Diagnosis
- Diagnosis is based on clinical features (rest tremor, rigidity, bradykinesia, postural instability) and response to dopaminergic therapy.
- PD is a clinical diagnosis and gold standard for diagnosis are history and neuropathologic exam.
- Generally, bradykinesia plus either tremor or rigidity must be present.
- Idiopathic rapid eye movement sleep behavior disorder is a possible prodrome for PD.
History
Symptoms are often subtle or attributed to aging.
- Decreased emotion displayed in facial features
- General motor slowing and stiffness (One or both arms do not swing with walk.)
- Resting tremor (often initially one hand)
- Speech soft/mumbling
- Falls/difficulty with balance; seen with disease progression
- Psychiatric symptoms including depression, anxiety, hallucinations, and dementia
- Urinary symptoms including increased frequency and urgency; constipation
Physical Exam
- Tremor
- Resting tremor (4 to 6 Hz) that is often asymmetric; disappears with voluntary movement; frequently emerges in a hand while walking and may present as pill rolling; may also present in jaw, chin, lips, and tongue
- Bradykinesia—generalized slowness of movements
- Rigidity: cogwheel (catching and releasing) or lead pipe (continuously rigid), tested by passively manipulating the limbs
- Postural instability—decreased ability to prevent falling
Differential Diagnosis
- Essential tremor: Bradykinesia is not present; often symmetric and occurs mostly during action or when holding hands outstretched, nonresponsive to levodopa (L-dopa).
- Depression can cause psychomotor slowing that may appear similar to bradykinesia in PD.
- Dementia with Lewy bodies: characterized clinically by visual hallucinations, fluctuating cognition, and parkinsonism; dementia occurs concomitantly with or before the development of parkinsonism.
- Multiple system atrophy: presets with parkinsonism and varying degrees of dysautonomia, cerebellar involvement, and pyramidal signs; poor response to L-dopa.
- Progressive supranuclear palsy: impairment in vertical eye movements (particularly down gaze), hyperextension of neck, and early falling; pseudobulbar palsy
- Associated neurodegenerative disorders: late stages of Alzheimer disease, Huntington disease, frontotemporal dementia, spinocerebellar ataxias
- Secondary parkinsonism (drug induced: reversible; may take weeks/months after offending medication is stopped; often bilateral symptoms): neuroleptics (most common); antiemetics (e.g., prochlorperazine and promethazine), metoclopramide; SSRIs; calcium channel blockers; amiodarone; lithium/valproic acid; amphotericin B; estrogens
Diagnostic Tests & Interpretation
Initial Tests (lab, imaging)
- Diagnosis is mainly clinical, and there are no confirmatory physiologic or blood tests.
- Reduction in α-synuclein and DJ-1 protein can act as a qualitative feature in PD diagnosis.
- MRI of brain is nondiagnostic but can be used to rule out structural abnormalities.
Follow-Up Tests & Special Considerations
Single-photon emission computerized tomography (SPECT) scan might be helpful to differentiate PD from secondary parkinsonism.
Diagnostic Procedures/Other
PET and MR spectroscopy are not recommended.
Test Interpretation
Diagnosis is clinical and no tests are recommended to confirm diagnosis of PD.
From 5-Minute Clinical Consult, Svitlana Zhukivska, Medical Doctor Reviewed 04/2024
