Stroke (CNS Ischemia)

 

Stroke

Objectives:

  1. Define stroke and transient ischaemic attack
  2. Risk factors for stroke
  3. Describe the different aetiologies of ischaemic & hypertensive strokes
  4. Understand effects of hypertension on brain
  5. Describe gross and microscopic morphology of cerebral ischaemic

 

Cerebrovascular disease Injury to the brain, due to altered blood flow

  • ischaemic
  • Haemorrhagic
Stroke (brain)
  • sudden
  • Neurological event
  • Vascular origin
  • Lasts for > 24 hrs
Strokes
Transient Ischaemic Attack (TIA) ”mini-stroke”, with effects that last less then 24hrs
RIND Reversible Ischaemic Neurological Deficit
  • > 24hrs
  • Resolves
Partial non-progressive stroke
Progressive Stroke
Complete Stroke

 

Stroke:

  1. Haemorrhagic
    1. Bleed from vessel/aneurysm within brain —> causes downstream effects (nutrients do not get there)
  2. Ischaemic
    1. Problem with blood flow ( < / >)

 

Risk Factors for Stroke

(i.e “heart-attack” in the brain” ) —> similar to MI

Hypertension Hyperlipidemia
Smoking Diabetes
Heart disease and impaired cardiac function

  • CHD, A.Fibrillation,LVH, Valvular disease (prolapse)
 Obesity
Oral Contraceptives

  • increased coagulability
 Post-surgery

  • Hypercoagulability

 

Virchow’s Triad

  • causes formation of thrombus
  • Altered flow/turbulence

 

For patients younger than 59 years:

  1. Vessel wall disease
    1. Large
      1. Fibromuscular dysplasia
      2. Dissection
      3. Migraine
    2. Small
      1. Vasculitis
      2. Drug-induced
      3. Sickle cell anaemia
      4. Anti-phospholipid syndrome
  2. Heart
    1. Congenital Heart disease and complications
      1. Valve Prolapse
      2. Patent foramen ovale
      3. Ventricular septal defect (paradoxical embolism – goes on the other side of circulation) – deep vein thrombosis, instead of going to lungs go to brain

Focal Cerebral Ischemia  —> (sustained) —> infarction

Cerebral Infarction:

  • Reduction/Cessation of blood flow to a localised area of the brain due to arterial occlusion of hypoperfusion
    • Thrombosis (local)
    • Embolism (solid mass from elsewhere)
    • Vasculitis (inflammation of vessels)
  • Important in Watershed areas (deep); less collateral vessels
    • Thalamus; basal ganglia; deep white matter

 

 

Cerebral Infarction (tissue death due to inadequate blood flow)

  • 80% = non-haemorrhagic (Occlusion)
  • 20% = haemorrhagic (burst blood vessel – ICF)

Often initially non-haemorrhagic

—> become haemorrhagic due to ischaemia-reperfusion injury

  • The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than (or along with) restoration of normal function.

 

It is important to differentiate the source of cerebral Infarcts as the treatment is different:

  • non-haemorrhagic = remove blockage, increase/decrease blood flow etc.
  • Haemorrhagic = not much of a treatment…

 

Clinical Presentation

F ace unilateral facial weakness

  • droopy eyes and lips (cant smile)
A rms unilateral limb weakness  (brain “damage” on contralateral side)
S peech Slurred speech
T elephone ambulance …

 

Non-haemorrhagic (ischaemic) Stroke – brain

  1. Thrombosis
  2. Embolism (most common) – thromboembolism
  3. Systemic hypoperfusion

 

Thrombus: clotted blood (solid)

Embolism: Moving mass through vasculature: i.e. air, infection, blood clot(thrombus)

  • Can cause blockage

 

Thrombotic Ischemic Stroke
Causes
  • Atherosclerosis
  • Dissection
  • Vasculitis (inflammation)
  • Large vessel disease/ Small vessel disease
  • Changes to Hypertension
    • Arteriolar sclerosis, fibrinoid degeneration
  • Atheroma
Location Extracranial: common & internal carotids

