Due to differences in the site and size of cerebral infarction, collateral circulation compensatory capacity, and secondary cerebral edema, there can be different clinicopathologic types, and their treatment is highly variable, which requires rapid and accurate staging in the acute phase, especially in the ultra-early phase (within 3-6 h). The Oxfordshire Community Stroke Study Staging (OCSP) does not rely on imaging findings. It allows rapid staging based on clinical presentation before conventional CT and MRI can detect the lesion, and indicates the size and location of the occluded vessel and infarct, which is clinically simple and easy to use, and is of great value in guiding treatment and assessing prognosis. OCSP classifies ischemic stroke into four subtypes: complete anterior circulation infarction, partial anterior circulation infarction, posterior circulation infarction, and lacunar infarction. 1. Complete anterior circulation infarction (TACI) manifests as a triad of symptoms, i.e., the manifestations of complete middle cerebral artery (MCA) syndrome: (1) impairment of higher neural activity in the brain (impaired consciousness, aphasia, aphasia, spatial disorientation, etc.); (2) isotropic hemianopia; and (3) more severe motor and/or sensory impairment in three contralateral areas (face, upper and lower limbs). Most of the infarcts are in the proximal segment of the main stem of the MCA, and a few are large brain infarcts caused by occlusion of the siphon segment of the internal carotid artery. 2. Partial anterior circulation infarction (PACI) With two of the above triad signs, or only higher neural activity impairment, or sensory-motor deficit more limited than TACI. It is suggested that it is a medium or small infarct caused by the occlusion of the distal trunk of MCA, branches at all levels or ACA and branches. 3. Posterior circulation infarction (POCI) manifests as various degrees of vertebrobasilar syndrome: it may manifest as ipsilateral cerebral nerve palsy and contralateral sensorimotor deficits; bilateral sensorimotor deficits; bilateral synoptic activity and cerebellar dysfunction without conduction bundle or visual field deficits, etc. Brainstem and cerebellar infarcts of varying sizes caused by occlusion of vertebral-basilar arteries and branches. 4. Lacunar infarction (LACI) manifests as lacunar syndrome, such as pure motor light hemiparesis, pure sensory stroke, ataxic light hemiparesis, and clumsy hand – poor dysarthria syndrome. Mostly small luminal foci caused by lesions in the basal ganglia or small penetrating branches of the pons.