stroke

Definations

• WHO defines stroke as “the rapidly

developing clinical symptoms &/or
signs of focal (at times global)
disturbance of cerebral function,
with symptoms lasting more than
24hrs or leading to death with no
apparent cause other than that of
vascular origin.
 Transient ischemic attack
A TIA is a clinical syndrome characterized
by an acute loss of focal cerebral or
monocular function with symptoms lasting
<24 hrs & which is thought to be due to
inadequate cerebral or ocular blood supply
as a result of arterial thrombosis or
embolism associated with arterial, cardiac
or hematological disease regardless of
whether there is imaging evidence of new
permanent brain injury.
Reversible ischemic neurological deficit
{RIND}
• It refers to a neurological deficit that
disappears within 7 days, but
usually within 2-3 days of onset.
Stroke in Evolution
If a patient suffers
progressive neurological deficits
over a period of a few
hours or days that are not accounted
for by cerebral edema, it is said to
be a stroke in evolution.
 COMPLETED STROKE
• A completed stroke is the term applied to
the temporal profile of the stroke
syndrome in which the deficit is prolonged
and often permanent, causing
demonstrable parenchymatous changes.
STROKE CLASSIFICATION
 The Oxford Community Stroke Project classification
(OCSP, also known as the Bamford or Oxford classification

The stroke episode is classified as:

• Total anterior circulation stroke (TAC)
• Partial anterior circulation stroke (PAC)
• Lacunar stroke (LAC)
• Posterior circulation stroke (POC)
The type of stroke is then coded by adding a
final letter to the above:
• I – for infarct (e.g. TACI)
• H – for haemorrhage (e.g. TACH)
• S – for syndrome; intermediate pathogenesis,
prior to imaging (e.g. TACS)
Stroke Data Bank Subtype
(NINDS) Classification
• Derived from the Harvard Stroke Registry
classification, the National Institute of
Neurological Disorders and Stroke (NINDS)
Stroke Data Bank recognised 5 major groups
• Infarction of unknown cause
• Infarction with normal angiogram
• Infarction in association with arterial pathology
• Embolism from a cardiac source
• Infarction due to atherosclerosis
• Lacune infarct
• Parenchymatous or intracerebral haemorrhage
• All other strokes
•
The TOAST (Trial of Org 10172 in Acute Stroke
Treatment) classification
• Is based on clinical symptoms as well as
results of further investigations. Based on
this, a stroke is classified as being due to:
• Thrombosis or embolism due to
atherosclerosis of a large artery
• Embolism of cardiac origin
• Occlusion of a small blood vessel
• Other determined cause
• Undetermined cause
• a. Two possible causes
• b. No cause identified
• c. Incomplete investigation
 NATURAL HISTORY
• Approximately 1/3 of all ‘strokes’ are fatal.
• The age of the patient, the anatomical size of the
lesion, the degree of deficit and the underlying
cause all influence the outcome.
• In cerebral haemorrhage, mortality approaches
50%.
• Cerebral infarction fares better, with an immediate
mortality of less than 20%, fatal lesions being large
with associated oedema and brain shift.
• Embolic infarction carries a better outcome than
thrombotic infarction.
• The level of consciousnees on admission to
hospital gives a good indication to immediate
outcome. The deeper the conscious level the
graver the prognosis.
MECHANISM
Causes of Cerebral ischemia
and infarction
• Arterial wall disorders
 atherothromboembolism
 intracranial small vessel disease
 trauma
 dissection
 fibromuscular dysplasia
 congenital arterial anomalies
 moyamoya syndrome
 embolism from arterial aneurysm
 inflammatory vascular diseases
 infections
 continued
• Embolisation from heart
• Hematological disorders
• Miscallaneous
• pregnancy
• oral contraceptives
• cancer
• fat embolism
• nephrotic syndrome
Causes of Spontaneous
intracranial hemorrhage
1]primary intracerebral hemorrhage
 hypertension
 aneyrysms
 intracranial vascular malformations
 hemostatic failure
 inflammatory vascular disorders
 hemorrhagic transformation of
cerebral infarction
 Vascular tumors
 miscallaneous
• 2]Subarachnoid hemorrhage

