Progressive stroke is a topic that is never finished. In the past, some experts have said that, well, progressive stroke should be well typed, staged and stratified, with good etiological diagnosis and then targeted management, but now we have done that, but still some patients do continue to worsen. In the above patient, the left carotid artery is clearly occluded by MRA, and the infarct is clearly present through the anterior communicating artery compensating for the blood supply of the left middle cerebral artery. After removing other unfavorable factors such as the patient’s poor general condition, the question to be discussed now is why the patient progressively progressed and got progressively worse? In fact, it is to discuss why the semi-dark zone around the patient’s lesion is gradually enlarging, why the patient’s perifocal edema is gradually increasing, and why the patient’s neuronal cell death continues. While the patient loses the opportunity for thrombolytic therapy, the core of all treatment should be to reduce edema, promote recovery of nerve cell function, and prevent new stroke formation. Some experts have said that in patients who have lost thrombolytic therapy, all treatment is called secondary prevention; there is very little we can do about this stroke! All kinds of neurocytoprotective agents, neurotrophic agents, and nerve activators are considered to have no evidence-based medical evidence, but at the same time, experts are using them in large quantities. Until a definite nerve cell repair measure is available, the ideal recovery of stroke patients remains a beautiful dream. So, medicine is not infallible and there will always be a certain rate of patients who will continue to get worse! Just as many patients will have a second or third stroke despite having followed secondary prevention measures to the letter. This patient already had a clear infarct focus present and even though DSA revealed a left carotid occlusion, stenting could not be done immediately and even if a stent was done at the risk of great hyperperfusion, it would have no effect on this patient’s recovery. In conclusion, for progressive stroke, within the framework of existing knowledge, the diagnosis is accurate, the etiology is accurately diagnosed, the remaining comorbidities are actively controlled, the dialectical relationship between prevention of cerebral edema and prevention of hypoperfusion is well handled, the anticoagulation, antiplatelet and anti-lipid are in place, and the rest is up to Socrates!