PATOPHYSIOLOGY &

MANAGEMENT OF STROKE
Abdul Gofir
Neurology Department of
Medical Faculty
Gadjah Mada University

Stroke: Definition
Stroke is clinically defined as a
neurologic syndrome characterized
by acute disruption of blood flow to
an area of the brain and
corresponding onset of neurologic
deficits related to the concerned
area of the brain

Nurs Clin N Am 2002;37:35-57

Causes of Stroke

Definition of Ischemic Stroke

Almost 80% of
strokes are from
an emboli or a
thrombus
Embolic &
Thrombotic
strokes are
ISCHEMIC
< 15% of strokes
are from
hemorrhage, with
an even smaller
percentage
caused by
hypoperfusion

Ischemic
Injury
Apoptotic
Cell Death
Necrotic
Cell Death

Dr.J.Husada 11-2003

2 process in ischemic stroke:

1. Vascular : Aterosclerotic process
2. Biochemistry change /cellular
chemist
Aterosclerotic is a normal response to arterial
endotel injury
Aterosclerotic plaque forming, start in young
Clinical manifestation : acute and tent to occur one
time because sudden plaque rupture

Causes of Ischaemic
STROKE
Blockade of blood flow by ateroma, emboli,
and ateroscelerotic

Embolic

Once in your
brain, the
embolus
eventually travels
to a blood vessel
small enough to
block its passage
The embolus
lodges there,
blocking the
blood vessel and
causing a stroke

Potential Stroke Risk Reduction for Individuals

AHA Guidelines
Factor
Hypertens

ion
Smoking
Diabetes

Hyperlipidemia
Atrial

fibrillation
(non-valvular)

Risk

reduction with
treatment
30% - 40%
50%

within 1 year, baseline

after 5 years
44%

reduction in hypertensive
diabetics with tight blood pressure
control
20-30% with statins in patients
with known coronary heart disease
68%
21%

(warfarin)
(aspirin)

Adapted from Goldstein, et al. Circulation 2001;103:163-182.

Stroke: Classification
Ischemic stroke : Account for 80%. Results from
occlusion in the blood vessel supplying the brain
Thrombotic : Occlusion due to
atherothrombosis of small/large vessels
supplying the brain
Embolic : Occlusion due to embolus arising
either from heart (e.g. atrial fibrillation,
valvular disease) or blood vessel

Classification (cont.)
Hemorrhagic stroke : Account for 20%. Results from
rupture of blood vessels leading to bleeding in
brain
Intracerebral: Bleeding within the brain due to
rupture of small blood vessels. Occurs mainly
due to high blood pressure
Subarachnoid: Bleeding around the brain;
commonest cause is rupture of aneurysm.
Other causes: Head injury

Stroke: Predisposing factors

Age (risk doubles for

every decade > age 55)
Gender
(males>females)
Family history of
stroke/TIA
Hypertension
Diabetes
Hyperlipidemia
Hyperhomocysteinemia

Obesity
Smoking
Atrial fibrillation
Sedentary lifestyle
Drug abuse (e.g.
cocaine use)
Hormone
replacement therapy
Oral contraceptive

Risk Factors for Stroke

Non-Modifiable
Risk Factors for Stroke
Age
Sex
Race/ethnicity
Family history

Modifiable Risk
Factors for Stroke6
Hypertension
Diabetes
Smoking
Hyperlipidemia
Carotid stenosis
Atrial fibrillation

Stroke: Symptoms
Onset

of stroke symptoms
varies as per type of stroke:
Thrombotic stroke: Develop
more gradually
Embolic stroke: Hits suddenly
Hemorrhagic stroke: Hits
suddenly and continues to worsen

Stroke: Symptoms
(cont.)
Dizziness

Confusion
Loss of balance/coordination
Nausea/vomiting
Numbness/weakness on one side of the body
Seizure
Severe headache
Movement disorder/speech disorder/blindness etc
(depending on the area of brain affected)

Symptom and Sign

Consider stroke in any patient presenting with
acute
neurological deficit or any alteration in level of
consciousness.
Common signs of stroke include the following:
Acute hemiparesis or hemiplegia
Complete or partial hemianopia, monocular or
binocular visual loss, or diplopia
Dysarthria or aphasia
Ataxia, vertigo, or nystagmus
Sudden decrease in consciousness

