Severe stenosis or occlusion of the ICA is not uncommonly asymptomatic provided that the development of the plaques is slow, allowing sufficient time for a collateral circulation to be established, and no distal embolization occurs. In the case of ischemia, despite frequently similar clinical syndromes, the pathogenetic process and the pattern visible on the angiographic examination can differ, as detailed in the following section:

The MCA is the most frequently involved vessel in cerebral infarction. The pathogenesis is commonly artery-to-artery (carotid bifurcation) or cardiac embolism, which leads to occlusion of the M1 or of more distal branches (Figs. 15.9, 15.10, 15.11a–i, 18.​2, and 18.​3).

In some cases, after successful reopening of the vessel, it appears clear that the embolus has been arrested at the level of a stenosis of M1 due to a microatheroma (Fig. 15.10).

In occlusion of the M1, the perforators are always involved. The degree of involvement depends on the location of the embolus (in the proximal or more distal M1, morphological aspects of the M1, short or long, and the site of origin of the perforators) (see anatomy). Perforators are end arteries, and so their occlusion, even for a relatively short time, can lead to ischemia in their territories. This is confirmed in those cases where despite rapid reopening of the occluded M1 through the endovascular treatment, small ischemic lesions in the basal ganglia are frequently demonstrated in CT and MR (Bradac et al. 2008b) (Figs. 15.9a–d and 15.11c–e). Frequently, these patients remain asymptomatic or only minimal neurological deficit is present. This is a little surprising, since it is well known (De Long 2000) that the basal ganglia are involved in brain activity concerning movements, cognition, and behavior. A complementary functional MR study could be useful in the examination of these patients.

In other cases, in CT performed after successful endovascular reopening of the M1, small hemorrhages are recognizable in the basal ganglia following the hemorrhagic transformation of the ischemia in this area.

In proximal occlusion of MCA, the efficiency of the collateral circulation between branches of ACA, PCA, and distal branches of MCA plays an important role to protect the distal vascular territories. This, however, can be impaired by embolization involving the distal branches, which can be due to emboli arising from the thrombus lodged in the proximal MCA. Distal embolization can occur also during endovascular treatment with disruption or asportation of the thrombus lodged in the proximal MCA (Fig. 15.11f–i) Furthermore, distal branches can be selectively involved by small emboli, arising from ICA or hearth and passing through the proximal MCA (Figs. 18.​2 and 18.​3).

The therapeutic endovenous or selective intra-arterial pharmacological associated increasingly with mechanical thrombolysis using different devices has improved in many cases the prognosis of these patients (Arnold et al. 2002; Qureshi et al. 2001, 2002; Noser et al. 2005; Zaidat et al. 2005; Tauntopoulou et al. 2008; Eckert 2009; Choi et al. 2009; Roth et al. 2010; Moehlenbruch et al. 2012; Machi et al. 2012).

Microatheroma of the M1 (Caplan 1989; Bogousslavsky et al. 1991) is another less common cause of ischemia which directly involves the perforators. Distal cortical and white matter vascular territories can also be involved in these cases by either hypoperfusion or distal embolization. Stenosis of the M1, as with stenosis of other intracranial arteries, particularly of the terminal ICA and basilar artery when symptomatic and not responsive to medical therapy, is reported to have a bad prognosis (Thijs and Albers 2000; Wasid 2003). Endovascular treatment (angioplasty, stent) has opened new ways of therapy (Berkefeld et al. 2003; Gupta et al. 2003; Bose et al. 2007; Turk et al. 2008; Bradac et al. 2008b; Qureschi et al. 2008; Berkefeld and Zanella 2009; Miao et al. 2011; Dorn et al. 2012a) (Figs. 15.12 and 15.13) and produced promising results. The rate of complications with this treatment, however, is still relatively high. Hemorrhage due to vessel rupture or reperfusion, and new ischemic lesions can occur. The latter are commonly the result of occlusion of the perforating branches from the stent struts crossing their origin or displacement of microatheromatous material. Fortunately, and somewhat surprisingly, this is relatively seldom. Taking these considerations into account, the treatment should be performed only in selected patients in whom medical therapy has failed, especially when the stenosis is severe and not in the acute phase after stroke (Chaturvedi and Caplan 2003; Kurre et al. 2010). Another unsolved problem is the in “stent restenosis or thrombosis” which still occurs relatively frequently (Kurre et al. 2010). This negative evolution involves all treated intracranial stenosis, but it is reported to be more frequent in the anterior circulation and in this group in those of the intradural internal carotid artery especially in younger patients (Levy et al. 2007; Turk et al. 2008). Why this occurs is not known. It has been suggested that the intradural ICA stenosis in young patients represents a distinct pathology not linked to atherosclerosis but to an inflammatory disease (Levy et al. 2007; Turk et al. 2008) which reacts differently to the endovascular treatment.

