STROKE

2017
 Stroke Subtypes
Stroke

Ischemic Stroke - 80% Hemorrhagic Stroke - 20%

Intracerebral hemorrhage
Subarachnoid hemorrage

Large Artery Small Vessel Cardioembolism Other

Atherosclerosis Disease
(lacunar infarction)
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
 CBF Disturbances

• Normal : CBF 50 – 60ml/100 gr per mnts

• Ischemia : CBF < 30 ml/ 100 gr per mnts
• Penumbra : CBF 15 – 30 ml/100 gr per mnts
• Neuron death :CBF < 10 ml/100 gr per mnts
 Stroke: Predisposing factors
• Age (risk doubles • Obesity
for every decade > • Smoking
age 55)
• Atrial fibrillation
• Gender
(males>females) • Sedentary
• Family history of lifestyle
stroke/TIA • Drug abuse (e.g.
• Hypertension cocaine use)
• Diabetes • Hormone
• Hyperlipidemia replacement
• Hyperhomocystein therapy
emia • Oral
 Risk Factors for Stroke

Non-Modifiable Modifiable Risk Factors for

Risk Factors for Stroke Stroke6
• Age •Hypertension
• Sex •Diabetes
• Race/ethnicity •Smoking
• Family history
•Hyperlipidemia
•Carotid stenosis
•Atrial fibrillation
PART OF BRAIN
CONTROL CENTER OF BRAIN
Anterior Cerebral Artery

•Much rarer
•The classic presentation is proximal
arm/leg weakness with present of
distal strength, the so-called “man in
a barrel”
Middle Cerebral Artery

•Characterized by weakness of the

contralateral face with hemianopsia
and a preference of the eyes and
head toward the side of the
involved hemispere
•Aphasia in dominant hemisphere
injury
•Hemineglect
•Involvement restricted to branches
of the MCA may produces fragment
of this syndrome sparing of leg
strengh
Posterior Cerebral Artery
•Involves the brainstem, cerebellum,
thalamus & occipital lobes
•Present with bilateral limb
weakness or sensory disturbances,
cranial nerve defisit, ataxia, nausea,
and vomiting or coma
•occlusion of the basilar artery trunk
: Present with hemianopia, memory
disturbance, mild personality
disturbance
•Rarely; bilateral thalamus : a state
of decreased responsiveness and
apathy without motor, sensory or
visual impairment
 PICA,AICA,SCA :
~ Cerebellum

Posterior
Cerebellar artery
Superior
Cerebellar artery

Anterior and Posterior

Inferior Cerebellar artery
Blood Vessels in the Brain
 Common Stroke Patterns
• Left (Dominant) Hemisphere Stroke
– Aphasia
– Right hemiparesis
– Right-sided sensory loss
– Right visual field defect
– Apraxia
– Dysarthria
– Difficulty reading, writing, or calculating
 Common Stroke Patterns

• Right (Non-dominant) Hemisphere

Stroke
– Extinction of left-sided stimuli
– Left hemiparesis
– Left-sided sensory loss
– Left visual field defect
– Poor left conjugate gaze
– Spatial disorientation
 Common Stroke Patterns

• Brain Stem / Cerebellum / Posterior

Hemisphere Stroke:
Motor or sensory loss in all four limbs
– Limb or gait ataxia
– Dysarthria
– Dysconjugate gaze
– Nystagmus
– Amnesia
– Bilateral visual field defects
 Common Stroke Patterns
• Small Subcortical Hemisphere or Brain Stem (Pure
Motor) Stroke: Common Pattern
– Weakness of face and limbs on one side of the body
without abnormalities of higher brain function, sensation,
or vision

• Small Subcortical Hemisphere or Brain Stem (Pure

Sensory) Stroke: Common Pattern
– Decreased sensation of face and limbs on one side of the
body without abnormalities of higher brain function, motor
function, or vision
1
 (caspase apoptosis: programmed cell death)

(necrosis)

