eMedicine Specialties > Neurology > Movement and Neurodegenerative Diseases
Parkinson Disease: Differential Diagnoses & Workup
Updated: Oct 29, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Differential Diagnoses
Other Problems to Be Considered
Jakob-Creutzfeldt and other prion diseases
Parkinsonism can be caused by a variety of degenerative disorders, as well as toxins, infections, and vascular or structural lesions.
Parkinsonism also can be induced by medications that block dopamine receptors (eg, neuroleptics, antiemetics) or deplete intraneuronal dopamine stores (eg, reserpine, tetrabenazine).
Workup
Laboratory Studies
- No laboratory biomarkers exist for Parkinson disease.
- Serum ceruloplasmin concentration is obtained as a screening test for Wilson disease. It should be obtained in patients who present with parkinsonian symptoms when younger than 40 years. In cases in which Wilson disease is suspected, 24-hour urinary copper and slit lamp examination of the eyes also should be obtained.
Imaging Studies
- Magnetic resonance imaging (MRI) and computed tomography (CT) scan are unremarkable in Parkinson disease.
- No imaging study is required in patients with a typical presentation. Such patients are aged 55 years or older; have a slowly progressive, asymmetric parkinsonism with resting tremor and bradykinesia or rigidity; and demonstrate a good response to dopamine replacement therapy.
- MRI is useful to exclude multi-infarct state, hydrocephalus, and the lesions of Wilson disease.
- MRI should be obtained in patients whose clinical presentation does not allow a high degree of diagnostic certainty, including those who lack tremor, have an acute or stepwise progression, or are younger than 55 years.
- Positron emission tomography (PET) and single photon emission CT (SPECT) are useful diagnostic imaging studies. They are not widely available and may not be covered by insurance. Moreover, they are not needed for routine clinical diagnosis in patients with a typical presentation.
- At the onset of symptoms, patients with Parkinson disease show approximately 30% decrease in 18F-dopa uptake in the contralateral putamen.
- 18F-dopa is taken up by the terminals of dopamine neurons and converted to 18F-dopamine. The rate of striatal 18F accumulation reflects transport of 18F-dopa into dopamine neurons and its decarboxylation to 18F-dopamine.
- 11C-Nomifensine and cocaine analogues such as 123I-Beta-CIT bind to dopamine reuptake sites on nigrostriatal terminals and provide an index of the integrity of nigrostriatal projections.
- Deficits on fluorodopa PET or β-CIT SPECT indicate a dopamine deficiency syndrome but do not necessarily differentiate Parkinson disease from atypical parkinsonisms including multiple system atrophy and progressive supranuclear palsy.
More on Parkinson Disease |
| Overview: Parkinson Disease |
Differential Diagnoses & Workup: Parkinson Disease |
| Treatment & Medication: Parkinson Disease |
| Follow-up: Parkinson Disease |
| Multimedia: Parkinson Disease |
| References |
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Further Reading
Keywords
Parkinson disease, Parkinson's disease, parkinsonism, Parkinson syndrome, basal ganglia disease, movement disorder, shaking palsy, Parkinson disease treatment, Parkinson disease symptoms
Differential Diagnoses & Workup: Parkinson Disease