Pathophysiology

Strokes are divided into two main categories: Ischaemic and Haemorrhagic. Fig.1 illustrates the changes in an ischaemic stroke whilst Fig.2 illustrates the changes occuring in a haemorrhagic stroke.

Fig.1- Image showing the changes occurring in an ischaemic cerebrovascular accident.     

    

Fig.2- Image showing the changes occuring in a haemorrhagic cerebrovascular accident.

Ischaemic strokes are due to an interruption in the blood supply to a certain area of the brain which leads to the ischaemia, Infarction and eventual necrosis of tissue. Ischaemic strokes are further divided into global and focal strokes.

Global strokes affect either the whole brain, watershed regions (those most vulnerable to reduced blood supply) or selectively vulnerable areas.

Focal strokes are described as large (regional) or small (lacunar) and are directed to a particular area of the brain tissue. Focal strokes are very common in the region of the brain that is supplied by the Middle Cerebral Artery. Fig.3 shows a coronal section of brain and the supply territories of the major cerebral vessels.

Fig.3- Image showing the supply regions of the cerebrl vessels. ACA: Anterior cerebral artery; MCA: Middle cerebral artery; PCA: Posterior cerebral artery.

 

The following list highlights the common causes of ischaemic stroke:

  • Embolism of thrombus via or from the heart (30%)

Embolism is the abnormal passage of particulate material from one part of the circulation to another. Emboli of cardiac origin are common and those patients who suffer from Atrial Fibrillation, Infective Endocarditis, or have recently suffered a Myocardial Infarction are at a higher risk of developing thrombus within the heart and therefore have a higher risk of embolus. The embolised material may range from a thrombus (developed in areas of flow turbulence or at atherosclerotic points), fat (from bone marrow in a broken bone), air, cancer cells, or bacteria (usually from Infective Endocarditis).

  • Large Artery Atherothrombosis or thromboembolism (40-45%)

This is also called ‘large vessel stroke’. Atherosclerosis of the larger arteries leads to stenosis (narrowing) and possibly even full occlusion.Fig.4 shows the major vessels that contribute to the cerebrovascular system and that could be implicated in ‘large artery atherothrombosis’. Occlusio of the vessels causes a decrease in blood flow and therefore blood supply to the brain tissues. Atherosclerosis is much more common at the bifurcations of arteries in the Circle of Willis or the vertebral artery. It is also common in the carotid arteries (carotid stenosis)- Fig.5 illustrates a case of carotid stenosis.

Fig. 4- The Cerebrovascular system. Vessels at risk of ‘large vessel atherothrombosis’ include: Common Carotid artery, Vertebral arter and bifurcation points within the Circle of Willis.       

   

Fig.5- Image illustrating Common Carotid Stenosis

  •  Small artery microatheroma/ lipohyalinosis (25%)

This is also called ‘small vessel stroke’. Small lacunar infarcts of the deeper brain tissue occur due to occlusion (through the process of atherosclerosis) or rupture of the small penetrating cerebral vessels (the ‘end arteries’). The Lenticulostriate perforators are those smaller vessels commonly affected, which arise at the commencement of the middle cerebral artery. If they are damaged in anyway, it is the deep structures of the brain that they supply which are damaged and small cavity type lesions (~5mm) are very common.

Lipohyalinosis is one type of small vessel disease where hypertension is a strong causative factor. The deep perforating arteries are once again prone to occlusion from a build up of fatty hyaline matter within the vessels.

  • Other arteriopathies such as dissection and arteritis (5%)
  •  Haematological disorders causing a prothrombotic state (< 5%)

For example, sickle cell anaemia can cause blood to clump up and block vessels. Stroke is the second leading killer of people under the age of 20 who suffer from sickle-cell anaemia.

  • Other

Such as, cerebral venous sinus thrombosis- there is locally increased venous pressure, which exceeds the pressure generated by the arteries. In this case, infarcts are more likely to undergo haemorrhagic transformation (leaking of blood into a damaged area).

Systemic hypoperfusion- there is a reduction of blood flow to all parts of the body, commonly due to cardiac pump failure from cardiac arrest or arrhythmias.

 

Ischaemic Strokes are also classified according to the vessels involved:

  • TACI – Total Anterior Cerebral Infarction        17%
  • PACI – Posterior Anterior Cerebral Infarction 34%
  • POCI – Posterior Cerebral Infarction             24%
  • LACI – Lacunar Cerebral Infarction                25%

 

Total anterior cerebral infarctions (TACI) give hemiplegia contralateral to the brain lesion, hemianopia contralateral to the brain lesion and a new disturbance of higher function. They occur in occlusion of the middle cerebral artery trunks.

Partial Anterior Cerebral Infarctions (PACI) gives one or a combination of motor/sensory deficits, hemianopia and new higher cerebral dysfunction. They result in occlusion of the Middle Cerebral Artery trunk with good Anterior and Posterior Cerebral Artery Collaterals circulation.

Posterior Cerebral infarctions (POCI) give unequivocal brainstem features – isolated hemianopia or cortical blindness, ipsilateral cranial nerve palsy with contralateral motor/sensory deficits, bilateral motor/sensory deficits, disorders of conjugate eye movement and cerebellar dysfunction without ipsilateral long tract deficit.

Lacunar Cerebral Infarction (LACI) involve sensory and/or motor systems, they are specifically caused by occlusion of the lenticulostriate artery (small branches of the middle cerebral artery).

Fig.7 illustrates the Cerberal Vasculature. This is a simplified diagram of the Circle of Willis and it’s main vessels. By understanding the anatomy of the vasculature- you can usually locate the position of the damaged blood vessel according to a patients presentation.

 Fig.7- Cerebral Vasculature

 Haemorrhagic strokes are due to the rupture of a blood vessels leading to compression of brain tissue from an expanding haematoma. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction.

Intracerebral haemorrhage is the accumulation of blood anywhere within the brain, i.e. – intraparenchymal haemorrhage, intraventricular haemorrhage. This will form a gradually enlarging haematoma (blood pool). Intracerebral Haemorrhages can be caused by local vessel abnormalities (hypertension, vasculitis, vascular malformation) or systemic factors (drugs, trauma, tumours and sickle cell anaemia/leukaemia). Haemorrhaging directly damages brain tissue and raises intracranial pressure giving headaches, vomiting nausea and eventually coma and death.

Subarachnoid haemorrhage is the gradual collection of blood in the subarachnoid space of the Dura. These can be traumatic or spontaneous. Spontaneous haemorrhages occur through saccular (berry) aneurysms and through extensions of intracranial haemorrhaging or due to similar causes. Approximately one third of those who suffer a subarachnoid haemorrhage die. Fig. 8 illustrats the Dural layers of the brain- it is the subarachnoid space (highlighted in green) which can pathologically fill with blood.

Fig.8 – Image illustrating the Brain dura and venous drainage system.

Saccular (Berry) aneurysms are dilations of arteries on the base of the brain, typically occurring at an arterial branch on the circle of Willis. They may be congenital. They give a variety of effects from silent stroke to compressive and haemorrhagic disorders. Complications include vasospasm and hydrocephalus.

Diagram.1 illustrates the changes occuring in the Ischaemic cascade- which is a feature of both ischemic and haemorrhagic strokes. The end result of this pathway is neuronal damage- which causes the signs and symptoms highlighted in the next section.

 

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