Page created on October 5, 2018. Last updated on May 24, 2019 at 18:22
Stroke is an acute neurological condition due to a cerebrovascular event. We distinguish two types of stroke: ischaemic and haemorrhagic stroke.
Ischaemic stroke, or cerebral ischemia, occurs because of an occlusion of an artery. This is the most common type of stroke, and the extent of the damage depends on which artery was occluded and for how long. The artery occlusion causes ischaemic damage to the brain tissue.
We distinguish two types of cerebral ischemia. If the artery occlusion resolves itself quickly and symptoms resolve within 24 hours, we call the episode a transient ischaemic attack (TIA). In these cases is the chance of a reoccurrence of a stroke is high within two years of the episode.
If the occlusion doesn’t resolve itself within a short amount of time the prolonged ischemia will cause permanent complications.
Brain tissue is especially vulnerable to ischemia. Irreversible changes to individual cells occur after only 1.5 minutes of ischemia. Because of the plasticity of the brain can cortical functions still work after some cells have died. Cortical functions can therefore survive ischaemia for as long as 4-5 minutes.
Ischaemic stroke can either be regional in the brain (limited to a certain area), or global (rarer). The causes for the two are:
- Regional ischaemic stroke
- Subclavian steal syndrome
- From the heart or carotids
- Global ischaemic stroke
- Cardiac arrest
- 3rd degree AV block
- Ventricular arrhyhtmias
- Cardiac arrest
When there is a regional ischemia, there is an ischaemic or necrotic core that is most severely affected by the ischemia. Around this core is a region called the penumbra. Tissue in this area is only partially injured, and the functions of it can be restored if blood flow is restored quickly enough.
The process of damage is as follows:
- The reuptake of the excitatory neurotransmitter glutamate is inhibited (as this requires energy). This causes glutamate to be present in the synaptic clefts longer.
- The increased presence of glutamate causes glutamate receptors to get activated. This causes opening of ion-channels.
- Na+and Ca2+ enter the cells
- More Ca2+ enters the cytoplasm from intracellular stores and from outside
- The increased intracellular Ca2+ level activates intracellular pathways, enzymes and gene expressions
- Free radicals are produced
- Activated enzymes damage DNA and trigger cell death
- The areas that were only partially affected by ischemia may improve their condition.
- Most of the penumbra might regenerate
- Other parts of the brain can take over several functions of the necrotic tissue in the long term, due to the brains’ plasticity.
In haemorrhagic stroke an artery in the brain ruptures and starts to bleed. Because the skull limits the volume of the brain will a haemorrhage cause compression of the healthy brain. Depending on whether the bleeding occurs inside the parenchyme or under the arachnoid mater we call the occurrence intracerebral or parenchymal haemorrhage or a subarachnoid haemorrhage.
Causes of parenchymal haemorrhage include:
- Cerebral amyloid angiopathy
- Ruptured arteriovenous malformations
Causes of subarachnoid haemorrhage include:
- Ruptured berry aneurysm
- Ruptured arteriovenous malformations
In ischaemic stroke the vessels are also damaged. If the arterial occlusion that caused the ischaemic stroke is removed, then the reperfusion could break the damaged vessels and cause haemorrhage.
We distinguish four types of cerebral oedema:
Vasogenic cerebral oedema occurs when there is an impairment of the blood-brain barrier, often due to ischemia (could be secondary to an ischaemic stroke), or due to a tumour. The impairment of the BBB causes an increased permeability of Na+, water and proteins which start to accumulate in the brain tissue.
Cytotoxic cerebral oedema occurs due to a metabolic disorder that causes the Na+/K+ ATPase to dysfunction, causing cells to swell due to the influx of Na+ and water. This can occur due to ischemia, acidosis, toxins, hypoglycaemia, hyperglycaemia or uraemia.
Osmotic cerebral oedema occurs due to a change in the osmotic gradient. This can occur due to the extracellular space becoming hypotonic due to water intoxication or increased ADH.
Hydrostatic cerebral oedema occurs due to dysfunction of a hydrostatic pressure gradient, either due to too high or low pressure in the arteries of the brain. This can occur if the MAP exceeds 150 mmHg, or if a patient with chronic hypertension suddenly reduces the MAP to normal values (the chronic hypertension has shifted the autoregulation range upwards, so the CBF is decreased even at a normal MAP).
Neither cytotoxic or osmotic brain oedemas are real oedemas as the fluid accumulated inside the cells and not in the extracellular space. Nevertheless, are the consequences of all of them the same.
Because the brain lives in a closed space will an oedema in the brain cause increased intracranial pressure (ICP). The consequence of increased ICP can be:
- Visual disturbances
- Due to a cerebral herniation, even into the foramen magnum, where the brainstem that controls the circulation and breathing can be compressed.
Increased ICP also activates a reflex called Cushing’s reflex. The reflex causes bradycardia, pathological breathing pattern and systolic hypertension.
As ICP increases will the intracranial pressure eventually exceed the mean arterial pressure inside the cerebral arteries and arterioles. This causes the vessels in the brain to be compressed, which further decreases brain perfusion. By elevating the MAP will the Cushing’s reflex try to prevent the arteries from being compressed by increasesing the MAP. The reflex therefore protects the brain against the increased ICP.
2 thoughts on “22. Cerebral hypoxia, ischaemia, stroke”
what you here call process of damage, is that the same as exitoxicity from the topic on conciousness in pathophysio2?
I don’t think so.