Luminal cerebral infarction is a cerebral infarction caused by occlusion of deep penetrating branch arteries in the cerebral hemisphere or brainstem. On the basis of long-term hypertension, lesions occur in the vascular biscuit, leading to lumen occlusion and formation of small foci of infarction. The diameter of lesioned vessels is mostly 100-400um deep penetrating branches, which are made to leave foci of infarction by macrophagy, generally 0.2-15mm cystic lesions in diameter, often multiple, called luminal cerebral infarction. Clinical symptoms are related to the size and location of the luminal infarct foci, and the following types are common: (a) Pure motor stroke: manifested as paralysis of the face, tongue, and limbs to varying degrees, without sensory impairment, visual field loss, or aphasia. The lesions are located in the radial crown, internal capsule, basal ganglia, pons, and medulla oblongata. (b) Pure sensory stroke: The patient complains of hemianesthesia, and examination reveals hyperalgesia or loss of sensation in one limb or body. The lesion is in the contralateral thalamic posterior lateral nucleus. (iii) Ataxic mild hemiparesis: manifests as pure motor mild hemiparesis and cerebellar ataxia on the contralateral side of the lesion, with a predominance of the lower extremities, and may also have dysarthria and nystagmus. The corticobasal tract at the internal capsule or at the base of the cerebral bridge. (d) Sensorimotor stroke: Mostly hemianesthesia followed by mild hemiparesis. It is the posterior ventral nucleus of the thalamus and involves the posterior limb of the internal capsule. (v) Dysarthria hand clumsiness syndrome: The patient has severe dysarthria, dysphagia, central facial tongue palsy contralateral to the lesion, mild weakness of the hand on that side, inaccurate finger-nose test, unsteady gait, hyperactive tendon reflexes and positive pathological reflexes. The lesion was located at the base of the pontine brain or in the forelimb and knee of the internal capsule.