Akinesia is a delay in the initiation of voluntary movement, and bradykines
ia demotes a slowing-down of a movement that is already taking place. Akine
sia and bradykinesia are the main features of Parkinson's disease (PD) and
the symptoms with the closest correlation to the dopaminergic deficit. Howe
ver, akinesia and bradykinesia are not specific neither for PD nor for park
insonism. In parkinsonism akinesia and bradykinesia are more prominent in c
omplex than in simple movements. Self-initiated movements are slower than s
timulus-initiated movements. Parkinsonian akinesia and bradykinesia are inf
luenced by (external) motivation, in contrast to slowness in pyramidal trac
t lesions. Typical signs of parkinsonian bradykinesia are fatigue and an in
creased variability. The two extremes of pathological variability may be fr
eezing on the one hand and paradoxical kinesia on the other. Akinesia and b
radykinesia are clinically evaluated using subscores of the Unified Parkins
on's Disease Rating Scale and timed tests. Simple devices such as the Purdu
e pegboard or counters fora hand tapping test are useful for evaluating bra
dykinesia. EMG-based evaluations allow for accurate measurements of reactio
n time and movement time in simple or complex movements. The triphasic patt
ern of agonist-antagonist-agonist bursting in a ballistic movement is prese
rved. Larger movements last longer because more triphasic cycles are requir
ed. Computer-based movement analysis is possible with optoelectronic or ult
rasound systems or graphic tablets. These systems have a high temporal and
spatial resolution. Acceleration and velocity can be calculated. Analysis o
f hand or finger-tapping tests using a PC keyboard allows the analysis of r
eaction time (correlating with akinesia), intertap intervals (correlating w
ith bradykinesia), variability, and fatigue. In conclusion, clinical neurop
hysiology allows exact quantification of the kinematic parameters of akines
ia and bradykinesia.