Posted: October 17, 2010 by chao85 in Medicine

Definition of Stroke

“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 > 24 hours

or leading to death, with no apparent cause other than that of vascular origin”.

Definition of Transient Ischaemic Attack (TIA)

“A Clinical syndrome characterized by an acute loss of focal cerebral or monocular function with

symptoms lasting <  24 hours and which is thought to be due to inadequate cerebral or

ocular blood supply as a result of arterial thrombosis or embolism”.

Cause & Pathophysiology

3 main causes of ischemic stroke:

  1. Atherothromboembolism (50%)
  2. Intracranial small vessel disease (penetrating artery disease) (25%)
  3. Cardiogenic embolism (20%)
  4. Others ( arterial dissection, trauma, vasculitis (primary/secondary), metabolic disorders, congenital disorders and other less common causes such as migraine, pregnancy, oral contraceptives, etc.)


Atheroma affects mainly the large and medium sized arteries at places of confluence, branching or tortuosity of vessels.

The process begins in childhood as fatty streaks and progresses over years with gradual buildup of fibrolipid plaque and infiltration of inflammatory cells, eventually narrowing the vessel lumen. The final step occurs with ulceration and platelet-fibrin thrombus formation on the plaque surface.

The atherothrombotic plaque can grow to obstruct a vessel, with intraluminal propagation of the thrombus proximally or distally to cause occlusion, or embolism occurs from the plaque surface to occlude smaller distant vessel(s).

Intracranial small vessel disease is thought to be due to lipohyalinosis but other causes may include microatheroma and angionecrosis, or thromboembolism from a larger artery. The clinical syndrome caused by this is lacunar infarction due to occlusion of small perforating arteries.

Vascular risk factors associated with increased risk of stroke: (primary prevention therapy)

AGE – after 55 yo 

  • Aspirin 50mg q other day (>65yo women)

  • Treat medically if bp sys>140mmHg &/or dia >90mmHg
  • Lifestyle changes if bp sys 130-139mmHg &/or dia 80-90mmHg
  • Target bp for DM sys<130mmHg &/or dia <80mmHg
  • Hypertension should be treated in the very elderly (>70yo) to reduce the risk
SEX – male>female 

  • Post menopausal Hormone replacement therapy for female

  • Cessation of smoking

  • Strict bp control
  • Maintain tight glycemic control



  • High risk grp – keep LDL<2.6mmol/L
  • ≥1 risk factors: keep LDL<3.4mmol/L
  • No risk factor: keep LDL<4.2mmol/L

  • Avoid heavy alcohol consumption

Embolism from the heart causes approximately 20% of all ischaemic strokes. The most common causes are atrial fibrillation (AF) and valvular heart disease. Not all cardiac sources pose similar threat in causing stroke.

The steps to a diagnosis of ischaemic stroke and the various causes which need investigation to identify the underlying cause for the stroke:


Based on Oxfordshire Community Stroke Project (OCSP)

Total Anterior Circulation Stroke (TAC) All of 

  • Hemiplegia contralateral to the cerebral lesion, usually with ipsilateral hemisensory loss
  • Hemianopia contralateral to cerebral lesion
  • New disturbance of higher cerebral function (dysphasia, visuospatial)
Lacunar Stroke (LAC) Pathological definition 

  • Occlusion of a single deep (LS) perforating artery
  • 5% can be due to haemorrhage
  • Occurs at strategic sites
  • More likely seen on MRI than CT scan
  • Classical lacunar syndromes correlated with relevant lacunes at autopsy
Partial Anterior Circulation Stroke (PAC) Any of 

  • Motor / sensory deficit + hemianopia
  • Motor/sensory deficit + new higher cerebral dysfunction
  • New higher cerebral dysfunction + hemianopia
  • New higher cerebral dysfunction alone
  • A pure motor/sensory deficit less extensive than for LAC (eg. confined to one limb, or to face and hand but not to whole arm)
Posterior Circulation Stroke (POC) Any of 

  • Ipsilateral cranial nerve palsy (single / multiple) with contralateral motor and/or sensory deficit
  • Bilateral motor and/or sensory deficit
  • Disorder of conjugate eye movement (horizontal/vertical)
  • Cerebellar dysfunction without ipsilateral long tract sign
  • Isolated hemianopia or cortical blindness
  • Other signs include Horner’s sign, nystagmus, dysarthria, hearing loss, etc
Code last letter as follows:



Syndrome: Indeterminate pathogenesis, prior to imaging (e.g. TACS) 

Infarct (e.g., TACI)

Haemorrhage (e.g., TACH)


  1. History – from family members, witness, patient
  2. Physical examination (Full Neurological examination +  conscious level + higher mental function test)
  3. Supplemented with selected diagnostic tests

The diagnosis should provide answers to the following questions: ( 3 what, 1 where, 1 why)

1. What is the neurological deficit?

2. Where is the lesion?

3. What is the lesion?

4. Why has the lesion occurred?

5. What are the potential complications and prognosis?

Clinical features of stroke:

The areas of the brain affected by the stroke depend on the particular artery that is affected: middle cerebral artery (pink); posterior cerebral artery (green); and anterior cerebral artery (blue).