ISCHEMIC CORE AND ISCHEMIC PENUMBRA

(Friedlander 2003)
 Ischemic
Injury
Apoptotic
Cell Death
Necrotic
Cell Death

Dr.J.Husada 11-2003
 Ischemic Stroke
 Incidency : 70-85%
 Classification :
1. TIA (transient ischemic attack) : < 24 hours
2. RIND (Reversible Ischemic Neurological
Deficits) normal between 24 – 48 hours.
Prolonge-RIND normal in max. 3 – 4 days.
3. Stroke in evolution : worsen stroke ( > 48
hours)
4. Stroke complete : permanent neurologic
deficit
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
 Ischemic Stroke Infarct
• When a stroke
occurs, it kills brain
cells in that
immediate area
• This area of dead
cells is called an
infarct
• These cells usually
die within minutes to
a few hours after the
stroke starts
 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
 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
 Thrombotic
• A thrombotic
stroke is when a
blood clot forms
in one of the
arteries in the
brain, or
supplying the
brain, and grows
and grows until it
is large enough
to block blood
flow.
 Proses Aterosklerosis

Mediate area are insuficiently supplied with blood, and they die

 Dimulai luka sel endotel - permukaan tidak mulus lagi

– produksi molekul adesi (ICAM) – peningkatan NO -
terjadi ketidak seimbangan (Depolarisasi) - ggn tonus
vaskuler - aktivasi monosit menjadi makrofag yg
mengambil LDL - foam cell
 Foam Cell (sel busa) merupakan komponen penting
pembentuk struktur masa plak
Cause by rupture aneurysma, angioma,
atherosclerotic lession
Causes of Spontaneous ICH In young adults

Etiology %
Ruptured AVM 29,1%
Arterial hypertension 15,3%
Sympathomimetic drug abuse 9,7%
Tumor* 6,9%
Acute EtOH intoxication 4,2%
Pre-eclampsia/eclampsia 2,8%
Superior sagittal sinus 1,4%
thrombosis
Moyamoya 1,4%
Cryoglobulinemia 1,4%
Undetermined 23,6%
 Definition:

• Intracerebral
hemorrhage (ICH)
results from the rupture
of an intracerebral
vessel leading to the
development of a
hematoma in the
substance of the brain.
 Epidemilogy
Incidence
• USA
– ICH represents 10-15 percent of all strokes (approximately
70,000 new cases each year)1.
• Internationally
– Asian countries >> incidence of ICH (30%) 2
• It is twice as common as subarachnoid hemorrhage and carries an
equally poor prognosis 3
• .
1 Stroke. 1999; 30: 2523-2528.
2 Strokr.2003;34:2091-2096

3 J Neurosurg. 1993; 78: 188-191.

 Epidemiology
Mortality
– At 7 days: >20%
– At 1 month: >40%
– At 1 year: 53%
– Correlated with volume of ICH (>30 cc)

Functionally indipendence
– At 1 month: 10%
– At 6 months: 20%

Clev Clin J Med 2005;4:341-344

 Primary and Secondary
Causes of Intracerebral Hemorrhage

Primary Secondary
Hypertension Aneurysms
Amyloid angiopathy Arteriovenous malformations
Neoplasms
Trauma
Anticoagulation
Use of thrombolytics
Hemorrhagic conversion of
ischemic stroke
 Haemorrhage
Effects of blood Release
Increase Vasoconstrictor agen
toxic Intracranial press Serotonin, Prostaglandin,

Global ischemic
Influks Ca+

Influks Ca+ Vasospasme

Necrosis
Focal Ischemic
Neuron
 Vasospasme Process on Haemorrhage

vasoconstrictor agens & blood componen release

Vasospasme

Influks Ca+ smooth muscle

vasculer

Lumen stronge
vasculer Vasospasme

Ischemic + deficit neurologic

 Hasil optimal terapi Stroke perdarahan sampai 96
jam setelah onset
 Puncak vasospasme antara hari ke 5-10)
 Management
• Medical Management
• Surgical Management
 Management
• In emergency Room
– ABC rules
– BP continuous monitoring
– Continuous ECG monitoring
– O2 pulse oxymetry
– 2 IV lines (norma saline only)
– Blood (CBC, SMAC, RBS, PTT, INR)
– Save 6 ml of blood
– Facilitate transfer to the operating room or
ICU
 Treating Mass Effect
• Is there any benefit of medically treating
mass effect in ICH?
– Steroid
– Glyserol
– Mannitol
 Edema Serebri

