CT imaging of early ischemic stroke

CT scan is the most important and routine diagnostic test for neurological diseases. You must be very skilled in the CT performance of hemorrhagic cerebrovascular disease, but the CT imaging performance of ischemic cerebrovascular disease is still a bit difficult for beginners, which is precisely where the level can be demonstrated. Brain tissue is very sensitive to ischemia and hypoxia, and permanent neuronal necrosis can occur 10 min after complete blockage of local blood flow. Animal experiments and clinical studies have shown that persistent ischemia and hypoxia in the ischemic area can lead to cellular ion pump failure after 10 minutes, resulting in cytotoxic cerebral edema, and vasogenic cerebral edema can occur if blood supply is not restored. However, the CT value decreases by 2.5-2.6 HU for every 1% increase of water in brain tissue, so the infarct lesion can be shown on CT only when the cerebral edema reaches a certain level. Therefore, for patients with cerebral infarction within 24 h, early CT imaging changes, especially CT features of ultra-early large cerebral infarction combined with clinical manifestations, should be used to propose a treatment plan at an early stage. Ultra-early cerebral infarction can show the following CT signs: (1) Early hypointensity: It is a characteristic manifestation of cerebral infarction, which can occur in the cytotoxic cerebral edema phase after blood flow blockage, and is clinically associated with Horner’s sign on the ipsilateral side of the lesion, bilateral gaze palsy and early alteration of consciousness state. (2) Indistinct cortical and white matter demarcation: Because the cortical hippocampus and striatum are most sensitive to ischemia, hypointense changes appear in the early stage of ischemia. It makes the interface between the cortex and white matter appear blurred and uniform hypointense shadow. (3) Bean-shaped nucleus and insula band sign: The early stage of CT shows unclear border of the bean-shaped nucleus and the interface of the whole insula structure. (4) Changes in the sulcal gyrus, ventricles and ventricular pools: compression of the sulcus, subarachnoid pools, and even ventricular deformation and midline shift appear relatively late and at a lower rate than the above-mentioned CT changes, mainly related to the occupancy effect produced by brain tissue edema. (5) Increased density of blood vessels after occlusion of large vessels (“middle cerebral artery [MCA] hyperdensity sign”, which can also occur in basilar artery occlusion), etc. A good understanding of the early signs of acute cerebral ischemia on CT is an important clinical guidance for both neurologists and emergency physicians, and it is even more important for neurologists in primary hospitals without advanced imaging equipment such as MRI. We are now compiling some information on this subject and studying it together with our beginner friends and senior colleagues to review it together. The CT was done at 2 hours and 45 minutes after the onset of the disease and showed a high-density shadow of the right middle cerebral artery (arrow) and blurred boundaries of the basal ganglia and surrounding white matter (arrow). Case 2 The patient presented with left-sided hemiparesis. Two hours after onset, CT showed a high-density shadow of the right middle cerebral artery (arrow) and a decrease in contrast of gray and white matter in the right middle cerebral artery blood supply area. MRA 4 h after onset showed occlusion of the right middle cerebral artery, and DWI showed high signal shadow in the whole right middle cerebral artery supply area. Case 3 The patient started with left-sided hemiparesis. Five hours after onset, CT showed a high-density shadow in the right middle cerebral artery, while the left side was normal. Case 4 Patient with left-sided hemiparesis. a CT 2 hours after the onset of the disease shows a deformed right ventricle under pressure, cortical edema in the right middle cerebral artery supply area, blurred gyrus, and shallow or absent sulci. b CT 6 days after the onset of the disease shows a right paraventricular subcortical infarction with cortical edema in the right middle cerebral artery supply area. The patient was treated with intravenous rt-PA, and the NIH score 90 days after onset decreased from 17 to 11 at baseline on admission. Case 5 Patient presented with left-sided hemiparesis. a. CT 6 hours after onset showed a mild decrease in tissue density in the area supplied by the right pericallosal artery and a branch in the brain, loss of the cerebral sulcus, and a mild shift of the cerebral integrity to the left. b. CT 3 days after the onset of the disease shows a clear manifestation of cerebral infarction in the above corresponding area. Case 6 a shows the CT 2 h after the onset of the disease, which shows a high-density shadow of the left middle cerebral artery and its branches (long arrow), and the left insular cortex and the nucleus accumbens are indistinct, with a mild decrease in density. The left middle cerebral artery and its branches are still high-density, and the left insular cortex and nucleus accumbens are obviously low-density foci of infarction. Case 7 a is the CT 2.5 hours after the onset of disease, which shows a mild decrease in density in the blood supply area of the whole right middle cerebral artery, with indistinct cortical and white matter demarcation. b is the CT presentation 7 days after the onset of the disease, which shows obvious hypointense infarct foci in the blood supply area of the right middle cerebral artery.