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The basal ganglia (BG) including the caudate nucleus are well known for their motor functions. The BG nuclei are anatomically and functionally associated with each of the frontal-striatal-thalamic-frontal circuits or loops. The caudate nucleus assumes the shape of a comet, curving along the lateral wall of the lateral ventricle. The caudate nucleus receives its blood supply mainly through the deep penetrators arising from the anterior cerebral arteries (ACAs) and middle cerebral arteries (MCAs) although there are individual differences. The major risk factors for caudate nucleus infarcts are: hypertension, hypercholesterolemia, diabetes mellitus, previous myocardial infarct, and cigarette smoking. As caudate nucleus infarcts can develop from any stroke mechanisms including lipohyalinosis, branch atheromatous disease, large artery atherothrombosis, or embolism, treatment of patients with caudate nucleus infarcts depends on the underlying stroke mechanism. Caudate nucleus hemorrhages account for approximately 7% of all intracerebral hemorrhages (ICH) and are caused by rupture of penetrating arteries.
Pseudo-occlusions of the internal carotid artery (Newton & Couch, 1960) have been described in the literature as ‘a diagnostic trap’ (Gabrielson et al., 1981), and ‘a diagnostic and therapeutical challenge’ (Ringelstein et al., 1983a) referring to both the difficulty in the precise diagnosis and the potentially serious, clinical consequences inherent to these insidious and extreme internal carotid artery stenoses. These consequences do not only refer to the decision of medical surgical treatment, or the timing of carotid endarterectomy, but also to a carefully planned ophthalmological therapy in parallel to vascular surgery (see below). In the 1980s, the false indication for extracranial–intracranial bypass surgery in patients with pseudoocclusions had been another clinical problem (Sekhar et al., 1980).
Several synonyms of the term ‘pseudo-occlusion’ have been suggested in the literature, such as ‘radiographically occluded, anatomically patent carotid artery’ (Clark et al., 1971), ‘nearly occluded internal carotid artery’ (Gabrielson et al., 1981), ‘sténoses athéromateuses pseudo-occlusives’ (Batt et al., 1993), ‘spurious internal carotid hypoplasia’ (Lippman et al., 1970), ‘preocclusive stenoses’ (Hetzel et al., 1993; Mansour et al., 1995), ‘near occlusion of the carotid artery’ (Morgenstern et al., 1997), and, ‘subtotal carotid artery stenoses’ (Goertler et al., 1994). ‘Pseudo-occlusion’ is the most widely used and internationally accepted term which comprises both atheromatous disease, as well as dissections of the internal carotid artery (ICA) and some other, very rare diseases of the ICA.
Low-flow infarctions, also called ‘border zone infarctions’, are the result of a critically reduced cerebral perfusion pressure in far-downstream brain arteries that leads to a critically reduced cerebral blood flow and oxygen supply in certain vulnerable brain areas. These areas are defined by the specific angioarchitecture of the cerebrum. The term watershed infarction should be reserved for the cortical infarcts located in-between the territories of the major cerebral arteries, and should not be extended to the more common, subcortical type of low-flow infarction. The latter is located within the affected vascular distribution but in a zone of marginal irrigation (i.e. border zone) comparable to the ‘last field’ in a unidirectional (i.e. non-collateralized) agricultural watering system (Zülch & Behrend, 1961). The more general terms ‘low-flow infarction’, or ‘hemodynamically induced infarction’, are preferred, whereas terms like ‘deep watershed territory’-infarct (Angeloni et al., 1990) or ‘internal border zone territory’-infarct ((Angeloni et al., 1990) or ‘internal watershed infarctions’ (Bladin & Chambers, 1993) are misleading.
In a wider sense, all ischemic brain infarcts are the consequence of a critically reduced blood flow. The concept underlying low-flow infarctions, however, emphasizes a difference between them and thromboembolically caused infarcts. In the thromboembolically induced brain infarcts, the corresponding cerebral artery(ies) is(are) occluded (rarely stenosed) by embolisms of various origins or by in situ atherothrombosis. By contrast, in low-flow infarctions the local brain artery(ies) supplying the infarcted area is(are) not diseased.
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