Transient Ischemic Attack (TIA)

Mini stroke
Stroke symptoms last for less than 24 hours
(usually 10 to 15 mins)
Result as a brief interruption in blood flow to
brain
Every TIA is an emergency
TIA may be a warning sign of a larger stroke
Patients with possible TIA should be evaluated
by a physician

Diagnosis of acute ischemic

stroke

Physical examination & Neurological

Examination
Brain imaging (cranial CT and/or MRI): Detect
small vessel disease. Helps to effectively
discriminate between ischemic and hemorrhagic
stroke, and stroke from brain tumours
Doppler ultrasonography/Angiography: Detect
large vessel atherosclerosis
ECG/Echocardiography: Detect cardiac embolism
Exclusion of conditions mimicking stroke
(hypoglycemia, migraine, seizure)

Ischemic stroke diagnostic

algorithm
Excluded hypoglycemia, migraine

Acute focal brain deficit

with aura, post-seizure deficit

< 1 hour

Head CT

TIA (if CT/MR brain imaging

without ischemic lesion)

Ischemic Stroke
Cortical
syndrome
ECG
Echo
CARDIAC
EMBOLISM

Lacunar syndrome

Doppler
MRA
Angiogram

MRI
CT

Vasculopathy
Coagulopathy

LARGE ARTERY
SMALL
OTHER DETERMINED
ATHEROSCLEROSIS VESSEL DISEASE
CAUSE

CRYPTOGENIC
STROKE

Acute
Treatment

r-TPA

If a 3-hour window of treatment can

be met, thrombolytic therapy with
intravenous t-PA can be beneficial for
each of the major categories of
ischemic stroke:
atherothrombotic/atheroembolic,
cardioembolic, and small vessel
occlusive (lacunar) stroke

Intravenous Thrombolysis
Intravenous rtPA (0.9 mg/kg, maximum
dose 90 mg) is recommended for selected
patients who may be treated within 3
hours of onset of ischemic stroke (Class I,
Level of Evidence A).
Besides bleeding complications, physicians
should be aware of the potential side
effect of angioedema that may cause
partial airway obstruction (Class I, Level of
Evidence C).

The intravenous administration of

streptokinase for treatment of stroke is not
recommended (Class III, Level of Evidence
A).
The intravenous administration of ancrod,
tenecteplase,reteplase, desmoteplase,
urokinase, or other thrombolytic agents
outside the setting of a clinical trial is not
recommended (Class III, Level of Evidence
C).

Heparin for Cardioembolic

Stroke:
Stroke recurrence is low, much less
than 1%/day in first 2 weeks
Large stroke: wait 48-72 hours and
repeat CT
Small stroke: use judgment

Heparin
There is no large clinical trial in the
literature comparing i.v. heparin as
traditionally administered to placebo
International Stroke Trial: compared s.q.
heparin at comparable doses to asa and
neither in 19435 patients: result: heparin
was not beneficial
Lancet.

1997;349:1569-81

Heparinoids
TOAST trial: indicated no benefit for a
LMW heparinoid in stroke (ORG 10172)
Stroke.

1998;29:286

Management of acute
ischemic stroke

Systemic thrombolysis: Intravenous

recombinant tissue plasminogen activator
(rt-PA): Within 3 hrs of onset of stroke.
Dose 0.9 mg/kg, max 90 mg.
Antiplatelet agents: Aspirin 160-300 mg
within 24- 48 hrs (not during first 24 hrs
following thrombolytic therapy).
Clopidogrel a potential alternative.
Combination of clopidogrel and aspirin
currently being evaluated

Management of acute
ischemic stroke (contd.)

Anticoagulants: Heparin/LMWH are not

recommended in acute treatment of ischemic
stroke. Recommended in setting of atrial
fibrillation, acute MI risk, prosthetic
valves, coagulopathies and for
prevention of DVT.
Intra-arterial thrombolytics: An option for
treatment of selected patients with major
stroke of < 6 hrs duration due to large vessel
occlusion.

Emergency Medical Care for Neurologic

Emergencies
Provide reassurance.
Ensure proper airway and breathing.
Place the patient in a position of comfort.
If you suspect stroke, transport immediately and
notify hospital.
Assess and care for any injuries if you suspect any
type of trauma.