• Vasogenic :
– kerusakan vaskuler endotel kapiler, gangguan
tight junction, permeabilitas meningkat
• Cytotoxic :
– gangguan pompa Na, K, ATP ase, Na intrasel
meningkat
• Interstisial :
– Transudasi
Akibat Vasospasme
 Fungsi bagian otak yg disuplai arteri vasospasme akan
terganggu
 Disekitar hematoma dpt terjadi vasospasme lokal pd
arteri yg utuh (tidak pecah)
 Ada kemungkinan vasospasme lokal di dekat sumber
perdarahan berubah menjadi vasospasme difus
 Subarachnoid Hemorrhage
Seminar 1

• Incidence
• Genetic Factors
• Diagnosis
• Natural History
 What causes aneurysms to
rupture?
• The probability of rupture is related to the tension on the
aneurysm wall

• The law of La Place states that tension is determined by

the radius of the aneurysm and the pressure gradient
across the wall of the aneurysm

• Therefore, the rate of rupture is directly related to the

size of the aneurysm

• Aneurysms with a diameter of 5 mm or less have a 2%

risk of rupture, whereas 40% of those 6-10 mm have
already ruptured upon diagnosis
 SAH – The Problem
• They occur in young people
– 80% in 40-65 year olds
– 15% in 20-40 year olds

• It can kill quickly

– 25% die within 24 hours
– 50% will be dead at 6 months

• It causes significant disability

– Cognitive impairment
– Neurological disability depending on size of bleed &
complications encountered
 How are SAH graded?
World Federation Fischer grading
Neurosurgeons

GCS 15, only Grade 1 No blood

CN deficit if any
GCS 13-14, no Grade 2 Diffuse blood,
deficit no clots &
<1mm
GCS 13-14, with Grade 3 Clots & blood
deficit 1mm or more
GCS 7-12, +/- Grade 4 ICH or
deficit intraventricular
clots
GCS 3-6 +/- Grade 5
deficit
 Incidence of Aneurysmal
SAH
Studies suggest that the incidence in the USA and Europe is 10 to
11 cases per 100,000 population per year

Autopsy Series
Total # Percentage
Author #of Series of Cases with aneurysms Rupt’d Unrupt’d
Jellinger 12 87,772 1.6 (0.2 to 9) 1
0.6
Bannerman 8 51,360 1.43 1.09
0.34

Overall, it is a reasonable approximation that less than 2% of the

entire population will have an aneurysm; an intracranial
aneurysm will rupture in less than 1% of the population and will
be the cause of death in 0.5%
 Age and the Incidence of
Aneurysmal SAH

• Aneurysmal rupture is extremely rare in

the first decade of life
• Incidence gradually increases each
decade and peaks in the sixth decade
 Gender and the Incidence of
Aneurysmal SAH
• There is a clear female preponderance
overall; the ratio of females to males in the
Cooperative Study on Timing of Surgery
was 1.6: 1
• Before age 40 males and females were
equally affected; after age 40 there is an
increasingly strong predominance of
females
 Natural History
Prognosis for Surgically Untreated Saccular
Intracranial Aneurysms

OVERVIEW
• Highest mortality occurs immediately after the
hemorrhage and then decreases rapidly
• Rebleeding is estimated to occur in 50% of
ruptured aneurysms within 6 months of the
first hemorrhage, and afterwards at 3% per
year
• 50-60% of patients die after rebleeding and
25% are left disabled
Probably the best natural history data
come from S Pakarinen: (Incidence, aetiology, and
prognosis of primary subarachnoid hemorrhage: a study based on 589 cases
diagnosed in a defined urban population during a defined period. Neurol Scand
(Suppl) 1967; 29:1-128)

• Unselected series, involving the entire city of

Helsinki, from 1954 to 1961; minimal surgical
withdrawals; all sudden deaths were autopsied
• Mortality at 1 day was 32%
• Mortality at 1 week was 43%
• Mortality at 1 month was 56%
• Mortality at 6 months was 60%
 How do they present?
• Headache
– sudden onset & severe
– small leak may cause minor headache & may be
warning sign of rupture

