Ischaemic Stroke

Aetiology:

1. Embolic stroke (20%)

o Cardiac emboli (Atrial fibrillation, prosthetic heart valve, mitral stenosis)
o Atheroemboli
o Infectious emboli (bacterial endocarditis)
o Paradoxical embolism (right to left cardiac shunt)

2. Thrombotic stroke (40%)  Rupture of an atherosclerotic plaque and exposure of sub-

endothelial collagen, resulting in formation of a thrombus

o Large vessel occlusion

o Small vessel occlusion (lacunar infarct)

3. Global cerebral ischemia  result in Watershed infarct

o Systemic hypoperfusion (etc, shock or bilateral large artery atherosclerosis that can
result in watershed infarct)
o Hypoglycaemia
o Severe chronic hypoxia (respiratory arrest, cardiac arrest)

4. Other causes
o Hypercoagulable states (Polycythaemias, sickle cell disease, inherited thrombophilia)
o Vasculitis
o Collagen disease (SLE)

Risk factors:

Modifiable Non-modifiable
 Hypertension  Old age
 Diabetes mellitus  Male gender
 Cardiac disease (atrial fibrillation,  Family history
bacterial endocarditis)
 Increased haematocrit level
 Smoking
 Obesity
 Sedentary lifestyle
Clinical features:

Artery Involved Clinical Manifestation

Anterior cerebral artery - Contralateral weakness and sensory loss (LL>UL)
- Limb apraxia
- Frontal release signs
Middle cerebral artery - Contralateral weakness and sensory loss (UL>LL)
- Wernicke or Broca Aphasia, acalculia (dominant hemisphere)
- Hemineglect (non-dominant hemisphere)
- Contralateral hemianopia
- Eye deviation to normal limb
Posterior cerebral artery - Contralateral hemianopia
- Alexia without agraphia (dominant)
- Wernicke Aphasia
- Visual cortex syndrome  Agnosia, visual hallucinations
- Midbrain syndrome  3rd nerve palsy, hemiparesis
- Thalamic syndrome  hemisensory loss, spontaneous pain, choreoathetosis
Vertebrobasilar artery - Cranial nerve palsies
- Crossed sensory deficit (sensory involvement of the face on one side of the
body and the arm and leg on the other side. E.g., ipsilateral face and
contralateral body numbness)
- Diplopia, vertigo, nausea, vomiting, dysarthria, dysphagia, hiccup
- Ataxia, coma
- Eye deviation to affected limb
Penetrating vessels - Pure motor hemiparesis
(Lacunar syndrome) - Pure sensory deficit
- Pure sensori-motor deficit
- Ataxic hemiparesis
- Dysarthria clumsy hand syndrome (combination of facial weakness, severe
dysarthria, and dysphagia, with mild hand weakness and clumsiness)

Definition of neurological terms:

1. Frontal release sign

 Primitive reflexes that tends to disappear as brain matures (baby grow up)
 Certain condition disrupts inhibitory effect on these reflexes, hence reflex is
“released” from inhibition resulting in the reflexes elicited again
 Examples are: Palmar grasp (Baby naturally grabs objects placed in palm), sucking
reflex
2. Apraxia: inability to perform coordinated, purposeful, and/or learned movements
3. Acalculia: Inability to perform simple calculations
4. Broca Aphasia/Expressive Aphasia: Loss of ability to produce language, but can understand
other’s speech
5. Wernicke Aphasia/Receptive Aphasia: Loss of ability to understand other’s speech, but able
to speak (non-sense speech)
6. Hemineglect: patients fail to be aware of items to one side of space (attention disorder, not
physical loss of visual field)
7. Hemianopia: Physical loss of one side of visual field
8. Alexia: Partial or complete inability to read (comprehension is impaired)
 9. Agraphia: Inability to write
10. Agnosia: Inability to recognize objects, person, sounds, shapes or smells (no loss of memory
or no specific sense loss)
11. Ataxia: Mimic those being drunk (slurred speech, stumbling, falling, incoordination).
12. Dysarthria: Motor speech disorder, muscles to produce speech are damaged, paralyzed or
weakened.
13. Choreoathetosis: occurrence of involuntary movements in a combination of chorea
(irregular migrating contractions) and athetosis (twisting and writhing)
14. Cortical sign (due to stroke in cerebral cortex): Aphasia, neglect, agnosia, apraxia,
hemianopsia
15. Lacunar syndromes:
 Noncortical infarcts characterized by the absence of cortical signs
 Most commonly occur in ischemic stroke, but also can arise from microbleeds
 There is no cortical sign in any of the lacunar stroke
16. Watershed infarct sign:
 Caused by sudden decrease in blood pressure or cessation of blood flow through
both vessels → ischemia in the susceptible region between two vascular territories
 Clinical features are:
i. Bilateral visual loss
ii. Stupor (state of near unconsciousness)
iii. Weakness of the upper limbs with sparing the face, hands and feet (“man-
in-the-barrel syndrome”)
17. Paresis vs Plegia:
 Paresis  describe weakness
 Plegia  describe loss of all voluntary movement
 Hemi  One side of body is affected
 Di  All 4 limbs affected, but lower limbs more affected than upper limbs
 Para  Lower limbs are affected
 Quadri  All 4 limbs affected
 Monoplegia  Only 1 limb affected
 Tri  3 limbs are involved

