What is the first pathophysiological event at a cellular level during stroke?
Loss of cerebral perfusion leading to neuronal depolarisation.
What happens to cellular energy supply during stroke?
ATP is depleted.
Why is ATP depletion harmful to neurons?
Membrane ion transport systems fail.
What happens to membrane ion balance when transport systems fail?
Excess calcium (Ca²⁺) enters the neuron.
Which neurotransmitter is released in excess during stroke?
Glutamate.
Why is excess glutamate dangerous?
It is a powerful neurotoxin.
How does glutamate worsen neuronal injury?
It activates excitatory receptors on neighbouring neurons, causing further depolarisation and Ca²⁺ influx.
What is excitotoxicity?
Neuronal injury caused by excessive glutamate-mediated excitation and calcium influx.
How does excitotoxicity affect the ischaemic area?
It expands the area of ischaemia.
What cellular damage results from excessive calcium influx?
Activation of destructive enzymes, production of free radicals, and release of harmful chemical mediators.
What is the ischaemic penumbra?
The area of injured but potentially salvageable brain tissue surrounding the infarct core.
Why is the penumbra clinically important?
It can recover if perfusion is restored in time.
What determines the clinical presentation of a stroke?
The site and extent of brain tissue affected.
Can stroke affect both grey and white matter?
Yes.
What is the aim of neuroprotective research in stroke?
To inhibit these damaging pathophysiological processes.