Letter to the Editor | Published:

Functional neuroimaging in Prader–Willi syndrome

International Journal of Obesity volume 31, pages 390391 (2007) | Download Citation

We welcome DelParigi, Chen and Reiman's comments about our paper,1 suggesting caution in the interpretation of our findings. Indeed, we have already discussed the points relating to the control group and medications in the paper itself. Although differences in cerebral blood flow across separate imaging sessions can contribute to the effects observed, it is not clear how such nonspecific differences could have produced the particular pattern of activation found. Importantly, this study design was adopted specifically to avoid order effects, which can produce far more serious confounds in imaging studies.2 DelParigi and colleagues have themselves noted (e.g. Tataranni et al.3) that within-session designs do not allow one to exclude the possibility that the data could be partly attributable to an interaction between scan order and fasting state. In future studies, both scan order and between-session effects should be accounted for in the statistical model applied and functional magnetic resonance imaging is particularly promising in this respect.

The lack of activation in satiety-related areas following food intake in those with Prader–Willi syndrome (PWS) is unlikely to be owing to a limitation in power, given that more participants were included in the PWS group than in the control study (n=12) and, more importantly, that a region of interest analysis was employed, based on previous studies. Whereas a corrected whole brain analysis was reported, the peaks of activation associated with satiety, both by Hinton et al.4 and from Tataranni et al.,3 were also investigated in the PWS data. This investigation found no activation in any of these regions, even when a less conservative threshold was chosen. With this in mind, we believe that our interpretation of the imaging data is justified in the light of recent behavioural (e.g. Lindgren et al.5) and functional imaging research6 that has suggested that the process of satiety is impaired in PWS rather than hunger. This is one of the first published studies to use neuroimaging to study hunger and satiety in PWS and we welcome further research, which will aid the interpretation of these findings through replication, and expand our understanding of this disorder using different paradigms.

References

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    , , , , , , . Neural representations of hunger and satiety in Prader–Willi syndrome. Int J Obes 2006; 30: 313–321.

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    , , , , . Scan order effects in PET activation studies are caused by motion artefact. Neuroimage 1999; 9: S56.

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    , , , , , et al. Neuroanatomical correlates of hunger and satiation in humans using positron emission tomography. Proc Natl Acad Sci USA 1999; 96: 4569–4574.

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    , , , , , . Neural contributions to the motivational control of appetite in humans. Eur J Neurosci 2004; 20: 1411–1418.

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    , , , , , . Eating behavior in Prader–Willi syndrome, normal weight, and obese control groups. J Pediatr 2000; 137: 50–55.

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    , , , , , . Satiety dysfunction in Prader–Willi syndrome demonstrated by fMRI. J Neurol Neurosurg Psychiatry 2005; 76: 260–262.

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Affiliations

  1. School of Psychology, Cardiff University, Cardiff, UK

    • E C Hinton
  2. Section of Developmental Psychiatry, University of Cambridge, Cambridge, UK

    • A J Holland
  3. MRC-Cognition and Brain Sciences Unit, Cambridge, UK

    • A M Owen

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Correspondence to E C Hinton.

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DOI

https://doi.org/10.1038/sj.ijo.0803412

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