Pathology

Cerebrovascular lesions

 

CT, MRI and angiography are the three main methods used in the diagnosis of ischaemic and haemorrhagic lesions of vascular origin. CT is the most important method because it is capable of distinguishing between infarction and fresh intracerebral haemorrhage. Clinically these conditions are collectively referred to as stroke. It is difficult to distinguish between infarction and fresh bleeding using MRI and the role of MRI in this area of neuroradiology is still not entirely clear. The importance of MRI, however, is likely to increase. Angiography gives specific information about the anatomy of the vessels prior to surgical procedures for aneurysm or stenosis.

lnfarction

Infarction can be classified as large infarction, lacunar infarction and subcortical atherosclertic encephalopathy (Binswanger's disease ). Other

Figure 6. Schematic CT scan of different types of infarction. Within the right cerebral hemisphere, infarction corresponding to the regions supplied by the middle cerebral and posterior cerebral arteries, respectively, as well as central lacunar infarcts within the basal ganglia. In the left cerebral hemisphere, central infarction (caput nucleus caudatus), as well as infarction in the border zone between the area of supply of the middle cerebral and posterior cerebral arteries (watershed infarction).

 

Figure 7. CT scan of a large right-sided middle cerebral artery infarction.

types of infarction occur at the junction between areas supplied by different vessels (so called watershed infarctions). In addition, infarction occurs secondary to vein or sinus thrombosis. Infarction can also display a haemorrhagic component. Fig. 6 shows schematically the different types of common infarction.

CT can demonstrate an infarct after approximately six hours but some infarcts are not visible on CT for one or sometimes two days. Occasionally, as a very early sign of infarction, the thromboembolus itself can be seen in the vessel as a hyperdense structure. Areas of infarction can be seen earlier with MRI than with CT. The larger infarcts are confined to specific vessel areas and of these infarction confined to the area supplied by middle cerebral artery is the most common (Fig. 7). This type of infarction involves both white and grey matter. Initially, CT shows a diffuse hypodensity and MRI hyperintensity with T2-weighted images. These changes occur because of oedema. During the subsequent 3-5 days the oedema becomes more obvious and the infarct's borders more clearly defined. At this stage, the area of infarction reaches its maximum size and its effect on surrounding structures is at its greatest. The part of the ventricular system nearest to the infarction is compressed. A large infarct can give rise to considerable swelling and result in displacement of mid-line structures and herniation. The swelling begins to reduce after approximately one week and disappears after 2-3 weeks. At a certain stage the area of infarct can be more or less isodense with the surrounding structures. Later the area of infarction becomes clearly defined and atrophic changes appear. Clinically, there is no re as on in most cases to monitor the development of the infarction with CT. The first examination is usually diagnostic in combination with history and examination. An infarct can develop haemorrhagic components some days after onset and these can be recognized as hyperdense areas within the infarction at CT (Fig. 8).

Figure 8. Infarction of the left occipital lobe with haemorrhagic components.

 

Figure 9. Lacunar infarction in the left thalamus (arrow).

Injection of contrast medium is only used when it is difficult to differentiate between infarction and other lesions. At infarction, damage to the blood-brain barrier is seen and this is most obvious after 2-3 weeks and can remain for a long time.

Lacunar infarctions are small (less than 15 mm) and usually situated in the area of the internal capsule. Infarctions as small as 5 mm in diameter can be demonstrated (Fig. 9). It can, however, take more than a week before they are detected. In the brain stem they are difficult or impossible to demonstrate with CT and in this region the use of MRI can be helpful.

In Binswanger's syndrome (Fig. 10) a diffuse hypodensity is seen in the white matter within the centrum semiovale, mainly periventricularly. This hypodensity can be accompanied by lacunar infarctions. The changes are usually bilateral but can be asymmetrical and are best shown with MRI using T2-weighted images.

The appearances of cerebellar infarction may resemble those of tumour of low attenuation. Considerable swelling can occur with compression of the 4th ventricle and development of hydrocephalus.

Infarcts arising as a result of thrombosis within the superior sagittal sinus are usually situated parasagittally. These can also be haemorrhagic. At CT, the thrombus itself can sometimes be demonstrated in the early stages as a lesion of high attenuation and the diagnosis can be confirmed

Figure 10. CT scan of Binswanger's disease with diffuse hypodensity in the white matter and widening of the lateral ventricles.

by injection of contrast medium. However, to be absolutely certain angiography needs to be performed. Experience with MRI and MR angiography suggests that these methods will replace CT and conventional angiography in the diagnosis of thrombosis.

lntracerebral haematoma

Spontaneous intracerebral haematoma can occur in hypertension or at rupture of arterial, mycotic or arteriovenous aneurysms. Haemorrhage can also occur in infarction and in tumours or metastases.

