What is stroke

Stroke is the result of obstruction of the cerebral blood vessels and deprivation of oxygen, glucose and other essential nutrients to the supplied vascular territory, which leads to cell death, through liquefactive necrosis (Colledge, Walker and Ralston., 2010, p. 1181). This is because brain tissue functioning stops, if deprivation of oxygen lasts longer than 60 to 90 seconds. If blood circulation is not re-established irreversible damage will be done to the affected area of the brain, causing it to lose function and can lead to visual impairment, inability to comprehend or formulate speech, move one or multiple limbs and other physical, cognitive and emotional problems resulting in acquired disability. (Figure 1)

Figure 1 Post stroke disabilities (Genentech., 2014)

Hemiparesis is a movement impairment, resulting in weakness on one side of the body.

Aphasia is a communication disorder, which makes writing, reading and speaking difficult, but does not affect the patients intelligence.

Two major types of stroke are: ∙ Ischaemic sroke (Figure 2)

∙ Haemorrhagic stroke (Figure 3)

The majority of strokes are ischemic (87%), others are haemorrhagic. (Heart and stroke foundation of Canada, 2008)

Figure 2 Ischaemic Stroke (Heart and stroke foundation of Canada, 2008)	Figure 3 Haemorrhagic Stroke (Heart and stroke foundation of Canada, 2008)

Ischaemic stroke happens when a blockage in the artery supplying the brain occurs, leading to hypoxia. Explanations why ischaemic stroke can occur include:

• Thrombosis - thrombus (blood clot) forms locally, obstructing blood vessels within the brain, either veins or arteries.

• Systemic hypoperfusion – such as in shock , for example hypovolemic, which results from inadequate blood volume for the continuation of satisfactory cardiac output, blood pressure, and tissue perfusion.

• Cerebral embolism – embolus (blood clot) forms in any blood vessel within the body and travels to the brain.

• Cryptogenic stroke – obscure or of unknown origin, without any obvious explanations, occurs in 30-40% of ischaemic strokes.

H

• Cerebral venous sinus thrombosis

• Arteriovenous malformation

• Bleeding within a tumour

• Amyloid angiopathy

aemorrhagic strokes are intracerebral bleeds and can be caused by:

• Penetrating head trauma

• Depressed skull fractures

• Rupture of an aneurysm

• Acceleration-deceleration trauma

The risk factors for stroke can either be fixed or amendable and include: (Colledge, Walker and Ralston., 2010, p. 1181)

• A

  • High blood pressure

  • Heart disease (atrial fibrillation, heart failure)

  • Diabetes mellitus

  • Hyperlipidaemia

  • Smoking

  • Excess alcohol consumption (≥2/day)

  • Polycythaemia

  • Oral contraceptives

  • Social deprivation

  ge

• Gender (male > female, except in the very young and very old)

• Race (Afro-Carribean > Asian > European)

• Heredity

• High fibrinogen

• Previous vascular event, e.g. MI, stroke or peripheral embolism

• Menopause

A study by Nakano et al., (2011) demonstrates that susceptibility for haemorrhagic stroke can also be increased after infection with serotype k Streptococcus mutants that express collagen-binding protein (CBP). This is because the bacteria are able to bind to collagen fibres in the damaged blood vessels, as CBP prevents collagen-dependent platelet aggregation, therefore the blood vessel remains open and bleeding continues.

Molecular mechanisms of neuronal ischaemia and infarction are depicted in Figure 4 and occur in the following order:

1. Reduced blood flow decreases oxygen and glucose supply and therefore also decreasing ATP levels.

2. Without ATP, energy-dependent transmembrane ion transporters fail, leading to membrane depolarisation and cytotoxic oedema, which allows glutamate to be released and calcium to enter.

3. Glutamate-gated channels transport calcium into cells.

4. Calcium then activates lipid peroxidises, poteases and other destructive enzymes, which in turn destroy intracellular organelles and the phospholipid cell membrane by releasing of free radicals.

5. The release of free fatty acid activates coagulation, which intensifies local ischaemia.

6. Glial cells take up H⁺ions instead of extracellular glutamate. This lack of glutamate leads to apoptosis of glial cells. The release of inflammatory mediators by microglia and astrocytes lead to necrosis of all cell types in the whole arterial territory.