Bradykinezj

Bradykinezj, commonly referred to as bradykinesia in English, is marked slowness of voluntary movement. It affects initiation, speed, and size of movements, leading to difficulty with tasks such as walking, rising from a chair, or writing. It is a core feature of Parkinsonism and related disorders.

Most often caused by loss of dopamine-producing neurons in the substantia nigra pars compacta, bradykinezj results from disrupted basal ganglia circuits. Dopamine depletion shifts balance between the direct and indirect pathways, slowing movement initiation and reducing movement velocity and amplitude. It may appear with various parkinsonian syndromes.

Clinically, bradykinezj presents with delayed movement initiation, slow execution, reduced arm swing, micrographia, and short, shuffling steps. Facial expression may be reduced (hypomimia). The impairment is not simply muscle weakness; fatigue and cognitive load can worsen it, especially during complex or dual tasks.

Diagnosis is clinical. Bradykinezj together with tremor at rest, rigidity, or postural instability supports a diagnosis of Parkinsonism. A good, sustained response to dopaminergic therapy reinforces it. Other causes include drug-induced parkinsonism, vascular parkinsonism, normal-pressure hydrocephalus, and other neurodegenerative syndromes.

Treatments aim to restore dopamine signaling and maintain function. Levodopa–carbidopa is the most effective for bradykinezj; other options include MAO-B inhibitors, COMT inhibitors, and dopamine agonists. Non-pharmacologic strategies such as physical therapy and exercise help maintain mobility; deep brain stimulation is used for advanced, medication-refractory cases.