Stroke

Audrey Lee
 Stroke
a syndrome of rapid onset of cerebral deficit (usually focal) lasting >24 h or
leading to death, with no cause apparent other than a vascular one.
 Transient ischaemic attack (TIA)
a brief episode of neurological dysfunction due to temporary focal cerebral or
retinal ischaemia without infarction, e.g. a weak limb, aphasia or loss of vision,
usually lasting seconds or minutes with complete recovery. TIAs may herald a
stroke. The arbitrary time of <24 hours is no longer used.

Definition
  ICA – anterior brain
 VA, BA – posterior brain
 ACA , MCA – Frontal and parietal lobe
 PCA – Occipital lobe
 Communicating arteries - provide connections between the
anterior and posterior circulations and between left and right
hemispheres, creating protective anastomotic connections that
form the circle of Willis.
Arterial supply
of the brain
Classification of Stroke
Stroke
Syndomes
  caused by thromboembolic disease secondary to artherosclerosis
of the major extracranial arteries (carotid artery and aortic arch)
 After occlusion of a cerebral artery, infarction may be forestalled
by opening of anastomotic channels from other arterial territories
that restore perfusion to its territory.
 Reduction in perfusion pressure leads to compensatory
homeostatic changes to maintain tissue oxygenation
Cerebral  If failed, ischemia starts and ultimately leads to infarction unless
Infarction blood supply is restored
 If fall below threshold for maintenance of electrical activity,
neurological deficit develops
 At this level, neurons are still viable, if blood flow increases,
function returns and the patient will have TIA
 If blood flow continue to fall, a level is reached at which
irreversible cell death starts
 Failure of
ATP supply
Hypoxia reduced
membrane
pumps

Glutamate Release of Influx of sodium

opens excitatory
and water into
neurotransmitter
membrane glutamate to cell (cytotoxic
channel extracellular fluid edema)
Cerebral
Infarction
Activates Inflammatory
Influx of calcium mediators released by
intracellular enzyme
and more sodium that complete the
microglia and
into neurons astrocytes causes cell
destructive process death

Worsened by anaerobic
production of lactic
acid and consequent
fall in tissue pH
  Caused by rupture of a blood vessel within the brain
parenchyma
 Explosive entry of blood into the brain parenchyma causes
immediate cessation of function in that area
 Neurons are structurally disrupted and white matter fibre
tracts are split apart
Intracerebral  Cerebral edema and hematoma formed during the process
Haemorrhage will act like a mass lesion to cause progression of
neurological deficit
 If its big, can cause shift of the intracranial contents,
producing transtentorial coning/herniation and sometimes
rapid death
 If patient survives, the hematoma will gradually absorbed
and leave a hemosiderin-lined slit in the brain parenchyma
  Limb weakness on the opposite side to the
infarct develops over seconds, minutes of hours
 Contralateral hemiplegia or hemiparesis with
facial weakness
 Aphasia (if the dominant hemisphere is
Clinical affected)
Features  Consciousness is usually preserved
 After a variable interval, usually several days,
reflexes return and become exaggerated
 Babinski’s sign present
Clinical
features
Risk
Factors
 To confirm the diagnosis
To determine the stroke mechanism
Investigations To assess risk stratification and prognosis
To identify potentially treatable large
obstructive lesions of the cerebrovascular
circulation
Investigations
Investigations
General
Management
General
Management
  The concept of the existence of an ischaemic penumbra
is fundamental to the current approach to treatment of
ischaemic stroke:
although a core of infarct tissue might not be salvageable,
adjacent dysfunctional tissue might be saved if the circulation
is restored and metabolism is normalized.

• Intravenous Thrombolysis With rt-PA

Reperfusion of Intravenous rt-PA (0.9mg/kg, maximum 90mg), with 10% of
Ischemic Brain the dose given as a bolus followed by a 60-minute infusion, is
recommended within 4.5 hours of onset of ischaemic stroke.
Intravenous 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 haemorrhage.
Regimen for IV rtPA
  Start aspirin within 48 hours of stroke onset.
 Use of aspirin within 24 hours of rt-PA is not
recommended.
Aspirin  Reduces the risk of early recurrence and has a
small but clinically worthwhile effect on long-
term outcome
  Every hospital should set up a stroke unit.
 Stroke units significantly reduces death,
dependency, institutionalisation and length of
hospital stay.
Stroke Unit  A stroke unit should be managed by a
multidisciplinary stroke team.
 An efficient referral and rehabilitation network
should be established to ensure the success of
stroke units.
  Kumar and Clark’s Clinical Medicine 8th Edition
References  Davidsons Principles and Practice of Medicine 22nd Edition
 Malaysian CPG Management of Stroke 2nd Edition