A triple distinction of cerebellar function for oculomotor learning and fatigue compensation.

The cerebellum implements error-based motor learning via synaptic gain adaptation of an inverse model, i.e. the mapping of a spatial movement goal onto a motor command. Recently, we modeled the motor and perceptual changes during learning of saccadic eye movements, showing that learning is actually a threefold process. Besides motor recalibration of (1) the inverse model, learning also comprises perceptual recalibration of (2) the visuospatial target map and (3) of a forward dynamics model that estimates the saccade size from corollary discharge. Yet, the site of perceptual recalibration remains unclear. Here we dissociate cerebellar contributions to the three stages of learning by modeling the learning data of eight cerebellar patients and eight healthy controls. Results showed that cerebellar pathology restrains short-term recalibration of the inverse model while the forward dynamics model is well informed about the reduced saccade change. Adaptation of the visuospatial target map trended in learning direction only in control subjects, yet without reaching significance. Moreover, some patients showed a tendency for uncompensated oculomotor fatigue caused by insufficient upregulation of saccade duration. According to our model, this could induce long-term perceptual compensation, consistent with the overestimation of target eccentricity found in the patients' baseline data. We conclude that the cerebellum mediates short-term adaptation of the inverse model, especially by control of saccade duration, while the forward dynamics model was not affected by cerebellar pathology.

How visual attention span and phonological skills contribute to N170 print tuning: An EEG study in French dyslexic students.

Developmental dyslexia is a disorder characterized by a sustainable learning deficit in reading. Based on ERP-driven approaches focusing on the visual word form area, electrophysiological studies have pointed a lack of visual expertise for written word recognition in dyslexic readers by contrasting the left-lateralized N170 amplitudes elicited by alphabetic versus non-alphabetic stimuli. Here, we investigated in 22 dyslexic participants and 22 age-matched control subjects how two behavioural abilities potentially affected in dyslexic readers (phonological and visual attention skills) contributed to the N170 expertise during a word detection task. Consistent with literature, dyslexic participants exhibited poorer performance in these both abilities as compared to healthy subjects. At the brain level, we observed (1) an unexpected preservation of the N170 expertise in the dyslexic group suggesting a possible compensatory mechanism and (2) a modulation of this expertise only by phonological skills, providing evidence for the phonological mapping deficit hypothesis.

Neural substrates of saccadic adaptation: Plastic changes versus error processing and forward versus backward learning.

Previous behavioral, clinical, and neuroimaging studies suggest that the neural substrates of adaptation of saccadic eye movements involve, beyond the central role of the cerebellum, several, still incompletely determined, cortical areas. Furthermore, no neuroimaging study has yet tackled the differences between saccade lengthening ("forward adaptation") and shortening ("backward adaptation") and neither between their two main components, i.e. error processing and oculomotor changes. The present fMRI study was designed to fill these gaps. Blood-oxygen-level-dependent (BOLD) signal and eye movements of 24 healthy volunteers were acquired while performing reactive saccades under 4 conditions repeated in short blocks of 16 trials: systematic target jump during the saccade and in the saccade direction (forward: FW) or in the opposite direction (backward: BW), randomly directed FW or BW target jump during the saccade (random: RND) and no intra-saccadic target jump (stationary: STA). BOLD signals were analyzed both through general linear model (GLM) approaches applied at the whole-brain level and through sensitive Multi-Variate Pattern Analyses (MVPA) applied to 34 regions of interest (ROIs) identified from independent 'Saccade Localizer' functional data. Oculomotor data were consistent with successful induction of forward and backward adaptation in FW and BW blocks, respectively. The different analyses of voxel activation patterns (MVPAs) disclosed the involvement of 1) a set of ROIs specifically related to adaptation in the right occipital cortex, right and left MT/MST, right FEF and right pallidum; 2) several ROIs specifically involved in error signal processing in the left occipital cortex, left PEF, left precuneus, Medial Cingulate cortex (MCC), left inferior and right superior cerebellum; 3) ROIs specific to the direction of adaptation in the occipital cortex and MT/MST (left and right hemispheres for FW and BW, respectively) and in the pallidum of the right hemisphere (FW). The involvement of the left PEF and of the (left and right) occipital cortex were further supported and qualified by the whole brain GLM analysis: clusters of increased activity were found in PEF for the RND versus STA contrast (related to error processing) and in the left (right) occipital cortex for the FW (BW) versus STA contrasts [related to the FW (BW) direction of error and/or adaptation]. The present study both adds complementary data to the growing literature supporting a role of the cerebral cortex in saccadic adaptation through feedback and feedforward relationships with the cerebellum and provides the basis for improving conceptual frameworks of oculomotor plasticity and of its link with spatial cognition.

Cerebellar signals drive motor adjustments and visual perceptual changes during forward and backward adaptation of reactive saccades.

Saccadic adaptation ($SA$) is a cerebellar-dependent learning of motor commands ($MC$), which aims at preserving saccade accuracy. Since $SA$ alters visual localization during fixation and even more so across saccades, it could also involve changes of target and/or saccade visuospatial representations, the latter ($CDv$) resulting from a motor-to-visual transformation (forward dynamics model) of the corollary discharge of the $MC$. In the present study, we investigated if, in addition to its established role in adaptive adjustment of $MC$, the cerebellum could contribute to the adaptation-associated perceptual changes. Transfer of backward and forward adaptation to spatial perceptual performance (during ocular fixation and trans-saccadically) was assessed in eight cerebellar patients and eight healthy volunteers. In healthy participants, both types of $SA$ altered $MC$ as well as internal representations of the saccade target and of the saccadic eye displacement. In patients, adaptation-related adjustments of $MC$ and adaptation transfer to localization were strongly reduced relative to healthy participants, unraveling abnormal adaptation-related changes of target and $CDv$. Importantly, the estimated changes of $CDv$ were totally abolished following forward session but mainly preserved in backward session, suggesting that an internal model ensuring trans-saccadic localization could be located in the adaptation-related cerebellar networks or in downstream networks, respectively.

The posterior parietal cortex processes visuo-spatial and extra-retinal information for saccadic remapping: A case study.

Optimally collecting information and controlling behaviour require that we constantly scan our visual environment through eye movements. How the dynamic interaction between short-lived retinal images and extra-retinal signals of eye motion results in our subjective experience of visual stability remains a major issue in Cognitive Neuroscience. The present study aimed to assess and determine the nature of the contribution of the posterior parietal cortex (PPC) to the saccadic remapping mechanisms which contribute to such perceptual visual constancy. Perceptual responses in transsaccadic visual localization tasks were measured in a patient presenting with a PPC lesion and manifesting optic ataxia in the left hemifield with no neglect. Two perceptual localization tasks, each with versus without an intervening saccade, were used: the saccadic suppression of displacement (SSD) task (Ostendorf, Liebermann, & Ploner, 2010) and the peri-saccadic flash localization (LOC) task (Zimmerman & Lappe, 2010). Compared to a group of age-matched healthy subjects, the patient showed a specific pattern of perceptual deficits in the ataxic (left) hemifield. First, a significant impairment occurred in the stationary eye conditions, attesting for an alteration of visuo-spatial encoding. Second, in the saccade conditions, an additional perceptual deficit (an error of ~5° along the saccade direction) was observed in both tasks and mainly in conditions where extra-retinal signals are thought to be critically involved, revealing a constant underestimation by extra-retinal signals of the saccade size, despite preserved saccade accuracy. These findings highlight a crucial role of the PPC in saccadic remapping processes underlying perceptual visual constancy and provide empirical evidence for models such as Ziesche and Hamker's (2014).