Management of acute
ischemic stroke (contd.)

BP management: Should be kept within higher

normal limits since low BP could precipitate
perfusion failure. Markedly elevated BP
(>220/110mmHg) managed with nitroglycerin,
clonidine, labetalol, sodium nitroprusside. More
aggressive approach is taken if thrombolytic
therapy is instituted
Blood glucose management: Should be kept
within physiological levels using oral or IV
glucose (in case of hypoglycemia)/insulin (in
case of hyperglycemia)
Elevated body temperature management:
Antipyretics and use of cooling device can
improve the prognosis

UPDATE ON MANAGEMENT OF
ICH (Pouratian 2003)
Medical interventions
- Cardiopulmonary optimization
(ABCSS)
- Blood pressure control
- ICP reduction
- Ultra-early hemostatic therapy

Surgical interventions

MEDICAL MANAGEMENT OF ICH

(Pouratian 2003)
Cardiopulmonary optimization ( Airway, Breathing,
Circulation,skin, seizures)
Reversing coagulation defects (coagulopathies and platelet
disorders)
Blood pressure control (Labetolol & nicardipine IV,
nitroprusside not often used brain edema).
ICP reduction:
- Ventriculostomy as therapeutic means of reducing ICP
- Head-of-bed elevated at 30 0, patients neck in neutral
position maximize venous outflow.
- Minimize agitation: sedatives
- Hyperosmolar fluids (mannitol, hypertonic saline)
- Hyperventilation used only as temporary measures
- Barbiturate-induced coma : rarely
- Vasogenic edema with mass effect: corticosteroids
(controversial)
Ultra-early hemostatic therapy:
- Antifibrinolytic tranexamic acid, aprotinin, activated
recombinant factor VII (rFVIIa)

BLOOD PRESSURE MANAGEMENT IN ICH

(Broderick 1999)
- If SBP > 230 mm Hg or DBP > 140 mm Hg on 2
readings 5 minutes apart nitroprusside 0.5-10
g/kg/min.
- If SBP is 180-230 mm Hg, DBP 105-140 mm Hg, or
mean arterial BP 130 mm Hg on 2 readings 20
minutes apart labetolol, esmolol, enalapril, or
other smaller doses of titrabble IV medications eg
diltiazem, lisinopril, or verapamil.
- If SBP is < 180 mm Hg and DBP < 105 mm Hg, defer
antihypertensive therapy.
- If ICP monitoring is available, cerebral perfusion
pressure should be kept at > 70 mm Hg.

Labetolol: 5-100 mg/h by intermittent bolus doses of 10-40 mg or continuous drip (2-8
mg/min).
Esmolol: 500 g/kg as a load, maintenance use, 50-200 g/kg/min.
Hydralazine: 10-20 mg Q 4-6 h
Enalapril: 0.625-1.2 mg Q 6 h as needed.

Management of Acute
hemorrhagic stroke

Analgesics/Antianxiety agents: To relieve

headache. Analgesics having sedative
properties are beneficial for patients having
sustained trauma (e.g. morphine sulphate)
Antihypertensives:(e.g. sodium
nitroprusside, labetolol)
Hyperosmotic agents (e.g. mannitol,
glycerol, furosemide): To reduce cerebral
edema, and raised intracranial pressure.
Adequate hydration is necessary
Surgical intervention may occasionally
be life saving

RECOMMENDATIONS FOR
SURGICAL TREATMENT OF ICH
(Broderick 1999)

NON SURGICAL CANDIDATES

1. Small hemorrhages (<10 cm3) or minimal
neurological deficits.
2. GCS score 4. Except for cerebellar hemorrhage
with brainstem compression for livesaving surgery.
SURGICAL CANDIDATES
1. Cerebellar hemorrhage > 3 cm who are
neurologically deteriorating or who have brainstem
compression and hydrocepahalus from ventricular
obstruction.
2. ICH with structural lesion eg aneurysm, AVM, or
cavernous angioma.
3. Young patients with a moderate or large lobar
hemorrhage who are clinically deteriorating.

