STROKE

SSSUUUDDDEEENNNN

ONSET
BRAIN ATTACK
PROGRESSION IN MINUTES
TO HOURS
FOCAL VASCULAR CAUSE
 ANTERIOR CEREBRAL ARTERY
• HEMIPARESIS, SENSORY LOSS (LEG MORE
AFFECTED THAN ARM)
• IMPAIRED RESPONSIVENESS (ABULIA,
AKINETIC MUTISM), ESP. BILATERAL
• LEFT SIDED IDEOMOTOR APRAXIA OR TACTILE
ANOMIA
 MIDDLE CEREBRAL ARTERY
• MAIN TRUNK • UPPER DIVISION
• HEMIPLEGIA • HEMIPARESIS, SENSORY
• HEMIANESTHESIA LOSS (ARM, FACE> LEG)
• HEMIANOPIA • BROCA APHASIA/
• APHASIA (D) HEMINEGLECT
• HEMINEGLECT (ND)
• LOWER DIVISION
• WERNICKE APHASIA,
BEHAVIOR DISORDER
 MIDDLE CEREBRAL ARTERY
• SUPPLIES THE LATERAL SURFACE OF
HEMISPHERE EXCEPT FOR:
• FRONTAL LOBE
• STRIP ALONG SUPEROMEDIAL BORDER OF
FRONTAL LOBE
• LOWEST TEMPORAL CONVOLUTIONS
• MOST FREQUENTLY AFFECTED IN EMBOLIC
AND THROMBOTIC STROKE
 POSTERIOR CEREBRAL ARTERY
BILATERAL MIDBRAIN DAMAGE
• CORTICAL BLINDNESS • HEMIPARESIS
• TUNNEL VISION • ATAXIA
• POOR EYE HAND • RETRACTORY NYSTAGMUS
COORDINATION
• MEMORY DISTURBANCE
 COMMON STROKE PATTERNS
LEFT (DOMINANT)
• APHASIA
• RIGHT HEMIPARESIS
• RIGHT SIDED SENSORY LOSS
• RIGHT VISUAL FIELD DEFECT
• POOR RIGHT CONJUGATE
GAZE
• DYSARTHRIA
• DIFFICULTY
READING,WRITING,
CALCULATING
RIGHT (NON DOMINANT)
• NEGLECT OF LVF
• EXTINCTION OF LEFT SIDED
• STIMULI
• LEFT HEMIPARESIS
• LEFT SIDED SENSORY LOSS
• LEFT VISUAL FIELD DEFECT
• POOR LEFT CONJUGATE GAZE
• DYSARTHRIA
• SPATIAL DISORIENTATION
 POSTERIOR CIRCULATION STROKE
• ATAXIA, GAIT ABNORMALITIES
• DIPLOPIA, OSCILLOPSIA, NYSTAGMUS
• DYSCONJUGATE EYE MOVEMENTS
• NAUSEA AND VOMITING( AREA POSTREMA)
• CROSSED HEMIPARESIS, HEMISENSORY
DEFICITS
• HEADACHE MORE COMMON
CEREBRAL ISCHEMIA (INFARCTION)
FOCAL NEUROLOGIC DEFICIT
NO SIGNS OF INCREASED
INTRACRANIAL PRESSURE AT ONSET
 SSP CLASSIFICATION OF ACUTE STROKE BASED ON CLINICAL SEVERITY
Mild Stroke Moderate Stroke Severe Stroke
Alert patients with any or a Awake patient with significant Deep Stupor or
combination of the motor and/or sensory and/or comatose patient
following: language and/or visual deficit with non-purposeful
1. Mild pure motor response,
weakness of one OR decorticate, or
side of the body, defined as: decerebrate
can
Disoriented, drowsy or light posturing to painful
raise arm above shoulder,
stupor with purposeful stimuli
has
clumsy hand, or can response to painful stimuli
ambulate OR
without assistance
2. Pure sensory deficit Comatose patient with
3. Slurred but intelligible no response to painful
speech stimuli
4. Vertigo with
incoordination (e.g., gait
disturbance, unsteadiness
or clumsy hand)
5. Visual field defects alone

