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@ARTICLE{Poeppl:865238,
      author       = {Poeppl, Timm B. and Mokros, Andreas and Bzdok, Danilo and
                      Eickhoff, Simon B.},
      title        = {{W}hat matters and what is possible in neuroimaging
                      meta-analyses (of psychopathy)},
      journal      = {Molecular psychiatry},
      volume       = {25},
      issn         = {1476-5578},
      address      = {London},
      publisher    = {Macmillan},
      reportid     = {FZJ-2019-04769},
      pages        = {3125–3126},
      year         = {2019},
      abstract     = {We thank Robert Latzmann, Christopher Patrick, and Scott
                      Lilienfeld for their interest in and thoughtful comment [1]
                      on our paper [2]. The commentary provides the opportunity
                      for clarification, to prevent possible misunderstanding
                      regarding the potential of neuroimaging meta-analyses of
                      (not only) psychopathy with this response.First, the authors
                      of the comment briefly mention “a failure to distinguish
                      among alternative measures of a target construct (i.e.,
                      psychopathy) and collapsing across non-interchangeable
                      dependent measures (i.e., MRI-brain activations from
                      different tasks)”, which they regard as limitations. We
                      concur that our meta-analyses did not assess putative
                      differences between measures that literally purport to
                      capture the same entity (so-called psychopathy scales) or
                      between various tasks performed by subjects with the same
                      disorder (i.e., psychopathy). That is, our intention was not
                      to isolate task-related differences in neural activity
                      response in psychopathy nor to isolate neural differences
                      between competing psychopathy concepts. Rather, the
                      objective of our meta-analytic study was to identify brain
                      regions showing aberrant activity associated with
                      psychopathy across the whole neuroimaging literature.
                      Indeed, it also seems interesting to investigate if
                      above-mentioned differences can in fact be spotted.
                      Unfortunately, there are simply not enough experiments
                      available to disentangle such subtle effects in valid
                      subanalyses presently (cf., work by Eickhoff et al. [3]).
                      For instance, only 14 of the 24 experiments using an
                      alternative measure of psychopathy (the Psychopathic
                      Personality Inventory [4]) found any (i.e., either positive
                      or negative) association of brain activity with the scale at
                      all. From these 14 experiments, seven showed a positive and
                      seven a negative relationship. Data underlying the
                      experiments were collected in only four independent studies
                      (i.e., samples). However, at least about 20 independent
                      experiments would be needed for a valid activation
                      likelihood estimation meta-analysis [3].The main criticism
                      raised by Latzman and colleagues, however, is the
                      “treatment of this condition as a unitary construct,
                      largely neglecting its heterogeneity”. To illustrate the
                      relevance to neuroimaging, they quote three individual
                      studies in which diverging activity corresponding to
                      psychopathy subdimensions was found within the same brain
                      regions.In fact, there is a heated debate whether
                      psychopathy is of a multidimensional or a unidimensional
                      nature. Although there are arguments for its
                      multidimensionality, there is also strong evidence against.
                      The Psychopathy Checklist-Revised (PCL-R) as well as its
                      derivative, the Psychopathy Checklist: Screening Version
                      (PCL:SV), are arguably the most important psychometric
                      instruments for assessing psychopathy. Most of the studies
                      included in our meta-analyses relied on the PCL (113 out of
                      155 experiments). Both the PCL-R [5] and the PCL:SV [6] have
                      been shown to be commensurate with a bifactor model of
                      psychopathy that includes a general (g) factor [6]. One of
                      the first applications of such a model to the PCL-R
                      instruments was published by Patrick et al. [5]. According
                      to these models [5, 6], the items of the PCL-R/SV
                      instruments load onto a common factor, with specific
                      portions of variance relegated to nuisance factors.
                      Moreover, taxometric research [7] indicates that the
                      disorder as such (i.e., psychopathy) is a dimensional trait,
                      not a taxon. From this point of view, it may even be
                      regarded as implausible to hypothesize that there should be
                      subtraits of the disorder that do not add up to a common
                      core and that have unique correlates in the brain. However,
                      neuroimaging meta-analyses (of psychopathy subscales) could
                      indeed serve as a useful tool to test if proposed subtraits
                      are neurobiologically founded. Also for this purpose, there
                      are unfortunately not enough experiments available from the
                      literature.Irrespective of the dimensionality discussion, it
                      has to be noted that the very same regions (where aforesaid
                      studies located diverging activity) emerged in our
                      meta-analyses. This militates against the concern that
                      subdivisions of psychopathy scales would lead to divergent
                      psychopathic subgroups or distinct traits which, in turn,
                      could cancel each other out with respect to neural
                      correlates. Apart from that, this issue does not apply to
                      the analyses in our paper, which was looking for convergence
                      in brain associations with psychopathy (scales).
                      Interestingly, there was indeed strong concordance in
                      several regions. Be it that the commentators’ argument of
                      subscales neutralizing each other is valid, then why have
                      these scales converging neural correlates?Moreover, our
                      findings provide robust evidence for neural alterations
                      associated with psychopathy and hence validate this
                      psychological construct using rigorous neurobiological
                      mapping. This result seems even more intriguing as similar
                      attempts with respect to other disorders, such as
                      depression, did not succeed [8]. In this context, we want to
                      mention that—contrary to the presentation by Latzman and
                      colleagues—we did not claim “that certain neural
                      activation patterns are “pathognomonic” of
                      psychopathy”. Rather, we used a general approach, which
                      avoids a priori assumptions about (putative differences
                      between) psychological constructs and their relationship
                      among one another as well as to neurobiology, to
                      meta-analyze brain activation changes associated with
                      psychopathy. In a second step, we characterized the ensuing
                      regions functionally using independent data from healthy
                      subjects. These analyses indicated that brain regions
                      showing aberrant activity in psychopaths fulfill mental
                      functions in healthy subjects which, in turn, happen to be
                      disturbed in psychopaths. We thus stated that these mental
                      functions correspond with the deviant behavioral patterns
                      that are characteristic and pathognomonic of psychopathy.
                      This reverse approach hence validated that the neural
                      aberrances were associated with (the overarching construct
                      of) psychopathy (and not with epiphenomena).Although we
                      provided robust evidence for a general neurobiological
                      foundation of psychopathy, we agree that further
                      investigations into particular aspects of this disorder are
                      desirable. Therefore, we will wait together with Latzman and
                      colleagues for “finer-grained meta-analyses”—for
                      instance on psychopathy subdimensions. Many more individual
                      studies on this topic, however, are necessary to constitute
                      a solid basis for such endeavors. Until then, our
                      consolidating results, establishing the robustness of a
                      neural signature underlying common conceptualization of
                      psychopathy, can provide guidance for future studies on the
                      potential heterogeneity in psychopathic traits, once
                      sufficiently large consortium datasets will be available in
                      the future},
      cin          = {INM-7 / JARA-BRAIN},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-7-20090406 / $I:(DE-82)080010_20140620$},
      pnm          = {574 - Theory, modelling and simulation (POF3-574)},
      pid          = {G:(DE-HGF)POF3-574},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {31481757},
      UT           = {WOS:000608499700006},
      doi          = {10.1038/s41380-019-0515-0},
      url          = {https://juser.fz-juelich.de/record/865238},
}