CEREBROVASCULAR DISEASE

DEPARTEMEN NEUROLOGI
FAKULTAS KEDOKTERAN
UNIVERSITAS ISLAM SUMATERA UTARA
 The brain and stroke

• How the brain works

• Understanding stroke
• Stroke risk factors
• Effects of stroke
• Stroke recovery

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• How the brain works
 Brain functions

• Movement – motor functions and the

coordination of movement
• Perception – how we interpret information
from our senses
• Sensation – such as touch
• Vision – how we see
• Cognition – thinking, remembering,
understanding, planning,
reasoning and problem-
solving
• Communication – speaking and
understanding
• Personality – including emotions and
behaviour

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The two sides of the brain control different functions

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Understanding stroke
 Understanding stroke
Stroke
• A sudden injury to part of the brain caused
when blood flow in an artery stops.
• The affected area of the brain is deprived
of oxygen and nutrients. This damages the
neurons and the functions they control.
• Neurons that die cannot be replaced or
restored.
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 Stroke Facts

 Stroke is the fourth leading cause of death in the

United States
 795,000 people in the U.S. suffer strokes each year
 133,000 deaths in the U.S. each year
– From 1998 to 2008, the stroke death rate fell
approximately 35 percent and number of deaths fell
by 19 percent
 7,000,000 stroke survivors

© 2011 National Stroke Association

What Is the Impact of Stroke?
 Stroke is the third leading cause of death
in the United States
• On average, someone suffers a stroke every 40
seconds
• About 795,000 Americans suffer a stroke each
year
• About every 4 minutes, someone dies of a stroke
 Stroke is a leading cause of serious, long
Disability (A leading cause of adult disability)
 Up to 80 percent of all strokes are preventable
through risk factor management
 On average, someone suffers a stroke every
40 seconds in the United States
 About 6.4 million Americans are stroke survivors
 Americans will pay about $73.7 billion in 2010 for
 stroke-related medical costs and lost
productivitylong-term
 Women & Stroke
 Stroke kills more than twice as many American
women every year as breast cancer
 More women than men die from stroke and risk is
higher for women due to higher life expectancy
 Women suffer greater disability after stroke then
men
 Women ages 45 to 54 are experiencing a stroke surge,
mainly due to increased risk factors and lack of
prevention knowledge

© 2011 National Stroke Association

What Are the Types of Stroke ?

 Ischemic Stroke (Blockage)

• Caused by a blockage in blood vessels
in brain
 Hemorrhagic Stroke (Bleeding)
• Caused by burst or leaking blood
vessels in brain
 Sudden brain damage
 Lack of blood flow to the brain caused by a clot or
rupture of a blood vessel

Ischemic = Clot
(makes up approximately
87 percent of all strokes)

Hemorrhagic = Bleed
Thrombotic

- Bleeding around brain

- Bleeding into brain
© 2011 National Stroke Association
 Three Stroke Types
Ischemic Intracerebral Subarachnoid
Stroke Hemorrhage Hemorrhage

Clot occluding Bleeding Bleeding around

artery into brain brain
85% 10% 5%
www.acponline.org/about_acp/chapters/o
k/gordon.ppt
Stroke Data Bank Subtype Classification
Derived from the Harvard Stroke Registry classification [1],
the National Institute of Neurological Disorders and Stroke
(NINDS), Stroke Data Bank recognized 5 major groups:
1. brain hemorrhage;
2. brain infarctions, and among them atherothrombotic
and tandem arterial pathological abnormalities;
3. cardioembolic stroke
4. lacunar stroke
5. stroke from rare causes or undetermined etiology
 Etiology of Ischemic Strokes
LARGE VESSEL THROMBOTIC:
Virchow’s Triad….
• Blood vessel injury
- HTN, Atherosclerosis, Vasculitis
• Stasis/turbulent blood flow
- Atherosclerosis, A. fib., Valve disorders
• Hypercoagulable state
- Increased number of platelets
- Deficiency of anti-coagulation factors
- Presence of pro-coagulation factors
- Cancer
 Etiology Of Ischemic Stroke:

LARGE VESSEL EMBOLIC:

• The Heart
– Valve diseases, A. Fib, Dilated cardiomyopathy, Myxoma

• Arterial Circulation (artery to artery emboli)

– Atherosclerosis of carotid, Arterial dissection, Vasculitis

• The Venous Circulation

– PFO w/R to L shunt, Emboli
 Determining the Location
• Large Vessel:
– Look for cortical signs