DDx:

 Neurologic
o Transient ischemic attack (complete recovery with no residual abnormalities,
resolved within 24 hours, no evidence of infarction on imaging)
o Postictal paralysis (Todd’s paralysis)
o Brain tumor
o Hemiplegic migraine
 Toxic/metabolic
o Hyponatremia
o Hypoglycemia
o DKA
o Alcohol withdrawal
o Drug intoxication (e.g., heroin, barbiturates)
  Infectious
o Meningitis
o Encephalitis
o Meningoencephalitis
o Cerebral/epidural abscess
 Trauma
o Traumatic brain injury
o Subdural hematoma
o Epidural hematoma
 Paraneoplastic syndromes/autoimmune disorders
o Multiple sclerosis
o Bell palsy
o Guillain-Barré syndrome
o Lung cancer (Lambert-Eaton myasthenic syndrome)

Investigation:
Aim of investigation are to identify mechanism of stroke and underlying risk factors causing stroke.
1. Emergent non-contrast CT brain (TRO haemorrhagic stroke)
2. MRI brain (if CT brain negative or CT not able to differentiate ischaemic or haemorrhagic
stroke, but clinical suspicion of acute stroke is high)
3. CT angiography (CTA) / MRI angiography (MRA)
- Indicated if CT or MRI show no ischaemic changes, but suspicion of stroke is high
- For candidate before undergoing mechanical thrombectomy
4. Lumbar puncture (if subarachnoid haemorrhage is suspected and CT scan is –ve)
5. Lab studies
a. FBC
 To assess for high haematocrit level (polycythaemia), risk factor for stroke
b. Serum electrolytes and creatinine
 Exclude electrolyte imbalance
c. Coagulation profile
 TRO hypercoagulation status (thrombophilia)
d. Blood glucose level
 TRO hypoglycaemia
e. Lipid profile (assess for risk factor)
f. ABG (if hypoxia is suspected)
g. ANA, lupus anticoagulant, anticardiolipin antibody (if SLE suspected)
6. ECG (TRO atrial fibrillation and MI)
7. Chest X-ray
8. Echocardiography (cardiac embolism is suspected, with abnormal ECG or CXR findings)
9. Carotid Doppler studies (to be performed for patient going for carotid endarterectomy)

