Hypertension and Brain Damage by Antonio Coca

Author:Antonio Coca
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

9.2.1.1 CT Imaging in the Hyperacute Stage (0–6 h)

Within the first minutes of ischaemia, rising lactic acid levels and the failure of cellular membrane ion pumps result in the redistribution of water from extracellular to intracellular spaces. Radiologists can measure these changes by delineating the field of cytotoxic oedema, which may reduce brain tissue radiodensity on CT scans. Ischaemic foci become hypodense compared to normal white and grey matter due to increased water uptake. The radiodensity of the ischaemic field theoretically decreases by 2 Hounsfield units (HU) every 2.5 h during stroke evolution, but these discrepancies may be imperceptible to inexperienced observers [2, 3].

In the first 6 h of ischaemic stroke, brain CT images seem to be unaffected in about 50 % of cases [3], and therefore, the negative predictive value is low (27 %) [4]. In the European Cooperative Acute Stroke Study, the sensitivity of CT during the first 6 h of cerebral ischaemia reached 64 %, with an accuracy of 67 % [5]. Blockage of the proximal M1 segment of the MCA causes abnormal CT findings within 3 h in 75 % of cases [6]. On the other hand, in the case of lacunar infarction, there is only a 50 % chance of a confirmed diagnosis within 48 h [4]. Therefore, the lack of radiological manifestations in early CT studies does not exclude stroke [7].

Hyperacute stroke syndromes usually appear in the MCA, the most common stroke localization. The signs include loss of the insular ribbon, obscuration of the lentiform nucleus, loss of grey-white matter differentiation, sulci effacement and a hyperdense MCA sign [8]. All are considered as indirect ischaemic symptoms on CT imaging. Cytotoxic oedema of the insular cortex, which is susceptible to early and irreversible ischaemic damage, generates local hypo-attenuation, which results in the so-called insular ribbon sign (Fig. 9.1). Lack of flow to the lenticulostriate arteries causes cytotoxic oedema in the basal ganglia. The associated radiological finding is known as obscuration of the lentiform nucleus (Fig. 9.1). This phenomenon is due to occlusion of the MCA proximal M1 segment and can be seen as early as one hour post onset.

Fig. 9.1(a, b) Unenhanced CT images show hypodensity and obscuration of the right lentiform nucleus, which appears abnormal in comparison with the left lentiform nucleus. Additionally, these scans demonstrate the loss of grey-white matter differentiation in medial margins of the right insula (insular ribbon sign)

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