Cerebellar ataxia, also known as Marie’s ataxia, is one of the lesions of the crestal medullary cerebellar degenerative diseases and is characterized by cerebellar atrophy and involvement of its neurotransmission pathways, along with varying degrees of other sensory and motor system disorders. Anatomically, the cerebellum can be divided into three parts. One part is the primitive cerebellum composed of lobules and nodules, also known as the vestibular cerebellum, which is closely related to the balance function and appears as limb ataxia, hypotonia, tremor, etc.; the other part is composed of the conus, pontine, parietal, and uvula lobes, also known as the paleocerebellum or crestal cerebellum, which is related to the trunk and other postural reflexes and appears as difficulty in rising and walking, etc.; the other part is composed of the pontine nucleus, inferior olivary nucleus, reticular fibers, and cerebellum. The other part consists of pontine nucleus, inferior olivary nucleus, reticular fibers and cerebellar hemispheres, also known as neocerebellum, with symptoms and signs such as low muscle tone, tremor, poor rotation and poor distance discrimination. Patients with cerebellar ataxia usually develop between the ages of 40 and 50 years old and exhibit a slowly progressive ataxic movement disorder starting from the lower extremities, such as unstable walking and a gait that resembles that of a “drunk”. This is followed by slurred speech, intermittent or staccato speech, often referred to as “cerebellar speech”. Later, upper limb activities are also affected, mainly fine hand movements, resulting in impairment of writing, drawing, threading needles, fastening buttons, and other activities. In addition, patients may have resting tremor of the head, limbs and trunk, and less frequently nystagmus. Myotonia is normal or mildly reduced, and is usually not accompanied by symptoms of the cone system, extrapyramidal system and sensory system, and there are no abnormal changes of intelligence. 2. Ancillary diagnosis By pathological examination, atrophic changes are visible to the naked eye affecting the cerebellar cortex, cerebellar peduncles and the base of the pontine brain. The number of deep neurons such as Purkinje cells, cerebellar cortical cells and dentate nucleus cells is significantly reduced under microscope, and the cerebellar earthworm, choroid and olivary body are also involved. atrophy of the above mentioned structures can also be detected by CT or MRI, but MRI is more clearly visible. The electrophysiological laboratory examination of the disease sometimes reveals slow eye movement changes in nystagmography (ENG), absence of gaze evoked nystagmus, and abnormal changes in somatosensory evoked and magnetic stimulation evoked potentials. The prognosis of this disease is better than that of cerebral atrophy diseases because there is no special treatment for this disease, but the late stage is less likely to affect intelligence and cause paralysis. The prognosis is better than that of cerebral atrophy diseases. Over the years, some people have tried butylphthalide or ritalin, edibenzoquinone and other drugs to treat the disease, which have a certain slowing effect.