On the role of V1 in avoiding obstacles

Constanze Hesse, Jutta Billino, Thomas Schenk (Corresponding Author)

Research output: Contribution to journalComment/debate

3 Citations (Scopus)
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Abstract

This commentary is the next in a chain of events. First, Striemer, Chapman, and Goodale (2009) argued, on the basis of a single case study testing a patient with hemianopia, that the primary visual cortex (V1) is not essential for successful obstacle avoidance behaviour. In the Cortex special issue on the “what and how-pathways”, we (Ross, Schenk, Billino, MacLeod, & Hesse, 2016) examined six patients suffering from hemianopia and came to the conclusion that obstacle avoidance during reaching crucially relies on input from V1. Subsequently, Striemer, Chapman, and Goodale (2017) have claimed that we misunderstood their original report. Clearly it is time that we get to the bottom of these misunderstandings and explore opportunities for finding common ground. In the introduction of our study (Ross et al., 2016) we presented several reasons for why Striemer et al.’s (2009) single-case study requires corroboration from similar findings in a group of patients with damage to their occipital cortex but intact subcortical visual pathways. Striemer et al (2017, section 2, 1st paragraph). accept that our failure to replicate their original findings in a group of six patients (Ross et al., 2016) might constitute a serious challenge to the validity of their conclusions - but only if our study can be considered to be a fair test of their claims. In the rest of their commentary, Striemer et al. (2017) provide three main reasons for why our study does not provide such a fair test in their opinion. Firstly, they question the evidence from our patient study on the basis that our patients fail to fulfil the relevant conditions required for testing our hypothesis. Secondly, they suggest that we designed our experiments in ways that ensured a failure to replicate their original findings. Lastly, they argue that we misrepresented their position and attacked a straw man. In this commentary, we aim to demonstrate that (1) the disqualified evidence from our study can be recovered, (2) the methods used in our experiment have more redeeming aspects than granted; and finally, we assess the theoretical implications of Striemer et al.’s commentary for their original findings as well as for our study (3).
Original languageEnglish
Pages (from-to)276-282
Number of pages7
JournalCortex
Volume98
Early online date15 Nov 2017
DOIs
Publication statusPublished - Jan 2018

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Hemianopsia
Avoidance Learning
Occipital Lobe
Visual Pathways
Visual Cortex

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On the role of V1 in avoiding obstacles. / Hesse, Constanze; Billino, Jutta; Schenk, Thomas (Corresponding Author).

In: Cortex, Vol. 98, 01.2018, p. 276-282.

Research output: Contribution to journalComment/debate

Hesse, Constanze ; Billino, Jutta ; Schenk, Thomas. / On the role of V1 in avoiding obstacles. In: Cortex. 2018 ; Vol. 98. pp. 276-282.
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abstract = "This commentary is the next in a chain of events. First, Striemer, Chapman, and Goodale (2009) argued, on the basis of a single case study testing a patient with hemianopia, that the primary visual cortex (V1) is not essential for successful obstacle avoidance behaviour. In the Cortex special issue on the “what and how-pathways”, we (Ross, Schenk, Billino, MacLeod, & Hesse, 2016) examined six patients suffering from hemianopia and came to the conclusion that obstacle avoidance during reaching crucially relies on input from V1. Subsequently, Striemer, Chapman, and Goodale (2017) have claimed that we misunderstood their original report. Clearly it is time that we get to the bottom of these misunderstandings and explore opportunities for finding common ground. In the introduction of our study (Ross et al., 2016) we presented several reasons for why Striemer et al.’s (2009) single-case study requires corroboration from similar findings in a group of patients with damage to their occipital cortex but intact subcortical visual pathways. Striemer et al (2017, section 2, 1st paragraph). accept that our failure to replicate their original findings in a group of six patients (Ross et al., 2016) might constitute a serious challenge to the validity of their conclusions - but only if our study can be considered to be a fair test of their claims. In the rest of their commentary, Striemer et al. (2017) provide three main reasons for why our study does not provide such a fair test in their opinion. Firstly, they question the evidence from our patient study on the basis that our patients fail to fulfil the relevant conditions required for testing our hypothesis. Secondly, they suggest that we designed our experiments in ways that ensured a failure to replicate their original findings. Lastly, they argue that we misrepresented their position and attacked a straw man. In this commentary, we aim to demonstrate that (1) the disqualified evidence from our study can be recovered, (2) the methods used in our experiment have more redeeming aspects than granted; and finally, we assess the theoretical implications of Striemer et al.’s commentary for their original findings as well as for our study (3).",
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