Superior temporal gyrus: a neglected cortical area?
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Journal Article↗
Biomedical subjects
G Di Pellegrino
Publications and source records attributed to G Di Pellegrino.
Spatial extinction on double asynchronous stimulation.
Despite the fact that visual extinction is widely considered a space-based disturbance of selective attention, there has been little theoretical consensus about the nature of its pathogenic mechanism. A specific disruption in the ability to disengage attention from ipsilesional stimuli, or a loss of weight with which contralesional objects compete for visual selection, have been hypothesized to account for the disorder. We tested the merits of these two explanations in a right-hemisphere-lesioned patient, FB, who failed to recognize a contralesional target only when it was shown concurrently to an ipsilesional target (i.e. visual extinction). His task was to report two target letters presented in rapid succession to the left and right of the fixation point. The order of stimulus presentation (Left-First vs Right-First), and the intertarget interval (stimulus onset asynchrony) were varied systematically. We showed that contralesional extinction may occur for successively presented targets, not just for stimuli displayed at the same time. Of most importance, FB was seriously and equally impaired in dealing with a contralesional stimulus when this either preceded the ipsilesional stimulus or followed it by an interval less than about 600 msec. The data appear to contradict the disengagement hypothesis, which predicted a substantial reduction of extinction when a stimulus was displayed first into the lesioned side of space. We suggest that a competitive model of visual selective attention fits the data quite well.
Aged↗
Clock-drawing in a case of left visuo-spatial neglect: a deficit of disengagement?
A patient (C.B.) with severe left visuo-spatial neglect and hemianopia after right hemisphere stroke was tested on three conditions of a clock-drawing task. Either on spontaneous drawing or when the number sequence was provided by the experimenter, C.B. drew a clockface with left-sided numbers transposed to the right side of the dial. By contrast, when each number was drawn on a separate dial, its location was correct and there was no transposition. Directional hypokinesia or a representational deficit cannot explain these effects. It is proposed that a deficit in disengaging attention from right-sided visual stimuli plays a critical role in some forms of number transpositions.
Aged↗
An experimental investigation on the nature of extinction.
Under conditions of bilateral simultaneous presentation a right brain-damaged patient consistently extinguished visual stimuli presented for 200 msec to the left visual field. He was submitted to a series of experiments aimed at assessing the variables that influence this phenomenon. Extinction persisted unmodified when stimulus presentation was lengthened to 500 msec, when the size of the left stimulus was four-fold that of the right stimulus and for whatever position the stimuli occupied on the two halves of the display. Single stimuli were always perceived, but their localization was transposed rightward. The only condition in which extinction was partially reduced was when the instructions called for total disregard of the right stimulus. The patient also extinguished the leftmost of two stimuli presented in the left space, while he always perceived both stimuli when they were presented in the right space. However, if attention was covertly moved to a point in the right space and two stimuli were displayed to either side of it, left stimuli were neglected 70% of the time. Though a left stimulus was never perceived, it slowed the RT to the identification of a right stimulus. These data are interpreted in the frame of the directional bias theory, which attributes extinction to a shift of attention towards the side ipsilateral to the lesion, caused by the imbalance between the opponent turning processors, controlled by the right and left hemisphere. However, the striking difference in the rate of extinction when both stimuli were presented to the left or to the right field implies a stepwise decrement in the deployment of attention by the damaged processor, when it enters in the opposite space.
Attention↗
Primate premotor cortex: dissociation of visuomotor from sensory signals.
1. If we assume adequate control for attention, memory, and stimulus location, a bona fide sensory response would be unaffected by whether a visuospatial stimulus instructs (1) one limb movement versus another or (2) limb movement versus a shift in spatial attention or memory. Two behavioral methods tested whether apparently sensory responses in the monkey's premotor cortex are strictly that, or, alternatively, whether they reflect the action instructed by a stimulus. 2. When an identical stimulus leads to two different responses, phasic discharge after a visuospatial stimulus is significantly, often dramatically, affected by the response. Similarly, premotor cortex neurons discharge more after a stimulus instructs a limb movement than after the same stimulus instructs a shift in spatial attention or memory. Thus, for the majority of premotor cortex neurons, the hypothesis that phasic poststimulus activity modulation represents a sensory response can be rejected.
Animals↗
[Opsoclonus-ataxia syndrome. Description of a case].
This report describes an 18-year-old woman who, after a febrile illness, developed opsoclonus, truncal ataxia and mild body tremulousness. The oculomotor disorder was documented by electro-oculography. The results of extensive neurological investigations, including CT scan, visual, auditory and somesthetic evoked potentials, nuclear magnetic resonance and complete cerebrospinal fluid evaluation, were negative. The patient recovered completely within about 1 month. After having thoroughly analyzed the pertinent literature, we conclude that the pathogenetic hypothesis of direct encephalitic damage is unproved, and that these peculiar unwanted ocular movements can be explained by assuming an abnormality of "pause" cell control over saccadic "burst" neurons.
Adolescent↗