Stroke is caused by an obstruction or rupture of blood vessels in the brain. Ischemic strokes account for 85% of cases and are caused by a blockage, while hemorrhagic strokes account for 15% and are caused by a rupture. Risk factors include age, hypertension, smoking, diabetes and heart disease. Symptoms depend on the area of brain affected and may include weakness, speech problems, or visual issues. Diagnostic tests include CT, MRI, and angiography. Treatment involves managing risk factors, blood pressure control, thrombolysis if given early, and rehabilitation. Prevention focuses on controlling risk factors and lifestyle changes like quitting smoking.

1. Stroke
Jyothi Lia Johnson

2. Definition
• Abrupt onset of neurological deficit that is attributable to a focal
vascular cause.
• Incidence increases with age
• Common medical emergency

3. • Ischemic stroke accounts
for 85% cases
• As a result of obstruction
within a blood vessel
supplying blood to brain
• Hemorrhagic accounts for
15% cases
• It results from weakened
vessel that rupture and
bleeds into surrounding
area

4. Risk factors
• Fixed risk factors ● Modifiable risk factors
1. Age
2. Gender
3. Race
4. Previous vascular event:
• MI
• Peripheral vascular disease
5. Heredity
6. Sickle cell disease
7. High fibrinogen
1. Hypertension
2. Cigarette smoking
3. Hyperlipidemia
4. DM
5. Heart Disease : Atrial fibrillation,
CCF, IE
6. Excessive alcohol intake
7. OCPs, HRT
8. Polycythemia

5. Pathophysiology
Cerebral infarction
• Mostly caused by thromboembolic disease secondary to
atherosclerosis
• Acute occlusion -> reductn in blood flow to brain
• The magnitude of flow reduction is function of collateral blood flow
and this depends on individual vascular anatomy, the site of occlusion
and systemic BP.
• As cerebral blood flow declines -> neuronal function fails
• Blood flow below threshold -> neuronal deficit develops

6. • If blood flow is retained prior to significant amount of cell death ->
transient symptoms -> TIA
• Between ischemic core and normally perfused brain at periphery lies
the ischemic penumbra, zone of moderately reduced cerebral blood
flow
• If blood falls further, hypoxia->ATP decreases -> sodium & water influx
-> glutamate release-> Ca influx; release of free radicals and
ultimately cellular destruction.

7. Intracerebral hemorrhage
• Bleeding within the brain caused by rupture of vessel
• Explosive entry of blood -> cessation of functions, as neurons are
disrupted and white matter fibre tracts are split apart
• Hematoma growth -> neurological deterioration
• Perihematoma brain edema, primary cause of neurological
deterioration after first day of bleed

9. Transient ischemic attack
• Abrupt onset focal neurological deficit of presumed vascular etiology not
lasting longer than 24hrs
• Most TIAs resolve in less than 30mins
• TIA implies an active plaque in the major
feeding artery & is a warning sign of stroke
Features
Carotid territory
• I/L mono ocular blindness
• Weakness & heaviness of C/L arm, face leg
• Numbness & paraesthesia
• Bradykinesia, dysphagia
Vertebro basilar territory
• Vertigo
• Tinnitus
• Ataxia
• Dysarthria
• Hemianopia
• diplopia
• Sudden fall
• Dysphagia

10. RISK ASSESSMENT OF
STROKE
Highest incidence of stroke in
TIA occurs within first 48hrs
0 -3 low risk
4-5 moderate risk
6-7 high risk
Score 7 -> 22% chance of
developing stroke

11. Symptoms suggestive of TIA/ Stroke
• Sudden onset of facial weakness
• Arm weakness
• Speech deficit
• Time delay implies max damage to neurons

12. Investigations
• Full blood count, ESR
• Blood glucose, urea, proteins
• CXR, ECG
• Echocardiography
• Lipid profile
• Carotid doppler
• Homocysteine
Treatment
• DAPT – Dual antiplatelet theraphy
Aspirin 75mg to 300mg
Clopidogrel 75mg to 300mg
• Noval oral anticoagulants -> Rivaroxaban, Dabigatrin
Carotid territory TIA, >70%
stenosis in carotid imaging
• Carotid endarterectomy
• Carotid stenting

13. CORTICAL STROKE
Cerebral cortex involvement ->
• Aphasia
• Apraxia (Altered voluntary movement)
• Visual field defect
• Memory deficits -> temporal lobe involvement
• Hemi neglect -> parietal lobe involvement
• Disorganised thinking, confusion -> frontal lobe involvement
• Anosognosia( inability to appreciate severity of cognition defect)

14. PARIETAL LOBE
In right handed person dominant lobe is left and non dominant lobe is right.
• Nondominant parietal lobe -> Visuospatial skills
• Right parietal lobe lesion leads to loss of visuospatial skills -> Constructional Aparxia
• Dominant parietal lobe lesion ->
• Acalculia
• Agraphia
• Left to Right disorientation
• Finger agnosia
• Global aphasia
Gertsmann syndrome

15. TEMPORAL LOBE
• Hippocampus -> short term memory
• Neo cortex-> long term memory
• Temporal lobe lesion
• Antegrade amnesia – loss of short term memory
• Prosopagnosia – impaired memory of faces
• Complex hallucination – smell of rotten fish/dead rat, metallic taste in mouth,
hearing music
• Deja vu – undue familiarity
• Jamai vu - unfamiliarity

