What is Cerebral Infarction?

Cerebral Infarction described here together with ischaemia. Infarction and ischaemia of the brain are closely associated with conditions that lead to focal necrosis of the nervous tissue in the ischaemic area, usually corresponding to the distribution of an arterial vessel. The main causes of infarction are atherosclerotic occlusion of large vessels, embolic occlusion of distal vessels, vasculitis and arterial spasm following subarachnoid haemorrhage. The common clinical presentation is stroke, with different neurological syndromes according to the functions located in the involved region. From dense unilateral hemiplegia to focal aphasias, from sudden coma to hemianopia, from hemispheric cerebellar ataxia to diplopia, from a Wallenberg syndrome to hemiballism, almost any neurological syndrome may be produced by a focal ischaemia with infarction of the brain tissue.

Ischaemia is a prerequisite of infarction but may still be reversible; if permanent, irreversible damage to the nervous tissue results. Not all the ischaemic nerve cells die and different cell types have varying sensitivity to ischaemia; in an ischaemic region a peripheral area of so-called "penumbra" is usually present, in which cells remain viable for several hours but at risk if circulation is not re-established. Neurones are the most sensitive to ischaemia, followed by astrocytes, oligodendroglia, microglia and endothelial cells. When a vessel is occluded, the entire supplied region does not become ischaemic because efficient collateral circulation may develop very rapidly, if not immediately. This happens through anastomoses that are either permanently or potentially patent; the circle of Willis and the external-internal carotid arteries anastomoses are examples of permanent and efficient collateral circulation, while the cortico-cortical anastomoses are an example of collateral circulation that opens up when the arterial pressure drops on one side.

Some deep areas of the brain are border zones between the terminal capillary beds of the major cerebral arteries in the cortex and receive the lowest cerebral blood flow; these zones, called watershed areas, are the first to suffer ischaemia and infarction during generalized systemic hypotension.


When a patient presents with stroke or transient ischaemic attack or neurological signs indicating a possible vascular ischaemic aetiology, a CT scan must be performed first (Fig.1). If there is a discrepancy between the clinical status and the CT finding, or if the patient is a candidate for aggressive thrombolitic therapy in a stroke unit, it will be necessary to perform MRI, including diffusion and perfusion studies (Fig.2) and angio MRI, eventually followed by angiography, if intra-arterial thrombolysis is envisaged.

The role of immediate CT is twofold: diagnose or exclude any other cause that may have mimicked clinically a stroke, mainly haemorrhage; and to recognize the extent of ischaemia and the significance of mass effect when present, over the adjacent structures.

Three phases may be identified: acute, subacute and chronic. In the acute phase about 60% of scans may be considered normal within the first few hours; however, some subtle early signs may be detected such as loss of grey-white matter interface, obscuration of the lentiform nucleus and hyperdensity of the horizontal portion of the middle cerebral artery within the sylvian fissure. A rapid development of the picture may be seen after 6-8 hours with the development of cytotoxic oedema. The infarcted area becomes markedly hypodense with involvement of both grey and white matter, usually in a wedge-shaped area corresponding to the region of distribution of the occluded vessel. In about 15-20% of cases haemorrhagic foci may be detected after 24-48 hours (Fig. 3), particularly in the basal ganglia in cases of occlusion of the middle cerebral artery. Enhancement following contrast injection may be observed as early as 3-4 days and may persist for as much as 2 months. While moving towards the chronic phase in which a porencephalic cavity with CSF density may result, the infarcted area goes through a short phase of isodensity around the second and third week in which the oedema and mass effect disappear.

At MRI detection of infarction usually occurs earlier than with both SE sequences and in particular with diffusion-weighted images. Absence of flow void in the vessels leading to the infarcted area and early gyral oedema with T2 hyperintensity subsequently involving also the white matter are among early signs.

Diffusion-weighted images show very early - within the first 2 hours - hyperintense areas due to a reduced diffusion coefficient in the infarcted area in the presence of cytotoxic oedema.

Angiography, when performed, shows the occluded vessel, extra- or intracranially and, eventually any resulting collateral circulation.

Imaging Examples

Infarction, cerebral, Fig.1 (a)
Infarction, cerebral, Fig.1 (b)
Infarction, cerebral, Fig.1 (c)
Infarction, cerebral, Fig.2 (a)
Infarction, cerebral, Fig.2 (b)
Infarction, cerebral, Fig.2 (c)
Infarction, cerebral, Fig.3 (a)
Infarction, cerebral, Fig.3 (b)

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Last Updated: Jan 22, 2014

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