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Biomedical subjects

S Rivaud

Publications and source records attributed to S Rivaud.

At least 37 records · Page 2Linked to original sources
PubMed1994

Influence of visual information on cerebellar saccadic dysmetria.

We compared the accuracy of saccades made to seen or remembered visual targets in 3 patients with saccadic dysmetria due to cerebellar lesions. Saccadic dysmetria was worse for saccades to remembered targets and for saccades to flashed targets visible for only 150 msec (i.e., invisible at the time of saccade). Furthermore, no corrective saccades were made if the target was not visible. These results have implications for testing saccadic dysmetria and suggest new hypotheses about the control of saccadic amplitude.

Aged↗
PubMed1994

Eye movements in parkinsonian syndromes.

Eye movements were recorded in 14 patients with Parkinson's disease (PD) in the "off" condition, 14 patients with striatonigral degeneration (SND), 10 patients with corticobasal degeneration (CBD), and 10 patients with progressive supranuclear palsy (PSP), with comparison with 12 control subjects. Vertical saccade paralysis was not observed in the PD, SND, and CBD groups but was present in 9 patients of 10 in the PSP group. In the PD and SND groups, horizontal reflexive visually guided saccade latency and accuracy were similar, and differed only slightly from those of controls. In the CBD group, saccade latency was significantly increased and correlated to an "apraxia score"; whereas, in the PSP group, saccade amplitude was significantly decreased. Thus, the abnormalities of both horizontal saccade parameters in the PSP group contrasted with those observed in the CBD group. The percentage of errors in the antisaccade task, an index of prefrontal dysfunction, was markedly increased only in the PSP group. The smooth pursuit gain was decreased in all groups but more severely in the PSP group. It may be concluded that saccade abnormalities are clearly different in SND, CBD, and PSP, and might help in early differential diagnosis in individual patients, but that SND cannot be differentiated from PD on the simple basis of eye movement abnormalities.

Aged↗
PubMed1994

Sequences of memory-guided saccades in Parkinson's disease.

Sequences of ocular saccades were studied in 8 patients with Parkinson's disease, with (i.e., "on") and without (i.e., "off") levodopa treatment. The amplitude of single saccades was decreased and not improved by treatment. The chronology of saccades during sequences was impaired in patients in the "off" state, but significantly improved during the "on" period. These results are compatible with a decreased activation of the supplementary motor area, which can be reversed by levodopa.

Electrooculography↗
PubMed1994

Impairment of extraretinal eye position signals after central thalamic lesions in humans.

Accuracy of four different types of memory-guided saccades was studied in two patients with a small central thalamic lesion, probably involving the region of the internal medullary lamina (IML), and in a control group. In the first paradigm, the eyes and head remained immobile between the time of the presentation of the visual target to be remembered and the memory-guided saccade. In the other three paradigms, the eyes were displaced during the same period (before the memory-guided saccade) by either visually-guided saccades, a smooth pursuit eye movement or a body movement (with vestibulo-ocular reflex suppression). Therefore, in these three paradigms, the initial eye displacement required the use of extraretinal eye position to produce accurate memory-guided saccades. Compared with the control group, the two patients had normal accuracy in the first memory-guided saccade paradigm, in which there was no initial eye displacement, but markedly impaired saccade accuracy in the other three paradigms. These results suggest that the cortical areas triggering saccades did not receive correct extraretinal eye position signals. They are consistent with an impairment of the efference copy, which could be distributed to the cortical ocular motor areas by the IML.

Cerebral Infarction↗
PubMed1994

Eye movement disorders after frontal eye field lesions in humans.