• Reduced consciousness

• Meningism
– Vomiting
– Neck stiffness
– Photophobia

• Seizures
 SAH of Unknown Etiology
(Subarachnoid Hemorrhage of Unknown Etiology. AH Friedman. Chapter 235 in Neurosurgery,
2nd Ed., Vol II, Edited by RH Wilkins and SS Rengachary, McGraw-Hill, 1966)

• With modern imaging, 75-80% of cases of spontaneous SAH will be found to

have an aneurysm. AVM, including dural fistulae, spinal cause, and a variety
of rare causes occur, but in some cases no cause for the SAH is ever found
• Many of these cases will show a predominance of perimesencephalic SAH on
CT scan. These patients are more likely to have negative CT scans, and are
less likely to show SAH in the sylvian and interhemispheric fissures
• Hypertension is the only known risk factor for such cases
• Patients tend to be in better clinical condition: 75% are Hunt-Hess Grades I-II,
while only 49% of cases with an aneurysm are Hunt-Hess Grades I-II
• 80% will have a good outcome, with return to work (compared to 50% with an
aneurysmal SAH)
• Repeat angiography is controversial. ACA and MCA are likeliest sites to find
an aneurysm. 3.6% of modern series show an aneurysm on repeat
angiography. Without a second angiogram, 4% of patients with rebleed early
(<3 months) and 0.8% per year for at least the next 3 years
• Friedman’s group recommends selective repeat angiography when: 1)
Vasospasm compromised the first study; 2) Part of the cerebral circulation is
not well seen; 3) CT shows large amount of diffuse or focal SAH; 4) A
second SAH occurs
 Unruptured Aneurysms:
A Different Perspective from ISUIA:
(S. Juvela, M. Porras & K. Poussa. Natural history of unruptured intracranial aneursyms:
probability of and risk factors for aneurysm rupture. J. Neurosurg, 93: 379-387, 2000)

• 142 patients with 181 unruptured aneurysms, followed from the 1950’s until
death, SAH or 1997-98 (mean 19.7 yrs). No surgical selection.
• Asymptomatic incidental aneurysms - 5 patients
Symptomatic intact aneurysms - 6 patients
SAH from another repaired aneurysm - 131 patients
(How did they determine the rupture site pre-CT? WST comment)
• In 2575 person-years of FU, 33 first-time episodes of SAH from previously
unruptured aneurysms for an average annual incidence of 1.3%. SAH fatal in
17 cases.
• The cumulative rate of bleeding was 10.5% at 10 yrs, 23% at 20 yrs and
30.3% at 30 yrs.
• Risk factors:
– Diameter of the aneurysm
– Patient age at diagnosis (inverse)
– Active smoking status at the time of diagnosis
 Treatment

• Main aim is damage control – want to

prevent further bleeding & try to avoid the
complications that SAH patients get

• SAH patients will vary greatly from GCS

15/15 to GCS 3/15
 To coil or clip?
• Coiling
– Endovascular technique done
• Clipping
in angiography by – Craniotomy & careful
interventional radiologists dissection using
under GA
microscope to reach
aneurysm & clip usually at
– May be best if small necked
aneurysm
neck

– Used in particularly sensitive – May be performed after

areas e.g. basilar tip failed clipping

– Must be able to access the

aneurysm (e.g. any stenosis – If aneurysm can’t be
or tortuous vessels) reached by the
endovascular root
– Like dome:neck ratio to be 2:1
or greater
 That’s Dandy
• First to clip an
aneursym
successfully in
1937

• Walter Dandy
Operative microscope
•
 Complications with SAH
1. Re-bleeding

2. Hydrocephalus

3. Vasospasm

4. Hyponatraemia

5. Seizures

6. VTE
 Complications with SAH
• Re-bleeding
– 80% mortality if re-bleed

– Greatest risk is in the first 24 hours after the

initial bleed

– Aim to prevent by controlling BP to avoid

dramatic changes & isolate the aneurysm
from the circulation (coil or clip)
 Complications with SAH
• Hydrocephalus
– Obstructive
• Blood enters the ventricles & can block the flow of CSF e.g.
at the aqueduct or outlet of the 4th ventricle

– Communicating
• Due to blood blocking reabsorption of CSF through the
arachnoid granules

– May need an extraventricular drain to treat

– Keep head of bed at 300 (promote CSF flow & venous

return)
 Complications with SAH
• Vasospasm
– Blood vessel goes into spasm causing ischaemia - stroke