• Small Vessel:
– No cortical signs on exam

• Posterior Circulation:
– Crossed signs
– Cranial nerve findings

• Watershed:
– Look at watershed and borderzone areas
– Hypo-perfusion
 Stroke Symptoms

Sudden and severe

headache Sudden confusion
Trouble speaking
Trouble seeing
in one or both eyes Sudden numbness
or weakness of
Sudden dizziness face, arm or leg
Trouble walking

If you observe any of these symptoms,

CALL 9-1-1 IMMEDIATELY
Every minute matters!
© 2011 National Stroke Association
http://www.phillystroke.org/content/learn
_about_stroke/act_fast.asp
 Cortical Signs

RIGHT BRAIN: LEFT BRAIN:

- Right gaze preference - Left gaze preference

- Neglect - Aphasia

• If present, think LARGE VESSEL stroke

 Large Vessel Stroke Syndromes

• MCA:
– Arm>leg weakness
– LMCA cognitive: Aphasia
– RMCA cognitive: Neglect,, topographical difficulty, apraxia,
constructional impairment
• ACA:
– Leg>arm weakness, grasp
– Cognitive: muteness, perseveration, abulia, disinhibition
• PCA:
– Hemianopia
– Cognitive: memory loss/confusion, alexia
• Cerebellum:
– Ipsilateral ataxia
 Aphasia

• Broca’s
– Expressive aphasia
– Left posterior inferior
frontal gyrus

• Wernicke’s
– Receptive aphasia
– Posterior part of the superior temporal gyrus
– Located on the dominant side (left) of the brain
 Intracranial Hemorrhages
(ICH)

Etiology of ICH
• Traumatic
• Spontaneous
– Hypertensive
– Amyloid angiopathy
– Aneurysmal rupture
– Arteriovenous malformation rupture
– Bleeding into tumor
– Cocaine and amphetamine use
Causes of ICH

http://spinwarp.ucsd.edu/neuroweb/Text/n
on-trauma-ER.htm
 Hypertensive ICH

• Spontaneous rupture of a small artery deep in the brain

• Typical sites
– Basal Ganglia
– Cerebellum
– Pons
• Typical clinical presentation
– Patient typically awake and often stressed, then abrupt
onset of symptoms with acute decompensation
 Ganglionic Bleed

• Contralateral hemiparesis
• Hemisensory loss
• Homonymous hemianopia
• Conjugate deviation of eyes toward the side of the bleed or
downward
• AMS (stupor, coma)
Cerebral Hemorrhage

JPG
 Cerebellar Hemorrhage

• Vomiting (more common in ICH than SAH or Ischemic CVA)

• Ataxia
• Eye deviation toward the opposite side of the bleed
• Small sluggish pupils
• AMS
Cerebellar Hemorrhage
 Pontine Hemorrhage

• Pin-point but reactive pupils

• Abrupt onset of coma
• Decerebrate posturing or flaccidity
• Ataxic breathing pattern
Pontine Hemorrhage
 Subarachnoid Hemorrhage

• “Worst headache of my life”

• AMS
• Photophobia
• Nuchal rigidity
• Seizures
• Nausea and vomiting
Subarachnoid Hemorrhage
 Management
Airway

• Most likely related to decreased level of consciousness (LOC),

dysarthria, dysphagia
• GCS < 8 - INTUBATE
• Avoid Hyperventilation or Hypoventilation
• NPO until swallow assessment completed- high aspiration risk
• Begin mobilization as soon as clinically safe
• Keep HOB greater than 30 degrees
Stroke Algorithm
 Imaging

• CT scan • MRI
• Non- contrast CTH remains • Superior for showing
the gold standard as it is
superior for showing IVH underlying structural
and ICH lesions
• CT with contrast may help • Contraindications
identify aneurysms, AVMs,
or tumors but is not
required to determine
whether or not the patient
is a tPa candidate
 Acute (4 hours) Subacute (4 days)
Infarction Infarction
R L R L

Subtle blurring of gray-white Obvious dark changes &

junction & sulcal effacement “mass effect” (e.g.,
ventricle compression)
www.acponline.org/about_acp/chapters/o
k/gordon.ppt
SIRIRAJ SCORE

(2.5 X KESADARAN) + (2 X MUNTAH) + (0.1 X

TEKANAN DARAH SISTOLIK) + ) + (2 X NYERI KEPALA)
– (3 X PENANDA ATHEROMA) – 12 = …….

