STROKE By

Siti Nur Shafiqah Binti Fazil

Mohammad Hazim Fikri Bin Adnan
Mohd. Amirul Hafifi Bin Khairulzaman
Nor Akma Binti Sulaiman
Norashikin Binti Naim
Zafirah Hani Binti Ramli
Atika Azura Binti Abdul Rashed
 Definition:
 Public: weakness, usually permanent on one
side, often with loss of speech.
“Stroke is a clinical syndrome characterized by rapidly
developing clinical symptoms and/or signs of focal, and at
times global, loss of cerebral function, with symptoms
lasting more than 24 hours or leading to death, with no
apparent cause other than that of vascular origin”.

~ Academy of Medicine, Malaysia

 Classification
Ischemic Hemorrhage

- Sudden loss of fx dt loss of blood - results from a weakened

supply to an area that controls that vessel that ruptures and
fx. bleeds into the surrounding
- Usually caused by brain.
partial/complete blockage of an - blood accumulates and
artery that supplies the brain. compresses the surrounding
 STROKE

Ischemic Hemorrhagic
(85%) - Thrombosis (15%)
- Embolism
- Subarachnoid
hemorrhage
Lacuna - Intracerebral hemorrhage
Cortico r
l
Brainstem
Small
arteries
Large vessel hypertension - Embolism
- atheroma
- Mesothelioma
Anterior Posterior
circulation circulation
 Risk Factors.
NON-MODIFIABLE MODIFIABLE
Age Hypertension (systolic and diastolic)
Sex Cigarette smoking
Ethnicity/race Diabetes Mellitus
Family history of stroke Atrial fibrillation
Coronary heart disease
Hyperlipidemia
Obesity and physical inactivity
Raised homocysteine level
High dietary salt intake
Heavy alcohol consumption
Previous stroke
 Causes.
Three main causes of ischaemic stroke are:
1. Atherothromboembolism (50%)

2. Intracranial small vessel disease (penetrating artery

disease) (25%)
3. Cardiogenic embolism (20%)

Other causes:
 Arterial dissection

 Trauma

 Vasculitis

 Metabolic disorder

 Congenital disorder
PATHOPHYSIOLOGY OF
STROKE
 Ischemic Stroke
 Caused by :
 Extracranial embolism
 Intracranial thrombosis
 Decreased cerebral blood

flow

Initiate ischaemic cascade

Necrosis of brain tissue

Cerebral infarction

Stroke
1- Embolism
 May arise from the heart or extracranial arteries
 Sources of cardiogenic emboli :
 Valvular thrombi (MS, IE, prosthetic valve)
 Mural thrombi ( MI, AF)
2- Thrombosis
 Large vessels (including carotid artery system)
 Small vessels (comprising intracerebral arteries,
including the Circle of Willis & posterior circulation)
3- Flow disturbances
• Inadequate cerebral blood flow due to :
 Decreased cerebral perfusion pressure
 Hematologic hyperviscosity ( sickle cell disease,
multiple myeloma, polycythemia vera)
• Less common cause :
 polycythemia, sickle cell anemia, protein C deficiency,
fibromuscular dysplasia of the cerebral arteries, and
prolonged vasoconstriction from migraine headache
disorders.
 Any process that causes dissection of the cerebral arteries
(trauma, thoracic aortic dissection, arteritis)
 Ischemic cascade
• Loss of perfusion to a portion of the brain 
unleashed the ischemic cascade
• On cellular level :
Ischemic neurons become depolarized (ATP depleted)

Membrane ion-transport systems fail

Calcium influx  release neurotransmitters (including

glutamate)

Activates N-methyl-D-Aspartate (NMDA) & other

excitatory receptors on other neurons
 Neurons become depolarized

Further calcium influx

Further glutamate release

Local amplification of initial ischemic insult

+ Massive calcium influx  activates various degradative

enzymes  destruction of the cell membrane and
other essential neuronal structures
+ Free radicals, arachidonic acid, and nitric oxide are
generated by this process  further neuronal damage
 Hemorrhagic Stroke
 Intracerebral and subarachnoid hemorrhage
 Blood vessel ruptures

Explosive entry of blood into the brain parenchyma.

The extravasation forms a roughly circular or oval mass

that disrupts the tissue and grows in volume as the
bleeding continues.

Swelling of brain tissue (cerebral edema)

Adjacent brain tissue is distorted and compressed.

Neurological deficit
1- Intracranial hemorrhage
• Common : chronic high BP
• Weakens the arteries  burst

2- Subarachnoid hemorrhage
• Common : ruptured
aneurysm
 CLINICAL
MANIFESTATION
 Presentation of patient of stroke varies from
mild confusion to altered level of
consciousness, coma and death.

