Relationship between Structural Changes and Functional Activity in Emotion Recognition Paradigm in Huntington’s Disease

I Dogan; CF Saß; S Mirzazade; A Kleiman; CJ Werner; F Binkofski; J Schiefer; JB Schulz; NJ Shah; K Reetz

doi:10.1055/s-0032-1301613

Klinische Neurophysiologie, Table of Contents

Relationship between Structural Changes and Functional Activity in Emotion Recognition Paradigm in Huntington’s Disease

I Dogan ¹, CF Saß ², S Mirzazade ³, A Kleiman ³, CJ Werner ¹, F Binkofski ⁴, J Schiefer ³, JB Schulz ³, NJ Shah ⁵, K Reetz ¹

¹Neurologische Klinik, Universitätsklinikum RWTH Aachen, Aachen
²Klinik und Poliklinik für Neurologie, Universitätsklinikum Münster, Münster
³Klinik für Neurologie, RWTH Aachen, Universitätsklinik, Aachen
⁴Sektion für klinische Kognitionsforschung an der Neurologischen Klinik, Aachen
⁵Institut für Neurowissenschaften und Medizin 4, Forschungszentrum Jülich, Jülich

Abstract

Objective: The neural correlates of emotion processing in Huntington’s Disease (HD) have only been investigated in premanifest HD by means of functional MRI (fMRI) focusing on disgust processing¹. Using an fMRI paradigm with more emotional valences, we aimed to investigate the functional correlates of emotion perception in manifest HD, while taking account of structural atrophy. Methods: Event-related fMRI and anatomical images were acquired with a 3T Siemens MR Scanner in 14 HD patients (stages² I-III) and 14 age- and gender-matched healthy controls. An emotion recognition task displayed video-sequences of trained actors performing one of six facial expressions (sadness, happiness, disgust, fear, anger, neutral). Structural changes between patients and controls were assessed by means of voxel-based morphometry. Differences in BOLD-response were analyzed for emotion-related regions of interest (ROI) with and without including grey matter values of respective ROIs as covariates (SPM8). Results: HD patients performed significantly worse than controls in recognizing negative emotions. During the perception of sadness, the amygdala, parahippocampal gyrus, putamen and posterior cingulate showed increased activity in patients compared to controls. The insula was more strongly recruited during disgust and sadness. Less activity was observed in parahippocampal regions for happiness, in orbitofrontal and lateral prefrontal cortices for all emotions. Taking account of grey matter changes, hyperactivity in most regions decreased, while hypoactivity remained constant and was further observed in the amygdala and parahippocampal gyrus for fear. Conclusion: Increased emotion-related activity seems to represent primarily dysfunctions due to degeneration processes in limbic regions³, which may along with frontal hypoactivity underlie emotion processing deficits in HD. Our results emphasize the need of considering structural changes in the investigation of functional activity in HD.

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