Bradykinesia

Bradykinesia is the slowness of voluntary movement and a reduced ability to initiate and execute movements. It is a core motor symptom of Parkinson's disease and other forms of parkinsonism. Patients commonly experience slowed finger tapping, dragging of the feet during walking, reduced arm swing, and progressively smaller handwriting (micrographia). Facial expression and spontaneous movements may be diminished, contributing to a mask-like face.

Pathophysiology is rooted in the loss of dopamine-producing neurons in the substantia nigra pars compacta, which disrupts the normal function of basal ganglia circuits. Dopamine depletion increases inhibitory output from the internal globus pallidus and substantia nigra pars reticulata to the thalamus, reducing thalamocortical activation and slowing voluntary movements. The degree of bradykinesia often correlates with overall dopaminergic deficit and disease progression.

Diagnosis is primarily clinical. Bradykinesia must be persistent and associated with impairment in at least two of the following: rest tremor, muscular rigidity, and postural instability, with a progressive course suggesting Parkinson's disease. Bradykinesia also occurs in other conditions, including drug-induced parkinsonism, vascular parkinsonism, normal pressure hydrocephalus, progressive supranuclear palsy, and multiple system atrophy. Neuroimaging may be used to rule out other causes or support a diagnosis in atypical cases.

Treatment aims to improve motor function and quality of life. Pharmacologic therapy often starts with levodopa combined with carbidopa, which alleviates bradykinesia for many patients. Other medicines include dopamine agonists, MAO-B inhibitors, and COMT inhibitors. Nonpharmacologic approaches such as physical therapy and regular exercise are important components of care. Deep brain stimulation is considered for select individuals with advanced disease and motor fluctuations. Outcomes vary and daytime fluctuations are common.