NIHSS score = 0 – 5 NIHSS score = 6 – 21 NIHSS score > 22

 ISCHEMIC PENUMBRA
• BLOOD FLOW < 50 ML – 20ML /100 G OF
BRAIN TISSUE – NO INFARCTION UNLESS
LASTING FOR HOURS OR DAYS
• SAVE THE ISCHEMIC PENUMBRA
PENUMBRA
• Cells of the penumbra are metabolically active
and are potentially salvageable with timely
intervention
• The infarction expands over time into the
penumbra increasing the area of irreversible
brain damage
• Interruption of this process is associated with
functional improvement
`
Stroke.2006;37:263-266
ISCHEMIC CASCADE Neuronal death

Hypoxia

Activation of lipases, NO synthase,

peroxidases

Na – K+ pump failure

 Intracellular Ca

K leak , Depolarization
Opening of
Ca channels

Glutamate & Activation of NMDA, AMPA

neurotransmitter release receptors
PATHOPHYSIOLOGY OF ISCHEMIC STROKE

• EMBOLISM
• THROMBOSIS
• STENOSIS
Intracranial Stenos is More Common Than
Extracranial Stenosis Among Asians

Caucasians Blacks, Hispanics, Asians

Origin of the ICA from the CCA Carotid siphon, prox MCA, ACA
Prevalence of IAS Chinese, Taiwanese, Japanese, Koreans with Stroke/TIA:
33 to 67%. Extracranial and ICA disease in 3-19%.

Leung TW, Wong KS. Int J Stroke. 2006,Feb1;1:20-5

RISK FACTORS FOR STROKE
 THROMBOTIC STROKE
• ATHEROSCLEROSIS- THE COMMONEST
PATHOLOGY OF VASCULAR
OBSTRUCTION OF LARGE VESSEL
THROMBOSIS ALSO SMALL VESSEL
• LIPOHYALINOSIS- SMALL VESSEL (LACULAR
STROKE)
 CARDIOEMBOLIC STROKE
• ~20% of all ischemic strokes
• THROMBOTIC MATERIAL FROM ATRIAL OR
VENTRICULAR WALL OR LEFT HEART VALVES
• EMBOLI FROM HEART USU. LODGE OVER
ICA,MCA, POST. CEREBRAL ARTERY
• MOST COMMON CAUSE NONVALVULAR AF;
OTHER CAUSES MI, PROSTHETIC VALVES, RHD,
ISCHEMIC CARDIOMYOPATHY
TREATMENT
 ACUTE ISCHEMIC STROKE TREATMENT

• MEDICAL SUPPORT
• IV THROMBOLYSIS
• ENDOVASCULAR REVASCULARIZATION
• ANTITHROMBOTIC TREATMENT
• NEUROPROTECTION
• STROKE CENTERS AND REHABILITATION
 MEDICAL SUPPORT
• PREVENT COMPLICATION OF BEDRIDDEN
PATIENT- INFECTION(PNEUMONIA, UTI,
SKIN)DVT WITH PULMONARY EMBOLISM
• LOWER BP IF:
• IF BP> 185/110
• MI, CHF, AORTIC DISSECTION
• SUGAR < 10MMOL/L
• CONTROL FEVER
IV Rtpa for AIS
ADMINISTRATION OF rTPA
IV Rtpa FOR AIS
 IV RTPA
COMPLICATION ADVANTAGE
• INTRACRANIAL • 12% ABSOLUTE INCREASE
HEMORRHAGE- 6.4 % AND IN PATIENTS WITH MINIMAL
0.6% ON PLACEBO
 ANTITHROMBOTIC TREATMENT
• A. PLATELET INHIBITION
• ASPIRIN DIPYRIDAMOLE
• CLOPIDOGREL
• CILOSTAZOL
• B. ANTICOAGULATION- NOT RECOMMENDED
FOR ATHEROTHROMBOTIC CEREBRAL ISCHEMIA
• TREATMENT OF CHOICE FOR CARDIOEMBOLIC
STROKE INR RANGE 2-3
 ASPIRIN
• ONLY ANTIPLATELET AGENT PROVEN FOR THE
ACUTE TREATMENT OF ISCHE3MIC STROKE
• 9/1000 DEATHS OR NON FATAL STROKE
RECURRENCES PREVE3NTED IN THE FIRST FEW
WEEKS
• ~13 FEWER PATIENTS WILL BE DEAD OR
DEPENDENT AT 6 MONTHS
 ENDOVASCULAR SURGERY
• INTRA ARTERIAL PROUROKINASE
• ENDOVASCULAR THROMBECTOMY DEVICE
GOOD DAY
STROKE
HEMORRHAGIC STROKES

