STROKE

Prepared by Adnan Ali

Lecture objectives
 Definitions
 Normal cerebral blood flow- circle of Willis
 TIA & stroke patient identification & management
 Classification
 Clinical manifestations
 ABCD2 criteria for risk stratification
 Stroke
 Definition: A stroke is any process that disrupts the flow
of oxygen and substrate-rich blood to the brain
 Commonly an infarcted area of brain is surrounded by a
region of tenuous blood flow, the ischemic penumbra.
 The focus of stroke management is to maintain the
blood supply to this region, thereby limiting infarct size.
 Overall, 85% of strokes are ischemic and 15% are
hemorrhagic
Anatomy of Cerebral Blood Flow (CBF)

A. Anterior circulation (from carotid arteries, 80%

of CBF)
 Frontoparietal lobes
 Anterior aspect of temporal lobes
 Optic nerve and retina
B. Posterior circulation (from vertebrobasilar arteries,
20% of CBF):
 Medial aspect of temporal lobes
 Thalamus
 Brainstem
 Upper spinal cord
 Cerebellum

Circle of Willis:
 Connection between anterior and posterior circulations
Cerebral blood flow
types

Stroke

Ischemic Hemorrhagic
stroke: stroke:
85% 15%
Ischemic Stroke
 Ischemic stroke may be divided into three types:
 A. thrombotic
 B. cardio-embolic
 C. hypoperfusion states
A. Thrombotic Stroke
 Causes:
 Thrombosis is the most common cause of stroke in

the U.S
 typically results from clot formation at the site of

an ulcerated atherosclerotic plaque.

 Other causes include:

 Vessel narrowing from vasculitis, dissection,

infectious disease, vasospasm
 Thrombophilia from hypercoagulable states
 Sickle cell disease
 Symptoms generally come on gradually and may be
preceded by transient ischemic attacks (TIAs)
affecting the same region as the stroke.
 Lacunar stroke :A subset of thrombotic stroke.
 This is a stroke of a small terminal vessel, typically
deep in the subcortical cerebrum, basal ganglia,
thalamus, corona radiate, or brainstem.
B. Cardioembolic Stroke
 Causes:

 Occurs when intravascular material (e.g., clot)

from a proximal source travels to the cerebral

circulation, causing obstruction –AF results in
blood stasis which becomes prone to clot
formation
 Types of emboli include:
 Cardiac (mural thrombus, valvular vegetations,

cardiac tumors)
 Venous thrombosis (in the presence of a ventricular

or atrial septal defect)

 Proximal aortic or carotid atherosclerotic plaque

 Fat (from a broken bone)

 Air (air embolism)

 Particulate matter (e.g., talc from injection drug use)

