Ischaemic Stroke: Pathophysiology, Signs and Treatment

  • Clinicals
  • Neurology
  • 2020-09-12 09:20:50
  • 4 minutes, 33 seconds

Ischaemic Stroke: Pathophysiology, Signs and Treatment

Acute ischaemic stroke is caused by the interrupted supply of blood to the brain as a result of thrombotic or embolic occlusion of a cerebral artery and is more common than hemorrhagic stroke accounting for about 85-90% while about 10–15% arise from haemorrhage into the brain substance or its surrounding spaces (hemorrhagic).

A stroke is a group of diseases that are of abrupt onset and cause neurological damage.

An injury to the brain can be caused by:

  • Sudden onset of inadequacies of blood flow to some or all of the brain (ischaemic stroke), or
  • Haemorrhage into brain tissue (parenchymatous hemorrhage) or spaces surrounding the brain, most frequently the subarachnoid space (hemorrhagic stroke.

If an ischaemic attack is brief with a duration of less than 24 hours it is known as a transient ischaemic attack (TIA) rather than a stroke.

Ischaemic stroke commonly arises from mural thrombi forming at the site of atherosclerotic lesions, blocking blood flow.

Alternatively, ulceration or rupture of an atherosclerotic plaque may lead to the formation of a clot and distal embolization, or still, haemorrhage into an atherosclerotic plaque may obstruct the artery.

Causes of Ischaemic stroke

  • Commonly, emboli arise from the left side of the heart, from mural thrombi, vegetations from infected heart valves, or arrhythmias.
  • Paradoxical emboli can arise from venous circulation and access cerebral circulation through the right to left cardiac shunts.
  • Cerebrovascular diseases commonly the thickening of atherosclerotic plaques and/or local increases in blood pressure

Risk factors for stroke

Important stroke risk factors include age over 55 years, with risk incidence doubling every decade after 55 years.

Men have a 30% greater risk than women.

Not surprisingly, genetic factors also play a significant role, probably affecting multiple risk factors for heart disease, atherosclerosis, and many others.

Because most strokes in the older population are attributable to atherosclerosis and cardiac disease.

Many risk factors can be modified by medication and lifestyle alteration. These factors include cardiac disease, hypertension, hyperlipidemia, cigarette smoking, diabetes mellitus, physical inactivity, and drug abuse.

Pathophysiology Of Ischaemic Shock

Acute ischemic strokes result from vascular occlusion secondary to thromboembolic disease. Ischemia causes cell hypoxia and depletion of cellular adenosine triphosphate (ATP).

Without ATP, there is no longer the energy to maintain ionic gradients across the cell membrane and cell depolarization. The influx of sodium and calcium ions and the passive inflow of water into the cell lead to cytotoxic edema.

Cerebral ischemia sufficient to cause clinical signs or symptoms, if severe, can produce irreversible injury to highly vulnerable neurons in 5 minutes.

Progressively longer duration of ischemia increases the probability of permanent damage. If cerebral ischemia persists for more than about 6 hours, infarction of part or all of the involved vascular territory is completed and the only strategies for treatment entail rehabilitation.

Whether clinical evidence of permanent brain injury from ischemia is detectable depends on the location of the brain tissue involved

Clinical Features of ischaemic stroke

Rapid onset of neuronal malfunction referable to the area of the brain for which blood supply is disrupted.

Common stroke signs and symptoms include the following:

  • Abrupt onset of hemiparesis, monoparesis, or (rarely) quadriparesis
  • Hemisensory deficits
  • Monocular or binocular visual loss
  • Visual field deficits
  • Diplopia
  • Dysarthria
  • Facial droop
  • Ataxia
  • Vertigo (rarely in isolation)
  • Nystagmus
  • Aphasia
  • A sudden decrease in the level of consciousness

Diagnostic investigations of ischaemic stroke

From history and physical examination of the patient, you should be able to obtain a clue.


Emergent brain imaging is for the evaluation of acute ischemic stroke.

Diffusion-weighted imaging (DWI) MRI is the best way to image acute stroke

Noncontrast computed tomography (CT) scanning-However, if done too early in the stroke, most CT scans will not detect signs of ischemia.

Cerebral angiography

A lumbar puncture is required to rule out meningitis or subarachnoid hemorrhage when the CT scan is negative.

Complete blood count (CBC): A baseline FHG may reveal a cause for the stroke eg, polycythemia.

Basic chemistry panel may reveal a stroke mimic (eg, hypoglycemia, hyponatremia).

Coagulation studies may reveal a coagulopathy.

Cardiac biomarkers are needed because of the association of cerebral vascular disease and coronary artery disease.

Treatment of ischaemic stroke

Assess airway, breathing, and circulation (ABCs) and stabilize the patient as necessary

Complete the initial evaluation and assessment, including imaging and laboratory studies

Reperfusion therapy eg, intravenous fibrinolysis with rt-PA (alteplase).

Thrombolytic therapy to dissolve the fibrin clots and are useful if initiated within 3 hours of the onset of symptoms.

Drugs used are intravenous tissue plasminogen activator (tPA), streptokinase, and intra-arterial recombinant prourokinase (rproUK).

Mechanical thrombectomy.

Treat comorbid conditions.

Because of the increased bleeding risk in patients treated with early thrombolysis, prophylaxis of subsequent ischaemic strokes with antiplatelets such as acetylsalicylic acid (ASA), also called secondary prevention, should be started not earlier than 24 hours after thrombolysis.

In patients with a contraindication for ASA, dipyridamole or clopidogrel can be used.

Neuroprotective therapy is designed to save the penumbra, or the area surrounding the core of the primary ischemia, from the damage caused by reduced blood flow to this region.

Neuroprotection targets include:

  • Calcium channels
  • Glutamate receptors
  • Free radicals
  • Nitric oxide
  • Proteases
  • Cell membrane components
  • Apoptotic pathway molecules (e.g. Bcl-2 promoters)

Prevention of stroke

Primary stroke prevention of individuals with no previous history of stroke by:

  • Use of platelet antiaggregants
  • Statins use.
  • Exercise and physical activity.
  • Lifestyle modifications like smoking cessation and alcohol moderation.

Secondary prevention of individuals who have already had a stroke:

  • Platelet antiaggregants
  • Antihypertensives to treat hypertension
  • Statins use
  • Lifestyle modifications.


Daniel Ogera

Medical educator, passionate about simplifying difficult medical concepts for easier understanding and mastery by nursing and medical students.

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About this article:
  • Topic:Clinicals
  • Duration:4 minutes, 33 seconds
  • Subtopic:Neurology

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