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ULY CLINIC
ULY CLINIC
21 Septemba 2025, 03:02:09
Bradykinesia
Bradykinesia refers to the slowness of all voluntary movements and speech, resulting from impaired initiation and execution of motor activity. It is a hallmark feature of parkinsonism and other extrapyramidal or cerebellar disorders.
Pathophysiology
Bradykinesia occurs due to reduced dopamine levels in the basal ganglia, particularly the substantia nigra pars compacta.
Dopamine depletion disrupts the normal excitatory and inhibitory circuits of the basal ganglia-thalamo-cortical pathways, leading to:
Slowed movement initiation (akinesia)
Reduced amplitude of voluntary movements (hypokinesia)
Impaired coordination of sequential motor tasks
Secondary causes may include drug-induced extrapyramidal effects, cerebellar lesions, or post-hypoxic neuronal injury.
Examination Technique
Observation: Watch the patient perform routine tasks such as walking, rising from a chair, or writing.
Timed tasks: Ask the patient to:
Tap fingers or hands rapidly
Perform repetitive hand movements
Open and close the mouth or repeat syllables (“pa-ta-ka”)
Assessment: Note slowness, decreased movement amplitude, or delayed initiation.
Interpretation: Significant reduction in speed or fluidity of movement indicates bradykinesia.
Clinical Utility
Diagnostic indicator: Bradykinesia is essential for the diagnosis of Parkinson’s disease, along with rigidity and resting tremor.
Severity assessment: The degree of bradykinesia can be quantified using scales such as Unified Parkinson’s Disease Rating Scale (UPDRS).
Monitoring progression: Useful in tracking disease progression and response to therapy.
Differential Diagnosis
Cause / Condition | Key Features | Mechanism / Notes |
Parkinson’s disease | Tremor at rest, rigidity, shuffling gait, postural instability | Dopamine depletion in basal ganglia, leading to impaired motor circuits |
Drug-induced parkinsonism | Bradykinesia, rigidity; often symmetrical | Caused by dopamine receptor antagonists (e.g., antipsychotics) |
Extrapyramidal syndromes | Rigidity, tremor, abnormal postures | Basal ganglia dysfunction due to neurodegeneration or toxins |
Cerebellar disorders | Ataxia, dysmetria, hypotonia | Impaired coordination may mimic slowness, but cerebellar signs predominate |
Post-hypoxic injury | Bradykinesia with cognitive impairment | Diffuse neuronal injury affecting basal ganglia and cortical motor areas |
Normal aging | Mild slowness of movement | Reduced neuromuscular efficiency; distinguished from pathological bradykinesia |
Management
Pharmacologic:
Levodopa/carbidopa for dopamine replacement in Parkinson’s disease
Dopamine agonists (e.g., pramipexole, ropinirole)
MAO-B inhibitors (e.g., selegiline, rasagiline)
Physical therapy: Exercises to improve mobility, balance, and speed of movement
Occupational therapy: Training in activities of daily living
Medication review: Discontinue or adjust dopamine-blocking drugs causing bradykinesia
Advanced interventions: Deep brain stimulation for severe, medication-resistant cases
Pediatric considerations
Rare in children, typically following hypoxic brain injury.
Early recognition is critical for rehabilitation and motor skill retraining.
Geriatric considerations
Most commonly occurs in adults over 50 years.
Early detection aids in slowing progression, improving quality of life, and preventing falls.
Limitations
Bradykinesia may be subtle in early disease and requires careful observation.
Can be masked by voluntary effort or comorbid musculoskeletal limitations.
Should always be interpreted alongside rigidity, tremor, and postural instability to confirm parkinsonism.
Patient counseling
Explain the nature of movement slowness and its underlying cause.
Encourage consistent exercise and participation in physical therapy programs.
Discuss medication adherence, potential side effects, and the importance of follow-up.
Conclusion
Bradykinesia is a core motor symptom in Parkinson’s disease and related disorders. Recognition through careful clinical assessment aids in early diagnosis, monitoring disease progression, and guiding therapy. Awareness of differential diagnoses and contributing factors ensures accurate evaluation and management.
References
Jankovic J. Parkinson’s disease: clinical features and diagnosis. J Neurol Neurosurg Psychiatry. 2008;79:368–376.
Kalia LV, Lang AE. Parkinson’s disease. Lancet. 2015;386:896–912.
Buttaro TM, Tybulski J, Bailey PP, Sandberg-Cook J. Primary Care: A Collaborative Practice. St. Louis (MO): Mosby Elsevier; 2008. p. 444–447.
McFarland NR, Hess CW. Bradykinesia: clinical assessment and pathophysiology. Mov Disord Clin Pract. 2017;4(1):7–18.
Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy. 9th ed. Philadelphia, PA: Wolters Kluwer; 2020.
