Bradykinesia

Bradykinesia is characterized by slowness in the initiation and execution of movement, along with decrement in amplitude or speed with repetitive actions (decrementing amplitude on finger tapping or hand opening/closing). It is one of the four cardinal signs of Parkinsonism, along with resting tremor, rigidity (often cogwheel), and postural instability. Bradykinesia is required for the diagnosis of Parkinson disease per the UK Brain Bank and MDS criteria, typically combined with either resting tremor or rigidity.

Pathophysiology: Loss of dopaminergic neurons in the substantia nigra pars compacta leads to decreased dopamine input to the striatum, disrupting the direct and indirect basal ganglia pathways. This results in excessive inhibition of the thalamus and reduced excitatory drive to the motor cortex, causing slowed initiation and execution of movement.

Clinical manifestations include: micrographia (progressively smaller handwriting), hypomimia (masked facies), hypophonia (soft, monotone speech), reduced arm swing while walking, shuffling gait with short steps, difficulty rising from a chair, and slowness in activities of daily living (buttoning shirts, cutting food).

Clinical significance: Bradykinesia helps distinguish Parkinson disease from essential tremor (which lacks bradykinesia). It is also seen in other parkinsonian syndromes (multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, drug-induced parkinsonism from antipsychotics/antiemetics that block dopamine receptors). Assessment includes finger tapping, hand movements, leg agility, and gait observation.

Treatment: Levodopa/carbidopa is the most effective therapy for bradykinesia and other motor symptoms. Dopamine agonists (pramipexole, ropinirole), MAO-B inhibitors (selegiline, rasagiline), and COMT inhibitors (entacapone) are also used. Deep brain stimulation of the subthalamic nucleus or globus pallidus interna can help in advanced disease.