stroke evolution

• Hyperacute: <6 hours: best described as cytotoxicoedema represented by the shift of waterin neurons. Because this is a relatively modest change, the CT in this stage is usually negative. On occasion, a CT scan obtainedin the hyperacute phase can give direct signs(e.g., vessel hyperdensity, subtle parenchymalhypodensity) or indirect signals (e.g., sulcaleffacement, gyral swelling, ventricular compression,fading of the white matter/grey matter interface)of hyperacute ischaemia. Such findingshave a negative prognostic value and are directlyassociated with the degree of neurological disability. Vessel hyperdensity in major cerebralarteries or one of their branches (the middlecerebral artery is the most commonly affected)can be observed within the first minutes following the onset of neurological signs andsymptoms and takes place before the appearanceof CT findings of the parenchymal infarct inthe corresponding territory. This increasein intravascular density, which is visible on CT without the use of contrast agents, appearsto be caused by the formation of an endoluminalclot, either by arterial thrombosis orembolism

Acute: – The acute phase of ischaemia occurs within the first 24 hours of the event, but typically begins within 6 hours after the stroke onset. From a neuropathological point of view, vasogenic oedema is present as supported by the filling of the extracellular spaces of the brain due to a blood-brain barrier breakdown. 

Subacute:  

24 hours after the event and continues until six weeks from the onset. From a neuropathological

point of view, beginning in the start of the second week there is an increase in   the vasogenic oedema as  in CT by an area with increasingly low attenuation coefficients, better defined margins and mass effect (internal cerebral herniations are possible,especially in cases of massive ischaemia) the ischaemic area appears most clearlytwo to three days after clinical onset of stroke.From the second week after the event, the oedemaand mass effect gradually subside and the area of hypodensity becomes less clear in some cases it disappears altogetherand the ischaemic area becomes difficultor impossible to distinguish from the normalbrain surrounding it. This is the so-called“fogging effect”, which is supported neuropathologicallyby an increase in cellularity dueto the invasion of microphages and the proliferation of capillaries 

Chronic: the chronic stage of ischaemiacoincides with the start of the sixth week from the onset of the clinical stroke and ischaracterized by repair processes. Parenchyma lhypodensity with well-defined marginsappears with attenuation values in the CSF range