PREDICTORS OF EARLY
NEUROLOGIC
DETERIORATION IN ICH (Leira
2004)
Early neurologic deterioration (END) occurred in 22.9 % patients.

On admission:
Body temperature > 37.5 C (37.3 0.7 vs 36.4 0.5)
Neutrophil count by 1000-unit increase (10.8 2.9 vs 6.3 4.3)
Serum fibrinogen > 525 mg/dL (546 126 vs 396 119)

Within 48 hours:
Early ICH growth (48.2 vs 20.7)
Intraventricular bleeding (46.4 vs 29.5)
High systolic blood pressure (192 21 vs 179 27)
Source : Neurology 2004; 63: 461-467

POOR OUTCOME IN ICH

Pouratian 2003
Volume of the hematoma ( 30 cc)
Neurologic status (GCS score 8)
Intraventricular extension of the clot
Hydrocephalus
Subarachnoid extension
Anticoagulation agents
Relative edema
Davis WSC 2004
Infratentorial lesion
Coronary heart disease
Hyperthermia

Cerebral oedema This is an abnormal accumulation of fluid

in the cerebral parenchyma.It is usually the result of
breakdown of the bloodbrain barrier, and it may occur
following damage initiated by several different
causes:Ischaemia, e.g. from infarction.Trauma,e.g.
from head injury.Inflammation encephalitis or meningitis.
Oveproduction of CSF by choroid plexus neoplasms

Back

Edem serebri vasogenik merupakan akibat primer dari

meningkatnya permeabilitas blood brain barier

Edem serebri sitotoksik terjadi sekunder dari kerusakan

elemen seluler serebri, terlepasnya faktor-faktor toksik
dari netrofil dan bakteri. Sehingga terjadi peningkatan
kandungan air intraseluler, dimana terjadi kebocoran
potasium, glukosa digunakan melalui glikolisis anae
robik, produksilaktat.

Edem serebri interstitial terjadi sekunder dari obstruksi

aliran LCS akibat inflamasi ruang subarakhnoid, seperti
hidrosefalus.
Back

Brain Edema

Cytotoxic edema : BBB is closed, no protein extravasation, no

enhancement in CT, cell swell
Vasogenic edema : BBB is disrupted, leaks of protein, enhance in
imaging, cell are stable, extracellular space expands,
Interstitial : Transudasi

Perdarahan
Efek toksik
darah

Peningkatan
TIK

Pelepasan agen
vasokonstriktor
Serotonin, Prostaglandin, darah

Iskemia
global

Influks Ca+

Nekrosis
Neuron

Influks Ca+

Vasospsme

Iskemia Fokal

Proses Vasospasme Pada Perdarahan

Pelepasan zat vasokonstriktor dan komponen darah

Vasospasme

Influks Ca

Lumen
vasa darah

Sel otot polos

pembuluh darah

Vasospasme
kuat

Iskemik + defisit neurologik

The Ischaemic Cellular Cascade and Targets for Novel Stroke

Therapeutic Agents

Cerebral Ischaemia
pH

Na+

Reperfusion
(4)

Cl-

cytokines
Neuron depolarisation
molecules

adhesion
Glutamate release
(1)

VGCC open

Intracellular Ca
PLA2
Activation

Leukocyte
adhesion

(2)
++

mitochondria

(3)

NOS

Oxidative
stress
Organelle
damage

Neuronal death

(5)

Tissue
response

inflammation
Agents stroke iskemik :
1. NMDA & AMPA receptor antagonists,
Mg+
2. Ca A
3. NOS inhibitors
4. Anti-oxidants
5. Adhesion molecule antibodies
VGCC: Voltage gated calcium channels
PLA2 : Fosfolipase A2

Epidemiology of SAH
Incidence about 10/100,000/yr
Mean age of onset 51 years
55% women
men predominate until age 50, then
more women

Risk factors
cigarette smoking
hypertension
family history

Diagnostic approach to
SAH
Wide range of symptoms and
signs
CT scanning
Limited role of lumbar puncture
Angiography
conventional vs. spiral CT vs. MRA
identification of multiple aneurysms
SAH without aneurysm

Diagnostic approach to
SAH
Screening of certain hight risk
populations for unruptured
aneurysms is of uncertain value.
Digital Subtraction angiography
(DSA) remains the gold standard
for diagnosis for Unruptured
aneurysms. (Class II b, Leve;l of
Evidence B)

