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Introduction
Bradykinesia refers to the slowness in executing simple and complex voluntary movements, whereas hypokinesia and akinesia refer to a reduction in amplitude or loss of voluntary and spontaneous movement, such as reduced arm swing and decreased stride length, or slow reaction time. 1 2 A characteristic feature of bradykinesia in Parkinson's disease (PD) is the progressive slowness in speed or a decrease in amplitude of sequential movements (ie, 'sequence effect' or decrement). 3 Bradykinesia and hypokinesia have been extensively investigated in the upper limbs in PD and in atypical parkinsonism (ie, progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and corticobasal degeneration (CBD)) in clinical 2 and neurophysiological studies. 1-3 In contrast to the many studies of limb bradykinesia, few studies have investigated facial bradykinesia in PD and in atypical parkinsonism. This is surprising as facial motor impairment (ie, reduction or loss of spontaneous and emotional facial expression-hypomimia) is an important clinical sign of PD, PSP and MSA, and is commonly rated in scales assessing severity of motor impairment in these conditions.
In comparison with upper limbs, the facial motor control system has several distinctive physiological features. Facial motor neurones receive neither reciprocal nor recurrent inhibition. 4 5 Unlike limb muscles, facial muscles do not act on joints and have few or no proprioceptors. 6 Equally important, the moving part shows lower inertia during facial movements than during arm movements. 7 Facial and arm movements differ in terms of electromyographic (EMG) muscle activation in that the triphasic EMG pattern that characterises arm movements is not a feature of facial movements. 1 7 Moreover, other factors that can potentially contribute to bradykinesia, including rigidity and tremor, scarcely affect the face. 1 Finally, facial movements may be not only voluntary, but also spontaneous and emotional in contrast with the predominantly voluntary limb movement. For these reasons, the clinical and pathophysiological features of facial bradykinesia differ from those in the limbs in PD and atypical parkinsonism.
In this paper, we first review the major findings about the physiological mechanisms underlying facial motor control. Then we present clinical and experimental evidence describing facial bradykinesia in PD and other causes of parkinsonism, highlighting the pathophysiological mechanisms.
Physiological basis of facial motor control
In the early 1950s, Penfield and Jasper...