I
INTRAPARENCHYMAL HEMORRHAGE
AND SUBARACHNOID HEMORRHAGE
FOCAL NEUROLOGIC DEFICIT
PLUS
SIGNS OF INCREASED
INTRACRANIAL PRESSURE
PROGRESSION IN MINUTES
TO HOURS
FOCAL VASCULAR CAUSE
SIGNS OF MENINGEAL
IRRITATION PLUS
SYMPTOMS OF INCREASE
INTRACRANIAL PRESSURE
SUBARACHNOID HEMORRHAGE
 CAUSES
• HEAD TRAUMA
• ANEURYSMAL RUPTURE
• AVM RUPTURE
 SACCULAR ANEURYSM
• RISK OF RUPTURE
• < 10 MM < 0.1 %
• >10 MM 0.5-1 %
• BIFURCATION OF LARGE TO MEDIUM INTRACRANIAL
ARTERIES 1. TERMICAL ICA, BIFURCATION OF MCA, TOP
OF BASILAR ARTERY
• 85% ANTERIOR CIRCULATION – CIRCLE OF WILLIS
• NECK - NO INTERNAL ELASTIC LAMINA
• DOME AND NECK-MEDIA THINS, CONNECTIVE TISSUE
REPLACE SMOOTH MUSCLE
 RISK OF RUPTURE
• BLEEDING AT THE DOME WHEN TEAR IS ABT <
OR = TO 0.5 MM LONG
• LOCATION TOP OF THE BASILAR, ORIGIN OF
POST. COMMUNICATING ARTERY
• GIANT ANEURYSM > 2.5 CM - 5%
• MULTIPLE – 20%
 CLUES
• 3RD NERVE PALSY PCA ANEURYSM
• 6TH NERVE PALSY- CAVERNUS SINUS
• VISUAL FIELD DEFECT- ACA OR SUPRACLINOID
ICA
• PAIN BEHIND THE EYE OR LOW TEMPLE- MCA
ANEURYSM
 CLINICAL MANIFESTATION
• LOSS OF • MENINGEAL SIGNS
CONSCIOUSNESS
• WORST HEADACHE
• SUDDEN IN ONSET NO
FOCAL NEUROLOGIC
DEFICIT
 DELAYED NEUROLOGIC DEFICITS
• RERUPTURE- FIRST MONTH 30% PEAK FIRST
SEVEN DAYS
• HYDROCEPHALUS
• VASOSPASM- 30% appear 4 to 14 days most
often at 7 days
• HYPONATREMIA- ATRIAL AND BRAIN
NATRIURETIC FACTOR
 INTRAPARENCHYMAL HEMORRHAGE

• INTRAPARENCHYMAL DEVELOP OVER 30-90

MINUTES
• ANTICOAGULANT THERAPY EVOLVE 24- 48
HOURS
• WITHIN 48 HOURS MACROPHAGES
PHAGOCYTIZE OUTER SURFACE
• 1 TO 6 MONTHS