 The presentation are dependant on what

portion of the brain is damage.

 The areas of the brain affected by the stroke

depend on the particular artery that is affected.
 Ischemic stroke
 Cortical
 Lacunar
 Brainstem

 Hemorrhagic stroke
Blood supply to the brain
 CORTICAL STROKE
Anterior (carotid) artery circulation

•Middlecerebral artery
Aphasia
Hemiparesis / plegia
Hemianopia

•Anteriorcerebral artery
personality changes
Posterior (vertebrobasilar) artery circulation

Supply:
•Brainstem
•Cerebellum
•Occipital
Symptoms:
 Dizziness

 Diplopia

 Dysarthria

 Dysphagia

 Dystaxia
 Cortical signs

 Aphasia
 Agnosia
 Apraxia
 hemineglect

 Loss of consciousness
 Drowsy
Clock drawing in neglect
 Lacunar Stroke

Definition:

strokes caused by the occlusion of a small branch of

a larger blood vessel. Because of the way blood
vessels divide in the brain, lacunar strokes tend to
occur in areas located away from the surface of the
brain, where many of the smaller blood vessel
branches are located.
 Alert
 Normal cognitive function (absence of cortical signs)
 Symptoms

 Pure motor stroke

 Pure Sensory
 Sensorimotor
 Ataxic Hemiparesis
 Dysarthria Clumsy-Hand Syndrome
Brainstem stroke
 distribution of the basilar or vertebral arteries
 "cardinal" feature of an ipsilateral peripheral
cranial nerve involvement, and a contralateral
weakness or sensory deficit
 dangerous: small portion but have many functions.
: most patient die.

 Wallenberg's syndrome
 Horner’s syndrome
 Hemiparesis : corticospinal tract
 Diplopia: occulomotor
 Facial numbness and weakness: 5th and 7th cranial
nerve
 Nystagmus and vertigo: vestibular
 Dysphagia and dysartria: 9th and 10th
 Haemorrhagic Stroke

 Dangerous within 24 hours.

 Clinical manifestation is almost the same, but usually
patient with hemorrhagic stroke present with severe
headache which sometimes preceed with vomitting.

 Differences between intracerebral and subarachnoid

can only be found radiologically. However, in severe
hemorrhage, it’s difficult to distinguish between the
two.

 Definite differences between hemorrhagic and

infarction can only be seen radiologically.
 DIAGNOSIS/DIFFERENTIAL DIAGNOSIS
• Metabolic/toxic encephalopathy
• Epileptic seizures ( Todd’s palsy)
• Hemiplegic migrain
• Structural intracranial lesion ( subdural hematoma,
brain tumor, AVM)
• Encephalitis
• Head injury
• Relapsing multiple sclerosis
• Conversion disorder
• Hyperviscosity syndrome
• Peripheral nerves lesion ( guillaine barre syndrome)
Investigations
 FBC, ESR, serum electrolytes, serum creatinine,
liver function test, blood glucose, lipid profile,
coagulation profile, ABG
- to detect common vascular risk factor and
markers of rarer causes such as atherosclerosis,
diabetis mellitus or blood clotting problem
 ECG, echocardiography, chest X-ray
- should be considered if cardiac embolism is
suspected
 Ct brain
-should be done as soon as possible in all patient
to exclude or confirm hemorrhage
 MRI brain and MRA
- should be considered if CT is negative (CT scan
unable to differentiate ischemic and
hemorrhagic stroke especially perfomed >10
days after stroke)
 Doppler or Duplex ultrasound scan  
- this is used to find out whether there has been
a narrowing of the blood vessels in the neck (the
carotid arteries), which supply blood to the
brain.
 Lumbar puncture
- should be done if subarachnoid hemorrhage is
suspected and CT brain is negative
 MANAGEMENT OF STROKE
 Acute management
 Long-term management
 Acute management (cont…)

Airway check the patient can protect can protect his/her airway and
swallow w/o evidence of aspiration
Breathing check that the patient is breathing adequately; check O2
saturation and give O2 if saturation < 95%
Circulation check peripheral perfusion, pulse, and blood pressure
adequate and treat w fluid replacement, anti-arrhythmics drug
and inotropic drug as appropriate
Hydration screen for sign of dehydration and give fluids parenterally or
by nasogastric tube if necessary
Nutrition assess nutritional status and provide nutritional supplements
if necessary; if dysphagia persist for a day or two, start feeding
via a nasogastric tube
Medication if the patient is dysphagic, consider alternative routes for
essential medications
 Acute management (cont…)

BP unless there is heart failure or renal failure, evidence of

hypertensive encephalopathy or aortic dissection, do not lower
the blood pressure in the fist few week since the cerebrel
perfusion may decrease. BP often returns towards the patient’s
normal level within the first few days