• 3]Intraventricular hemorrhage

• 4]Subdural hemorrhage
Cerebral circulation
 PHYSIOLOGY
• 2% of BW
• 20% of Total body oxygen
consumption
– (60% used for ATP formation)
• CMR O2 3-3.8mL /100 gm/min
– (50 ml /min in Adult)
• 15% 0f CO2
• Glucose consumption 5
mg/100gm/min
– (25% of total body)
consumption/min
• High oxygen consumption but
no reserve
• Grey matter of cerebral cortex
consumes more
• Directly proportional to
electrical activity
– (Hippocampus & cerebellum
most sensitive to hypoxic
injury)
CBF
GLOBAL 45-55ml/100g/min
CORTICAL 75-80ml/100g/min
SUBCORTICAL 20ml/100g/min

CMRO2 3-3.5ml/100g/min
CVR 2.1mmHg/100ml/
min/ml
Cerebral venous 32-44mmhg
Po2
Cerebral venous 55%-70%
So2
ICP(supine) 8-12mm Hg
Autoregulation of CBF
• Autoregulation refers to the
capacity of the cerebral
circulation to adjust its
resistance in order to
maintain CBF constant over
a wide range of mean
arterial pressure (MAP).
• In normal human subjects, the
limits of autoregulation occur
at MAPs of approximately 70
and 150 mm Hg
• Above and below the
autoregulatory plateau, CBF is
pressure dependent (pressure
passive) and varies linearly
with CPP.
Cerebral perfusion pressure
• MAP—ICP( or CVP whichever is greater)
• Normally 80 to 100mm Hg
• ICP is <10 mmHg so CPP primarily
dependent on MAP
• Increase in ICP>30 =CPP & CBF
compromise
• CPP<50 slowing of EEG
• 25-40 Flat EEG
• CPP <25 result in Irreversible brain
death
Middle cerebral artery
ACA AND PCA
 Stroke Syndromes
• Cluster of signs and symptoms produced
due to the occlusion of an artery(due to an
atherothrombotic lesion or an emboli or
dissection ) supplying a particular region of
the brain
 Classification
• Large vessel stroke within the anterior
circulation
• Large vessel stroke within the posterior
circulation
• Small vessel disease of either vascular
bed
 Stroke within the anterior
circulation
• Due to occlusion of Internal
carotid artery and its branches
• Middle cerebral artery, Anterior
cerebral artery and Anterior
choroidal artery
 Middle Cerebral Artery
• M1 segment(proximal)- deep
penetrating or lenticulostriate
branches– Internal capsule,
caudate nuclues, putamen and
outer pallidus
M1 Segment
Cerebral hemishere in coronal
section
 M2 Segment
• M2(distal)- superior and inferior divisions-
the entire superolateral surface of frontal
and parietal lobe except frontal pole, strip
along the superomedial frontal and parietal
cortex, occipital lobe convolutions and
medial temporal cortex
M2 segment
 Complete MCA Syndrome
• Contralateral hemiplegia
• Contralateral hemianaesthesia
• Contralateral homonymous hemianopia
• Gaze preference to the ipsilateral side
• If dominant hemisphere involved-Global
aphasia
• If non dominant hemisphere involved-
Hemispatial neglect, anasognosia and
constructional apraxia
 Partial syndromes
• M1 syndrome-occlusion of
lenticulostriate branches-
• If ischemia of internal capsule
produces pure motor or sensorymotor
stroke contralateral to the side of
lesion
• If ischemia of putamen, pallidus-
predominantly parkinsonian features
 M2 syndromes
• If superior division involved
• Brachial syndrome- weakness of hand and
arm
• Frontal opercular syndrome-Brocas
aphasia with facial weakness with or
without arm weakness
• proximal part of the superior division
involved- clinical features of motor
weakness, sensory disturbances and
brocas aphasia
 M2 syndromes
• If inferior division of M2 involved-
• If dominant hemisphere- Wernickes
aphasia without weakness with
contralateral homonymous superior
quadrantanopia
• If non dominant hemisphere- Hemispatial
neglect , spatial agonosia without
weakness
 Anterior cerebral artery

A1 segment- from internal carotid to anterior

communicating artery- branches to
anterior limb of internal capsule,
anteroinferior caudate, anterior
hypothalamus
A2 segment-distal to anterior communicating
artery- supplies frontal pole, entire medial
part of cerebral hemispheres
Precommunal A1 segment
Postcommunal A2 Segment
 A1 segment

• A1 segment occlusion rarely

produces clinical syndrome
because collateral flow
through anterior
communicating artery and
collaterals from MCA and PCA
 A2 syndromes
• Motor area for leg and foot-c/l paralysis of
foot and leg
• Sensory area for foot and leg-c/l cortical
sensory loss of foot and leg
• Sensorimotor area in paracentral lobule-
urinary incontinence
• Medial surface of posterior frontal lobe-c/l
grasp and suckling reflex
• Cingulate gyrus and the medial inferior
portions of frontal, parietal and temporal
lobes-abulia
 Anterior Choroidal Artery