More subtle
subarachnoid
hemorrhage
Interhemispheric
fissure
Sylvian
fissure

Complications of SAH
rebleeding
cerebral
vasospasm
volume
disturbances
osmolar
disturbances
seizures

arrhythmias
and other
cardiovascula
r
complications
CNS
infections
other
complications
of critical

Critical care issues: rebleeding

Unsecured aneurysms:
4% rebleed on day 0
then 1.5%/day for next 13 days [ 27% for 2 weeks]

Antifibrinolytic therapy
may be useful between presentation and early
surgery

Blood pressure management

labetalol, hydralazine, nicardipine

Analgesia
Minimal or no sedation to allow examination

Preventing Re-bleeding Recommendations

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (SAH)

Class I Recommendations
Blood pressure should be monitored and
controlled to balance the risk of strokes,
hypertension-related re-bleeding, and
maintenance of cerebral perfusion
pressure (LOE B)
Class II Recommendations
Bed rest alone is not enough to prevent rebleeding after SAH. It may be considered
as a component of a broader treatment
strategy along with more definitive
11/04/15 2009, American
measures (LOE B)Heart Association. All rights
reserved.

Preventing Re-bleeding Recommendations

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (SAH)

Class II Recommendations
Recent evidence suggests that early
treatment with antifibrinolytic
agents, when combined with a
program of early aneurysm treatment
followed by discontinuation of the
antifibrinolytic and prophylaxis
against hypovolemia and vasospasm
11/04/15 2009, American
Heart Association. All rights
reserved.
(LOE B)

Preventing Re-bleeding Recommendations

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (SAH)

Antifibrinolytic therapy to prevent

rebleeding may be considered in
certain clinical situations, e.g.,
patients with a low risk of
vasospasm and/or a beneficial
effect of delaying surgery (Level of
Evidence B)
11/04/15 2009, American
Heart Association. All rights
reserved.

Surgical and Endovascular

Management -- Recommendations
AHA/ASA Scientific Statement
Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (SAH)

Class I Recommendations
Surgical clipping or endovascular coiling is
strongly recommended to reduce the rate
of rebleeding after aneurysmal SAH (LOE
B)
Wrapped or coated aneurysms as well as
incompletely clipped or coiled aneurysms
have an increased risk of re-hemorrhage
compared to those completely occluded
and therefore require long-term follow-up
angiography. Complete obliteration
of the
11/04/15 2009, American
Association. All rights
aneurysm is recommendedHeart
whenever
reserved.
possible (LOE B)

Surgical and Endovascular

Management -- Recommendations
Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (SAH)

Class I Recommendations
For patients with ruptured aneurysms
judgedby an experienced teamof
cerebrovascular surgeons and
endovascular practitioners to be
technically amenable to both endovascular
coiling and neurosurgical clipping,
endovascular coiling can be beneficial (LOE
B)
Class II Recommendations
Individual characteristics of the patient
and the aneurysm must be considered in
deciding the best means of repair,
and
11/04/15 2009,
American
Heart Association. All rights
management of patients in centers
offering
reserved.
both techniques is probably recommended

Surgical and Endovascular

Management -- Recommendations
Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (SAH)

Class II Recommendations
Although previous studies showed that
overall outcome was not different for early
versus delayed surgery after SAH, early
treatment reduces the risk of rebleeding
after SAH, and newer methods may
increase the effectiveness of early
aneurysm treatment. Early aneurysm
treatment is reasonable and is probably
11/04/15 2009, American
indicated in the majority of cases
(LOEAllB)
Heart Association.
rights
reserved.

Left image arrow -Angio with Large aneurysm

Right image arrow Angio showing aneurysm
post clipping

11/04/15 2009, American

Heart Association. All rights
reserved.

Coil system embolization:

immediate result
Angio showing large ICA
aneurysm

Same aneurysm - Post GDC Coiling

11/04/15 2009, American

Heart Association. All rights
reserved.

