The pedunculopontine (PPN) region of the upper brainstem is known to play an important role in motor control. 1 In akinetic disorders such as progressive supranuclear palsy (PSP), multisystem atrophy (MSA) and Parkinson's disease, the pendunculo-pontine nucleus has been shown to degenerate. 2,3 Electrical and pharmacological stimulation of the PPN region in rats increase motor activity, and pharmacological inhibition decreases it. 4-7 Also, uptake of 2-deoxyglucose in this region is greatly increased in the MPTP-exposed primate, which implies that it receives greatly increased afferent activity, largely from the medial pallidum. 8 Thus, chronic depression of the upper brainstem pedunculopontine region is believed to be central to the genesis of akinesia in basal ganglia disease. We have shown that radio-frequency (RF) lesions in the PPN region in the normal macaque monkey lead to akinesia, which is temporary after unilateral lesions, but prolonged after bilateral ones. 9,10 However, since such lesions also destroy fibres of passage, we have also applied kainic acid to the PPN to selectively destroy only neuronal cell bodies. 11 These lesions caused akinetic states similar to those following the RF lesions, confirming the role of the pedunculopontine region in basal ganglia mechanisms of akinesia. The accompanying video illustrates how kainate lesions of the pedunculopontine region in a rhesus monkey (sites located by ventriculogaphy and confirmed histologically) depress activity which was recorded using a 24hour Doppler whole body activity meter.