A patient who suffered bilateral posterior brain damage exhibited disturbance of movement vision in a rather pure form. The patient had no impression of movement in depth, and could only discriminate between a stationary and a moving target in the periphery of her otherwise intact visual fields. She had some movement vision in the central part of her visual fields, provided that target velocity did not exceed 10 deg/s. Neither did she possess visual movement after effects nor apparent (phi) visual movement. In addition, visually guided eye and finger movements were impaired. In contrast to the disturbance of movement perception in the visual modality, movement perception elicited by acoustic and tactile stimuli was not impaired. On the basis of the localization of the cerebral damage (as judged by CT scanning and neuropsychological testing) it is concluded that the observed disorder in movement vision is due to bilateral cerebral lesions affecting the lateral temporo-occipital cortex and the underlying white matter. The selectivity of the visual disturbance supports the idea that movement vision is a separate visual function depending on neuronal mechanisms beyond the primary visual cortex.

Grip force adjustments to fluctuations of inertial loads induced by vertical arm movements with a grasped object were analysed during normal and impaired finger sensibility. Normally grip force is modulated in a highly economical way in parallel with fluctuations of load force. Two subjects performed vertical up and down movements of a grasped object, both with normal finger sensibility and then cutaneously anaesthetized finger sensibility. Short breaks were taken in between single movements, during which the object was held stationary. After digital anaesthesia was applied to the grasping fingers, both subjects substantially increased the grip force. The grip force amplitude and timing still anticipated changes in load force, although the established grip force had already overcome movement-induced load force peaks. This implies that the increase of grip force and consequently the elevated force ratio between maximum grip and maximum load force are not processed to alter the feedforward system of grip force control. Cutaneous afferent information from the grasping digits appears to be necessary for economic scaling of the grip force level, but it plays a subordinate role in the precise anticipatory temporal coupling of grip and load forces during voluntary object manipulation.

No abstract

In 1983 we reported in this Journal a patient who suffered a disturbance of movement vision in a relatively pure form. This uncommon cerebral visual deficit resulted as a consequence of bilateral brain damage affecting the lateral temporo-occipital cortex and the underlying white matter. In this paper we present further evidence for the selectivity of the movement vision deficit. Furthermore, follow-up examination did not reveal any significant change which indicates that the disorder appears irreversible. Magnetic Resonance Imaging (MRI) shows bilateral lesions involving the upper (cranial) part of the occipital gyri and the adjacent portion of the middle temporal gyri, with the main focus of damage in the upper (cranial) banks of the anterior occipital sulcus. In addition, cortico-cortical fibre pathways interconnecting occipital, temporal and parietal 'visual' areas are also affected bilaterally. The selectivity of the movement vision deficit and the irreversibility of the disorder strongly support the idea that movement vision is a separate function which is subserved by a visual pathway specialized for the processing of visual motion.