  1. Anterior artery circulation (carotid artery)
    1. Middle cerebral artery
      1. i.      Aphasia (dominant hemisphere)
      2. ii.      Hemiparesis / plegia
      3. iii.      Hemisensory loss/disturbance
      4. iv.      Homonymous hemianopia
      5. v.      Parietal lobe dysfunction, e.g. astereognosis, agraphaesthesia, impaired two-point discrimination, sensory and visual inattention, left-right dissociation and acalculia
  2. Anterior cerebral artery
    1. i.      Weakness of lower limb more than upper limb
  3. Posterior (vertebrobasilar) artery circulation

  1. i.      Homonymous hemianopia
  2. ii.      Cortical blindness
  3. iii.      Ataxia
  4. iv.      Dizziness or vertigo
  5. v.      Dysarthria
  6. vi.      Diplopia
  7. vii.      Dysphagia
  8. viii.      Horner’s syndrome
  9. ix.      Hemiparesis or hemisensory loss contralateral to the cranial nerves palsy
  10. x.      Cerebellar signs



  1. Confirm the diagnosis
  2. Determine the stroke mechanism
  3. Risk stratification and prognostication
  4. Identify potentially treatable large obstructive lesions of the cerebrovascular circulation

Blood investigations

FBC Exclude anemia, polycythaemia, thrombocytosis, thrombocytopenia, etc
Random Blood Glucose Exclude hypoglycaemia, new diagnosis of DM
Urea & Electrolyte Hydration status, excludes electrolyte imbalances
Clotting profile ( if thrombolysis is considered) Baseline
Lipid profile (fasting)
Glucose (fasting)
OPTIONAL TESTS (in selected patients)
Autoimmune screen ESR, ANA, RF, anti ds-DNA antibody, C3-C4 levels, etc
Thrombophilia screen & Lupus anticoagulants Serum fibrinogen, anti-thrombin III, Protein C, Protein S, factor IV leyden, Antiphospholipid Ab,
Homocysteine (fasting)

Other investigations

12 lead ECG Mandatory
Ambulatory ECG For suspected arrhythmias or SAN diease


CXR Mandatory
CT brain
  • The emergency neuroimaging scan of choice for all patients
  • Differentiates haemorrhage from infarction
  • Confirms site of lesion, cause of lesion, extent of brain affected
ECHO cardiography For suspected cardioembolism, assess cardiac function
MRI (magnetic resonance imaging)
  • Sensitive
  • Not available in emergency setting, limited by expense
  • Useful tool to select patients for thrombolysis where available
Carotid duplex Ultrasound Allows identification of extracranial vessel disease
Transcranial Doppler Ultrasound Identifies intracranial vessel disease with prognostic and therapeutic implications
MR angiography (MRA)
  • Non invasive tool to assess intra- and extra-cerebral circulation
  • Objective assessment of vessel stenosis
CT angiography (multislice CT scan)
  • Non invasive tool to assess intra- and extra-cerebral circulation.
  • Involves intravenous contrast injection
MR venography In suspected cerebral venous thrombosis
Contrast angiogram
  • Gold standard assessment of cerebral vasculature
  • Reserved for patients planned for intervention


  • Metabolic/toxic encephalopathy (hypoglycaemia, non-ketotic hyperglycaemia,
  • Wernicke-Korsakoff syndrome, drug intoxication)
  • Epileptic seizures (postictal Todd’s paresis)
  • Hemiplegic migraine
  • Structural intracranial lesions ( e.g. subdural haematoma, brain tumour, arteriovenous malformation)
  • Encephalitis (e.g. herpes simplex virus), brain abscess, tuberculoma
  • Head injury
  • Hypertensive encephalopathy
  • Relapsing Multiple Sclerosis
  • Conversion disorders
  • Hyperviscosity syndrome
  • Peripheral nerve lesions (e.g. Guillain-Barre Syndrome)



Aim: to save the adjacent dysfunctional tissue by restoration of circulation and normalization of the metabolism.


