We propose a new active vision system that mimics a saccadic movement of human eye. It is implemented based on a new computational model using neural networks. In this model, the visual pathway was divided in order to categorize a saccadic eye movement into three parts, each of which was then individually modeled using different neural networks to reflect a principal functionality of brain structures related with the saccadic eye movement in our brain. Initially, the visual cortex for saccadic eye movements was modeled using a self-organizing feature map, then a modified learning vector quantization network was applied to imitate the activity of the superior colliculus relative to a visual stimulus. In addition, a multilayer recurrent neural network, which is learned by an evolutionary computation algorithm, was used to model the visual pathway from the superior colliculus to the oculomotor neurons. Results from a computer simulation show that the proposed computational model is effective in mimicking the human eye movements during a saccade. Based on the proposed model, an active vision system using a CCD type camera and motor system was developed and demonstrated with experimental results.

With the advent of an aging society, the incidence of Alzheimer-type dementia (hereinafter referred to as AD for convenience) has drastically increased. Compared with classic cerebrovascular dementia, AD requires different therapeutic modalities. Despite such differences, it is difficult to establish a differential diagnosis of AD and cerebrovascular dementia. In the present paper, we analyze the neuropsychological symptoms and signs associated with AD, such as visual cognitive dysfunction, with particular attention to head and eye coordination. The subjects were allowed to gaze at targets disposed 1 m away and at a visual angle of 25 and 50 in order to compare healthy volunteers and patients with senile dementias such as multi-infarct dementia (MID). As a consequence, patients with AD presented clinical manifestations not seen in patients with other senile dementias; that is, (1) an increase in stepwise eye movement, (2) anisotropy in the velocity of right-directional and left-directional eye movements, (3) a decrease in the velocity of head movements (4) incomplete gaze, and (5) decreased head share.

To clarify the stereopsis disturbance in patients with Alzheimer's disease (AD), we analyzed binocular eye movement when subjects shifted their gaze between targets at different depths. Subjects are patients with Alzheimer's disease, Mluti-infarct dementia (MID), or Olivopontocerebellar atrophy (OPCA), and healthy controls. Targets are arranged in two ways: along the median plane and asymmetrically crossing the median plane, at distances from the eyes of 1000 mm and 300 mm. When the targets are switched at the onset of a beep, the subjects shifted their gaze to the lit target. The experiment is conducted in a dimly lit room whose structure is capable of providing good binocular cues for depth. In AD subjects, especially in the subjects whose symptoms are moderate (advanced stage), vergence is limited and the change in the convergence angle is small, unstable, and non-uniform. These results are different from those of other patients (MID) and OPCA) or healthy controls and suggest a disturbance of stereopsis in the parietal lobe where AD patients typically have dysfunctions.

We analyzed vergence change by moving both the target and the subject toward depth direction simultaneously. It has been suggested that the command for vergence movement caused by depth-direction-head-movement and that caused by target movement are generated separately, then combined in the oculomotor system.