Idiopathic PD must be distinguished from familial PD Parkinson syndrome Early atypical cases must be distinguished from genetic disease or degenerative disease with Parkinson syndrome. 1, familial PD about 10% of incomplete episomal rate autosomal dominant, available DNA blotting technology PCR and DNA sequence analysis; detection of alpha-synuclein gene Parkin gene mutation susceptibility gene analysis such as cytochrome P450-2D6 gene mutation, etc. 2, Parkinson syndrome has a clear cause; secondary to drugs, infection, poisoning, stroke Post-encephalitis syndromes such as trauma: Parkinson’s syndrome is often left behind after the epidemic of sleeping encephalitis in the first half of the 20th century, but is now rare. Drug or toxic syndromes: neuroleptics, rifampin, gastrofacial, alpha-methyldopa, lithium, flunarizine, etc. can cause Parkinson’s syndrome; manganese dust, carbon disulfide poisoning or welding fumes can also cause it. Arteriosclerotic syndrome: multiple cerebral infarction occasionally leads to syndrome, patients with hypertension, a history of arteriosclerosis and stroke, pseudobulbar palsy, pathological signs and neuroimaging can provide evidence. Traumatic such as boxing encephalopathy, others such as hypothyroidism, hepatocerebral degeneration, brain tumors and normal pressure hydrocephalus can lead to Parkinson’s syndrome. 3, genetic disease with syndrome Disseminated Lewy body disease: most commonly seen in 60 to 80 years old, dementia, hallucinations, Parkinson’s syndrome movement disorder as clinical features, early appearance of dementia, rapid progress, may have myoclonus, levodopa response is poor, but the side effects are extremely sensitive. Hepatomegaly: can cause Parkinson’s syndrome adolescent onset one or both upper extremities coarse tremor, muscle tonicity, slow or involuntary movements liver damage and corneal K-F ring serum copper copper cyanine copper oxidase activity is reduced urinary copper increased Huntington’s disease: movement disorders with muscle tonicity, movement reduction, easily misdiagnosed as PD 4. degenerative disease with syndrome multisystem atrophy: involving the basal ganglia brain bridge olive cerebellum and autonomic Progressive supranuclear palsy: there may be bradykinesia and myotonia, early postural instability and falls, inability to gaze vertically, frontotemporal dementia, pseudobulbar palsy, dysarthria and pyramidal fasciculus, tremor is not obvious, poor response to levodopa. Corticobasal ganglion degeneration: showing myotonia, bradykinesia, postural instability, dystonia and myoclonus, etc. There may be cortical compound sensory loss, neglect of one limb, loss of use, aphasia and dementia and other symptoms of cortical damage, eye movement disorders and pathological signs, and levodopa treatment is ineffective. 5, Alzheimer’s disease with Parkinson’s syndrome Depression: there may be a paucity of expression, monotonous speech, reduced voluntary movements, PD patients often coexist, depression without myotonia and tremor, antidepressant trial treatment may help to identify. Idiopathic tremor: mostly early onset, postural or motor tremor, affects the head causing nodding or shaking, PD typically affects the face, mouth and lips, the disease does not have myotonicity and motor retardation, about 1/3 of patients have a family history, drinking alcohol or taking tips on tremor significantly reduced.