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Jeromy Anglim
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It is not widely thought that impaired function or destruction of the fusiform is sufficient to produce prosoganosia. It is currently widely held that face processing involves a network of regions in the occipital and temporal lobes (e.g., the occipital face area, posterior superior temporal sulus, anterior superior temporal sulus, anterior collateral sulcus). For example, Bruno Rossion reports a patient with prosopagnoisa who has widespread damage to bilateral occipital and temporal brain regions but with a spared right FFA. Moreover, work by Marlene Behrmann has shown that people with developmental prosopagnosia have disrupted connections between the posterior temporal lobes (ie near the FFA) and the anterior temporal lobes. This is significant because there is growing evidence that there may be face selective regions in the anterior temporal lobes and that they are more directly involved in face recognition. Moreover there is some evidence that this anterior temporal region modulates the activity in the FFA (Nestor, Plaut, Behrmann, 2011 PNAS). So it might very well be that the FFA does show decreased activity in a face recognition task, but this might be due to impaired feedback to this region. On this view, lower activity in FFA is the effect of prosopagnosia not the cause, so making comparisons on levels of activity within one region might not be as meaningful as you think.

References

  • Nestor, A., Plaut, D.C., & Behrmann, M. (2011). Unraveling the distributed neural code of facial identity through spatiotemporal pattern analysis. Proceedings of the National Academy of Sciences, 108, 9998. LINK

It is not widely thought that impaired function or destruction of the fusiform is sufficient to produce prosoganosia. It is currently widely held that face processing involves a network of regions in the occipital and temporal lobes (e.g., the occipital face area, posterior superior temporal sulus, anterior superior temporal sulus, anterior collateral sulcus). For example, Bruno Rossion reports a patient with prosopagnoisa who has widespread damage to bilateral occipital and temporal brain regions but with a spared right FFA. Moreover, work by Marlene Behrmann has shown that people with developmental prosopagnosia have disrupted connections between the posterior temporal lobes (ie near the FFA) and the anterior temporal lobes. This is significant because there is growing evidence that there may be face selective regions in the anterior temporal lobes and that they are more directly involved in face recognition. Moreover there is some evidence that this anterior temporal region modulates the activity in the FFA (Nestor, Plaut, Behrmann, 2011 PNAS). So it might very well be that the FFA does show decreased activity in a face recognition task, but this might be due to impaired feedback to this region. On this view, lower activity in FFA is the effect of prosopagnosia not the cause, so making comparisons on levels of activity within one region might not be as meaningful as you think.

It is not widely thought that impaired function or destruction of the fusiform is sufficient to produce prosoganosia. It is currently widely held that face processing involves a network of regions in the occipital and temporal lobes (e.g., the occipital face area, posterior superior temporal sulus, anterior superior temporal sulus, anterior collateral sulcus). For example, Bruno Rossion reports a patient with prosopagnoisa who has widespread damage to bilateral occipital and temporal brain regions but with a spared right FFA. Moreover, work by Marlene Behrmann has shown that people with developmental prosopagnosia have disrupted connections between the posterior temporal lobes (ie near the FFA) and the anterior temporal lobes. This is significant because there is growing evidence that there may be face selective regions in the anterior temporal lobes and that they are more directly involved in face recognition. Moreover there is some evidence that this anterior temporal region modulates the activity in the FFA (Nestor, Plaut, Behrmann, 2011 PNAS). So it might very well be that the FFA does show decreased activity in a face recognition task, but this might be due to impaired feedback to this region. On this view, lower activity in FFA is the effect of prosopagnosia not the cause, so making comparisons on levels of activity within one region might not be as meaningful as you think.

References

  • Nestor, A., Plaut, D.C., & Behrmann, M. (2011). Unraveling the distributed neural code of facial identity through spatiotemporal pattern analysis. Proceedings of the National Academy of Sciences, 108, 9998. LINK
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Bronson
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It is not widely thought that impaired function or destruction of the fusiform is sufficient to produce prosoganosia. It is currently widely held that face processing involves a network of regions in the occipital and temporal lobes (e.g., the occipital face area, posterior superior temporal sulus, anterior superior temporal sulus, anterior collateral sulcus). For example, Bruno Rossion reports a patient with prosopagnoisa who has widespread damage to bilateral occipital and temporal brain regions but with a spared right FFA. Moreover, work by Marlene Behrmann has shown that people with developmental prosopagnosia have disrupted connections between the posterior temporal lobes (ie near the FFA) and the anterior temporal lobes. This is significant because there is growing evidence that there may be face selective regions in the anterior temporal lobes and that they are more directly involved in face recognition. Moreover there is some evidence that this anterior temporal region modulates the activity in the FFA (Nestor, Plaut, Behrmann, 2011 PNAS). So it might very well be that the FFA does show decreased activity in a face recognition task, but this might be due to impaired feedback to this region. On this view, lower activity in FFA is the effect of prosopagnosia not the cause, so making comparisons on levels of activity within one region might not be as meaningful as you think.