Effects Of Occlusion Of Arteries

Here, as in other parts, the effects of occlusion depend chiefly on whether the arteries concerned have sufficient anastomosing communications or not. The arteries of the circle of Willis anastomose freely, and occlusion of one of them leads only to a very temporary derangement of the circulation. The larger branches anastomose sparely, and occlusion of them has much more serious effects. The nutrient arteries do not anastomose at all, and occlusion of them has very evil results.

The most direct result of occlusion of arteries is Anaemia of the part supplied. As the occlusion in the case of embolism is sudden, there is often a very abrupt interference with the cerebral functions. In the case of a large artery, such as the main stem of the middle cerebral, there may be a very extensive anaemia, leading to a fatal issue before the anastomosing circulation can be established.

Softening of the brain substance (Bamollissement) is a further consequence. This is really a necrosis with fatty degeneration of the nervous tissue, and it only occurs when the conditions are such that the circulation is brought absolutely to a standstill. This is the case when any of the nutrient arteries are obstructed, as these are end-arteries. The nutrient arteries which come off from the first part of the middle cerebral are the most exposed to obstruction from embolism, and hence softening of the central parts of the brain, especially in the region of the corpus striatum, is of somewhat common occurrence. It is important to notice that, for reasons to be afterwards considered, it is these arteries also which most frequently give rise to haemorrhage.

But softening not infrequently occurs although the vessels occluded are not end-arteries. This is especially true where thrombosis is the cause of the occlusion. As we have already seen, thrombosis is common in connection with atheroma. Now this is a disease of old people, in whom the circulation is weak. Under these circumstances occlusion of a small peripheral artery may lead to softening, before the force of the blood has brought about an anastomosing circulation, all the more because many of the neighbouring arteries are also partially obstructed by atheroma. Even in the case of embolism there may be considerable cortical softening if the embolus has broken up and plugged several vessels at the same time, so as to interfere with the establishment of the anastomosing circulation.

The Changes in the brain substance in softening have already been incidentally considered. It will be a local lesion limited to the piece of brain substance to which the affected artery is distributed.

Softenings have often been distinguished according to the colour presented by the affected brain substance, so that white, yellow, and red softenings have been described. For the most part the colour depends on the blood mixed with the nervous tissue, and the amount and condition of the former can hardly be regarded as a chief characteristic of the softening; the colour is therefore not of primary importance.

We have seen already that softening of the brain substance is really due to a Necrosis. The result of the death of the nervous structures is their disintegration. The nerve fibres very rapidly break up; the myeline of the medullary sheath coagulates and escapes from the primitive sheath, and afterwards breaks up into fine fat granules. The ganglion cells are more resistant, but they also become granular and gradually disappear. The cells of the neuroglia and the cells of the walls of the vessels undergo fatty degeneration. These structures become filled with finely divided fat, so that the neuroglia cells are converted into characteristic Compound granular corpuscles and the cells of the vessels are converted into aggregates of fat granules at intervals along the vessels (Fig. 326). So far as the neuroglia cells are concerned it is probable that in some cases they pick up fat arising from the disintegrated myeline. It is not so clear that the cells of the blood-vessels do this, and there is here, probably always, a proper fatty degeneration. Besides the neuroglia cells there may be present in the part amoeboid cells, or these may pass into it after the occurrence of the necrosis, and these also become occupied by granular fat. In this way there are, frequently, large numbers of compound granular corpuscles which are very conspicuous when a piece of the softened tissue is examined in the fresh state under the microscope. A ready means of distinguishing true pathological softening from a mere post-mortem change is afforded by the presence of these cells. In true softenings they are present in large numbers and afford a highly characteristic appearance.

Fig. 326. - Fatty degeneration of the vessels in cerebral softening. (Paget).

In some cases, as already mentioned, the softened brain substance is largely mixed with blood. At first the blood gives a red colour to the softening. But as time goes on the colouring matter is dissolved out of the red corpuscles and diffused throughout the softened structures, as well as to some extent in the brain substance around. In that case the colour becomes less intense and merges into yellow, or the colour may be reddish yellow from the outset. It will be seen from this that red and yellow softening run together, and that the latter is often merely • a later stage of the former. If there is very little blood in the vessels of the softened part then the colour is white or grey. This is mostly seen when death has occurred very soon after the occlusion of an artery.

The ultimate disposal of the necrosed piece of brain substance occurs on principles already considered. The softened brain substance has ultimately the characters of a fatty emulsion, which is gradually absorbed. A chronic inflammation occurs around, just as in the case of a haemorrhage, and in a similar fashion connective tissue is produced, taking the form of a cyst or cicatrix, according to circumstances. The resulting cyst or cicatrix is not always to be distinguished from that of a cerebral haemorrhage. Usually the latter presents more distinct pigmentation^ but the former may also present pigment granules and crystals.

Other forms of softening are of less consequence than those from occlusion of arteries. Softenings are very frequent around extravasations of blood. They are partly due to mechanical destruction, but also to anaemia from the pressure of the blood. Softenings around tumours are similarly due to anaemia. There is occasionally a softening from localized inflammation, more especially such septic forms as lead on to abscess. A softening of the brain around the ventricles also occurs in connection with the hydrocephalus of tubercular meningitis (which see).

Occlusion Of Arteries And Other Conditions In Chorea

The frequent association of chorea with acute endocarditis has suggested the view that it may have its origin in embolism of the arteries and capillaries of the brain, multiple embolism with softening having been found in some cases, but not in all. Embolism, however, is only a coincidence related to the endocarditis, and not necessarily connected with the pathology of chorea. This, indeed, is evident from the fact that acute endocarditis is not infrequently absent in cases of chorea. Other changes in the vessels have been observed, such as dilatation of the arteries and veins throughout the substance of the brain and spinal cord, exudations or small haemorrhages, sometimes with blood crystals, around the vessels. These lesions, however, are by no means constant, and are to be regarded as consequences of irritation of the brain, or as coincident phenomena.

In chorea there is an irritant present in the blood, presumably the same irritant as that in acute rheumatism. It attacks the nervous system, producing hyperaernia and exudation from the vessels. While the whole central nervous system is more or less affected there are certain parts specially involved, these parts being what have been called the accessory portions of the nervous system. It may be supposed that the fundamental and simpler parts of the brain and cord are more stable than the accessory parts, and that when attacked by an irritant the latter will give way first. The anatomical distribution of the lesions suggests that this is so, and the symptoms of chorea indicate disorder in "movements which are acquired, and which are probably only learned by a long apprenticeship" (Hughlings Jackson). On the other hand, chorea has been regarded by some as due to an "infection," but so far there is not much evidence forthcoming in support of such a view, although, according to Osier, Pianese is said to have isolated a bacillus from the nervous system of a choreic patient, which when inoculated into animals caused death with muscular twitchings and convulsions. From the central nervous system of these animals the same bacillus could be obtained in pure culture. By others staphylococci have been obtained in fatal cases.