psychosis, while Angelman syndrome, a disorder of paternal overimprinting, should have the opposite. However, autism rates are substantially above those of the general population in PWS and similar to or below it in AS, while non-affective psychosis appears to occur at rates comparable to the general population in PWS. Indeed, it has been suggested that maternally imprinted cases of Prader-Willi syndrome have an elevated autism prevalence compared to all etiologies of the disorder, the exact opposite of the imprinted brain hypothesis. Despite being contradicted by other research, Crespi nonetheless claims that imprinting disorders as a rule fit his hypothesis. While Crespi and Badcock have claimed neuroimaging studies lend support to the imprinted brain hypothesis, other neuroimaging studies have found contradictory results. Several neurological findings are common to both autism and schizophrenia. The brain regions that distinguish schizophrenia from autism are also those at the centre of the controversy regarding neuroleptic medication, reducing the degree to which they can be used to distinguish the disorders; autistic subjects taking psychotropic medication share some of the altered neuroconnectivity that Crespi and Badcock ascribe to schizophrenia. The imprinting brain hypothesis has also been criticized for inaccurately presenting the schizophrenia spectrum and making claims about schizophrenic disorders that are at odds with their clinical profiles. The claim that milder schizophrenia-spectrum disorders are associated with intensified empathy and strong theory of mind is imperiled by research showing the opposite. The specific pattern of empathy deficits also appears to be consistent between autism and schizophrenia, with both demonstrating impaired cognitive empathy and relatively preserved affective empathy. Crespi and Badcock's attempt to conceptualize schizophrenia as a relatively homogenous disorder that slots neatly into one end of a spectrum has been criticized due to the clinical heterogeneity in even individual cases of schizophrenia, due to the different presentation and course of positive and negative symptoms. Crespi and Badcock have also been criticized for avoiding falsifiable claims, in addition to the falsification of those claims they do make. Responses to Crespi's major publications on the topic have noted the broad range of evidence it attempts to 'tie up' and explain, without considering the consequences such a sweeping conjecture would have for known traits and comorbidities that contradict the claims, and for avoiding the matter of what would constitute a falsification or disconfirmation. One of the most significant components of the hypothesis is that it predicts autism should be associated with