– To prevent keep them filled with at least 3L fluid day &

nimodipine IV/PO & insert central line to monitor central venous
pressure – aiming for 8-10

– Suspected with deteriorating GCS/new neurological deficit

– Treatment – Urgent CT brain to rule out a bleed as a cause of

the deterioration then urgent angiogram to diagnose & treat
vasospasm

– Greatest risk of vasospasm is days 4-7 but significant risk for first
3 weeks after bleed, therefore will use preventative measures for
at least 3 weeks
 Complications with SAH
• Hyponatraemia
– Susceptible due to being fluid loaded & cerebral salt
wasting

– Cerebral salt wasting = renal loss of sodium due to

intracranial pathology ? Cause. Loss of water & salt
(whereas SIADH is loss of salt & retention of water)

– Treat with normal or hypertonic saline

– If refractory may need a mineralocorticoid e.g.

fludrocortisone to stimulate renal reabsorption – but
this should only be used under instructions from
consultant endocrinologist
 Complications with SAH
• Seizures
– A seizure is a disturbance of sensation, movement or
consciousness

– All seizures originate from the surface of the brain –

cortex

– Blood is an irritant to the cortex

– Prophylaxis with phenytoin or levetiracetam

– Ensure phenytoin levels are therapeutic

– Treat as seizure from any cause & suspect re-bleed

 Complications with SAH
• VTE
– On bed rest

– TEDS

– Prophylactic enoxaparin as soon as consultant sees

fit

– Always keep VTE in the back of your mind

 Prognostic Factors in Aneurysmal SAH
(L Disney, B Weir, M Grace et al. Factors Influencing the Outcome of Aneurysm
Rupture in Poor Grade Patients: A Prospective Series. Neurosurgery 23: 1-9 1988)

Using a discriminant function analysis, the relative importance of

factors
prognostic for outcome was, in order of importance:
1. Whether the patient was treated surgically:
Patients subjected to definitive obliteration of the aneurysm (65%) did
much better than those whose aneurysms were not clipped, with a
mortality of 25% compared to 86% (P<0.001)
2. Neurological grade on admission:
a) Hunt and Hess: Mortality increased with worsening neurological
grade, being 23% for Grade III, 44% for Grade IV and 91% for Grade
V. Good outcome occurred in 30% of Grade III, 14% of Grade IV and
no Grade V patients (P<0.001)
b) GCS: Mortality was inversely related to admission GCS at 29% for
GCS 11 to 14, 42% for GCS 7 to 10 and 70% for GCS 3 to 6. Good
outcome occurred in 29% for GCS 11-14, 14% for GCS 7-10 and 7%
for GCS 3-6 (P=0.01)
Prognostic Factors in Aneurysmal SAH .../cont’d

3. Age:
Younger patients had more good outcomes and lower mortality.
The mean age for good outcome was 46 and for death, 58
years.
4. Initial systolic blood pressure:
When categorized by initial systolic BP (<141, 141-180, >180),
patients with higher systolic BP were less likely to have a good
outcome and had a higher mortality rate (P<0.05)
5. Aneurysm size:
A bad outcome was seen in 72% of patients with aneurysm
diameter >21 mm and 56% with aneurysm diameter 4-6 mm
Non Neurological:
Infection : Respiratory, Urinary, Septicaemia
Metabolic : Dehydration, Electrolyte Disturbance,
Hypoglycaemia
Drugs : Major and Minor Tranquillizers, Baclofen,
Lithium Toxicity, Antiemetics
Hypoxia : Pulmonary Embolism, Chronic Pulmonary
Disease, Pulmonary Oedema
Hypercapnoea: Chronic Pulmonary Disease
Others : Limb or Bowel Ischaemia in Patients
with a Cardiac or Aortic Arch Source of
Embolism
Neurological:
• Progression/completion of the stroke
• Extension/early recurrence
• Hemorrhagic transformation of an infarct
• Development of oedema around the infarct or hemorrhage
• Obstructive hydrocephalus in patients with stroke in the posterior
fossa, or after subarachnoid hemorrhage
• Epileptic seizures
• Delayed ischaemia (in subarachnoid hemorrhage)
• Incorrect diagnosis :
– Cerebral Tumor - Cerebral abscess
– Encephalitis - Chronic Subdural Haematoma
– Subdural empyema
• Conscious level, i.e. Glasgow Coma Scale
• Pupillary Responses
• Eye Movements
• Limb Movements
• Temperature
• Pulse Rate
• Blood Pressure
• Respiratory Rate
• Pulse Oximetry
• Fluid Balance
• Fever
• Agitation
• Purulent Urine
• Tender Abdomen
INDICATIONS FOR CT & MRI IN
STROKE

