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Biomedical subjects

B Gaymard

Publications and source records attributed to B Gaymard.

At least 37 records · Page 2Linked to original sources
PubMed1999

Neurology of saccades and smooth pursuit.

During the period covered by this review a number of papers have been published on saccade and smooth pursuit research, conducted experimentally in monkeys and clinically in humans. In monkeys, using mainly electrophysiological methods, the roles of the frontal eye field, parietal eye field and supplementary eye field at the cortical level, and those of the paramedian pontine reticular formation, nucleus prepositus hypoglossi, interstitial nucleus of Cajal and superior colliculus at the brainstem level have been studied in great detail. In humans the same cortical areas have also been examined, mainly using functional imaging resulting in new information on the location of these areas and new hypotheses on the role of the superior parietal lobule in visual attention and that of the posterior part of the anterior cingulate cortex in motivation. Saccades, smooth pursuit and clinical applications of eye movement research are dealt with separately.

Animals↗
PubMed1998

Eye movement abnormalities correlate with genotype in autosomal dominant cerebellar ataxia type I.

We compared horizontal eye movements (visually guided saccades, antisaccades, and smooth pursuit) in control subjects (n = 14) and patients with three forms of autosomal dominant cerebellar ataxias type I: spinocerebellar ataxias 1 and 2 (SCA1, n = 11; SCA2, n = 10) and SCA3/Machado-Joseph disease (MJD) (n = 16). In SCA1, saccade amplitude was significantly increased, resulting in hypermetria. The smooth pursuit gain was decreased. In SCA2, saccade velocity was markedly decreased. The percentage of errors in antisaccades was greatly increased and was significantly correlated with age at disease onset. In addition, a correlation between smooth pursuit gain and the number of trinucleotide repeats was found. In SCA3, gaze-evoked nystagmus was often present as was saccade hypometria and smooth pursuit gain was markedly decreased. Three major criteria, saccade amplitude, saccade velocity, and presence of gaze-evoked nystagmus, permitted the correct assignment of 90% of the SCA1, 90% of the SCA2, and 93% of the patients with SCA3 to their genetically confirmed patient group and, therefore, may help orient diagnoses of SCA1, SCA2, and SCA3 at early clinical stages of the diseases.

Adolescent↗
PubMed1998

Effects of anterior cingulate cortex lesions on ocular saccades in humans.

Cerebral blood flow studies in humans suggest that the anterior cingulate cortex (ACC) could be involved in eye movement control. In two patients with a small infarction affecting the posterior part of this area (on the right side) and in ten control subjects, we studied several paradigms of saccadic eye movements: gap task, overlap task, antisaccades (using either a 5 degrees or 25 degrees lateral target), memory-guided saccades with a short (1 s) or long (7 s) delay, and sequences of memory-guided saccades. Compared with controls, patients had normal latency in the gap task but increased latency in the other tasks. The gain of memory-guided saccades was markedly decreased, bilaterally, whatever the duration of the delay. Patients made more errors than controls in the antisaccade task when the 5 degrees lateral target was used, and a higher percentage of chronological errors in the sequences of saccades. These results show that the posterior part of the right ACC plays an important role in eye movement control and suggest that this area could correspond to a "cingulate eye field" (CEF). The role of this hypothetical CEF could be an early activation exerted on the frontal ocular motor areas involved in intentional saccades and also a direct action on brainstem ocular premotor structures.

Adult↗
PubMed1998

Cortical control of saccades.

Saccadic eye movements are controlled by a cortical network composed of several oculomotor areas that are now accurately localized. Clinical and experimental studies have enabled us to understand their specific roles better. These areas are: (1) the parietal eye field (PEF) located in the intraparietal sulcus involved in visuospatial integration and in reflexive saccade triggering; (2) the frontal eye field (FEF), located in the precentral gyrus, involved in the preparation and the triggering of purposive saccades; and (3) the supplementary eye field (SEF) on the medial wall of the frontal lobe, probably involved in the temporal control of sequences of visually guided saccades and in eye-hand coordination. A putative cingulate eye field (CEF), located in the anterior cingulate cortex, would be involved in motivational modulation of voluntary saccades. Besides these motor areas, the dorsolateral prefrontal cortex (dlPFC) in the midfrontal gyrus is involved in reflexive saccade inhibition and visual short-term memory.

Cerebral Cortex↗
PubMed1998

Temporal limits of spatial working memory in humans.

