Progressive supranuclear palsy (PSP), also known as the syndrome, is a rare neurodegenerative disorder. Progressive supranuclear palsy (PSP) usually begins in late middle age and presents with an inability to turn the eyes upward. Due to the concomitant symptoms of Parkinson’s disease, patients may develop severe tonicity and loss of mobility as the disease progresses. The disease destroys the basal ganglia and brainstem, and its etiology is unknown and easily confused with Parkinson’s disease. There is no effective treatment available. Drugs used to treat Parkinson’s disease can sometimes reduce its symptoms. The disease does not yet have specific biological markers, so diagnosis remains a major challenge in the early stages or in the absence of some characteristic signs and symptoms. Although recent advances have been made in the recognition of some genetic factors in progressive supranuclear palsy, the etiology remains unclear. Brain biochemical studies in patients with progressive supranuclear palsy provide a potentially useful guide to further improve the understanding of the features of this disease. Posey (1904) first reported this disease, and in 1963 Richardson, together with Steele and Olszewski, treated progressive supranuclear palsy as a separate disease of clinical pathology. In 1972 Steele described in detail the clinicopathologic features of this disease, also known as the Steele-Richardson-Olszewski syndrome. Clinical manifestations 1. Movement disorders Early manifestations include gait instability and balance disorders, repeated falls, and walking with a large gait. Both lower extremities are heavily affected, with both knees stiffened, and even when sitting on a chair, the body leans back and both feet leave the ground. Tremor is less frequent and can be reduced. Another important feature, cervical dystonia is an important symptom of the disease. A specific posture of neck hyperextension, face tilting, and chin protrusion occurs. The head, neck and trunk muscles are obviously strong, the limbs are lighter, the facial expression is stereotyped, and the wrinkles deepen. 2. Oculomotor disorders are characteristic manifestations of the disease, with upward and downward gaze paralysis of both eyes. The patient cannot see his or her toes, the eyes are fixed in the median position, and walking is difficult. The reflex to light is present. 3. Pseudobulbar palsy manifests as dysarthria, dysphagia, enhanced jaw reflexes, enhanced tendon reflexes, and pathological reflexes may be present. There may be various non-constant cerebellar and pyramidal tract symptoms and signs. 4. Cognitive function and behavioral disorders occur later, with gradual personality changes, memory loss, intellectual decline, and reduced emotional activity, rarely to severe dementia. Imaging features Midbrain and pontine atrophy, predominantly midbrain, anterior and posterior midbrain diameter <15 mm. widening of the third ventricle and interpeduncular pool, enlargement of the lateral ventricles. MRIT1WI showed atrophy and flattening of the superior edge of the midbrain, with a "hummingbird sign" in the sagittal plane. Axial radiographs and T2WI showed that the anterior and posterior diameters of the midbrain had become smaller, the midbrain aqueducts were dilated, the tegmental pool was enlarged, and the midbrain had a "mouse ear" shape. These two points are characteristic manifestations of PSP.