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Treatment for Parkinson Disease

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Medications (i.e., neuroleptics)

Endocrine diseases (i.e., Hypoparathyrodism)

Heavy Metals (i.e.. Manganese)

Infectious Diseases (i.e.,Whipple's disease; Creut/feldt-

.Takob disease, HIV)

Normal Pressure Hydrocephalus

Vascular disease (i.e., multi-infarct; hypoxia)

Fig. 1. PSP, progressive supranuclear palsy; CBD, corticobasal degeneration; MSA, multiple system atrophy; DLB, dementia with Lewy bodies; FTDP-17, frontotemporal dementia with parkinsonism linked to chromosome 17; SCAs, spinocerebellar atrophy; NBIA, Neurodegeneration With Brain Iron Accumulation, previously called Hallervorden-Spatz Syndrome; HIV, human immunodeficiency virus.

Table 1

When Should an Atypical Parkinsonian Disorder be Suspected?

Features suggestive of an atypical parkinsonian disorder Motor

Rapid disease progression Early instability and falls

Absent, poor, or not maintained response to levodopa therapy

Myoclonus

Pyramidal signs

Cerebellar signs

Early dysarthria and/or dysphagia Early dystonia/contractures (unrelated to treatment) Autonomic Features

Impotence/decreased genital sensitivity in females Early orthostatic hypotension unrelated to treatment Early and/or severe urinary disturbances Oculomotor

Marked slowing of saccades

Difficulty initiating saccades, gaze (oculomotor apraxia) Supranuclear gaze palsy Nystagmus Cognitive and behavioral

Early and severe frontal or cortical dementia Visual hallucinations not induced by treatment Ideomotor apraxia

Sensory or visual neglect/cortical disturbances

Table 2

Progression of Various Parkinsonian Disorders

Table 2

Progression of Various Parkinsonian Disorders

Disorder

Sample Size (N)

Median Age at Onset

(yr)

Median HY II Latencies (mo)

Median HY III Latencies (mo)

Median HY IV Latencies (mo)

Median HY V Latencies (mo)

Median survival After HY V Onset (mo)

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