Critical care issues:

vasospasm and delayed
ischemic
damage
Potential mechanisms
oxyhemoglobin/nitric oxide
endothelins

Diagnosis
clinical
transcranial Doppler flow velocity
monitoring
electrophysiologic
radiologic

Vasospasm in acute
SAH
Initial angiogram

Repeat angiogram
showing vasospasm
(small arrows)

Hypertension/treatment
In general, antihypertensive drugs should be
withheld unless the calculated mean blood
pressure (the sum of the systolic pressure plus
double the diastolic pressure, divided by three) is
greater than 130 mm Hg or the systolic blood
pressure is greater than 220 mm Hg
Elevated blood pressure usually declines
spontaneously over the first 24 hours after stroke
onset and overzealous use of a calcium antagonist
and other antihypertensive drugs should be
avoided because they can further reduce cerebral
perfusion.

Antithypertensive
Treatment

Indicated for:

aortic dissection
acute myocardial infarction
heart failure
acute renal failure
hypertensive encephalopathy
thrombolytic therapy

When systolic pressure is 180 mm Hg or

higher or the diastolic pressure 105 mm
Hg or higher.

Blood Pressure and hemorrhage

Control of elevated blood pressure has
never been shown to decrease the risk
of ongoing or recurrent bleeding in
patients with intracerebral hemorrhage.
Recommend treatment of moderate and
severe elevations of blood pressure
(systolic blood pressure of greater than
180 mm Hg or mean arterial pressure of
greater than 130 mm Hg).

Hyperglycemia & Stroke

Persistent hyperglycemia (>140 mg/dL)

during the first 24 hours after stroke is
associated with poor outcomes.
Lower serum glucose concentrations
(possibly >140 to 185 mg/dL) probably
should trigger administration of insulin,
similar to the procedure in other acute
situations accompanied by hyperglycemia
(Class IIa, Levelof Evidence C).
Close monitoring

Temperature
Increase temp increases percentage
of poor outcome in stroke
Increase cerebral oxygen/substrate
consumption

Lancet 1996:422

Fever

There is general agreement to

recommend treatment of the sources of
fever and use of antipyretics to control
an elevated body temperature (Levels of
Evidence III through V, Grade C). There
are insufficient clinical data about the
use of hypothermia to recommend this
therapy.

Fever: Treatment
Treat any temperature elevations
Data is not in as to whether hypothermia
may be protective

CEREBRAL EDEMA
Hypo-osmolar fluids, such as 5%
dextrose in water, may worsen edema.
1/2NS or NS recommended

Mannitol
Mannitol (0.25 to 0.5 g/kg IV) given over
20 minutes rapidly lowers intracranial
pressure and can be given every 6
hours.57 The usual maximum daily dose
is 2 g/kg.57

Mannitol
Dose: - 25 to 50 g I.v. q 3-5 hrs.
Maximal dose of 2 g /KG/D.
Furosemide I.v. 20 to 80 mg q 4 to 12
hours to supplement mannitol.
Replacement fluids to maintain the
calculated serum osmolality at 300 to
320 mOsm per kilogram of water.

Aspirin Plus Dipyridamole Versus

Aspirin for Prevention of Vascular
Events After Stroke or TIA

This meta-analysis systematically reviewed randomized controlled

trials comparing aspirin plus dipyridamole with aspirin alone in
patients with stroke and TIA to determine the efficacy of these
agents in preventing recurrent cerebral and systemic vascular events

The combination of aspirin plus dipyridamole is more

effective than aspirin alone in preventing stroke and
other serious vascular events in patients with minor
stroke and TIAs. The risk reduction was greater and
statistically significant for studies using primarily
extended release dipyridamole, which may reflect a true
pharmacological effect or lack of statistical power in
studies using immediate release dipyridamole

Rehabilitation Program:
Physical therapy :

Mobilization
Walking
Major motor or sensory impairment of the
limbs
Prescription of devices, such as a cane or
walker

Occupational Therapy :

Fine movements of the hand

Arm function
Utilization of tools
Assistive devices
Ability to function independently

Diagnosis And Treatment Of Dizziness

In Cerebrovascular Disease
Abdul Gofir
Unit Stroke RS Sardjito/ Bagian Ilmu Penyakit Saraf
Fakultas Kedokteran Universitas Gadjah Mada, Yogyakarta

American Heart Association. All rights reserved.

