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A Structural MRI Study of Cortical Thickness in Depersonalisation Disorder [Oral Presentation]

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Original languageEnglish
JournalPsychiatry Research. Neuroimaging
Published4 Jul 2013

King's Authors


AIMS AND HYPOTHESES The neurobiological basis of depersonalisation disorder (DPD) has previously been examined using positron emission tomography (PET), functional magnetic resonance imaging (fMRI) and physiological measures. This study presents the first investigation of cortical thickness in DPD using structural MRI. BACKGROUND DPD is a psychiatric disorder characterized by emotional numbing and sensations of derealisation or unreality. Functional imaging has suggested dysfunction in the temporo-parietal regions, possibly underlying physical detachment, and the inferior frontal regions, perhaps linked to emotional blunting. METHODS Twenty-one patients with a diagnosis of DPD (mean age = 35.75, 20% females, 50% unmedicated) and 21 healthy controls (mean age = 27.20, 57.1% females) were scanned. Images were acquired on a GE 1.5 T HDx system and processed using FreeSurfer software to obtain measures of cortical thickness. Data were analysed with the SurfStat toolbox for MatLab and covaried for age and gender. RESULTS One participant from the patient group was excluded due to cortical atrophy. The predominant areas which were larger in controls than in patients at p < .01 were found in the right superior frontal gyrus (BA 10; t = -3.337), left inferior frontal gyrus (BA 47; t = -3.608), left inferior temporal gyrus (BA 20; t = -3.048), right inferior/middle temporal gyrus (BA 20/21; t = -3.279), and right cingulate gyrus (BA 24; t = - 3.647). The post-central gyrus was larger in patients than in controls (BA 3; t = 3.603). CONCLUSIONS The present findings overlap with discoveries of increased activation in patients over controls for frontal, temporal, parietal and cingulate, but not limbic areas among relevant fMRI and PET studies into DPD and depersonalisation-like experiences in post-traumatic stress disorder. This suggests some neural underpinning or vulnerability for the syndrome. We take this to support a dissociation- and emotional-numbing-based explanation of DPD, though a replication of our results is warranted.

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