What is bradykinesia?

Bradykinesia: Definition and Clinical Significance

Bradykinesia is the slowness of movement that represents an essential diagnostic feature of Parkinson's disease, characterized by reduced speed, decreased amplitude of movement, and progressive deterioration of movement with repetition. 1

Key Components of Bradykinesia

• Bradykinesia consists of several distinct manifestations including movement slowing, amplitude reduction, and gradual decrease of both speed and amplitude over multiple repetitions of the same movement 2

• It is one of the cardinal motor symptoms of Parkinson's disease and other parkinsonian syndromes, and must be present for a clinical diagnosis of Parkinson's disease along with either resting tremor, rigidity, or both 1

• Bradykinesia differs from hypokinesia, which refers to a reduced amount of movement over time; these are distinct motor features that follow different patterns of progression in Parkinson's disease 3

Clinical Characteristics

• Bradykinesia typically manifests as:

  • Slowness in initiating and executing voluntary movements 1
  • Decreased amplitude of movements, which is often disproportionately affected compared to speed 4
  • Sequential deterioration of repetitive movements (sequence effect), where movements become progressively slower and smaller with repetition 5

• The impairment in movement amplitude appears to correlate more strongly with clinical disability measures than impairment in movement speed 4

• Bradykinesia can affect all voluntary movements, including:

  • Fine motor tasks (e.g., buttoning clothes, writing)
  • Gross motor activities (e.g., walking, turning)
  • Facial expressions (reduced facial animation, hypomimia)
  • Speech (hypophonia, monotonous speech) 5

Pathophysiology

• Bradykinesia results from dysfunction in the basal ganglia network, particularly the loss of dopaminergic neurons in the substantia nigra 1

• Symptoms typically appear after approximately 40-50% of dopaminergic neurons have been lost, usually about 5 years after the initial neurodegeneration begins 1

• The pathophysiology involves not only the basal ganglia but also interconnected structures such as the primary motor cortex and cerebellum, as well as abnormal sensorimotor processing 5

• Bradykinesia may reflect a problem in generating appropriate movement forces to produce required end-point accuracy, rather than simply being a compensatory mechanism for defective preparatory processes 6

Differential Diagnosis

• Bradykinesia must be distinguished from:
  • Drug-induced parkinsonism (e.g., from antipsychotics) 7
  • Other parkinsonian syndromes such as progressive supranuclear palsy, multiple system atrophy, and corticobasal degeneration 1
  • Negative symptoms in psychiatric disorders, which may sometimes be confused with bradykinesia 7

Treatment Response

• Levodopa therapy improves bradykinesia in Parkinson's disease, but treatment variably affects different features of bradykinesia 5

• Levodopa tends to normalize movement speed to a greater extent than movement amplitude 4

• Deep brain stimulation of the subthalamic nucleus can improve specific aspects of bradykinesia, including increasing movement amplitude and frequency, and decreasing variability 2

• Anticholinergic or mild dopaminergic agents (amantadine) are used to treat drug-induced parkinsonism symptoms, including bradykinesia 7

Clinical Assessment

• Bradykinesia is typically assessed through tasks that require rapid alternating movements, such as finger tapping, hand opening/closing, and pronation-supination movements 5

• The Unified Parkinson's Disease Rating Scale (UPDRS-III) is commonly used to evaluate bradykinesia, though it does not separately weigh impairments in speed and amplitude 4

• Advanced assessment techniques using electromagnetic tracking devices can help categorize impairments in speed and amplitude more precisely 4