Major or mild neurocognitive disorder due to Parkinson's disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2]

Overview

Major or Mild Neurocognitive Disorder Due to Parkinson's Disease

Epidemiology and Demographics

Prevalence

The prevalence of major or mild neurocognitive disorder due to parkinson's disease is:

75,000 per 100,000 (75%) major neurocognitive disorder.

27,000 per 100,000 (27%) mild neurocognitive disorder.[1]

Risk Factors

Risk factors for developing Cognitive impairment and dementia in Parkinson disease are: Duration of PD, severity of the disease, age of onset >60 years, old age, presence of rapid eye movement sleep behavior disorder, autonomic dysfunction, gait problem and hyposmia.[2][3][4][5][6][7][8][9][10]

Differential Diagnosis

Dementia with Lewy bodies

Dementia will finally occurs in the most cases of Parkinson disease but the timing of dementia in PD is after full developing of PD and mostly after at least one year of disease start date. When dementia occurs with or before the signs and symptoms of Parkinson disease we will categorize it as dementia with lewy body.[11][12]

Multiple system atrophy

MSA is an idiopathic disease[13] characterized by autonomic problems such as urogenital dysfunction, ataxia and parkinsonism symptoms.[14] MSA patients have resting tremor in arms, rigidity and bradykinesia.[15] The underlying pathophysiology of MSA is myelin dysfunction and inclusions in glial cell throughout CNS.[13][16]

Corticobasal degeneration

Clinical features of CBD is asymmetric movement disorders including rigidity, akinesia and dystonia.[17][18][19] cognitive disorder is very common in this disease and can be the presenting sign of it.[20][21] there are evidences of asymmetric frontoparietal cortical atrophy in autopsy in CBD patients. In microscopic evaluation there are neuronal loss, ballooned achromatic and gliosis.[22][23]

Progressive supranuclear palsy

Abnormal gait is the most common presentation of PSP disease. As opposed to idiopathic Parkinson disease, their trunk is extended and arms are abducted. They commonly fall from behind leading to bruises and lacerations.[24] They can also have supranuclear ophthalmoparesis or ophtalmoplegia.[25]

Idiopathic and familial basal ganglia calcification

Accumulation of calcium in some brain regions and the basal ganglia is known as idiopathic basal ganglia calcification or bilateral striatopallidodentate calcinosis. Some of these patients can have parkinsonism symptoms such as dystonia, ataxia and chorea mostly between ages 20_60.[26][27] The autosomal dominant form of the disease which is known as familial form[28] can be the result of several mutations such as: The SLC20A2 gene on chromosome 8p11.2[29], the PDGFRB gene on chromosome 5q32[30], the PDGFB gene on chromosome 22q13.1[31][32] and the XPR1 gene on chromosome 1q25.3.[33]

Secondary parkinsonism


References

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