Thalamic infarction mainly leads to abnormalities in consciousness and somatic sensation and movement, and the clinical symptoms are more diverse and complex depending on the specific site of involvement, as follows: 1. Thalamic nodal artery supply area infarction: manifested as anterior thalamic infarction, with varying degrees of altered consciousness and silence, and personality changes may occur at later stages of development; 2. Thalamic penetrating artery infarction: manifested as thalamic ventral medial syndrome, mainly manifested as reduced level of consciousness, cognitive and behavioral abnormalities, and the triad of vertical gaze disorder. 3. Infarction of the thalamic geniculate artery: Patients with posterior lateral thalamic infarction may present with thalamic syndrome, with symptoms of contralateral hemianesthesia, contralateral hemianesthesia spontaneous pain, transient mild hemiparesis, and hemianopic ataxia; 4. Infarction of the posterior choroidal artery: Dorsal thalamic infarction leads to contralateral neglect, and involvement of the lateral geniculate body may present with quadrant wedge-shaped or fan-shaped visual field defects, and thalamic occipital involvement may present with tremor, dystonia, myoclonus, and chorea. If thalamic infarction is present, active treatment such as antiplatelet aggregation and lipid regulation can be started in the early stage of the disease, and the symptoms can be relieved within two weeks to one month, and the prognosis is good. However, if the treatment is not timely or the vascular condition is poor, the prognosis is poor, and hemiparesis, impaired consciousness, cognitive and behavioral abnormalities may persist, and some cases may be disabling or even fatal.