Eye movements were recorded electro-oculographically in three patients with a small ischemic lesion affecting the left frontal eye field (FEF) and in 12 control subjects. Reflexive visually guided saccades (gap and overlap tasks), antisaccades, predictive saccades, memory-guided saccades, smooth pursuit and optokinetic nystagmus (OKN) were studied in the three patients. Staircase saccades and double step saccades were also studied in one of the three patients. For both leftward and rightward saccades, latency in the overlap task (but not in the gap task) and that of correct antisaccades and of memory-guided saccades was significantly increased, compared with the results of controls. There was a significant decrease in the amplitude gain of all rightward saccades programmed using retinotopic coordinates (gap and overlap tasks, predictive and memory-guided saccades), whereas the amplitude gain of corresponding leftward saccades was preserved. Such an asymmetry between leftward and rightward saccades was significant. In the staircase paradigm as well as for the first saccade in the double step paradigm (with the use of retinotopic coordinates in both cases), the amplitude gain of rightward saccades was also significantly lower than that of leftward saccades. Moreover, in the double step paradigm, the amplitude gain of the first rightward saccade was significantly lower than that of the second rightward saccade (programmed using extraretinal signals), which was preserved. The percentage of errors in the antisaccade task did not differ significantly from that of normal subjects. In the predictive saccade paradigm, the percentage of predictive rightward saccades was significantly decreased. The left smooth pursuit gain for all tested velocities, the right smooth pursuit gain for higher velocities, and the left OKN gain were significantly decreased. The results show, for the first time in humans, that the FEF plays an important role in (1) the disengagement from central fixation, (2) the control of contralateral saccades programmed using retinotopic coordinates, (3) saccade prediction and (4) the control of smooth pursuit and OKN, mainly ipsilaterally. In contrast, the left FEF did not appear to be crucial for the control of the only type of saccades programmed using extraretinal signals studied here.

Brain↗
PubMed1994

The role of the right medial temporal lobe in the control of memory-guided saccades.

The role of the hippocampal formation in the control of memory-guided saccades is unclear. We tested two types of memory-guided saccades with short memorization delay in three patients with a lesion affecting the right medial temporal lobe and involving the hippocampal formation. In single memory-guided saccades, testing spatial working memory, the gain of the patient group did not differ from that of an age-matched control group. In contrast, in sequences of memory-guided saccades, testing chronological working memory, there was a marked and significant increase in the percentage of erroneous sequences in patients, compared to controls. These results suggest an important role of the hippocampal formation in the memorization of the chronological order of saccade sequences. In contrast, this structure does not appear to be crucial for spatial working memory, used in single memory-guided saccades.

Aged↗
PubMed1994

Role of pontine nuclei damage in smooth pursuit impairment of progressive supranuclear palsy: a clinical-pathologic study.

We performed a quantitative study of the pontine nuclei in the basis pontis and a semiquantitative study of extrapontine structures involved in smooth pursuit in four patients with severe impairment of horizontal smooth pursuit and histopathologically confirmed diagnosis of progressive supranuclear palsy (PSP). There were only slight changes in the extrapontine structures involved in smooth pursuit, but there was a significant neuronal loss--massive in three patients and mild in one patient--in all nuclei of the basis pontis. Our results suggest that degenerative lesions affecting the pontine nuclei are largely responsible for the horizontal smooth pursuit impairment in PSP.

Aged↗
PubMed1993

Role of the left and right supplementary motor areas in memory-guided saccade sequences.

Six right-handed patients with a lesion affecting the left (3 patients) or right (3 patients) supplementary motor area were studied using single and sequential memory-guided saccade paradigms. Accuracy of single saccades was preserved in both groups, compared to control subjects, and the chronology of saccade sequences was disturbed in the group with the left lesion but not in the group with the right lesion. The results suggest that neither side of the supplementary motor area is involved in spatial memory, and that the left supplementary motor area plays a greater role in motor sequencing than does the right supplementary motor area.

Adult↗
PubMed1993

Role of the different frontal lobe areas in the control of the horizontal component of memory-guided saccades in man.

Two paradigms of memory-guided saccades were studied in 14 patients with focal vascular lesions affecting either the frontal eye field (FEF), or the supplementary eye field (SEF) or Brodmann's area 46 in the prefrontal cortex (PFC), and in 13 age-matched control subjects. In the first paradigm, the subject had to remember the position of a visual target with the body immobile and, in the second, the position towards which gaze was directed before a body rotation, i.e. with a vestibular input. In control subjects, the percentage of error in saccade accuracy (horizontal component) was greater in the second than in the first paradigm (37% and 14% on average, respectively). Compared with controls, amplitude error was significantly increased in the FEF group for the first paradigm only, in the SEF group for the second paradigm only, and in the PFC group for both paradigms. These results are consistent with (1) the PFC providing an improvement in the utilization by the saccade system of the visual and vestibular signals used in the two paradigms, and (2) the FEF and SEF providing an improvement in the utilization of visual signals in the first paradigm and vestibular signals in the second paradigm, respectively. Furthermore, from these findings and experimental data, it may be hypothesized (1) that the PFC is a part of the network contributing to short-term memorization of both visual and vestibular signals, and (2) that the FEF and SEF control two different types of memory-guided saccades, with separate calculation modes to determine their amplitude.