An essential feature attributed to working memory is the labile and transient nature of its representations. Using an oculomotor task, we examined the stability of spatial working memory in 16 normal human subjects. Eye movements towards remembered spatial cues (memory-guided saccades) were electro-oculographically recorded after memorization delays that varied unpredictably between 0.5 and 30s. A peaked time-course of saccadic targeting errors, with maximal errors around 20s delay, was found, showing that delay-dependent decay of spatial information in working memory occurs, but is time-limited and reverts significantly beyond delays of about 20s. These data (i) indicate temporal limits of spatial working memory and (ii) provide the first behavioural evidence for the existence of two parallely generated mental representations of space that successively control memory-guided behaviour in humans.

Adult↗
PubMed1997

Cerebral ocular motor signs.

Eye movement disturbances resulting from cerebral lesions are reviewed and the specific roles of the different ocular motor areas are summarized. Three cortical areas may trigger saccades: the frontal eye field (FEF), the supplementary eye field (SEF) and the parietal eye field (PEF). The FEF could be involved mainly in intentional visual exploration (intentional saccades), the PEF mainly in reflexive visual exploration (reflexive saccades) and the SEF in the preparation of motor programs (sequences of saccades). Only bilateral lesions affecting these areas result in visible saccade disturbances (at bedside examination), as manifested in Balint's syndrome after parietal lesions, and ocular motor apraxia after fronto-parietal lesions. Other cortical areas prepare saccades: the posterior parietal cortex (near the PEF) controls visuomotor integration; the prefrontal cortex (i.e. area 46 of Brodmann) is involved in inhibition of unwanted reflexive saccades, prediction (predictive saccades) and spatial memory. Smooth pursuit is controlled by the FEF and the medial superior temporal area, located in the posterior part of the cerebral hemisphere. Eye movement disorders resulting from basal ganglia lesions are also reviewed. Lastly, the contribution of eye movement recordings in early diagnosis of some cerebral degenerative diseases (such as progressive supranuclear palsy or corticobasal degeneration) is emphasized.

Brain Diseases↗
PubMed1997

[Electrophysiologic study in a patient presenting with expanding cerebral lacunae].

A 42-year-old man was affected with multiple cerebral lesions suggesting expanding lacunae. He had suffered for about 15 years of headaches and blurred vision. Neurological examination showed a Parinaud syndrome and a skew deviation. Magnetic resonance imaging showed an enlargement of the third and lateral ventricles and multiple intraparenchymatous lesions with a signal similar to that of the cerebrospinal fluid. These lesions were located in the mesencephalon and right thalamic region. Important discrepancies between the topography of the lesion and the clinical data were observed. Neurological examination, ocular movements during wake and neuropsychological testing suggested sub-cortical dysfunction. These results suggest functional rather than lesional repercussion of expansive lacunae.

Adult↗
PubMed1996

Saccade disturbances after bilateral lentiform nucleus lesions in humans.

OBJECTIVE: To determine the roles of the putamen and pallidum in ocular motor control. METHODS: Eye movements were recorded electro-oculographically in nine patients with bilateral focal lesions affecting the lentiform nucleus, and in 12 age matched control subjects. Reflexive visually guided saccades (gap task), antisaccades, memorised sequences of saccades, memory guided saccades (with visual input only, and with both visual and vestibular inputs), and predictive saccades (with and without gap) were studied. RESULTS: Latency and accuracy of visually guided saccades were normal. The percentage of errors in the antisaccade task and latency of correct antisaccades did not differ significantly from the results of controls. The percentage of errors in saccade sequences was significantly increased. Accuracy of the two types of memory guided saccades was impaired bilaterally. The percentage of predictive saccades was significantly decreased when a gap existed, but unchanged without a gap, compared with controls. Therefore, saccades made immediately in response to an external target (reflexive visually guided saccades and antisaccades) were performed without difficulty, whereas those requiring an internal representation of such a target (such as memory guided saccades, predictive saccades, and saccade sequences) were performed with significant disturbances. CONCLUSIONS: The lentiform nucleus influences the cortical areas involved in the control of saccades when the experimental paradigm requires the use of an internal representation of the target for correct planning and execution of the ensuing saccade.

Adult↗
PubMed1996

Effects of single-pulse transcranial magnetic stimulation over the prefrontal and posterior parietal cortices during memory-guided saccades in humans.