• Supplies posterior limb of internal capsule,

retrolentiform and sublentiform parts
• Complete syndrome rare due to collaterals
from MCA, PCA, and ICA
• Syndrome comprises
• c/l hemiplegia
• c/l hemianaesthesia
• c/l homonymous hemianopia
 others
 Internal carotid artery
 Common carotid artery
 Stroke within Posterior
Circulation
• Paired Vertebral arteries
• Basilar artery
• Paired Posterior cerebral arteries
• Gives small penetrating branches and
short and long circumferential
branches
Posterior Circulation

Supplies
Cerebellum
Medulla
Pons
Midbrain
Thalamus
Subthalamus
Hippocampus
Medial part of
temporal lobe
Occipital lobe
 Posterior cerbral artery

• P1 segment-Precommunal-
Midbrain, thalamus and
subthalamus
• P2 segment-Temporal and
occipital cortex
 P1 syndrome

• Due to the involvement of

ipsilateral subthalamus,
cerebral peduncles and
midbrain
 P1 syndrome
• Midbrain
• Claudes- 3rd nerve palsy with c/l ataxia-
Red nuclues
• Webers- 3rd nerve palsy with c/l
hemiplegia-Cerebral peduncle
• Subthalamus-c/l hemiballismus
• Thalamus- Thalamic dejerine Roussy
syndrome- c/l hemisensory loss followed
later by severe agonising pain
Midbrain syndromes
 P2 syndromes

• Infarction of medial temporal and occipital

lobes
• Occipital lobe-c/l homonymous
hemianopia with macular sparing, if visual
association area spared, patient aware of
visual defect
• Medial temporal lobe- Memory
impairement
• Visual hallucinations
 P2 syndromes
• Antons syndrome-bilateral occlusion
in distal PCAs – bilateral occipital
lobe infarction- cortical blindness and
patient often unaware and even deny
it
• Balints syndrome-bilateral visual
association areas- palinopsia and
asimultagnosia
P2 syndromes
vertebral [v4] and PICA
 V4 AND PICA
• V1 and V4- prone for
atherothrombosis
• If V1 occlusion
• If occlusion is in subclavian artery
proximal to origin of vertebral artery-
subclavian steal syndrome
 Lateral medullary syndrome
[wallenburgs]
• Caused due to occlusion of V4 segment or PICA
• Descending tract and nucleus of trigeminal nerve- Pain,
numbness and abnormal sensation over one half of face
• Vestibular nucleus-Vertigo, nausea, vomiting and
diplopia
• Issuing fibres of 9th and 10th nerve nucleus- Dysphagia,
hoarseness, palatal paralysis
• Restiform body, and cerebellar hemispheres-Ataxia of
limbs
• Descending sympathetic tract-Horners syndrome
• Spinothalamic tract- c/l loss of pain and temperature
Medullary syndromes
 Medial Medullary Syndrome
• Infarction of pyramid- c/l hemiplegia
of arm and leg, sparing face
• If medial lemniscus-c/l loss of tactile
and proprioception
• If hypoglossal nerve nucleus
involved- ipsilateral LMN hypoglossal
nerve palsy – atrophy of half of
tongue.
 BASILAR ARTERY
• Paramedian- wedge of pons in
midline
• Short circumerential- lateral two thirds
of pons and middle and superior
cerebellar peduncles
• Long circumferential- Superior and
anterior inferior cerebellar
 BASILAR ARTERY
SYNDROMES
• Occlusion of basilar artery-b/l
brainstem signs
• Occlusion of basilar branch artery-
unilateral motor, sensory and cranial
nerves
 BASILAR ARTERY
SYNDROMES
• Complete basilar artery
occlusion(Locked in state)-b/l long
tract(sensory/motor) with cranial
nerve and cerebellar dysfunction-
preserved consciousness,
quadriplegia and cranial nerve
signs
Differential diagnosis of acute
stroke
• Intracranial tumor
• Subdural hematoma
• Epileptic seizure
• Cerbral abscess
• Metabolic /toxic encephalopathy
• Viral encephalitis
• Hypertensive encephalopathy
• Multiple sclerosis
• Head injury
• Psychogenic
• Creutzfeldt jacob disease
 Baseline non imaging
investigations for stroke patients
• Full blood count
• ESR/CRP
• ELECTROLYTES
• Urea
• Plasma glucose
• Plasma lipids
• Urine analysis
• electrocardiogram
 Imaging studies
• CT radiographic images identify or exclude hemorrhage
as the cause of stroke, and they identify
extraparenchymal hemorrhages, neoplasms, abscesses,
and other conditions masquerading as stroke. Brain CT
scans obtained in the first several hours after an
infarction generally show no abnormality, and the infarct
may not be seen reliably for 24–48 hours. CT may fail to
show small ischemic strokes in the posterior fossa
because of bone artifact; small infarcts on the cortical
surface may also be missed.
• Contrast-enhanced CT scans add specificity by showing
contrast enhancement of subacute infarcts and allow
visualization of venous structures.
• CT angiography (CTA) can be performed
with administration of IV iodinated contrast
allowing visualization of the cervical and
intracranial arteries, intracranial veins,
aortic arch, and even the coronary arteries
in one imaging session. Carotid disease
and intracranial vascular occlusions are
readily identified with this method.
• CT Perfusion Imaging
 MRI