Blood check blood glucose and treat w insulin when levels are > 11.1
glucose mmol/L. monitor closely to avoid hypoglycemia
Temperature check for pyrexia and investigate and treat underlying cause ;
give antipyretics since raised brain temperature may increase
infarct volume
Pressures check pressure areas and introduce measures to reduce the risk
area for bedsores : treat infection, maintain nutrition, provide a
pressure-relieving mattress, turn immobile patient regularly
 Acute management (cont…)

Incontinenc check for constipation and urinary retention and treat

e appropriately; avoid urinary catheterization unless the patient is
in acute urinary retention or incontinence is threatening pressure
areas
Investigatio CT/MRI, blood glucose, urea n electrolyte, FBC, INR, ESR, ECG
n
 Long-term management
 Further management of the stroke patient
centre on identification and treatment of risk
factor and rehabilitation to restore function.
 Primary prevention (ie before a stroke)
 Secondary prevention (ie preventing further stroke)
 1st prevention
 Medical therapy
 Risk factor should be identified and addressed
 Risk factor are :
 HPT – treat and monitor
 Smoking – stop
 Lifestyle – more active (exercise)
 Alcohol – moderate intake/stop
 High cholesterol – statins, diet
 Raised hematocrit – reduce
 Atrial fibrillation – anticoagulate
 Obesity – weight reduction
 Diabetes – good control
 Severe carotid stenosis - surgery
 Sleep apnoea - treat
 2nd prevention
 Antihypertensive therapy
 Recognition and good control of high BP is the major factor in both 1st and 2nd
stroke prevention. Transient HPT often seen following stroke usually does not
require treatment provided diastolic pressure does not rise > 100 mmHg.
Sustained severe HPT needs treatment. BP should be lowered slowly to avoid any
sudden fall in perfusion.

 Antiplatelet therapy
 Long-term soluble aspirin(75 mg daily) reduces substantially the incidence of
further infarction following thromboembolic TIA or stroke.
 Clopidogrel and dipyrimadole are also used
 Combined aspirin 75 mg daily and dipytidamole 200 mg twice daily possibly
provide optimal prophylaxis against further thromboembolic stroke or TIA.

 Anticoagulants
 Heparin and warfarin shoud be given when there is atrial fibrillation
 2nd prevention (cont…)
 Other measures
 Polycythaemia and any clotting abnormalities should be treated.
Statin therapy should be given for all

 Surgical approaches
 Internal carotid endarterectomy
 Surgery is recommended in TIA or stroke patient with internal carotid
stenosis >70%.
 Successful surgery reduces the risk of further TIA/stroke by around
75%.
 Endarterectomy has a mortality around 3% and a similar risk of stroke.
 Percutanous transluminal angioplasty (stenting) is an alternative.
 The value of surgery for asymtomatic carotid stenosis is debatable.
 2nd prevention (cont…)

 Rehabilitation after stroke

 Optimal care is on a stroke rehabilitation unit that
provides multidisciplinary services, coordinates
disability-related medical care and trains caregivers.
 Physiotherapy*
 Speech therapy*
 Occupational therapy*
 physiotherapy
 Is particularly useful in the few weeks in
reducing spasticity, relieving contractures and
teaching patients to use walking aids.
 The benefits of physiotherapy for longer-term
outcome are still inadequately researched.
 Baclofen and/or botulinum toxin are
sometimes helpful in the management of
severe spasticity.
 Speech therapy
 Speech therapists have a vital understanding of
aphasic patients’ problem and frustration.
 Return of speech is hastened by conversation
generally.
 If swallowing is unsafe because of the risk of
aspiration, either nasogastric feeding or
percutanous gastrostomy will be needed.
 Video-fluoroscopy while attempting to
swallow is helpful.
 Occupational therapy
 Following recovery, the occupational therapists
play a valuable role in assessing the
requirement for and arranging the provision of
various aids and modifications in the home,
such as stair rails, hoists or wheelchairs.
Pharmacology agents used in treatment of
stroke
 Anti-platelet- aspirin, clopidogrel, ticlopidine
 Anticoagulants-heparin, warfarin
 Thrombolytics-streptokinase, urokinase,t-PA
 Antihypertensive agents
 ACE inhibitors
 Beta-blockers
 Hydralazine
 Lipid lowering drugs
 MOA
ANTIPLATELETS
 Inhibition of prostaglandin mechanism
 Aspirin
 Inhibition of ADP-induced platelet aggregation
 Ticlodipine, clopidogrel
 Blockade of GP llb/llla receptors on platelets
 Abciximab, integrelin
 Aspirin
 irreversibly inactivates platelet cyclooxygenase
1 (through acetylation)and suppresses the
production of thromboxane A2
 Interfere with platelet aggregation
 Anuclear platelet cannot synthesize new
enzyme during its 10 day lifetime
 Clopidogrel, Ticlodipine
 Irreversibly inhibit binding of ADP to its
receptors on platelets
 Thus, inhibit activation of GP llb/IIIa receptors
required for platelets to bind to fibrinogen and
to each other
 MOA
ANTICOAGULANTS
 Heparin
 serve as a calatytic template to accelerate the
antithrombin reaction
 antithrombin inhibits clotting factor proteases by
forming stable complexes with them
 it interacts with activated factors (thrombin)IIa,
IXa,Xa, providing anticoagulant effect within
minutes
 Warfarin
 Antagonist of vitamin K
 inhibit the synthesis of Vitamin K dependent clotting
factors:
 factor II
 factor VII
 factor IX
 factor X
 MOA
THROMBOLYTICS
 Streptokinase
 Combines with ciculating plasminogen to form an
activator complex: convert plasminogenplasmin
 t-PA (Alteplase, Reteplase)
 Preferentially activate plasminogen bound to fibrin
 confines fibrinolysis to the formed thrombus and
avoids systemic activation
 MOA
 ANTIHYPERTESIVE AGENTS
 IV betablockers
 hydralazine are recommended
 ACE inhibitors