Brain Mapping↗
PubMed1993

Upbeat nystagmus in a patient with a small medullary infarct.

A 43 year old man presented with decreased sensitivity in the left side of the face and both upper limbs, and with upbeat nystagmus and skew deviation. MRI demonstrated a well defined lesion compatible with an infarct in the left side of the medulla, caudal and ventral to the vestibular nuclei, possibly involving the most caudal of the perihypoglossal nuclei, the nucleus intercalatus. Ocular motor studies, using an infrared system, showed that the nystagmus slow phase decayed exponentially, suggesting a failure of integration for vertical eye movements. Vertical integration might, therefore, be performed partly in the nucleus intercalatus.

Adult↗
PubMed1993

Smooth pursuit eye movement deficits after pontine nuclei lesions in humans.

Eye movements were recorded electroculographically in four patients with basal pontine lesions, demonstrated by MRI. The most prominent eye movement abnormality observed was mild to severe impairment of smooth pursuit and optokinetic nystagmus, mainly ipsilateral to the lesion. This abnormality is thought to result from damage to the pontine nuclei, which form a crucial relay between the cerebral cortex and the cerebellum controlling smooth pursuit. Abnormalities of saccades and the vestibulo-ocular reflex in one patient are also discussed.

Adult↗
PubMed1991

Cortical control of memory-guided saccades in man.

Memory-guided saccades were electro-oculographically recorded in 30 patients with limited unilateral cerebral infarction, documented by computerized tomographic scan and/or magnetic resonance imaging. The lesions affected either (1) the posterior parietal cortex (PPC), (2) the dorsolateral frontal cortex (DLFC), involving the frontal eye field (FEF) and/or the prefrontal cortex (PFC) (area 46 of Brodmann), or (3) the supplementary motor area in the dorsomedial frontal cortex (DMFC). Patients were divided into 6 groups according to the location (PPC, DLFC, DMFC) and side of the lesions. Both latency and accuracy (expressed as percentage of error in amplitude) of memory-guided saccades were compared in each group of patients to values obtained from 20 age-matched normal subjects. Latency was significantly increased, for both directions of saccades in the two DLFC groups and in the right PPC group, and for leftward saccades in the left PPC group. The percentage of error in amplitude was also significantly increased for both directions of saccades in the right PPC group and the left DLFC group, and for leftward saccades in the right DLFC group. Results were near the normal values in patients with lesions affecting the DMFC. Thus, both the PPC (essentially on the right side) and the DLFC appear to play a role in the control of memory-guided saccades. It is suggested that the cortical pathway involved in these saccades includes the PPC, the PFC and the FEF, successively. The PPC could have a dual role: visuospatial integration, and early selection and preparation of certain collicular cells by pre-excitation. Both functions could be ensured by two different types of cells, corresponding, in the monkey, to area 7a and to lateral intraparietal area, respectively. The DLFC could also have a dual role: memorization of visuospatial information by the PFC, and triggering of memory-guided saccades by the FEF.

Cerebral Cortex↗
PubMed1991

Cortical control of reflexive visually-guided saccades.

