SMALL VESSEL
LACUNAR STROKE
What is Stroke?
Definition
Clinical syndrome.
Characterized by rapidly developing clinical symptoms and/or
signs of focal, and at times global, loss of cerebral function.
Symptoms lasting more than 24 hours or leading to death.
No apparent cause other than that of vascular origin.
Stroke Facts
Stroke is a global health problem and is the second
commonest cause of death and a leading cause of adult
long term disability worldwide.
20% of survivors require institutional care after 3
months and 15% to 30% are permanently disabled.
Life-changing event that affects both stroke patients
and caregivers.
Effective prevention remains the best approach for
reducing the burden of stroke.
Those who practice a healthy lifestyle have an 80%
lower risk of first stroke compared with those who do
not.
Risk Factors for Stroke That Cannot
Be Changed
Increased age
Being male
Race (e.g., African-Americans)
Diabetes mellitus
Prior stroke/transient ischemic attacks
Family history of stroke
Asymptomatic carotid bruit
Risk Factor For Stroke: Treatable
Major
Hypertension
Heart disease, esp. atrial fibrillation
Cigarette smoking
Transient ischemic attacks
Dyslipidemia
Physical inactivity
Obesity
Less Well Documented
Excessive alcohol intake / drug abuse
Acute infection*
Types of Stroke
Ischemic, 80%
- thrombosis, 50% (small & large-vessel)
- embolism, 30%
Hemorrhagic, 20%
- intracerebral (HTN as risk)
- subarachnoid (aneurysm)
Transient Ischemic Attack vs
Ischemic Stroke
American Stroke Association (2009): TIA
A transient episode of neurological dysfunction caused by focal
brain, spinal cord, or retinal ischemia without acute infarction.
Clinical Practice Guidelines for Management of Ischemic
Stroke (2012):
A Clinical syndrome characterized by an acute loss of focal
cerebral or monocular function with symptoms lasting less than
24 hours
due to inadequate cerebral or ocular blood supply as a result of
arterial thrombosis or embolism
Ischemic stroke
Anischemic strokemay be due
to:
1. Cerebral thrombosis: blood
clot (thrombus) forms in a main
artery leading to the brain,
cutting off body supply.
2. Cerebral embolism: blood clot
forms in a blood vessel
elsewhere in the body, and is
carried in the bloodstream to the
brain.
3. Intracranial small vessel
Etiology of Ischemic Stroke
LARGE VESSEL THROMBOTIC (most common cause):
Virchows Triad
Blood vessel injury: Hypertension, Atherosclerosis,
Vasculitis
Stasis/turbulent blood flow: Atherosclerosis, Atrial
fibrillation, Valvular disorders, decreased myocardial
contractility, massive hemorrhage, others.
Hypercoagulable state:
Increased number of platelets
Deficiency of anti-coagulation factors
Presence of pro-coagulation factors
Cancer
Pathophysiology
The brain is protected against focal interruption of
blood supply by a number of extra- and intracranial
collateral vessels.
Actual size of the cerebral ischemia depends on:
Number and vascular tone of collateral channels.
Blood viscocity
Blood perfusion pressure
Atherothrombotic
occlusion of larger
arteries
Embolism: Artery-to
artrey, cardiogenic
Primary small vessel
disease
(lipohyalinosis)
Pathophysiology
TIME IS BRAIN:
SAVE THE PENUMBRA
Penumbra
Penumbra is zone of
reversible ischemia
around core of irreversible
infarctionsalvageable in
first few hours after
ischemic stroke onset
Penumbra damaged by:
Hypoperfusion
Hyperglycemia
Fever
Seizure
Core
Clot in
Artery
Symptoms
Signs and symptoms depend on: type, location and
the extent of the affected brain tissue.
Usually presents with sudden or rapid onset of focal
neurological symptoms, within minutes to an hour.
Some may have a stepwise or gradual worsening or
waxing and waning symptoms.
A third of all strokes occur during night sleep, therefore,
the symptoms are first noted on awakening.
Symptoms
The most common stroke symptoms
are:
Sudden numbness or weakness of face, arm or leg,
especially on one side of the body
Sudden confusion, trouble speaking or understanding
Sudden blurred vision in one or both eyes
Sudden trouble walking, dizziness, loss of balance or
coordination
Sudden severe headache with no known cause
Major Blood Vessels Of The Brain
Circle of Willis
Anterior
circulation- MCA,
ACA, and Anterior
choroidal artery
Posterior
circulationVertebral artery,
Basilar artery and
Posterior cerebral
artery
Lacunes are caused by occlusion of a single penetrating
artery.
