Resting tremor is the first symptom of PD in about 70% of cases, and the tremor can be attenuated or completely controlled by anticholinergic and levodopa agents. There is usually a clear history of encephalitis, traumatic brain injury, and toxic poisoning (e.g., CO). Pharmacogenic PDS (especially phenothiazines and butylphenols) is common in those on long-term medication. Differentiation from vascular Parkinson’s syndrome in the elderly: in the elderly with lacunar or multiple cerebral infarcts, there is a stepwise clinical exacerbation or fluctuation, and limb paresis, bulbar palsy and hyperreflexia, and cone bundle signs are common; VP imaging features (1) multiple lacunar cerebral infarcts in the basal ganglia; (2) VP may be accompanied by infarcts and hypointense changes in the subcortical white matter and peri-lateral ventricles, mainly in the frontal lobe; (3) whole brain atrophy is common in VP; (4) nigrostriatal The width of the dense band (WPCSN) was significantly narrower in PD than in VP and normal controls, and the narrowing was more pronounced as the disease worsened; the degree of WPCSN narrowing in the VP group was less pronounced than in the PD group, and was not related to the severity of the disease, presumably as a result of retrograde degeneration of the striatal pathway in the substantia nigra based on striatal infarction. The distinction between Parkinson s disease and Parkinsonism is actually quite simple: a common variant of Parkinson s syndrome occurs without an obvious cause, an idiosyncratic form known as Parkinson s disease or tremor palsy. This means that the former is an idiopathic form of the latter, which also includes many other types for which a cause can be found, these being lethargic encephalitis, drug or toxin induced, occurring in association with other neurological diseases, and familial. In idiopathic Parkinson’s syndrome, or Parkinson’s disease, pathological examination shows loss of pigment and cells in the substantia nigra and other brainstem centers, loss of pale globules and shell nuclei, and the presence of filamentous eosinophilic intra-neuronal inclusion body particles (Lewy vesicles) in the basal nucleus, brainstem, spinal cord, and sympathetic ganglia with alpha-conjugated nucleoproteins. These inclusion bodies are not seen in post-encephalitic Parkinson’s syndrome, whereas there may be nonspecific neuronal fiber degeneration in many mesencephalic structures, as well as nigrostriatal changes. The diagnosis is not specific and the clinical manifestations are all characterized by tremor, decreased movement, tonicity, gait and postural abnormalities. Treatment is symptomatic in the former and symptomatic in the latter along with etiologic treatment. Chunhui Zhou, Department of Neurosurgery, Naval General Hospital