Reflexive visually-guided saccade triggering may be facilitated or inhibited by the cerebral cortex. To study this control, saccades made towards suddenly appearing visual targets (saccade task) or away from them (antisaccade task) were recorded electro-oculographically in 45 patients with limited unilateral cerebral infarction. Lesions affected (1) the superior part of the angular gyrus (area 39 of Brodmann) in the posterior parietal cortex (PPC), (2) the dorsolateral prefrontal cortex (PFC) (area 46 of Brodmann), (3) the frontal eye field (FEF), or (4) the supplementary motor area (SMA). As these 4 types of lesions were located either in the right or the left cerebral hemisphere, patients were divided into 8 groups. Saccade latency, in the saccade task, and the percentage of errors (misdirected saccades made towards the visual target), in the antisaccade task, were compared in each group of patients with the values of 20 control subjects. In the saccade task, saccade latency was significantly increased bilaterally in the right PPC group. In the left PPC group, the increase in latency was less marked, and significant only for saccades made contralaterally to the lesion. In the different frontal groups, latency was unchanged or only slightly increased. These results confirm that the main area facilitating the triggering of reflexive visually-guided saccades is located in the PPC, in or near the superior part of the angular gyrus. The difference between right and left parietal lesions could be due to the predominance of the right hemisphere in the control of these saccades. In the antisaccade task, the percentage of errors was significantly increased bilaterally in both PFC groups compared with the control group and also to the FEF and SMA groups. These results suggest that the PFC is the main area in the cerebral hemisphere inhibiting reflexive visually-guided saccades.

Cerebral Cortex↗
PubMed1991

Saccade deficits after a unilateral lesion affecting the superior colliculus.

A 70 year old patient with a small haematoma largely restricted to the area of the right superior and inferior colliculi is reported. Eye movements were electro-oculographically recorded 17 and 80 days after the onset of the haematoma. At the first examination, latency of lateral reflexive visually-guided saccades was asymmetrical, both in the gap task (central fixation point switched off 200 ms before the onset of the lateral target) and in the overlap task (central fixation point remaining switched on). Furthermore, latency of leftward saccades in the overlap task was increased, and accuracy of these saccades was impaired, at both examinations. In the immobility task (fixation straight ahead while lateral targets suddenly occurred) and in the anti-saccade task (saccade made away from the lateral target), the percentages of errors (saccades made to the target) were high at the first examination, and noticeably lower at the second. These results suggest that the superior colliculus plays an important role both in the triggering and inhibition of reflexive visually-guided saccades.

Aged↗
PubMed1990

Impairment of sequences of memory-guided saccades after supplementary motor area lesions.

Different paradigms of saccades were recorded electro-oculographically in 2 patients with infarction affecting the left supplementary motor area. Saccades made toward visual targets (visually-guided saccades) or away from them (antisaccades) were normal in both patients. Memory-guided saccades, made to the remembered position of a flash occurring 2 seconds before, were preserved in 1 patient and only slightly impaired in the other. However, sequences of two or three memory-guided saccades were severely impaired in both patients. It has previously been reported that the supplementary motor area plays an important role in programming sequential limb movements. Our data suggest that this area plays a similar role in the control of sequential eye movements.

Adult↗
PubMed1989

Lateral visually-guided saccades in progressive supranuclear palsy.

Lateral visually-guided saccades were studied electro-oculographically in 40 patients with progressive supranuclear palsy (PSP) in order to increase understanding of the pathophysiology of the oculomotor syndrome and the suprareticular control of saccades. In the two main paradigms used, the central fixation point was removed just before the appearance of a lateral target, the subject being told either to look at the target (gap task) or, particularly to test frontal lobe influence, in the direction opposite to the target (antisaccade task). Saccade latency distribution in the gap task was significantly more scattered in patients as compared with 40 normal control subjects, although mean latencies did not differ greatly. In particular, many patients had latencies shorter or longer than those of control subjects. In the PSP group, the percentage of errors in the antisaccade task (misdirected saccades made towards the target) was strongly correlated with latency in the gap task, high percentages of errors corresponding to short latencies. There was also a correlation between latency and the frontal dysfunction evaluated by neuropsychological tests. These correlations suggest that short latencies could result from a severe impairment of the frontal inhibitory system involved in saccade initiation. Long latencies would result from damage to diverse excitatory suprareticular pathways (such as the superior colliculus) or to circuits responsible for shifts in visual attention. Lastly, 20 patients were followed longitudinally (for 3-12 months). The initially great intersubject variability of saccade latency in the gap task significantly decreased over a period of several months. This finding could result from a secondary balance between the impairment of the frontal inhibitory system and that of the diverse excitatory pathways.

Aged↗