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Preserved prism adaptation in bilateral optic ataxia: strategic versus adaptive reaction to prisms

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Abstract

To date the anatomical substrate(s) of prism adaptation remain(s) particularly debated, with two main candidates emerging from the literature: the posterior parietal cortex (PPC) and the cerebellum. The functional processes involved in the acquisition of the adaptive aftereffects also remain largely unknown. The main result shown here is that a patient with a bilateral optic ataxia can adapt to an optical deviation, which allows us to make a step forward on these two issues. First, it demonstrates that the corresponding part of the PPC is not a necessary substrate for prism adaptation. Second, since this patient exhibits deficit for fast visuo-motor guidance, it provides direct evidence for a dissociation between on-line visuo-motor control and visuo-motor plasticity. Since the intermanual transfer rate of adaptation is larger in this patient than in control subjects, the PPC may still have an influence on adaptation under normal conditions. We propose a model of the relative contribution of the PPC and the cerebellum during prism exposure, associating these two structures with the two interacting behavioural components of prism adaptation described by previous psychophysical experiments: the strategic component would be linked to the PPC and the adaptive component to the cerebellum. In this model, the strategic component enters in conflict with the development and the generalisation of the adaptive aftereffects. This idea is compatible with the fact that a lesion of the PPC increases the transfer rate and the generalisation of the adaptation, as is also observed in unilateral neglect.

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Notes

  1. Clower et al. (1996) identified their activation site as area PEG, which is along the intraparietal sulcus in the angular gyrus (upper part of Brodmann area 39, see Fig. 1) according to the classification of Eidelberg and Galaburda (1984) and whose lesion leads to optic ataxia referring to the lesion superimposition work of Perenin and Vighetto (1988). However, re-plotting of the Talairach coordinates of the Clower et al. (1996) study led to rather locate the activation within Brodmann area 40 (supramarginal gyrus), which does not pertain to the focus of lesion leading to optic ataxia (Perenin and Vighetto 1988). We wish to thank an anonymous referee, Isabelle Faillenot and Christine Baleydier for raising and discussing this issue.

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Acknowledgements

The authors wish to thank patient I.G. for her kind participation and Isabelle Faillenot for her help in the neuroanatomical reading of the MRI scans of the patient. This work was supported by INSERM (Progrès) and ACI plasticité.

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Correspondence to Y. Rossetti.

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Pisella, L., Michel, C., Gréa, H. et al. Preserved prism adaptation in bilateral optic ataxia: strategic versus adaptive reaction to prisms. Exp Brain Res 156, 399–408 (2004). https://doi.org/10.1007/s00221-003-1746-4

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