In the Basso Laboratory our research interest focuses on understanding the neurophysiological underpinnings of movement disorders.  In particular, we are interested in understanding the role of a set of forebrain structures called the basal ganglia (BG) in the generation of volitional movements and how the functioning of these structures goes awry in movement disordered states such as Parkinson’s disease, Huntington’s disease and dystonia.  An overlying principle that guides the research performed in the laboratory is that the disorders of volitional movement involving the BG are not motor per se, but rather reflect faulty perceptual or higher cognitive processes that are required for the generation of volitional movement.  For example, Parkinsonian (PD) patients frequently exhibit paradoxical movement.  If a late-stage Parkinsonian patient is asked to walk voluntarily, they have difficulty.  This is a hallmark of the disease called akinesia (meaning "lack of movement"). However, if horizontal lines are drawn on the floor and the same patient is asked to step over the lines, gait can be initiated normally. This phenomenon implies that there is something about generating the movement internally that is faulty, since the movement guided by the presence of the visual stimuli (the horizontal bars) appears normal.  

A similar phenomenon can be revealed in eye movements.  We can ask a PD patient to fixate their eyes on a visual target and in the periphery we present another visual target. We can then ask the patient to look at this target.  If we measure the eye movements, we find that in early stages of the disease process, the eye movements look normal. The same patient can then fixate while we flash a target in the periphery and remove it. We then ask the patient to look at the location where the target was and we find that the eye movements are not normal. They are slow and inaccurate.  Thus, the problem is not one of seeing, nor is it one of moving, but rather it is a problem of reconstructing the target from memory.  It is these kinds of higher perceptual/cognitive processes and their role in producing some of the more enigmatic symptoms seen in BG disordered states that we are trying to understand. Our approach to these problems is based on three facts.  First, saccades, those rapid eye movements serving to realign the direction of gaze, are a simple motor behavior requiring coordination of only six extraocular muscles in each eye. Second, much is known about the brainstem circuits involved in saccade initiation, making this system an elegant model to study processes that precede movement initiation.  Third, volitional saccades align the center of gaze to objects of interest and therefore are closely linked to the visual system and perceptual processing. In addition to studies with humans, we are very fortunate to have an animal model, the Rhesus monkey, in which to study these processes. 

Dr. Basso and the members of her lab believe in the importance of maintaining a link between clinicians who diagnose, treat and perhaps cure people with debilitating diseases of the brain and basic science developing non-human primate models of brain diseased states with which to create better diagnostic tests, better treatments and perhaps develop cures. Our goal is to keep the laboratory firmly focused on issues that are of both scientific and clinical importance.