  • In selected patients presenting within 3 hours:
  • IV bolus 10% rt-pa (0.9mg/kg, maximum 90mg) followed by an infusion over 1hr.
  • Start aspirin within 48 hrs of stroke onset.
  • Use of aspirin within 24 hours of rt-PA is not recommended
  • The use of heparins (unfractionated heparin, LMW heparin or heparinoids) is not routinely recommended as it does not reduce the mortality in patients with acute ischaemic stroke.


  • A large number of clinical trials testing a variety of neuroprotective agents have been completed.
  • These trials have thus far produced negative results.
  • To date, no agent with neuroprotective effects can be recommended for the treatment of patient with acute ischaemic stroke at this time.

Regime for treatment of Acute Ischemic Stroke with Intravenous Thrombolysis rt-PA (recombinant tissue PA – alteplase)

  • IV bolus over 1 min rt-PA 10% (0.9mg/kg, maximum 90mg);
  • Followed by an infusion over 1hr is recommended for carefully selected patients within 3hrs of the acute onset of ischaemic stroke.
  • Admit the patient to an ICU or a **stroke unit for monitoring.
  • Perform neurological assessments q 15 min during the infusion of rt-PA (1 hr) and q 30 min for the next 6 hrs and then q hr until 24 hr from Rx.
  • If the patient develops severe headache, acute hypertension, nausea or vomiting discontinue the infusion if agent is still being administered and obtain a CT scan of brain.
  • Measure bp q 15 min for the 1st 2 hrs, q 30 min for the next 6 hrs and then q hr until 24 hrs from Rx.
  • If B.p systolic > 180mm Hg or diastolic >105mm Hg, administer anti-hypertensive medications to maintain bp at or below these levels.
  • Delay placement of nasogastric tubes, indwelling bladder catheters or intra-arterial pressure catheters.
  • Avoid antiplatelet drugs for the first 24 hrs after administration of rt-PA.

* C/I of streptokinase in acute ischemic stroke because of poor clinical outcome*

**STROKE UNIT – unit in the hospital only managing stroke patients. The core disciplines of the stroke team are: medical (neurologist, geriatrician or general physicians with interest in stroke), nursing, physiotherapy, occupational therapy and speech therapy. In bigger centres, it may include neurosurgeon, social worker and dietitian.

IV rt-PA can be given ONLY if the following is available:

1. A physician with expertise in the diagnosis and management of stroke.

2. Appropriate neuroimaging tests are available 24 hours a day

3. Capability to manage the complications of thrombolysis, particularly intracranial


Characteristics of Patients with Ischaemic Stroke Who Could Be Treated With rt-PA

1. Diagnosis of ischaemic stroke causing measurable neurological deficit

2. The neurological signs should not be clearing spontaneously, minor and isolated

3. Caution should be exercised in treating a patient with major deficits

4. Onset of symptoms ❤ hours before beginning treatment

5. No contraindication for thrombolytic therapy

6. Sys Bp < 185mm Hg and/or dia. Bp < 110mm Hg

7. Brain CT is normal

8. The patient or family understand the potential risks and benefits from treatment

Contraindications for intravenous thrombolytic therapy

1. Current use of oral anticoagulant or PT > 15sec (INR > 1.7)

2. Use of heparin in the previous 48 hrs and a prolonged aPTT

3. A platelet count < 100,000/mm3

4. Another stroke or any serious head injury in the previous 3/12

5. Major surgery within the preceding 14 days

6. Arterial puncture at noncompressible site within the last 21 days

7. Pre-treatment sys. bp > 185mmHg or dia. bp > 110mmHg

8. Neurological signs that are improving rapidly

9. Isolated mild neurological deficits, such as ataxia alone, sensory loss alone, dysarthria alone or minimal weakness

10. Prior intracranial haemorrhage

11. A blood glucose < 2.7mmol/l or > 22.2mmol/l

12. Seizure at the onset of stroke

13. GIT or UT bleeding within the preceding 24 days

14. Recent MI


  • Supportive care
  • Treatment of acute complications.

This is important to improve mortality and functional disability.

