Akinesia or lack of movement, tremor and rigidity are hallmark symptoms seen in patients with Parkinson’s disease (PD). Another common characteristic is a shuffling pattern of gait. Patients often walk with very small and frequent steps. Interestingly, if these patients are given visual cues such as high contrast lines on the floor, the gait pattern can be normalized. This phenomenon is called paradoxical movement [71
] Paradoxical movement exists in the saccadic system as well as the skeletal motor system. For example, it is generally understood that visually-guided saccades in patients with PD are difficult to distinguish from those of healthy controls. Memory-guided saccades in contrast, are often impaired compared to those of healthy controls [73
]. Work in the monkey basal ganglia confirms these clinical observations. For example, electrical stimulation of the nigra preferentially alters memory-guided saccades but leaves visually-guided saccades relatively unaltered [67
]. Recordings in the nigra reveal that neuronal activity is preferentially linked to memory-guided elbow movements [74
]. In pallidal neurons, decreases in activity are more commonly seen during sensory-guided reaching whereas increases are more commonly seen during memory-guided reaching [75
]. Thus, the basal ganglia of both patients and monkeys appear to play a preferential role in cognitive processes leading to action.
It is easy to imagine that alterations in the neuronal activity of basal ganglia neurons such as those described above might underlie some of the deficits seen in patients with basal ganglia disease, in particular the inability to produce movement guided by mechanisms associated with memory. What is less clear is through what circuitry visual information arises to provide support for movement in the diseased basal ganglia. One prominent hypothesis is that the cerebellum compensates for a damaged basal ganglia and assists in sensory-guided movement [71
]. A second possibility that arises in light of recent anatomical studies is that visual information reaches the basal ganglia via the projection from the superior colliculus to the dopamine containing neurons of the pars compacta, the ventral tegmental area and the subthalamic nucleus [76
; ]. Visual information could reach the striatum via the nigrostriatal pathway, but also through thalamic inputs to the striatum [81
]. Understanding the functional significance of these newly identified loops through the basal ganglia involving subcortical areas is an important area for future investigation.
In addition to basic science informing clinical medicine, the study of the basal ganglia is one area in which insights obtained from the clinic also directly impact basic science. For example, a number of lines of evidence support the hypothesis that oscillations in the β band among neurons within basal ganglia circuits underlie the symptoms of akinesia and rigidity in PD [82
]. Using advances in multiple neuron recording techniques and statistical techniques, it was shown that neurons in the striatum as well as the external and internal divisions of the pallidum in monkeys display synchronous activity occurring within the β band frequency (12–30Hz). The synchronized activity of neurons is more likely to occur in the Parkinsonian state than in the healthy state [83
]. However, work in the caudate of monkeys performing a saccade task shows that β band oscillations are present even in the healthy caudate [85
]. Interestingly, the synchronous activity among neurons was decreased around the time of a saccade. These new approaches to understanding brain activity highlight the possible role of temporal information contained in the trains of action potentials rather than rate information. Although interesting, it remains to be explored what relationship these synchronous discharges have to oculomotor behavior and more importantly, how timing information is ultimately converted to the rate code required by motoneurons for all types of action.