Management:
1. Ensure clear airway and adequate oxygenation.
2. Elective intubation if GCS score <8.
3. High suspicion of stroke (with clinical assessment and history OR NIHSS score >6) 
emergent non-contract CT brain TRO haemorrhage.
4. Perform ECG (atrial fibrillation/MI), echocardiography, lab studies to evaluate for causes of
symptoms.
5. Reperfusion therapy:
a. After ruling out haemorrhage, determine eligibility of patient for IV rtPA.
b. If time of onset <4.5 hours and fulfil all criteria for IV rtPA, begin reperfusion therapy
immediately.
c. If patient not fulfilling rtPA criteria, consider criteria for mechanical thrombectomy.
d. If time of onset <6 hours and fulfil all criteria for thrombectomy, go for
thrombectomy.
e. Intra-arterial mechanical thrombectomy can be considered for patient time of onset
between 6 to 24 hours and imaging studies showed visible penumbra.
6. For all stroke patient (including those without undergoing reperfusion therapy), they will be
kept under monitoring and stabilization.
7. Monitoring and stabilization:
a. Monitor pulmonary function (pulse oximeter), continuous cardiac monitoring for at
least 24 hours.
b. Monitor NIHSS score, GCS score of patient.
c. Maintain fluid balance using normal saline to prevent dehydration. Hypotonic saline
should be avoided to prevent cerebral oedema.
d. Maintain blood glucose level between 7.8 mmol/L to 10.0 mmol/L. Insulin therapy
should be indicated if glucose level >10.
e. Body temperature should be kept <37.5 C.
f. Patient who are unconscious, not able to sit upright, not able to swallow should be
fed by NG tube.
g. DVT can be prevented by intermittent pneumatic compression device (IPC) or
anticoagulation. (IPC compress the leg from ankle to hip, to help venous return)
h. Rehabilitation appropriate to patient’s level of disabilities should be stared soon as
patient is stable.

8. BP management:
a. Elevated blood pressure is generally allowed in ischemic stroke (permissive
hypertension). This is to prevent further development of cerebral ischemia due to f.
b. If severe HTN (>220mmHg/ >120mmHg):
i. Reduce BP by 15% within first 24 hours of stroke onset
ii. For patient to undergo tPA administering, BP should be reduced to
<185mmHg/ <100mmHg prior to tPA.
c. Drugs of choice are IV labetalol, nitroglycerin patch, IV sodium nitroprusside.
d. Hypotension should be corrected if present.

9. Treatment for raised ICP and cerebral oedema:

a. Cerebral oedema is maximum in 24 to 72 hours.
b. Elevate head of bed by 30 degree to help venous drainage.
c. Hyperventilate to lower ICP.
d. IV mannitol or frusemide can be helpful to treat cerebral oedema.
e. Craniectomy should be considered for patient with large infarctions of cerebral
hemisphere.
 10. Antithrombotic agents:
a. Aspirin given within 48 hours onset of ischemic stroke. Initial dose of 150-300 mg
and maintenance dose of 75 to 150 mg daily.
b. If there is aspirin allergy, use clopidogrel as alternative.
c. If patient already on aspirin, add on second agent usually aspirin + dipyridamole.
d. For patients who have undergone tPA reperfusion therapy, aspirin only initiated
after 24 to 48 hours of tPA administration.

Secondary stroke prevention:

Strategies for stroke prevention include antithrombotic therapy, pharmacological treatment of
comorbid conditions that predispose to stroke, lifestyle modifications and therapy for specific
problems.
1. Antithrombotic therapy
a. Anticoagulation agents recommended for all patients with TIA/ stroke as a result of
cardiac emboli, thrombophilia and cerebral venous thrombosis.
b. Choice of anticoagulation agents are direct oral anticoagulants (DOACs) and
warfarin.
c. When warfarin used, it must be initiated at 3-5 mg/ day, INR monitored daily at
target of 2 to 3.
d. DOACs example are dabigatran, apixaban, rivaroxaban.
e. Patients who are contraindicated for anticoagulation agents should be given
antiplatelet agents.
f. Aspirin is most commonly prescribed antiplatelet agent.
g. Clopidogrel is more effective than aspirin and used as alternative to aspirin in patient
have aspirin allergy.
h. Combination of aspirin + dipyridamole is very efficacious in preventing recurrent
stroke event.

2. BP control:
a. BP reduction should only be initiated 1 to 2 weeks after a stroke event unless BP
become >220/ 120mmHg.
b. In hypertensive patient with stroke/ TIA, BP should be kept <130/80 mmHg but not
lower than 120/70 mmHg, once acute stage is over.

3. Cholesterol reduction
a. Treatment with statins should be given at a sufficient dose to reduce LDL level at
least 40 to 60 mg/dL.
b. Treatment should be continued for lifelong.

4. Control of diabetes mellitus

5. Hormone replacement therapy should not be prescribed to women having stroke.
6. Lifestyle modification:
a. Weight reduction
b. Smoking cessation
c. Increased physical activity
d. Moderate alcohol intake
e. Dietary modification (low salt, low saturated fat, high fiber)