  1. Oxygen and Airway Support
  • To prevent hypoxia and potential worsening of the neurological injury.

  1. Regular Observation
  • To recognise impaired pulmonary function (pulse oxymeter), circulatory function (PR, bp) and to recognise complications from mass effect.
  1. Mobilisation
  • First treated with bed rest, but mobilisation should begin as soon as the patient’s condition is judged to be stable.
  • This involves passive and full-range-of-motion exercises, frequent turning, the use of alternating pressure mattresses (ripple mattress), and close surveillance of the skin. Measures to avoid falls are an important part of mobilisation.
  1. Blood Pressure
  • Hypertension following stroke is quite common.
  • However, its optimal management has not been established.
  • Very high blood pressure should be reduced gradually.
  • Proposed drugs: Labetolol 10-20 mg boluses at 10 min intervals up to 150-300 mg or 1 mg/ml infusion, 1-3 mg/min or Captopril 6.25-12.5 mg orally.
  • Sublingual use of a calcium antagonist, such as nifedipine, should be avoided because of rapid decline in blood pressure.

  1. Blood Glucose
  • Hyperglycaemia following acute stroke is strongly associated with subsequent mortality and impaired neurological recovery.
  • This applies to diabetics and non-diabetics.
  1. Nutrition
  • Sustaining nutrition is important as malnutrition after a stroke might interfere with recovery.
  • Persons with infarctions of the brain stem, multiple strokes, large hemispheric lesions, or depressed consciousness are at the greatest risk for aspiration.
  • Swallowing impairments are associated with an increased mortality.
  • Early initiation of PEG feeding has not been shown to improve long-term outcome.
  • A water swallow test should be performed before the patient is allowed to eat or drink.
  • A wet voice after swallowing, incomplete oral-labial closure, or coughing reflex on swallowing indicates high risk of developing aspiration.
  • A videofluoroscopic modified barium swallow examination can be performed later if indicated.
  • If the patient fails the swallowing test, a nasogastric tube should be inserted to prevent aspiration.
  • Percutaneous placement of an endogastric (PEG) tube is superior to nasogastric tube feeding if a prolonged need for devices is anticipated.
  1. Infection
  • The commonest complication = pneumonia and UTI.
  • The appearance of fever should prompt a search for infection and appropriate antibiotic therapy should be administered early. Bladder catheters should be avoided if possible.

  1. Fever
  • A meta-analysis suggested that fever after stroke onset is associated with marked increase in mortality and morbidity.
  • Anti-pyretics should be used to control elevated temperatures in acute stroke patients.

  1. Raised Intracranial Pressure
  • Cerebral oedema and increased intracranial pressure largely occur with large cerebral infarctions.
  • The head of the bed can be elevated by 20 to 30 degrees in an attempt to help venous drainage.
  • Hyperventilation is an emergency measure that acts almost immediately; a reduction of the PCO2 by 5 to 10 mm Hg can lower intracranial pressure by 25% to 30%.
  • Mannitol (0.25 to 0.5 g/kg) IV administered over 20 minutes lowers intracranial pressure and can be given 1 6 hrs.
  • The usual max daily dose is 2 g/kg.
  • If hydrocephalus is present, drainage of CSF via an intraventricular catheter can rapidly lower intracranial pressure.
  • Hemicraniectomy and temporal lobe resection have been used to control intracranial pressure and prevent herniation among those patients with very large infarctions of the cerebral hemisphere.
  • Ventriculostomy and suboccipital craniectomy is effective in relieving hydrocephalus and brain stem compression caused by large cerebellar infarctions


  • Haemorrhagic transformation should be considered as a cause of neurological deterioration following the use of a thrombolytic agent.
  • If an urgent brain CT confirms a haemorrhage, stop the rt-Pa infusion.
  • Obtain blood samples for coagulation tests, infuse fresh frozen plasma and cryoprecipitate, and seek immediate neurosurgical opinion.


  • Depends on the stroke type, size and location.
  • Haemorrhagic stroke has a higher mortality than ischaemic stroke. However patients with haemorrhagic stroke show a better neurological and functional recovery.
  • Brainstem infarct, large hemispheric infarct and cardio embolic stroke also carry a poor prognosis.
  • Lacunar infarct has the lowest mortality rate.

  1. gerardloh says:

    welcome to the club…awesome post

  2. Dr Faravee says:

    Very nice ,thoughtful presentation.i think it would be helpful,if u put referrances of def & give classification of stroke

  3. Great article.
    I would like to add that the ABCD2 score is a simple and very useful tool to assess the prognosis of TIA. It helps to classify mild, moderate, and high risk TIA, and hence determine the urgency of referring.
    Patients with TIA should always have their carotid arteries assessed by vascular surgeons. Large clinical trials show that patients with symptomatic carotid stenosis of 70% or more benefit from carotid endarterectomy (CEA), which is still the preferred treatment option, compared to stenting.
    CEA is a very common operation performed when I was in the UK.

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