When the internal carotid artery is suddenly blocked, the ipsilateral ophthalmic artery is involved, resulting in monocular vision loss or even blindness on the side of the lesion, ipsilateral Horner’s sign, contralateral hemiparesis, and cortical sensory impairment (form sense, two-point discrimination) on the contralateral limb. When the anterior cerebral artery is blocked at the proximal part of the anterior communicating artery, no obvious symptoms and signs may appear. In the former, there is paralysis of the contralateral lower leg and foot (below the knee), low muscle tone, active knee and ankle reflexes, positive cone bundle sign, and sensory disturbance, as well as psychiatric symptoms, mental retardation, urinary disturbance, and strong grip reflex and sucking reflex; in the latter, paralysis of the face and proximal upper limb is the main symptom. In the latter case, facial and proximal paralysis of the upper extremities are the main symptoms, and other symptoms mentioned above are also seen. In the latter case, facial and proximal paralysis of the upper extremities are predominant, and other symptoms are also seen. In the case of occlusion of the cortical branch of the middle cerebral artery, the manifestation varies depending on the location, except for the contralateral facial, upper limb and lower limb paralysis (upper limb more than lower limb). In addition to sensory aphasia, aphasia in reading, aphasia in writing, deafness, etc., the parietal lobe damage syndrome (Gerstmann’s sign: aphasia, aphasia, aphasia in finger recognition, aphasia in left and right recognition, etc.) may also occur; in the case of parietal lobe damage, somatotopic disorders such as hemianopia, hemiplegia, and aphasia and aphasia may occur; in the case of deep temporal lobe damage, the contralateral isotropic quadrant may occur. Blindness. If the main trunk of the middle cerebral artery is occluded, contralateral hemiparesis, hemianesthesia, and isotropic hemianopsia (triple hemianopia) may occur; aphasia is often seen in the primary hemisphere, and disuse, dyscognition, and somatotopic impairment are seen in the secondary hemisphere. Patients with this type are prone to life-threatening brain herniation due to the large lesions and significant cerebral edema. The occurrence of watershed cerebral infarction is mostly seen in the marginal area or watershed area of the above-mentioned large arterial vascular innervation area, which can be divided into the following types in combination with CT: ① precortical type: it is a watershed cerebral infarction in the blood supply area of the anterior cerebral artery and middle cerebral artery, with the appearance of central hemiparesis and hemianesthesia mainly in the upper limbs, usually without facial palsy and tongue palsy, and may have affective disorder, strong grip reflex and focal epilepsy; the main side The primary lesion may show motor speech dysfunction; bilateral lesions may show tetraplegia, intellectual disability or dementia. (2) Posterior cortical type: the lesion is located in the junctional area of temporal, parietal and occipital lobes, and is a watershed infarction between the middle cerebral artery and the posterior cerebral artery, or the cortical branches of the anterior middle and posterior cerebral artery, with hemianopia being the most common, mainly in the lower quadrant, and may have cortical sensory impairment, slight or queasy hemiparesis, emotional indifference and memory loss in about half of the cases, and Gerstmann syndrome may also appear. The primary hemisphere lesion has difficulty in word recognition and sensory aphasia, while the non-primary hemisphere lesion occasionally has somatosensory impairment. (3) Subcortical type: Infarction in the watershed area between the cortical branches of the anterior, middle and posterior cerebral arteries and the deep penetrating branches or between the return branch of the anterior cerebral artery (Heutmet. artery) and the doublestem artery, a branch of the middle cerebral artery, with lesions located in the deep white matter of the brain, the nucleus accumbens and the caudate nucleus. The anterior choroidal artery obstruction is less common, but its appearance can be seen as contralateral limb hemiparesis and hemianesthesia, but the duration is relatively short; ipsilateral hemianopia and pupil dilatation, blunted light response can also be seen, and generally speaking, hemianopia persists. The posterior cerebral artery is responsible for the blood supply to the posterior part of the cerebral hemispheres, the thalamus and the upper brainstem. When one side is blocked, ipsilateral hemianopia (with macular avoidance) and transient visual impairment such as blackout may occur. Visual distortion and visual loss may also occur. In the case of posterior cortical damage in the primary hemisphere, reading loss, writing loss, or a combination of both may occur; color loss, amnesic aphasia, and near memory impairment may also occur. Lesions in the posterior part of the supplementary hemisphere may have somatosensory deficits. Deep penetrating branch lesions involving the thalamus and upper brainstem present with thalamic syndromes (manifested by contralateral hemianesthesia, such as sensory abnormalities, hyperalgesia, and thalamic pain) and partial midbrain syndromes (e.g., Weber syndrome, Benedikt syndrome). The damage to the vertebral basilar artery may lead to medial, lateral, combined medial and lateral, and dorsolateral syndromes depending on the branching arteries that are blocked; lower and medial, lateral, central and medial and lateral, and upper and medial and external syndromes of the pons; and the midbrain may also be involved, with the midbrain tegmental, parietal, and ventral syndromes and the inferior red nucleus syndrome. In addition, although basilar artery trunk obstruction is rare, it occurs as basilar artery syndrome, which is extremely dangerous and has a very poor prognosis. The clinical manifestations of cerebral embolism include: the age range of onset is large, with rheumatic heart disease affecting more middle-aged and young people, and coronary heart disease and large artery lesions causing more middle-aged and old people. There is no obvious cause, and the onset of the disease can occur both in quiet and in activity. The onset of stroke is rapid, with symptoms peaking within seconds to minutes, mostly complete. Half of the patients have transient impairment of consciousness of varying degrees at onset. Headache and seizures are more common, mostly headache on the affected side and contralateral hemiplegia or limited convulsions, and if generalized tonic clonic seizures occur, the embolism is more extensive. Other conditions such as hemiparesis, aphasia, hemianesthesia and hemianopsia are determined by the location of the lesion. See the previous section on this topic. Cardiogenic embolism is usually associated with signs and symptoms of heart disease or a history of cardiac surgery. Fat embolism often occurs after fracture or surgery of the long bone diaphysis, and is often preceded by pulmonary symptoms, such as dyspnea, chest pain, hemoptysis, etc. Thereafter, neuropsychiatric symptoms appear, manifesting as mental abnormalities, irritability, headache, vomiting, drowsiness, coma, convulsions and other manifestations, with few restrictive signs and brown bruises visible on the skin, and a high mortality rate.