The deep penetrating arteries are small, nonbranching
end arteries (usually smaller than 500 m in diameter)
Arise directly from much larger arteries (eg, the middle
cerebral artery, anterior choroidal artery, anterior
cerebral artery, posterior cerebral artery, posterior
communicating artery, cerebellar arteries, basilar
artery).
Control Centers of the Brain
Large vessel stroke syndromes (anterior
circulation) assuming left hemispheric dominance
Vascular territory
Signs and Symptoms
Internal Carotid
Artery
- Combined ACA + MCA
- Ipsilateral monocular visual loss ( amurosis)
secondary to CRAO
Left ACA
- Right leg numbness and weakness
- Transcortical motor aphasia
- Ideomotor apraxia
Right ACA
- Let leg numbess and weakness
- Motor neglect
- Possibly ideomotor apraxia
Left MCA
- Right face/arm > leg numbness and
weakness
- Aphasia
- Left gaze preference
Right MCA
Left face/arm > leg numbness and weakness
Left hemispatial neglect
Right gaze preference
Agraphesthesia / astereoagnosia
Motor/Broca aphasia localized to posterior inferior
frontal lobe
Sensory/Wernickes aphasia posterior superior
temporal/inferior parietal
Lacunar syndromes
Syndrome
Signs/Symptom
s
Localization
Vascular supply
Pure motor
Contralesional
hemiparesis
- Internal
capsule
posterior limb
- Corona
radiata
- Basis pontis
Pure sensory
Contralesional
hemisensory
loss
- VPL nucleus of
thalamus
-Lenticulostriate
branches of the
MCA or
-perforating
arteries from
basilar artery
- Lenticulostriat
e branches of
MCA
- Small
thalamoperfo
rators of PCA
Sensorimotor
Contralesional
weakness and
- Thalamus and
adjacent
Lenticulostriate
Lacunar syndromescontn.
Syndrome
Signs/Symptoms
Localization
Vascular supply
Dysarthia-clumsy
hand
Slurred speech and
weakness of
contralateral hand
(fine motor)
- Basis pontis
( between rostral
1/3rd and caudal
2/3rd )
- Basillar artery
perforators
Ataxia- hemiparesis
Contralesional
Hemiparesis and
ataxia out of
proportion to
weakness
Contralesional limb
flailing / dyskinesis
- Subthalamic
nucleus
Hemiballismus/
Hemichorea
Internal capsuleposterior limb
Basis pontis
Lenticulostritae
branches of MCA
Perforating
arteries of basilar
artery
Perforating
arteries of
anterior choroidal or
PCOM
-
Lacunar strokes present with fluctuating
symptoms capsular warning
syndrome
Often thrombolysis withheld due to
rapidly improving symptoms
Classification of Stroke
For prognostic purposes
Guides cost effective investigations for underlying
cause
Aids decisions for therapy and secondary stroke
prevention strategies
Aids in epidemiological studies.
Eg : Oxfordshire Community stroke Project Classification
(OCSP)
Oxfordshire Community Stroke
Project (OCSP)
Categorizes stroke syndromes into 4
subtypes:
total anterior circulation infarcts (TACI),
partial anterior circulation infarcts
(PACI),
lacunar infarcts (LACI),
posterior circulation infarcts (POCI).
used to predict early mortality, functional outcome, and whether
the infarct was likely due to large- or small-vessel occlusion.