16. FRONTAL LOBE
• Frontal lobe damage
• Aggressive ,antisocial behaviour
• Personality changes
• Urge incontinence ( damage to paracentral lobule)
• Apathy(lack of interest in self care)
• Abulia (lack of desire to speak)
• Primitive reflexes present- grasp reflex, rooting reflex

17. OCCIPITAL LOBE
• Visual hallucination
• Palinopsia- persistence of an image even when the object is removed
• Asimultagnosia- Simultaneous visual information is not processed by
brain
• Homonymous hemianopia
Anton syndrome -> B/L distal PCA obstruction -> cortical blindness ->
Gun barrel vision

19. MIDBRAIN ANATOMY
Weber Syndrome

20. Claude syndrome
Benedikt Syndrome

21. Nothnagel syndrome
Parinaud’s syndrome

23. Medullary syndromes
1. Medial medullary syndrome
• Vessel involved – vertebral artery, anterior spinal artery
• Structures affected – Corticospinal tract
Medial lemniscus
Medial longitudinal fasciculus
Hypoglossal nucleus
• Clinical features- C/L hemiplegia
C/L loss of position and vibration
Internuclear ophthalmoplegia
I/L 12th nerve palsy( deviation of tongue towards same side of lesion)

24. 2. Lateral medullary syndrome
• Vessel involved – Posterior inferior cerebellar artery
• Structures affected – Inferior cerebellar peduncle
Vestibular nucleus
Trigeminal nucleus
Nucleus Ambiguus
Lateral spinothalamic tract
Descending fibres of Sympathetic chain
• Clinical features – I/L ataxia
I/L nystagmus and vertigo
I/L facial numbess
I/L palatal palsy
Horners syndrome
C/L loss of pain, touch and temperature

25. LACUNAR STROKE
• Internal capsule -> Anterior limb, genu, Posterior limb
• Corticospinal tract conducts impulse from brain to spinal cord
• Due to occlusion of lenticulo striate artery(small penetrating artery)
• Lipohyalinosis of small vessels feeding the internal capsule
• Pure motor stroke- Lesion of posterior limb of internal capsule
hemiparesis or hemiplegia typically affects
face,arms and leg equally
motor aphasia-> lesion in genu & anterior capsule

26. • Ataxic hemiparesis- combination of cerebellar & motor symptoms-> weakness &
clumsiness on I/L side of body
Most frequent site of infarction – posterior limb, basis
pontis, corona radiata
• Pure sensory stroke- persistent/ transient numbness and/or tingling on 1side of
body
Frequent site of infarction- thalamus
• Mixed sensorimotor stroke- hemiparesis/hemiplegia with I/L sensory impairment
Infarct usually in thalamus and adjacent posterior
internal capsule

28. Investigations
• Initial evaluation
• BP, Cardiac function and ECG
• Degree of neurological deficit and vascular territory involved
• Metabolic status -> Blood sugar, hypoxia, RFT, Electrolyte status
• Hematological parameters-> Hb, coagulation parameters
• Other investigations
• CT- to confirm infarct
• MRI
• CT angiography & MR angiography
• CXR

29. Treatment
• General measures
• Adequate airway
• Give O2 if saturation <95%
• Treat hyperglycemia with insulin if serum glucose>200mg/dL
• Avoid hyperthermia
• Skincare by changing position once in 2hrs to prevent bed sore
• Assess nutritional status and provide supplements if needed, nasogastric tube
if unable to swallow
• Signs of dehydration give fluids parenterally or via nasogastric tube
• Bladder catheterisation if continence or retention has occurred
• Passive movements of limbs to prevent contractures, edema of limb,venous
stasis and pulmonary embolism

30. • Blood pressure
• Urgent reduction is required only if
• SBP>220mmHg
• DBP>120mmHg
• MAP>130mmHg
• BP not elevated to that extent but patient has pulmonary edema, renal failure, acute MI etc,
antihypertensives required
• Candidates of thrombolytic therapy, Antihypertensives are recommended if SBP>185mmHg
or DBP>110mmHg
• Anti edema measures
• Mannitol 20% iv over 20mins, 3 to 4 times daily
• Glycerol 30ml orally 3 to 4 times daily
• Furosemide 20mg iv 3 times a day

31. • Thrombolytic therapy
• Reteplase, Alteplase
• Intravenoulsy within 4.5hrs of onset of symptoms
• Dissolve blood clot and restore blood flow
• Dose 0.9mg/kg with 10% of tot dose bolus and rest over 1 hour
• Intra arterial rTPA can be given in selected patients
• Anticoagulant
• Aspirin, heparin, warfarin
• Subcutaneous administration is recommended for treatment of immbolised patients to
prevent DVT
If patient presents, 4.5 -6hrs after onset of symptoms -> mechanical
thrombectomy

32. Prevention
• Cessation of smoking
• Control of diabetes
• Diet (low fat, high fiber)
• Lowering SBP by 10mmHg is associated with a reduction in the risk of
stroke by about 1/3rd, irrespective of baseline BP levels
• Antiplatelet agents and anticoagulants in patients with atrial fibrillation
• Reducing LDL cholesterol to 100mg/dL using statin
• For asymptomatic patients who are detected to have carotid artery
stenosis of 60-99%, carotid endarterectomy may be considered.

33. • Later management includes rehabilitation, adequate control and
maintenance of risk factors
• Rehabilitation should involve family members, and includes motor
sensory, cognitive and psychological measures and attempts at
occupational rehabilitation.

35. THANK YOU