1. We used single-pulse transcranial magnetic stimulation (TMS) to explore the temporal organization of the cortical control of memory-guided saccades in eight humans. The posterior parietal cortex (PPC) or the dorsolateral prefrontal cortex (DPFC), which are both known to be involved in the control of such saccades, were stimulated on the right side at different time intervals after the presentation of a flashed lateral visual target. The memorization delay was 2,000 ms. Single pulses were applied at 160, 260, and 360 ms after the flashed target, during the period of 700 and 1,500 ms, and finally at 2,100 ms, i.e., 100 ms after the extinguishing of the central fixation point. The effects of TMS were evaluated by calculating the percentage of error in amplitude (PEA) and latency of memory-guided saccades. The PEA was determined for the primary saccade (motor aspect) and the final eye position, i.e., after the end saccade (mnemonic aspect). Stimulation over the occipital cortex at the same time intervals served as control experiments. 2. After PPC stimulation, a significant increase in the PEA of the primary saccade and final eye position existed for contralateral saccades, compared with the PEA without stimulation, when stimulation was applied 260 ms after target presentation, but not at other time intervals. There was no significant effect on ipsilateral saccades. Latency was significantly increased bilaterally when stimulation was performed 2,100 ms after target presentation. 3. After prefrontal stimulation, a significant increase in the PEA of the primary saccade and final eye position existed for contralateral saccades, when stimulation was applied between 700 and 1,500 ms after target presentation, but not at other time intervals. There was no significant effect on ipsilateral saccades. Latency was not affected by prefrontal TMS at any stimulation times. 4. Occipital stimulation resulted in no significant effect on the PEA and latency of ipsilateral or contralateral saccades, in particular including the application at 260 ms after target presentation or during the memorization phase. 5. From these results it may be concluded that the observed effects of TMS on saccade accuracy were specific to the stimulated region and specific to the stimulation time. The PPC seems to be involved in the preparation of saccade amplitude, during the early phase of the paradigm, i.e., the sensorimotor processing period, whereas the DPFC could play a role during the later phase of the paradigm, i.e., the memorization period. Therefore in humans these results support the experimental findings suggesting that sensorimotor integration is controlled by the PPC and spatial memory by the DPFC. Furthermore, our results suggest that the PPC, although not the DPFC, plays a role in saccade triggering.

Adult↗
PubMed1995

Cortical control of saccades.

A scheme for the cortical control of saccadic eye movements is proposed based partly on defects revealed by specific test paradigms in humans with discrete lesions. Three different cortical areas are capable of triggering saccades. The frontal eye field disengages fixation, and triggers intentional saccades to visible targets, to remembered target locations, or to the location where it is predicted that the target will reappear (i.e., saccades concerned with intentional exploration of the visual environment). The parietal eye field triggers saccades made reflexively on the sudden appearance of visual targets (i.e., saccades concerned with reflexive exploration of the visual environment). The supplementary eye field is important for triggering sequences of saccades and in controlling saccades made during head or body movement (i.e., saccades concerned with complex motor programming). Three other areas contribute to the preparation of certain types of saccades. The prefrontal cortex (area 46 of Brodmann) plays a crucial role for planning saccades to remembered target locations. The inferior parietal lobule is involved in the visuospatial integration used for calculating saccade amplitude. The hippocampus appears to control the temporal working memory required for memorization of the chronological order of sequences of saccades.

Cerebral Cortex↗
PubMed1995

Cortical control of vestibular-guided saccades in man.

Memory-guided saccades, made to a remembered location to which gaze was directed before a passive body rotation (i.e. with a vestibular input), were electro-oculographically recorded in 24 patients with various cortical lesions and in 18 control subjects. Anticipation and latency, direction errors and accuracy of the first saccade, stability of eye position in darkness and final eye position were quantified. Patients were divided into small groups, each with lesions affecting one of the following cortical areas: left or right frontal eye field (FEF), left or right prefrontal cortex (area 46 of Brodmann) (PFC), left supplementary eye field (SEF), left or right posterior parietal cortex (PPC) and right parieto-temporal cortex (PTC). There were some abnormalities in the results of the right FEF group, concerning anticipation, direction errors and latency of the first saccade, but no abnormality in the accuracy of the first saccade or of the final eye position. Results in the left FEF group were normal. Accuracy of the first saccade was impaired in the SEF group, bilaterally. Final eye position was also inaccurate in the SEF group. In both PFC groups, significant and, in general, bilateral abnormalities existed for all tested parameters. Accuracy of the first saccade was impaired in the PTC group, leftwards. In contrast, the results in both PPC groups were not significantly different from those of control subjects. Our results suggest that (i) the PFC is involved in the memorization of saccade goals probably encoded in spatiotopic coordinates; (ii) the SEF, but not the FEF, is involved in the control of accuracy of these vestibular-derived goal-directed saccades; (iii) the PTC (i.e. the vestibular cortex), but not the PPC, is involved in the control of such saccades. Therefore, a cortical network different from that involved in the control of memory-guided saccades made to visual targets, with only the PFC in common, could control vestibular-derived goal-directed saccades.

Adult↗
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

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↗