Diagnosis
History
Physical examinations:
Vital signs, general assessments
Full neurological examinations
Diagnostic tests
To determine
whether
ischemic or
hemorrhagic
stroke
Plain CT-Brain Scan (the primary diagnostic test for stroke)
Additional studies:
Lab investigation (Eg: FBC, Coagulation profile, Electrolytes, blood sugar, renal and hepatic
profile, lipid profile, etc)
To identify
Lipid profile
source of
ECG/ Echocardiogram
thrombi or
Carorit ultrasound
Cerebral angiography
emboli
Transcranial Doppler flow studies
Magnetic resonance imaging (MRI) of the brain, neck, or
both
Xenon-enhanced CT scan
single photon emission CT (SPECT) scan
Acute Treatment
General management (supportive care and prevention of
complications)
Oxygen and airway support prevent hypoxia, aspiration
Observation
Mobilisation early to prevent complications
Blood sugar control Hyperglycemia associated with
subsequent mortality and impaired neurological recovery
Temperature prevent/treat fever
Nutrition check gag reflex and water swallow test
Prevent raised intracranial pressure head up 20-30 to help
venous drainage, hyperventilate, mannitol, surgical drainage
BP Control in Acute Ischemic
Stroke
High BP can be due :
Stress of cerebrovascular event
Full bladder
Nausea, pain,
Preexisting hypertension
Physiological response to hypoxia to perfuse penumbra
Response to increased intracranial pressure
Failure to canalize results in high BP and poor
neurological outcome.
Lowering BP drastically reduces perfusion in penumbra
and worsens outcome.
BP Control in Acute Ischemic
Stroke
No data to suggest BP >220/120 is dangerous & requires
immediate treatment.
Evidence that BP lowering worsens outcomes is
concerning.
Goal is to avoid overtreating until definitive data available
Only definite indications to reduce BP emergently in AIS:
AMI, CHF, Aorta dissection, ARF, or HTN encephalopathy
Candidate for thrombolysis and BP > 185/110
BP Control in Acute Ischemic
Stroke
Clinical Practice Guidelines for Management of Ischemic
Stroke (2012):
Do not treat hypertension if < 220mmHg systolic or <
120mmHg diastolic. Mild hypertension is desirable at 160180/90-100 mmHg.
Blood pressure reduction should not be drastic.
Proposed substances:
Labetolol 10-20mg boluses at 10 minute intervals up to 150-300mg or
1mg/ml infusion (rate 1-3mg/min)
Captopril 6.25-12.5mg orally
BP Control in Acute Ischemic
Stroke
Reperfusion Therapy
IV thrombolytic therapy
Restore circulation to penumbra and normalize metabolism to
prevent further damage.
Recommended agent: Recombinant Tissue Plasminogen
Activator (rt-PA)
rt-PAShould only be given if:
A physician with expertise in the diagnosis and management
of stroke.
Appropriate neuroimaging tests are available 24 hours a day
Capability to manage the complications of thrombolysis,
particularly intracranial haemorrhage.
Indication of rt-PA
Reperfusion Therapy
Intra-arterial thrombolysis
an option for the treatment of selected patients who have
major stroke of <6 hours duration due to occlusions of the
middle cerebral artery, internal carotid and carotid terminus
who are not otherwise candidates for intravenous rtPA.
Endovascular mechanical thrombectomy
may be performed up to 8 hours duration in selected patients
with major stroke syndrome and ineligible for or failing
intravenous thrombolysis. T
the utility of the device in improving outcomes after stroke is
unclear.
Rehabilitation and Outpatient
Care
Lessening disability and attaining optimal functioning.
Respiratory system: prevent obstruction, aspiration
Musculoskeletal system: prevent contracture, muscle wasting
physiotherapy and occupational therapy
Integumentary system: susceptible to breakdown due to loss
of sensation, reduced circulation and immobility regular
position change, skin hygiene, early mobilisation
GI tract and nutrition oral hygiene
Communication speech therapy, depression
Education self-care, enhance family coping, secondary
prevention
Primary Prevention
Goals
Health management for the well individual
Education and management of modifiable risk factors to
prevent a stroke
Antiplatelet drugs are usually the chosen treatment to
prevent further stroke in patients who have had a TIA
Aspirin is the most frequently used antiplatelet drug
Anti-Thrombotic Therapy
High-flow states:
platelets cause clots
large-artery
atherosclerosis
small-artery
disease
Low-flow & hypercoagulable states:
clotting factors cause clots
cardioembolism
ANTIPLATELET AGENT
aspirin 81-325/d
clopidogrel 75/d
aspirin + dipyridamole XR 25/200 twice/d
hypercoagulable
state
ANTICOAGULANT
warfarin
INR 2.0-3.0
or
INR 2.5-3.5
Antiplatelet Agents
Recommended by Clinical Practice Guidelines
for
Management of Ischemic Stroke (2012):
Aspirin
Ticlodipine : superior to aspirin. SE:
neutropenia
Clopidogrel
Triflusal
Cilostazol
Double/ combined therapy
Thank You