Infarcts in the territory of the anterior choroidal artery (AchA) are frequently associated with ischemia in other vascular territories, especially the MCA and PCA. The pathogenesis is carotid or cardiac embolism, or atheroma in the terminal ICA (Helgason et al. 1986; Boiten and Lodder 1991; Hupperts et al. 1994; Levy et al. 1995). Involvement of the AchA in T Occlusion has already been described (Sect. 15.4.1). Finally, also isolated embolization (Fig. 15.14), as well of cases of ischemia due to an inadvertent occlusion of the artery (Friedman et al. 2001) in surgical or endovascular treatment of aneurysm in this area, can occur. As already described, the vascular territories of the AchA can be replaced by other arteries. Furthermore, there are many anastomoses with branches of the PCA, and this explains the irregular presence of ischemic lesions in cases of occlusion of the AchA.

Infarcts in the territory of the ACA are commonly associated with ischemia in other vascular territories after carotid or cardiac embolism (Figs. 15.15 and 18.​2). Embolization is not infrequently associated with variants in the anterior portion of the circle of Willis, which favors the passage in the ACA (Kazui et al. 1993). The vascular territories of perforators and/or peripheral branches in varying combinations can be involved depending on the proximal or more distal location of the occlusion.

Considering especially the artery of Heubner, its involvement, also in proximal occlusion, can vary due to its possible different site of origin (see also Chap. 4). Also, the inadvertent occlusion of the artery of Heubner in treating aneurysm of the ACA can lead to ischemia.

Microatheroma typically located in the pericallosal segment can be another rare cause of ischemia (Fig. 15.16).

These infarcts are due to involvement of the deep perforators supplying the basal ganglia and capsula interna and perforators supplying the superficial and deep white matter, which are called medullary arteries. As already described, these arteries do not anastomose to each other, and neither are connections between the deep perforators and medullary arteries present (De Reuck 1972; Moody et al. 1988, 1990, 1991). Both vascular territories or only one can be involved. This pathological condition, also called small vessel disease, presents with clinical symptoms which depend on the site and extension of the damaged parenchyma. Isolated lesions can be asymptomatic. Strokes can occur followed by improvement. Multiple lesions can develop presenting with or without strokes leading to a progressive decline of different neurological function with cognitive impairment and finally to dementia.

A frequent pathogenesis is a special form of atherosclerosis occurring particularly, but not always, in patients with hypertension and diabetes called lipohyalinosis, characterized by fibrinoid changes followed by collagenous fibrosis. This leads to stenosis or occlusion of the artery causing ischemia and sometimes to rupture of the wall and hemorrhage. The lesions can be very numerous and disseminated in both hemispheres. MR demonstrates on T2-weighted images the hyperintense ischemic lesions not rarely associated with small hypointense foci due to old microhemorrhage well defined with T2*-weighted gradient-echo and SW-weighted images. Pathological examinations disclose infarcts, commonly small (less than 20 mm in diameter) in the basal ganglia and white matter. In this latter, also areas of rarefaction due to destruction of fibers and area of gliosis have been demonstrated (Pantoni et al. 1996). No pathological changes of the arteries can be detected on the angiogram in many of these patients.

Another cause of ischemia is severe stenosis or occlusion of the ICA leading to hypoperfusion (Weiller et al. 1991; Waterston et al. 1990; Bogousslavsky et al. 1991; Boiten and Lodder 1991; Bogousslavsky and Regli 1992; Bladin and Chambers 1993; Horowitz and Tuhrim 1997; Boiten et al. 1997; Read et al. 1998; Bradac et al. 2008b). In this condition, the vascular territory of the medullary arteries is commonly more affected than that of the deep perforators (Fig. 15.8).