(narrowing of the branches)
Intracranial: Circle of Willis / proximal branches

  • Small penetrating arteries from distal vertebral art.
  • Basilar artery
  • MCA

 

Case:

Atherosclerosis at the internal carotids

  • treatment: Carotid endarterectomy (removal of plaque)
  • Risk : removal of neointima layer, endothelial of vessels is one cell thick —> accidental removal can cause loss of function (dilation)

 

Embolism Ischemic Stroke
  1. Cardiac Mural Thrombi (attaches to lining of vessel/heart)
  • Things that causes stasis in the heart

Predisposition to cardinal mural thrombi:

Atrial Fibrillation (pumping becomes “bag-of-worms”) —> turbulent flow
MI Necrotic tissue —> Scar—> weaken walls = “bag” —> stasis
Valvular disease Turbulent flow
Aneurysm (vessels) Turbulent flow

 

  1. Thromboemboli from arteries (esp. carotids)
  • Recent MI, Deep vein thrombosis(long sitting periods), Post-surgery, obesity
  1. Emboli of other material: tumour, fat, air, bone marrow

 

Systemic Hypoperfusion

Systemic low blood pressure —> diffused ischaemic/hypoxic encephalopathy(brain damage)

  • global, non-focal signs; bilateral signs (weakness)

 

General reduction of cerebral perfusion (cardiac arrest, shock, severe hypotension)

Most sensitive neurons in the brain; pyramidal layer of hippo campus, cerebellar purkinje cells, pyramidal neurons in cerebral cortex.

 

Describe gross and microscopic morphology of cerebral ischemia

Macroscopic Microscopic
  • Cerebral Oedema
  • Poor demarcation of grey and white matter
  • Widen gyri and flattened sulci (pressured against meninges)
 12-24 hrs.: “Red dead neurones” then infiltration by neutrophils (nypoxic)
24 hrs.-2 wks.: Necrosis (brain = liquefactive), macrophage influx, vascular proliferation, reactive gliosis
>2 wks.: loss of normal CNS architecture with gliosis

 

Hypertensive Cerebrovascular Disease

  1. Lacunar infarcts
  2. Slit haemorrhages
  3. Hypertensive encephalopathy
  4. Intracerebral haemorrhage/haemorrhagic stroke

 

Hypertensive Cerebrovascular Disease: Lacunar Infarcts
“Lacunar” = small spaces
AoE: HTN affects deep penetrating arteries and arterioles that supply the basal ganglia, hemispheric white matter and brainstem.

  • Vessels develop arteriolar sclerosis (hardening) and may become occluded
  • Develops into single/multiple small cavitary infarcts (lacunes)

 

Hypertensive Cerebrovascular Disease: Slit Haemorrhages
Microaneurysm → slit haemorrhage “pin-point” haemorrhage

  • Rupture of small penetrating vessels → small haemorrhages
  • In time, these haemorrhages resolve and leave behind a slit-like cavity (slit haemorrhage) surrounded by brown-ish discolouration

 

Hypertensive Cerebrovascular Disease: Hypertensive Encephalopathy
Encephalopathy = “brain-malfunction”
Syndrome consisting of a sudden elevation of arterial pressure

  • A clinicopathological syndrome that arises in the setting of malignant HTN
  • Diffuse cerebral dysfunction: headaches, confusion, vomiting, convulsions → coma
  • Medical emergency

 

Hypertensive Cerebrovascular Disease: Intracerebral Haemorrhage
(intracerebral = mostly caused by high BP, not berry aneurysm- subarachnoid space)

  • Rupture of deep (larger) vessels
  • AoE: Basal Ganglia, Thalamus, Cerebellum (central zone)
  • Charcot-Bouchard microaneurysms

 

Summary

  1. Stroke a major cause of mortality and morbidity worldwide
  2. Stroke may be ischaemic or haemorrhagic; ischaemic is more common
  3. Hypertension is a major risk factor for different types of cerebrovascular disease