Bradykinesia in Parkinson's Disease
Bradykinesia is the essential diagnostic feature of Parkinson's disease, defined as slowness of movement initiation and execution with reduced amplitude of repetitive movements, and must be present alongside at least one other cardinal sign (resting tremor or rigidity) to establish the diagnosis. 1, 2, 3
Definition and Core Components
Bradykinesia represents a complex of motor alterations that includes three distinct features:
- Slowness (reduced speed) of movement initiation and execution 1, 2
- Hypokinesia (decreased amplitude) with reduced size of movements 4, 5
- Sequence effect: progressive reduction in speed and amplitude during repetitive movements 4, 5, 6
The amplitude impairment is typically more severely affected than speed impairment in the "off" medication state, and amplitude correlates more strongly with overall disability than speed does 7. This distinction is clinically important because levodopa normalizes speed to a greater extent than amplitude 7.
Clinical Manifestations
Bradykinesia affects multiple domains of voluntary movement:
- Fine motor tasks: difficulty buttoning clothes, writing (micrographia), manipulating small objects 1
- Gross motor activities: slowness in walking, turning, rising from a chair 1
- Facial expressions: reduced spontaneous facial movements (hypomimia) 1
- Speech: reduced volume and articulation 1
Motor symptoms typically appear approximately 5 years after initial dopaminergic neuron loss begins, by which time 40-50% of dopaminergic neurons in the substantia nigra have already been lost 1, 2.
Assessment Methods
Clinical Examination
To properly assess bradykinesia, test repetitive movements (finger tapping, hand opening/closing, foot tapping) and observe for three key features: initial slowness, reduced amplitude, and progressive decrement with repetition. 4, 5
Specific examination techniques include:
- Finger tapping: Have the patient tap thumb and index finger together rapidly with maximum amplitude, observing for slowness, small amplitude, and progressive decrement 4, 5
- Hand movements: Ask the patient to open and close their hand repeatedly as fully and quickly as possible 5
- Foot tapping: Assess heel tapping on the floor with maximum amplitude 4
- Pronation-supination: Test rapid alternating hand rotations 8
Standardized Rating Scales
- The Unified Parkinson's Disease Rating Scale (UPDRS) or Movement Disorder Society-UPDRS (MDS-UPDRS) should be used for standardized assessment, which includes motor examination components that specifically evaluate bradykinesia 1, 3
- The MDS-UPDRS provides improved evaluation of motor aspects including freezing of gait and tremor subtypes 1
Objective Kinematic Assessment
While not routinely used clinically, kinematic techniques using electromagnetic tracking devices or optical fiber gloves can objectively quantify speed, amplitude, and sequence effect during functional MRI or clinical research 4, 5, 7. These methods provide precise measurements but are primarily research tools.
Pathophysiology and Neural Correlates
Bradykinesia arises from dysfunction of the basal ganglia-thalamo-cortical circuit network, with reduced activity in motor planning areas (supplementary motor area, cingulum) and motor execution regions (cerebellum, pallidum/thalamus) correlating with both hypokinesia and sequence effect. 5, 6
Key pathophysiological findings include:
- Reduced activity in fronto-parietal areas, middle cingulum/supplementary motor area, parahippocampus, pallidum/thalamus, and motor cerebellar areas 5
- Compensatory increased activity in cognitive brain areas (superior temporal gyrus, posterior cingulum, cerebellum crus I) 5
- Abnormal connectivity between thalamus and motor cortex 6
- Contribution of abnormal sensorimotor processing 6
First-Line Treatment Options
Dopaminergic Therapy
Levodopa remains the gold standard first-line treatment for bradykinesia, improving both movement speed and amplitude, though it affects speed more than amplitude and does not significantly modify the sequence effect. 7, 6
- Levodopa normalizes speed to a greater extent than amplitude 7
- The sequence effect (progressive decrement with repetition) is not significantly modified by levodopa therapy 4, 6
- Treatment variably affects different bradykinesia features 6
Alternative First-Line Agents
- Selegiline (10 mg daily) improves both movement speed and amplitude in early Parkinson's disease, though it does not influence the sequence effect 4
- Amantadine can be used as a mild dopaminergic agent, particularly for drug-induced parkinsonism 1
Advanced Treatment Options
Deep Brain Stimulation
Subthalamic nucleus (STN) deep brain stimulation improves specific components of bradykinesia—increasing movement amplitude and frequency while decreasing variability—but does not affect short-term within-trial decrement that may reflect muscular fatigue. 8
Specific effects of STN-DBS include:
- Increased movement amplitude 8
- Increased movement frequency 8
- Decreased movement variability 8
- Reduced across-trial decrement (long-term fatigue) 8
- No effect on within-trial decrement (short-term fatigue) 8
Differential Diagnosis Considerations
When evaluating bradykinesia, distinguish Parkinson's disease from:
- Atypical parkinsonisms (PSP, MSA, CBD): These conditions show bradykinesia but the sequence effect is less common 6
- Drug-induced parkinsonism: Caused by antipsychotics or other dopamine-blocking agents; treat with anticholinergics or amantadine 1
- Essential tremor: Presents with postural/action tremor without true bradykinesia 2
- Vascular parkinsonism: Look for multiple lacunar infarcts or diffuse white matter disease on MRI 1
Diagnostic Imaging When Diagnosis is Uncertain
If clinical diagnosis remains uncertain after examination, obtain MRI brain without contrast first to exclude structural causes, followed by I-123 ioflupane SPECT/CT (DaTscan) to differentiate true Parkinsonian syndromes from mimics like essential tremor or drug-induced parkinsonism. 1, 3
- A normal DaTscan essentially excludes Parkinsonian syndromes 1, 3
- DaTscan shows decreased radiotracer uptake in the striatum, typically progressing from putamen to caudate 1
- Drug-induced parkinsonism typically yields a normal DaTscan 1
Critical Pitfalls to Avoid
- Do not diagnose Parkinson's disease without confirming bradykinesia is present—it is the essential diagnostic feature 1, 3
- Do not assume all components of bradykinesia respond equally to treatment—speed improves more than amplitude with levodopa, and sequence effect is largely treatment-resistant 7, 6
- Do not skip neurologist confirmation of diagnosis—correctly diagnosing parkinsonian syndromes on clinical features alone is challenging, and atypical syndromes (PSP, MSA, CBD) have different prognoses and treatment responses 1
- Do not order functional imaging (DaTscan) before structural imaging (MRI)—structural causes must be excluded first 1
- Do not confuse voluntary muscle contraction with rigidity during examination—ensure the patient is completely relaxed when testing for rigidity 1