• MRI reliably documents the extent and location

of infarction in all areas of the brain, including
the posterior fossa and cortical surface. It also
identifies intracranial hemorrhage and other
abnormalities but is less sensitive than CT for
detecting acute blood.
• Diffusion-weighted imaging is more sensitive for
early brain infarction than standard MR
sequences or CT as is fluid-attenuated
inversion recovery (FLAIR) imaging
 Ultrasound techniques

• Stenosis at the origin of the internal carotid

artery can be identified and quantified
reliably by ultrasonography 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

• Xenon CT
• PET Scan
• Single-photon emission computed
tomography (SPECT)
• MR perfusion
• Plain CT scan with CT perfusion scan
• MR Perfusion combined with MR diffusion
imaging
 Management Of Cerebral
infarction
Treatment Aims
[Link] progression of present
event
2. Prevent development of
complication (e.g.
aspiration pneumonia, pressure
sores, deep vein thrombosis)
[Link] rehabilitate the patient
4. Prevent the development of
subsequent event
 Reverse or Lessen the
infarction
• Medical Support
• IV Thrombolysis
• Endovascular Techniques
• Antithrombotic Treatment
• Neuroprotection
• Stroke centres and Rehabilitation
 MEDICAL SUPPORT

• Lower blood pressure (BP) to < 185/110

mm Hg before rtPA
• Airway support if necessary
• Treat hyperthermia
• No O2 if not hypoxic
• Maintain adequate hydration(normal saline
being the fluid of choice)
• Maintain euglycemia
 A PRACTICAL APPRACH TO ELEVATED BP In
PTS. WITH ACUTE ISCHEMIC STROKE-
Recommendations from STROKE COUNCIL of
ASA:

• BP MANAGEMENT
A] NOT ELIGIBLE FOR OBSERVE

THROMBOLYSIS & UNLESS

SBP≤22O MM HG OTHER END
OR ORGAN
DBP≤120 MMHG DAMAGE
 SBP>22O &/OR DBP>120
LABETELOL 10-20 mg IV OVER 1-2 min.
REPEAT OR DOUBLE EVERY 10 min.
MAX. DOSE:300mg
NICARDIPINE INFUSION
5 mg/[Link] TO DESIRED EFFECT
BY INCREASING BY2.5mg/Hr EVERY
MIN. MAX.15mg/hr
TARGET:10-15% DROP
DBP>140 MMHG
NITROPRUSSIDE DRIP
-5mcg/kg/min.
TITRATE.
TARGET-10-15% DROP

[Link] FOR THROMBOLYSIS

SBP>180 OR DBP>110
LABETELOL-10-20 Mg IV.
REPEAT AS NECESSARY.
NITROPRUSSIDE
 Administration of Intravenous
Recombinant Tissue Plasminogen
Activator (Rtpa) for Acute
Indication Contraindication
Ischemic
Clinical diagnosis of stroke
Stroke
Sustained BP >185/110 mm Hg despite
Onset of symptoms to time of drug treatment
administration ≤3 h Platelets <100,000; HCT <25%; glucose <50
CT scan showing no hemorrhage or edema or >400 mg/dL
of >1/3 of the MCA territory Use of heparin within 48 h and prolonged
Age≥ 18 years PTT, or elevated INR
Consent by patient or surrogate Rapidly improving symptoms
Prior stroke or head injury within 3 months;
prior intracranial hemorrhage
Major surgery in preceding 14 days
Minor stroke symptoms
Gastrointestinal bleeding in preceding 21
days
Recent myocardial infarction
Coma or stupor
 Administration of rtPA
• Intravenous access with two peripheral IV lines (avoid
arterial or central line placement)
• Review eligibility for rtPA
• Administer 0.9 mg/kg IV (maximum 90 mg) IV as 10% of
total dose by bolus, followed by remainder of total dose
over 1 h
• Frequent cuff blood pressure monitoring
• No other antithrombotic treatment for 24 h
• For decline in neurologic status or uncontrolled blood
pressure, stop infusion, give cryoprecipitate, and reimage
brain emergently
• Avoid urethral catheterization for ≥2 hr
 Endovascular Techniques
• Intraarterial urokinase is being used by
some stroke centres.
• 1 out of 7 treated patients is benefited
from this technique currently(as per
PROACT 1 AND PROACT2 TRIALS)
• Not approved by US FDA Till date
• Endovascular mechanical thrombectomy
 Antiplatelet Therapy