 limited effect on cerebral circulation

 MOA of ACE inhibitor and Angiotensin receptor
blocker
angiotensinogen
Captopril, enapril, lisinopril, ramipril
ACE inhibitors
Angiotensin 1 Inhibit peptidyl dipeptidase enzyme
•Decreased formation of angiotensin 2
•Decreased breakdown of bradykinin
Angiotensin 2
Angiotension
receptor blocker
Losartan, valsartan, irbesartan,candesartan
Angiotensin 2 receptor •Block angiotensin 2 receptor
•Do not have effect on bradykinin
•Similar benefits like ACE inhibitor
vasoconstriction Aldosterone secretion

Increase peripheral Increased sodium,

vascular resistance Increase water retention

Increased blood pressure

 Beta-blockers
 Labetalol
 Hydralazine
 This drug causes direct vasodilation, acting
primarily on arteries and arterioles.
 This results in a decreased peripheral
resistance, which in turn prompts a reflex
elevation in heart rate and cardiac output.
LIPID LOWERING DRUGS
 HMG CoA Reductase Inhibitor

 Bile acids binding resin

 Nicotinic acid

 Fibric acid derivatives

 Cholesterol absorption inhibitors

HMG CoA reductase inhibitor
Lovastatin, simvastatin, pravastatin, fluvastatin
MOA: - analogs of 3-hydroxy-3-methylglutarate
-competitive inhibitors of 3-H-3-M coenzyme A (HMG
CoA reductase) which catalyze mevalonate biosynthesis
HMG CoA mevalonate
HMG CoA reductase ihibitor

•Decreased de novo synthesis of cholesterol

•Increase LDL receptor number
•Increased LDL uptake by hepatocytes
•Decreased plasma LDL
Bile acid binding Nicotinic acid Fibrates (clofibrate, Cholesterol
resin (niacin) benzafibrate, absoprtion
(cholestyramine, gemfibrozil) inhibitor
cholestipol, (ezetimibe)
colesevelam)
MOA: binds to bile MOA: -decreased MOA: - activate MOA: inhibit
acid in the intestine intracellular lipase peroxixome intestinal absorption
and prevents activity proliferator- of dietry and biliary
reabsorbtion ; •Increased activated receptor cholesterol
•Enterohepatic lipoprotein lipase -Increased -reduce hepatic
cycling interupted activity expression of cholesterol stores
•More cholesterol •Decrease catabolic lipoprotein lipase -increase hepatic
neede to form bile rate of HDL -Increased uptake of LDL from
acid catabolism of VLDL plasma.
Outcome:
Increased de nove
synthesis of
cholesterol
Increased LDL
Psychosocial and financial impact on
patient
Phychosocial Financial
•Sexual relationships changed. •Need to buy some equipment for the
patients for example, wheel chair, air
•Most of the females lost interest in bed, medication, pampers.
their appearance, regardless of their
age. •The fees for physiotherapy and
speech therapist treatment.
•felt unable to prevent outbursts and
this compounded their feelings of •Many become unemployable, lose
guilt, low-esteem and despair. independence and are financially
embarrassed
•increase anger and feelings of
frustration.

•Loss of self esteem makes depression

common
 Patient education and counselling
 Family members must be educated about how
to take care of stroke patient
 Both the family and stroke patient must go for
counseling in order to over come the problem
 Physiotherapy and speech therapy have an
important psychological role, as it will increase
confidence of stroke patients to live their life.