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
1
 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 Risk reduction with

treatment
Hypertensio 30% - 40%
n
Smoking 50% within 1 year, baseline after
5 years

Diabetes 44% reduction in hypertensive

diabetics with tight blood pressure
control
Hyperlipidemia 20-30% with statins in patients with
known coronary heart disease

Atrial 68% (warfarin)

fibrillation 21% (aspirin)
(non-valvular)
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  Obesity
every decade > age 55)  Smoking
 Gender
(males>females)  Atrial fibrillation
 Family history of  Sedentary lifestyle
stroke/TIA  Drug abuse (e.g.
 Hypertension cocaine use)
 Diabetes  Hormone
 Hyperlipidemia replacement therapy
 Hyperhomocysteinemia  Oral contraceptive
 Risk Factors for Stroke

Non-Modifiable Modifiable Risk Factors

Risk Factors for Stroke for Stroke6
• Age Hypertension
• Sex
Diabetes
• Race/ethnicity
• Family history 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
Acute focal brain deficit Excluded hypoglycemia, migraine
with aura, post-seizure deficit

< 1 hour TIA (if CT/MR brain imaging

Head CT without ischemic lesion)

Ischemic Stroke

Lacunar syndrome
Cortical
syndrome
Doppler MRI Vasculopathy CRYPTOGENIC
MRA CT Coagulopathy STROKE
ECG Angiogram
Echo

CARDIAC LARGE ARTERY SMALL OTHER DETERMINED

EMBOLISM ATHEROSCLEROSIS VESSEL DISEASE CAUSE
 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 300, patient’s 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 > 37.5º 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
 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 • arrhythmias
• cerebral and other
vasospasm cardiovascular
• volume complications
disturbances • CNS infections
• osmolar • other
disturbances complications
• seizures of critical illness
 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 re-
bleeding after SAH. It may be considered as a
component of a broader treatment strategy
along with more definitive measures (LOE B)
4/1/2019© 2009, American 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 (LOE B)
4/1/2019© 2009, American Heart
Association. All rights reserved.
 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)
4/1/2019© 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 aneurysm is recommended
whenever possible (LOE B)
4/1/2019© 2009, American Heart
Association. All rights reserved.
 Surgical and Endovascular
Management -- Recommendations
Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (SAH)
Class I Recommendations
For patients with ruptured aneurysms judged by
an experienced team of 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 management of
patients in centers offering both techniques is
probably recommended (LOE B)
4/1/2019© 2009, American Heart
Association. All rights reserved.
 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
indicated in the majority of cases (LOE B)
4/1/2019© 2009, American Heart
Association. All rights reserved.
 Left image arrow -Angio with Large aneurysm
Right image arrow – Angio showing aneurysm post
clipping

4/1/2019© 2009, American Heart

Association. All rights reserved.
Coil system embolization: immediate
result
Angio showing large ICA Same aneurysm - Post GDC Coiling
aneurysm

4/1/2019© 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
Repeat angiogram
Initial angiogram showing vasospasm
(small arrows)
 Management of TIA
 Evaluation within hours after onset of
symptoms
 CT scan is necessary in all patients
 Antiplatelet therapy with aspirin (50-325
mg/d), consider use of clopidogrel,
ticlopidine, or aspirin-dipyridamole in
patients who are intolerant to aspirin or
those who experience TIA despite
aspirin use
 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
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.

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
 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 - Syncope - Presyncope
- Weak - Giddiness - Anxiety
- Anemia - Depression - 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

 Peripheral causes  Central causes

– canalithiasis (BPPV)-50%
– vestibular neuronitis
(labyrinthitis)-25%
– Meniere’s disease-10%
– trauma
– drugs (aminoglycosides)
– Cerebrovascular disease
(vertebrobasilar insufficiency)-50%
– demyelinating (multiple sclerosis)
– drugs (anticonvulsants, alcohol,
hypnotics)
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 Meniere’s 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
– Meniere’s 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 (50-325
mg/d), consider use of clopidogrel,
ticlopidine, or aspirin-dipyridamole in
patients who are intolerant to aspirin or
those who experience TIA despite
aspirin use