Parkinson’s superimposed syndrome includes a group of disorders in which patients may have resting tremor, tonicity, reduced motion, and postural instability similar to Parkinson’s disease, but also have atypical manifestations that are different from typical Parkinson’s disease, such as unremarkable or absent tremor and a lack of efficacy with levodopa. In addition to Parkinson’s syndrome, this group of patients also had other systemic degenerations, such as vegetative neurological failure, supranuclear ophthalmoplegia, striatal nigrostriatal degeneration, olivopontocerebellar atrophy, corticobasal ganglion degeneration, Alzheimer’s disease with Parkinson’s syndrome (including diffuse lewy body disease and Guam-Parkinson’s-dementia syndrome, primary progressive rigid gait syndrome and Kufor- Rakeb syndrome, etc.). The etiology of Parkinson’s superimposed syndrome is not well understood, but it may be a process of gradual degeneration of multiple neuronal systems in patients with the involvement of certain factors. The onset of olivopontocerebellar microcephaly has been reported to be associated with reduced glutamate dehydrogenase activity, and crystalline inclusion bodies have been observed in the cerebellar cortex, which is presumed to be associated with viral infection. Striatal substantia nigra degeneration is clinically ineffective with levodopa and is presumed to be distinct from Parkinson’s disease with impaired dopamine synthesis and release from the presynaptic membrane of striatal terminals. The pathogenesis of vegetative neurological failure is highly debated, and the original popular explanation of nerve cell degeneration due to ischemia and hypoxia in the CNS caused by recurrent upright hypotension is widely recognized as primary degeneration because the central nervous structures that are poorly tolerant to hypoxia are not affected instead and are not reasonably explained. In general, MSA occurs biochemically with depletion of multiple central nervous structures dopamine and adrenaline.