Hypoperfusion States
 CAUSES:
Cerebral perfusion pressure (CPP) is dependent on
mean arterial blood pressure (MAP) and
intracranial pressure (ICP), and is represented by
the formula: CPP = MAP – ICP.
 Hypoperfusion may logically result from an
increased ICP or decreased MAP.
Symptoms/Exam
 Symptom onset varies with stroke type.
 Sudden and maximal at onset with embolic
 More gradual or preceded by TIA with thrombotic
 Amaurosis fugax: Transient monocular blindness
from embolization of carotid plaque to the
ophthalmic artery
 Cont.
 Transient ischemic attack (TIA): Neurologic deficit that has
complete clinical resolution within 24 hours.
 Wernicke aphasia (receptive aphasia): There is inability to
comprehend language input.
 Speech is fluent but disorganized, due to ischemia/infarct in
Wernicke’s area of temporal lobe.
 Broca’s aphasia (expressive aphasia): There is inability to
communicate verbally.
 Speech is halting and produced with great effort, due to
infarct/ischemia of Broca’s area in the frontal lobe.
Area of Major findings Other findings
blockage
Anterior Contralateral weakness of leg > Altered mentation and
cerebral artery arm and face with minimal judgment
sensory findings Perseveration Primitive reflexes
(grasp and suck)
If both arteries originate from
occluded common trunk
(bilateral infarct) → paraplegia
and severe dysarthria
Middle Contralateral weakness and Homonymous hemianopsia
cerebral artery numbness of arm and face > leg Gaze preference toward side of
infarct
If dominant hemisphere:
Receptive/expressive
aphasia
Nondominant hemisphere:
Inattention and
neglect
Lacunar artery Pure motor or pure Clumsy hand—
sensory findings dysarthria syndrome
Posterior cerebral artery Contralateral visual field Memory loss
and light touch/
pinprick deficit with
minimal weakness
Vertebrobasilar artery Crossed deficits: Bilateral spasticity
Ipsilateral cranial nerve Syncope and drop
deficits with attacks
contralateral weakness
Distal vertebral or Crossed pain and Ipsilateral Horner
posterior temperature deficits: syndrome and cranial
inferior cerebellar artery Ipsilateral loss on face, nerve deficits may be
contralateral present Gait and limb
on body ataxia
Basilar artery “Locked in” syndrome
(complete paralysis
of voluntary muscles
except eye
movement; normal
level of consciousness)
Cerebellar Sudden inability to Lateralizing dysmetria
artery walk or stand with (e.g., finger-nose-finger)
headache,
nausea/vomiting and
cerebellar
findings
Diagnosis
 Suspect based on history and examination.
 Confirmed based on CT or MRI
 Appears as area of hypodensity on non-contrast CT
 Ischemic stroke will not be visible on non contrast
CT until >6 hours.
 Glucose to rule out hypoglycemia
 ECG to evaluate rhythm
 Coagulation studies if coagulopathy suspected
 Treatment
 ABCs (including intubation for decreased level of
consciousness)
 Hypotension: Restore euvolemia, then use pressors (if
necessary).
 Hypertension: Aggressive lowering of BP in chronically
hypertensive patients (who have cerebral auto regulation curve
shifted to right) may limit flow to the ischemic penumbra.
 Treat if BP persistently elevated (systolic >220 or diastolic
>140).
 Goal = BP ≤ 185/115 mmHg.
 Use titratable agent such as labetalol or nitroprusside.
 Glucose control:
 Treat hyperglycemia to keep blood glucose 100–200.
 Avoid IV solutions with glucose.
 Avoid steroids, if possible.
Systemic tPA (thrombolysis)
 Criteria:
 Symptoms <3 hours duration
 Age >18 years
 Blood pressure <185/110
 Meaningful neurologic deficit that is not resolving
 No finding on non contrast CT head scan or clear
ischemic penumbra
 Criteria for Intravenous Thrombolysis
in Ischemic Stroke
INCLUSION EXCLUSION*
Age 18 years or older Minor stroke symptoms
Clinical diagnosis of ischemic stroke Rapidly improving neurologic signs
Time since onset well established Prior intracranial hemorrhage
to be less than 3 hr.
Blood glucose <50 mg/dL or >400 mg/dL
Seizure at onset of stroke
GI or GU bleeding within preceding 21 days
Recent myocardial infarction
Major surgery within preceding 14 days
Sustained pretreatment
SBP >185 mmHg or
DBP >110 mmHg
Inclusion Exclusion
Previous stroke within preceding 90 days
Previous head injury within preceding 90
days
Current use of oral anticoagulants or PT >15
s or INR >1.7
Use of heparin within preceding 48 hr and a
prolonged PTT
Platelet count <100,000/μL
Treatment
 Antiplatelet agent (aspirin, clopidogrel or
ticlopidine) is primary therapy.
 Goal is prevention of stroke, based on suspected
underlying process
ABCD2 Score to Predict Subsequent
Stroke in Patients with TIA
Variable Points
Age >60 years 1
BP ≥140/90 mmHg 1
Unilateral weakness 2
Speech disturbance 1
without weakness
Duration ≥60 minutes 2
Duration 10—59 minutes 1
Diabetes 1
Hemorrhagic Stroke
 Can be divided into intracerebral hemorrhage and
subarachnoid hemorrhage
Intracerebral Hemorrhage (Ich)

 CAUSES: Intracerebral hemorrhage is an acute

bleed into the brain parenchyma as a result of:
 Chronic hypertension (most common)
 Cocaine or methamphetamine use
 Vascular malformation
 Anticoagulation or thrombolysis
Symptoms/Exam
 Characterized by sudden onset and rapid progression
of neurologic symptoms
 Headache
 Nausea, vomiting
 Patients usually present hypertensive.
Differential
 Hypoglycemia
 Todd paralysis
 complicated migraine
 mass lesion
Diagnosis
 Suspect based on history and examination.
 Confirm by non contrast CT scan
 Lumbar puncture is necessary to rule out
subarachnoid hemorrhage, when suspected.
Treatment
 Supportive therapy
 Elevated head of bed to 30º
 Hyperventilation (to PaCO2 of 30), mannitol and
furosemide if impending herniation
 Hypertension: Treat if severe (>220/120 mmHg)
with goal of gradually lowering BP to pre-
hemorrhage levels
 Use titratable agent—labetalol or nitroprusside.
 Seizure prophylaxis with phenytoin
 Neurosurgery consult: Especially for cerebellar
hemorrhage, which is associated with rapid
deterioration and herniation
 Thank you