• Should be treated with aspirin as soon as

practicable after brain imaging has
excluded hemorrhage
• Starting aspirin therapy within first 48 hrs
of acute ischemic stroke avoids death or
disability at 6 months for about 10 patients
per 1000 treated[CAST TRIAL 1997]
• Starting dose of 150-300 mg is adviced for
acute phase of ischemic stroke f/b long
term treatment with 75-150 mg /day
• Combination of aspirin and dipyridamole is
more effective than aspirin alone[ESPIRIT
STUDY GROUP2006]
• Combination of Aspirin and Clopidogrel
was not superior to clopidogrel alone
[MATCH TRIAL 2004]
However the risk of life threatening
hemorrhage was significantly higher in
combination antiplatelet group at 18
months
 ANTICOAGULATION
• Immediate therapy with systemic anticoagulants
like unfractionated
heparin,LMWH,Heparinoids,DTI is not a/w net
short or long term benefit[internatinal stroke trial
collaborative group 1997]
• Patients in AF who have a tia or stroke without
other clear etiology should be anticoagulated if
there is no contraindiaction[EAFSG 1993]
• Anticoagulation is not effective in secondary
prevention of stroke in pts with sinus
rhythm[SPIRIT TRIAL 1997][WARSS TRIAL]
[WASID TRIAL]
 Surgical decomprssion for malignant middle
cereberal artery infarction

• Malignant middle cerebral artery territory

infarction is defined as large MCA territory
infarct with marked edema and swelling
leading to raised ICPand high risk of
coning
• Decompressive surgery consisting of
hemicraniectomy and duroplasty
• Surgery within 48 hrs of stroke onset
reduced case fatality from 71 to 22 %
 Neuroprotective Interventions
 Hyperbaric oxygen not recommended, except for air
embolization
 Transcranial near-infrared laser therapy and other
neuroprotective drugs not recommended
 Metalloproteinase inhibitors are not found to be
effective in human studies
 Hypothermia is a powerful neuroprotective treatment in
patients with cardiac arrest and is neuroprotective in
animal models of stroke, but it has not been adequately
studied in patients with ischemic stroke.
 The Bottom Line: No trial has yet shown benefit for a
neuroprotective agent in acute stroke. A few agents
remain in trials, such as a phase 3 trial of magnesium
delivered in the field by paramedics.
 Treatment of acute intracerebral
hemorrhage
• Recombitant factor VIIa
• Cerebrospinal fluid drainage
• Hyperventilation
• Osmotic agents
• Use is not backed up by randomised trials
with clinical outcomes than pressure as
the outcome variable
 Blood pressure control in ICH

• SBP>220 OR MAP>150 MMHG

CONSIDER AGGRESSIVE MANAGEMENT
WITH IV INFUSION

SBP>180 OR MAP>130 WITH EVIDENCE

OF ELEVATED ICP
CONSIDER ICP MONITORING INFUSION
OR INTERMITTENT DOSES TO KEEP
CPP>60
[Link]>180 OR DBP>130 WITH NO
EVIDENCE OF ELEVATED ICP
Consider modest reduction of blood
pressure
 Surgical Treatment
• 4 possible ways
1] simple aspiration
2] craniotomy with open surgery
3]endoscopic evacuation
4]stereotactic evacuation

Open surgery remains the technique of

choice at present
 RECOVERY

Some degree of recovery occurs in majority

of patients after [Link] complete
recovery is possible,the prognosis is
difficult o predict in individual patient
Good prognostic signs include
young age ,an initially mild deficit,normal
conscious level, good sitting balance,lack
of cognitive impairment,urinary
continence,rapid improvement,social
support
• Thank you