KESADARAN ( CM = 0, SONOLANCE = 1, SOPOR =2,

COMA =3)
MUTAH (ADA = 1, TIDAK ADA = 0)
NYERI KEPALA (ADA = 1, TIDAK ADA = 0)
PENANDA ATHHEROMA (ADA = 1, TIDAK ADA = 0)
General Stroke Treatment
Content
Monitoring
Pulmonary and airway care
Fluid balance
Blood pressure
Glucose metabolism
Body temperature
Continuous monitoring
oHeart rate
oBreathing rate
oO2 saturation
Discontinuous monitoring
oBlood pressure
oBlood glucose
oVigilance (GCS), pupils
oNeurological status (e.g. NIH stroke scale
or Scandinavian stroke scale)
 Pulmonary function
Background
Adequate oxygenation is important
Improve blood oxygenation by administration of > 2 l O2
Risk for aspiration in patients with side positioning
Hypoventilation may be caused by pathological respiration
pattern
Risk of airway obstruction (vomiting, oropharyngeal muscular
hypotonia): mechanical airway protection
Background
Elevated in most patients with acute stroke
BP drops spontaneously during the first days after
stroke
Blood flow in the critical penumbra passively
dependent on the mean arterial pressure
There are no adequately sized randomised,
controlled studies guiding BP management
Specific issues
Elevated BP (e.g. up to 200mmHg systolic or
110mmHg diastolic) may be tolerated in the
acute phase of ischaemic stroke without
intervention
BP may be lowered if this is required by
cardiac conditions
Upper level of systolic BP in patients
undergoing thrombolytic therapy is
180mmHg Avoid and treat hypotension
Avoid drastic reduction in BP
Glucose metabolism
Background
High glucose levels in acute stroke may increase the
size of the infarction and reduce functional outcome
Hypoglycemia can mimic acute ischaemic infarction
Routine use of glucose potassium insulin (GKI) infusion
regimes in patients with mild to moderate
hyperglycaemia did not improve outcome1
It is common practise to treat hyperglycemia with insulin
when blood glucose exceeds 180mg/dl2 (10mmol/l)
 tPa
Tissue plasminogen activator
• Fast Facts • Contraindications
• Tissue plasminogen • Hemorrhage
activator • SBP > 185 or DBP > 110
• “clot buster” • Recent surgery, trauma or
• IV tpa window 3 hours stroke
• Coagulopathy
• IA tpa window 4.5 hours
• Seizure at onset of symptoms
• Disability risk  30% despite
• NIHSS >21
~5% symptomatic ICH risk
• Age?
• Glucose < 50
 Mechanical Thrombolysis
• Often used in adjunct with tPa
• MERCI (Mechanical Embolus Removal in
Cerebral Ischemia) Retrieval System is a
corkscrew-like apparatus designed to remove
clots from vessels
• PENUMBRA system aspirates the clot
 Blood Pressure Management

•BP Management
– The goal is to maintain cerebral perfusion!!
– CPP = MAP – ICP (needs to be at least 70)
– Higher BP goals with Ischemic stroke
– Lower BP goals with Hemorrhagic stroke (avoid hemorrhagic
expansion, especially in AVMs and aneurysms)
 BP-AIS Relationship
Penumbra
• BP increase is due to
arterial occlusion (i.e., an
Core
effort to perfuse
penumbra)
• Failure to recanalize (w/
or w/o thrombolytic
therapy) results in high BP
and poor neuro outcomes
• Lowering BP starves
penumbra, worsens Clot in
Artery
outcomes
www.acponline.org/about_acp/chapters/o
k/gordon.ppt
 Save the Penumbra!!
Normal
20 function

15
Neuronal CBF
PENUMBRA dysfunction 8-18
10

5 Neuronal CBF
CORE death <8

1 2 3
TIME (hours) CEREBRAL
BLOOD
FLOW
(ml/100g/min)
www.acponline.org/about_acp/chapters/o
k/gordon.ppt
 Supportive Therapy

• Glucose Management
– Infarction size and edema increase with acute and chronic
hyperglycemia
– Hyperglycemia is an independent risk factor for hemorrhage
when stroke is treated with t-PA
• Antiepileptic Drugs
– Seizures are common after hemorrhagic CVAs
– ICH related seizures are generally non-convulsive and are
associated to with higher NIHSS scores, a midline shift, and tend
to predict poorer outcomes
 Hyperthermia

• Treat fevers!
– Evidence shows that fevers > 37.5 C that persists
for > 24 hrs correlates with ventricular extension
and is found in 83% of patients with poor
outcomes
ASSALAMUALAI
KUM