Dizziness

Prevalence
1 in 5 adults report dizziness in last month
Increases in elderly
Worsened by decreased visual acuity,
proprioception and vestibular input

Dizziness
Non-specific term
Different meanings to different people
Could mean
-

Vertigo
Weak
Anemia

- Syncope
- Giddiness
- Depression

- Presyncope
- Anxiety
- Unsteady

Cerebrovascular Disease

Epidemiology of Cerebrovascular
Disease
5,500,000 stroke survivors are alive today
700,000 each year

500,000 of these are first attacks

200,000 are recurrent attacks.

30% to 50% of stroke survivors do not regain

functional independence
15% to 30% of all stroke survivors are
permanently disabled

Incidence of Cerebrovascular
Disease
Increases with age
28% are less than 65 yrs old
80% of cerebrobvascular disease
are preventable
19% greater in men than women
Women > 65 have higher incidence
than men

Vertebrobasilar insufficiency
Dizziness, diplopia, dysarthria, gait
ataxia and bilateral sensory & motor
disturbance
Transient ischemia - low stroke risk

Anatomi

American Heart Association. All rights reserved.

Arise from the subclavian

arteries
Run alongside the
medulla
Blood supply for
brainstem and cerebellum
Key Functional Areas:
Spinal cord tracts-pyramidal
and spinothalamic
Cranial nerves 3-12

1- Posterior Cerebral
2- Superior Cerebellar
3- Pontine Branches of
Basilar
4- Anterior Inferior Cerebellar
5- Internal Auditory
6- Vertebral
7- Posterior Inferior
Cerebellar
8- Anterior Spinal
9- Basilar

Dizziness

Central causes
Peripheral causes
canalithiasis (BPPV)-50%
Cerebrovascular disease
(vertebrobasilar insufficiency)-50%
vestibular neuronitis
demyelinating (multiple sclerosis)
(labyrinthitis)-25%
Menieres disease-10%
drugs (anticonvulsants, alcohol,
hypnotics)
trauma
drugs (aminoglycosides)

Vertigo vs. other types of

dizziness
Time course -- vertigo is never continuous
Provoking factors -- spontaneously or with

positional changes

Aggravating factors -- all vertigo is made

worse by moving the head

Establishing the cause of

dizziness

Time course

BPPV: lasts less than one minute, self-limited,

responds poorly to anti-vertigo drugs
Vascular: single episode lasting minutes to
hours; usually due to migraine or to transient
ischemia of the labyrinth or brainstem;
occasionally Menieres disease
Recent onset of more prolonged episodes
characteristic of vestibular neuronitis, multiple
sclerosis, vertebrobasilar ischemia

Establishing the cause of

dizziness

Associated symptoms
Vertebrobasilar disease / stroke: diplopia,
dysarthria, dysphagia, weakness, numbness
Menieres disease: aural fullness, deafness,
tinnitus
Psych/Panic attack: SOB, palpitations,
diaphoresis
Multiple sclerosis: vertigo preceded by other
neurologic dysfunction

Establishing the cause of

dizziness

Prior risk factors

Migraine
Hypertension, Diabetes Mellitus,
smoking, Peripheral Vascular Disease
Head injury
Psychiatric illness

Physical examination
Vestibular exam
Neurologic exam
Severity of postural instability
Hearing tests

Further studies to evaluate

dizziness
MRI/MRA -- distinguishing central causes
TCD
Audiometry -- distinguishing peripheral
causes

Brainstem evoked audiometry -- 90-95%

sensitivity for detecting acoustic neuroma

Transient Ischaemic Attack

(TIA) management
The risk of stroke post TIA is high
immediately after an event; up to 5%
in the first 2 days and 10% within the
first week

Those at high risk can be

discriminated from those at low risk
by means of clinical assessment (the
ABCD2 score).

Cont..

The ABCD2 scale is a 7-point scale

based on clinical data available
before neuroimaging, which can be
used to estimate the risk of stroke
after TIA

Johnston et al, Lancet 2007

Management of TIA

Evaluation within hours after onset

of symptoms
CT scan is necessary in all patients
Antiplatelet therapy with aspirin (50325 mg/d), consider use of
clopidogrel, ticlopidine, or aspirindipyridamole in patients who are
intolerant to aspirin or those who
experience TIA despite aspirin use