Patients with Parkinson disease (PD) often complain of painful sensations that may involve body parts affected and unaffected by dystonia.^1-7 Pain in nondystonic body parts may have cramping and arthralgic features, as well as features of peripheral or central neuropathic pain.^1,6 The high frequency of these pain disorders in the general population makes it hard to establish whether pain is more frequent among people with PD than among age-matched controls. Although the 3 pertinent controlled studies (1 published in abstract form alone)^5-7 found a higher frequency of pain among PD patients than among controls, they provided inconclusive results, owing to limitations in study design. Most important, they failed to distinguish between dystonic and nondystonic pain, used as controls a relatively small group of participants with diseases who may not have fully represented the variable of interest in the source population, and did not take into account the time between pain and PD onset.^5,6 Finally, 2 of 3 studies focused on back pain alone.^5,6

The aim of this paper is to summarise the main clinical and pathophysiological features of facial bradykinesia in Parkinson's disease (PD) and in atypical parkinsonism. Clinical observation suggests that reduced spontaneous and emotional facial expressions are features of facial bradykinesia in PD and atypical parkinsonism. In atypical parkinsonism, facial bradykinesia is complicated by additional dystonic features. Experimental studies evaluating spontaneous and emotional facial movements demonstrate that PD is characterised by a reduction in spontaneous blinking and emotional facial expression. In PD, neurophysiological studies show that voluntary orofacial movements are smaller in amplitude and slower in velocity. In contrast, movements of the upper face (eg, voluntary blinking) are normal in terms of velocity and amplitude but impaired in terms of switching between the closing and opening phases. In progressive supranuclear palsy (PSP), voluntary blinking is not only characterised by a severely impaired switching between the closing and opening phases of voluntary blinking, but is also slow in comparison with PD. In conclusion, in PD, facial bradykinesia reflects abnormalities of spontaneous, emotional and voluntary facial movements. In PSP, spontaneous and voluntary facial movements are abnormal but experimental studies on emotional facial movements are lacking. Data on facial bradykinesia in other atypical parkinsonism diseases, including multiple system atrophy and corticobasal degeneration, are limited. In PD, facial bradykinesia is primarily mediated by basal ganglia dysfunction whereas in PSP, facial bradykinesia is a consequence of a widespread degeneration involving the basal ganglia, cortical and brainstem structures.

Research from JAMA Neurology — Botulinum Toxin A Treatment for Primary Hemifacial Spasm — A 10-Year Multicenter Study