artery
occlusion; however, quadriparesis may result from
occlusion of the anterior spinal artery
Medial Medullary Syndrome
occurs with infarction of the pyramid and
contralateral hemiparesis of the arm and leg,
sparing the face.
• If the medial lemniscus and emerging
hypoglossal nerve fibers are involved,
contralateral loss of joint position sense
and ipsilateral tongue weakness occur.
• Only 4th segment gives rise to branches that supply the
brainstem and cerebellum.
• The Posterior inferior cerebellar artery (PICA) in its
proximal segment supplies the lateral medulla and, in its
distal branches, the inferior surface of the cerebellum.
• Atherothrombotic lesions mainly in V1 and V4
segments of the vertebral artery.
• The first segment may become diseased at the origin of
the vessel and may produce posterior circulation emboli
 Imaging studies
• CT scan: Identify Hemorrhage
Identify Extraparenchymal hemorrhages,
Neoplasms,
Abscesses etc.
• MRI: Extent and location of infarction in all areas of the
brain, including the posterior fossa and cortical surface & also
identifies intracranial hemorrhage and other abnormalities
• Cerebral Angiography : Gold standard for identifying and
quantifying atherosclerotic stenosis of the cerebral arteries
and for identifying and characterizing other
pathologies(aneurysms, vasospasm, intraluminal thrombi,
fibromuscular dysplasia, arteriovenous fistulae, vasculitis,
and collateral channels of blood flow)
• Ultrasound Techniques: stenosis at the origin of ICA can
be identified and quantified reliably by USG that
combines a B-mode ultrasound image with a Doppler
ultrasound assessment of flow velocity (“duplex”
ultrasound).
• Transcranial Doppler (TCD) assessment of MCA, ACA, and
PCA flow and of vertebrobasilar flow is also useful
• Perfusion Techniques: Both xenon techniques (principally
Xenon-CT) and PET quantify cerebral blood flow. Single-
photon emission computed tomography (SPECT) and MR
perfusion techniques report relative cerebral blood flow.
• MR perfusion can be combined with MR diffusion imaging
to identify the ischemic penumbra as the mismatch
between these two imaging sequences
Causes of Intracranial Hemorrhage
 ISCHEMIC STROKE
• Acute occlusion of an intracranial vessel causes
reduction in blood flow.
• Normal cerebral blood flow in an adult brain at
rest is 50-55mL/100g/min
• A decrease in cerebral blood flow to zero ,causes
death of brain tissue within 4–10 min;
• Values <16–18 mL/100 g tissue per minute cause
infarction within an hour; and
• Values <20 mL/100 g tissue per minute cause
ischemia without infarction unless prolonged for
several hours or days.
• If blood flow is restored to ischemic tissue before
significant infarction develops, the pt may
experience only transient symptoms, and the
clinical syndrome is called TIA.
• Ischemic Penumbra
Defined as ischemic but reversibly dysfunctional
tissue surrounding a core area of infarction.
• Ischemic Penumbra
It will eventually progress to infarction if no
change in flow occurs, and hence, saving the ischemic
penumbra is the goal of revascularization therapies
Causes of Ischemic Stroke
Three major mechanisms that underlie ischemic stroke:

(1) Occlusion of an intracranial vessel by an embolus

(e.g., cardiogenic sources such as atrial fibrillation or
artery-to-artery emboli from carotid atherosclerotic
plaque), often affecting the large intracranial vessels;

(2) In situ thrombosis of an intracranial vessel, typically

affecting the small penetrating arteries that arise from
the major intracranial arteries;

(3) Hypoperfusion caused by flow-limiting stenosis of a

major extracranial (e.g., internal carotid) or intracranial
vessel, often producing “watershed” ischemia.
phy angiogram of the common, internal, and external carotid art
Pathophysiology of Cerebral Ischemia
 Management
• The first goal is to prevent or reverse brain injury.
• Attend to the patient’s Airway, Breathing, and Circulation
(ABCs)
• Treat Hypoglycemia or Hyperglycemia.
• Perform an emergency noncontrast head CT scan to
differentiate between ischemic stroke and hemorrhagic
stroke
• There are no reliable clinical findings that conclusively
separate ischemia from hemorrhage, although a more
depressed level of consciousness, higher initial blood
pressure, or worsening of symptoms after onset favor
hemorrhage
• Treatments designed to reverse or lessen
the amount of tissue infarction and
improve clinical outcome fall within six
categories:
(1) Medical support,
(2) IV Thrombolysis,
(3) Endovascular revascularization,
(4) Antithrombotic treatment,
(5) Neuroprotection, and
(6) Stroke centers and rehabilitation
 Management
• If pt presents with weakness :
• Diagnose if it’s a Stroke / TIA
• If stroke elicit whether it is a thrombotic / embolic or
thromboembolic stroke from history assess if it can be
salvaged
• Endovascular intervention / thrombolysis
• But when in doubt , do a
➢ CT brain : to assess hemorrhage
➢ Diffusion weighted MRI (DWMRI):
• Normal : No stroke
• Hyperintensity : Infarct + t stroke
➢ Scope for salvagability & Penumbra
• <10 ml/mg/min : infarcted area
• >22ml/mg/min : normal cerebral blood flow
• 10-22 ml/mg/min : ischemic penumbra
 Penumbra
• Peripheral region of ischemia but salvageable tissue
surrounding a central core of irreversibly infarcted
tissue is referred as penumbra .
• Without adequate timely recanalization , infarction
expands to include penumbra
• To detect penumbra : do a perfusion weighted MRI
Penumbra
 Identification of Penumbra by PMR

• DWI shows area with

irreversible damage
(dead tissue) –marked
in red
• PWI shows area with
hypoperfusion –
marked in blue
• Diffusion perfusion
mismatch indicated in
green : this is the area
that may be salvaged
by therapy
• MR Angiogram : shows exact location of infarct /lesion
• If present in a large vessel /1st order branches : start
endovascular procedures for clot retrieval or stent for
stenosis
• Initially done within 6hrs but now is being done within
24hrs in some hospitals
• MR Angio shows lesion in an inaccessible vessel , then do
thrombolysis , provided that pt brought to hospital within
4-5hrs

Duration /time Prognosis & treatment

4.5hrs Golden hours of stroke

Thrombolysis can be done
>5hrs Thrombolysis is ineffective
 Thrombolysis
Indication :
• Clinical diagnosis of stroke
• Onset of symptoms to time of drug administration
<4.5hrs
• Age ≥18 yrs
• CT scan showing no haemorrhage or edema of
>1/3rd of MCA territory
Contraindications of thrombolysis :
• Sustained BP >185/110 mmHg despite
treatment
• Bleeding diathesis
• Recent head injury or ICH
• Major surgery in preceding 14 days
• Minor stroke symptoms
• Gastrointestinal bleeding in preceding 21days
• Recent MI
 Drugs used for thrombolysis
➢ Alteplase : Recombinant Tissue Plasminogen Activator
(rtPA)
0.9mg/kg : 10% of dose is given an IV bolus
90%given as infusion over 1hr
Recently , Tenecteplase is being approved
➢ Endovascular procedures preferred over thrombolysis
• At presentation : single Anti-platelet may be given
Aspirin 300mg stat dose f/b 150mg
maintainance which can be stepped down to 75mg
➢ Double anti-platelet therapy (DATP):
indications :
• TIA as it can develop into stroke
• Minor stroke
• Developed stroke while on a single
antiplatelet
➢ Anticoagulation : required only for
Cardioembolic stroke like in
. AF with MS
. Post mitral valve replacement
Recombinant Tissue Plasminogen Activator (rtPA)
Management of acute stroke