A fresh haemorrhage is hyperdense and well-defined at CT (Fig. 11). During the first days a hypodense zone of oedema appears around the haematoma. Large haemorrhages affect the ventricular system and can break through into the CSF contained within. Haematomas as small as a few mm. in diameter can be demonstrated.

The density of the haematoma decreases gradually from the periphery to the centre. Depending on its size it takes from 2-4 weeks before the hyperdense component has disappeared. After two months the haematoma is hypodense and resembles, as far as density is concerned, an old infarct.

At MRI, the haematoma increases gradually in signal intensity because the haemoglobin assumes changed paramagnetic qualities in the process of changing to methaemoglobin. The haemoglobin molecules break

Figure 11. CT scan of a fresh haemorrhage in the left putamen.

down and the effect this has on signal intensity is shown in Table l. When conversion to haemosiderin is complete the signal intensity becomes low. It is important to note that fresh bleeding can be overlooked at MRI.

Table 1. Breakdown of the haemoglobin molecule and resultant effects on the signal at MRI

Stage	Product	Effect on signal
acute	oxyhaemoglobin	insignificant
subacute	deoxyhaemoglobin methaemoglobin	slight shortening of T2 shortening of T1
chronic	haemosiderin	shortening of T2

Haematoma following rupture of an arterio-venous malformation is usually confined to the lobe in which the malformation is situated (Fig. 12). The possibility to diagnose such a malformation at CT depends on its size. The tortuous vessels have a characteristic appearance especially after injection of contrast medium and an impression of afferent and efferent vessels can be perceived. At MRI, vessel malformations display low intensity because of the blood flow within (signal void). For more detailed information of arterial supply and venous drainage of malformations angiography must be performed (Fig. 13). This information can
 

Figure 12. Haematoma (arrow) in association with arteriovenous malformation in the left occipital lobe (see Fig. 13 ). The haemorrhage has broken through into the ventricular system.

 

Figure 13. AP angiogram of arterio-venous malformation in the left occipital lobe (arrow).

also be obtained with MR angiography.

Rupture of an arterial aneurysm can, as well as causing subarachnoid haemorrhage (Fig. 14) cause an intracerebral haematoma. This latter haemorrhage, if it does occur, gives information about the vessel from which the bleeding has occurred. Even the distribution of blood in the subarachnoid space often gives an indication of the vessel involved.

Figure 14. CT scan of subarachnoid haemorrhage with blood in the basal cisterns and Sylvian fissures bilateraly and the interhemispheric sulcus.

 

Figure 15. Lateral angiogram in a patient with subarachnoid bleeding (see Fig. 14). Aneurysm of the pericallosal artery (arrow).

The commonest locations for aneurysms are the anterior communicating artery and the middle cerebral artery. In 20% of cases more than one aneurysm is evident. The accuracy of CT in cases of subarachonid haemorrhage depends on the size of the haemorrhage and the time of onset. In certain cases it is impossible to demonstrate the haemorrhage with CT. In these cases lumbar puncture is necessary to confirm the diagnosis. MRI is a poor method for detecting blood in the subarachnoid space. Larger aneurysms can be demonstrated with CT after injection of contrast or with MRI which displays low signal, or varying signal intensity if the aneurysm is partly thrombosed. Further information about the relevant anatomy can be obtained at angiography (Fig. 15) and in general all intracerebral vessel areas need to be examined in order to detect the

a   b Figure 16. Depressed fracture (arrow) in the left squama ossis temporalis. a) plain x-ray of the skull b) CT sea n with measuring points

presence or otherwise of additional aneurysms. The investigation should be performed immediately after the onset of bleeding because vessel spasm can occur after 2-3 days and this can last for approximately one week. If surgery is delayed the risk of a further episode of bleeding is increased.

Other vascular lesions

Dissection within the carotid or vertebral artery is an often overlooked cause of stroke. Dissection can occur spontaneously or as a consequence of trauma to the neck. The intra-mural haemorrhage and also the remaining vessel lumen can be visualized both with CT and MRI and if further information is required, angiography must be performed.

Cavernous haemangioma is best diagnosed at MRI and is seen as a small lesion containing haemorrhages of different ages. Calcium content is shown best with CT. A true cavernous haemangioma displays no increased vascularity at angiography but different combinations occur in the spectrum between cavernous haemangioma and arterio-venous mal

Figure 17. Schematic CT scan of the most common skull and brain injuries at trauma 1. Linear fracture 2. Depressed fracture 3. Foreign body of metal density 4. Pneumocranium and pneumocephalus 5. Contusion haematoma with oedema 6. Acute subdural haematoma 7. Chronic subdural haematoma with re-bleeding 8. Extradural haematoma formation.

Venous angioma is regarded as an insignificant anatomical variation with a collection of small veins joining to form a single large vein. In general the appearances are characteristic both at CT and MRI.

 

Kjell Bergström and Giuseppe Scotti