DIAGNOSTIC
1. Types of stroke (etiopathology)
2. Topical localisation (Anatomy)
3. Size & extension
4. Diff. Diag. to SOL, etc.
5. Monitoring : follow up, assesment of
treatment
(PERDOSSI, 1999)
Time sequence of histology and CT in infarction
Density : Hypodens < 40 ( 0 - 35 HU)
Isodens
Time CT Finding
1st 3 hours Normal (isodense)
3rd - 6th hour ILL-Defined hypodense
Area (Infarct. edema begins)
6th - 24 th hour Hypodensity ↑
Sharper demarct. infarct
24th - 48th hour SD-Effect & Intensity ↑
2nd - 7th day Max.So-effect of edema
7th day  weeks Cystic defect + scar

Fogging effect : Hypodensity disappears on > 10th day

(in 50% cases after onset)
 Acute Stroke Management
• Stroke Alert ( TIME IS BRAIN ! )
• Acute Diagnosis
– clinical
• level of consciousness
• location of stroke
• severity of stroke - NIH stroke scale
• ABC’s
 Diagnosis of acute ischemic stroke

• Physical examination: For carotid bruits

• 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)
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
 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

• 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.
 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
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
 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
 Secondary prevention of stroke
• Recurrence: Annual risk is 4.5 to 6%. Five year
recurrence rates range from 24 to 42%; one-
third occur within first 30 days, hence high
priority should be given to secondary
prevention.
• Patients with TIA or stroke have an increased
risk of MI or vascular event.
• Management of hypertension (goal <140/85 mm
Hg)
• Diabetes control (goal<126 mg/dL)
 Secondary prevention of stroke
• Lipid management: Statins (goal
cholesterol<200 mg/dL, LDL<100 mg/dL)
• Antiplatelet agents: Aspirin (50-325 mg),
clopidogrel (75 mg). A fixed dose combination
of the two drug may also be used
• Anticoagulants: Warfarin (target INR 2 to 3);
esp. recommended in patients with
cardioembolic stroke
• Appropriate life style modification (cessation of
smoking, exercise, diet etc)
 Surgical interventions

• Balloon angioplasty/stenting
• Carotid endarterectomy/Bypass
• Decompressive surgery
 Purpose of Rehabilitation

To reduce the worth consequence of pro

long in activity as contracture, ulcus
decubitus, muscle weakness, deep
end thrombosis, cardiopulmonar
complication, depression.
 Rehabilitation Started
• Stroke rehabilitation more effective when it
started in first day in hospital and the latest of 2-
3 days after onset.(Feigenson)
• Stroke patients result emboli/trombosis without
complication need to mobilization within 2-3 days,
but stroke patients result subarahnoid hemorrhage
have to stable previously during 10-14 days before
mobilization.(Swenson)
• Stroke patients with intracerebral hemorrhage
have to lie down during 3 weeks.(Toole JF)
 Rehabilitation

• EUSI Recommendations
1. Rehabilitation should be initiated early after
stroke (Level I)
2. Every patient should have access to
evaluation for rehabilitation (Level III)
3. Rehabilitation services should be provided by
a multidisciplinary team (Level III)
Rehabilitation Program:
 Physical therapy :
Speech Therapy :
• Mobilization
•Disorders of language
• Walking
•Disorders of articulation
• Major motor or sensory impairment
of the limbs •Disorders of swallowing
• 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
 Factors that Influence the
Successfully of Rehabilitation
• Cause of stroke
• Severity of stroke
• Location
• Age
• Self motivation
• Premorbide personality and mood
• Family
• Social economy
• Specific deficit neurology
• Onset, duration and intensity
• Rehabilitation team