The impairment of emotion recognition in Huntington’s disease extends to positive emotions

Robotham, Laura; Sauter, Disa; Bachoud‐Lévi, Anne‐Catherine; Trinkler, Iris

doi:10.1016/j.cortex.2011.02.014

Cited by 39 publications

(26 citation statements)

References 24 publications

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“…That is, there was nothing specific about the emotional content of the faces that differentiated the groups. This interpretation is consistent with a recent study assessing emotional response to auditory sounds in HD participants (Robotham et al, 2011), which reported performance decrements in HD across all emotion types, including positive valence sounds. However, given the use of a different modality (auditory as opposed to visual), and the lack of comparison between emotional and non-emotional sounds, it is difficult to translate the relevance to emotional face processing.…”

Section: Discussionsupporting

confidence: 92%

Emotion perception and electrophysiological correlates in Huntington’s disease

Croft¹,

McKernan²,

Gray³

et al. 2014

Clinical Neurophysiology

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Objective This study aimed to characterise, emotion perception deficits in symptomatic Huntington's disease (HD) via the use of event-related potentials (ERPs). Methods ERP data were recorded during a computerised facial expression task in 11 HD participants and 11 matched controls. Expression (scrambled, neutral, happy, angry, disgust) classification accuracy and intensity were assessed. Relationships between ERP indices and clinical disease characteristics were also examined. Results Accuracy was significantly lower for HD relative to controls, due to reduced performance for neutral, angry and disgust (but not happy) faces. Intensity ratings did not differ between groups. HD participants displayed significantly reduced visual processing amplitudes extending across pre-face (P100) and face-specific (N170) processing periods, whereas subsequent emotion processing amplitudes (N250) were similar across groups. Face-specific and emotionspecific derivations of the N170 and N250 ('neutral minus scrambled' and 'each emotion minus neutral', respectively) did not differ between groups. Conclusions Our data suggest that the facial emotion recognition performance deficits in HD are primarily related to neural degeneration underlying 'generalised' visual processing, rather than face or emotional specific processing. Significance ERPs are a useful tool to separate functionally discreet impairments in HD, and provide an important avenue for biomarker application that could more-selectively track disease progression.

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Section: Discussionsupporting

confidence: 92%

Emotion perception and electrophysiological correlates in Huntington’s disease

Croft¹,

McKernan²,

Gray³

et al. 2014

Clinical Neurophysiology

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show abstract

“…These findings suggest that functional MRI indices may be more sensitive than behavioural indices in tracking altered emotion processing in Huntington's disease, and raise the further possibility that the use of alternative, more finely differentiated stimuli might however reveal hitherto largely undetected deficits in processing positive-valence facial expressions. The detection of impaired recognition of vocal expressions of positive emotions in Huntington's disease in one previous study (Robotham et al , 2011) supports this assertion.…”

Section: Discussionsupporting

confidence: 68%

Altered brain mechanisms of emotion processing in pre-manifest Huntington's disease

Novak

Warren

Henley

et al. 2012

Brain

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Huntington's disease is an inherited neurodegenerative disease that causes motor, cognitive and psychiatric impairment, including an early decline in ability to recognize emotional states in others. The pathophysiology underlying the earliest manifestations of the disease is not fully understood; the objective of our study was to clarify this. We used functional magnetic resonance imaging to investigate changes in brain mechanisms of emotion recognition in pre-manifest carriers of the abnormal Huntington's disease gene (subjects with pre-manifest Huntington's disease): 16 subjects with pre-manifest Huntington's disease and 14 control subjects underwent 1.5 tesla magnetic resonance scanning while viewing pictures of facial expressions from the Ekman and Friesen series. Disgust, anger and happiness were chosen as emotions of interest. Disgust is the emotion in which recognition deficits have most commonly been detected in Huntington's disease; anger is the emotion in which impaired recognition was detected in the largest behavioural study of emotion recognition in pre-manifest Huntington's disease to date; and happiness is a positive emotion to contrast with disgust and anger. Ekman facial expressions were also used to quantify emotion recognition accuracy outside the scanner and structural magnetic resonance imaging with voxel-based morphometry was used to assess the relationship between emotion recognition accuracy and regional grey matter volume. Emotion processing in pre-manifest Huntington's disease was associated with reduced neural activity for all three emotions in partially separable functional networks. Furthermore, the Huntington's disease-associated modulation of disgust and happiness processing was negatively correlated with genetic markers of pre-manifest disease progression in distributed, largely extrastriatal networks. The modulated disgust network included insulae, cingulate cortices, pre- and postcentral gyri, precunei, cunei, bilateral putamena, right pallidum, right thalamus, cerebellum, middle frontal, middle occipital, right superior and left inferior temporal gyri, and left superior parietal lobule. The modulated happiness network included postcentral gyri, left caudate, right cingulate cortex, right superior and inferior parietal lobules, and right superior frontal, middle temporal, middle occipital and precentral gyri. These effects were not driven merely by striatal dysfunction. We did not find equivalent associations between brain structure and emotion recognition, and the pre-manifest Huntington's disease cohort did not have a behavioural deficit in out-of-scanner emotion recognition relative to controls. In addition, we found increased neural activity in the pre-manifest subjects in response to all three emotions in frontal regions, predominantly in the middle frontal gyri. Overall, these findings suggest that pathophysiological effects of Huntington's disease may precede the development of overt clinical symptoms and detectable cerebral atrophy.

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“…svPPA patients also have impaired comprehension of sarcasm based specifically on (primarily vocal) paralinguistic cues [24]. Additionally, HD patients show poor recognition of negative [12] as well as positive [25] vocal emotional signals. In contrast, AD patients’ ability to read emotions in both voice prosody and music is preserved [26].…”

Section: Perception Of Social and Emotional Signalsmentioning

confidence: 99%

Personality and social cognition in neurodegenerative disease

Shany‐Ur

Rankin

2011

Current Opinion in Neurology

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Purpose of review Neurodegenerative diseases often cause focal damage to brain structures mediating social cognition and personality, resulting in altered interpersonal communication and behavior. We review recent research describing this phenomenon in various aspects of social cognition. Recent findings Corresponding to their pervasive social-emotional deficits, patients with frontotemporal dementia perform poorly on lab-based tasks including recognizing emotions, attending to salient information that guides social behavior, representing social knowledge, comprehending others’ mental states, and maintaining insight to their own difficulties. Together with poor executive and regulation mechanisms, these social cognition deficits ultimately impact behavior. Patients with logopenic and nonfluent primary progressive aphasia have some deficits recognizing emotional prosody, while those with the semantic variant show more widespread deficits in social comprehension. While Alzheimer’s disease patients perform poorly on some social cognition tasks, this typically reflects general cognitive impairment, and their real-life social functioning is less affected than in diseases targeting frontotemporal structures. Studies in motor diseases such as Parkinson’s suggest some degradation of emotion recognition and social comprehension which should be investigated further. Summary We summarize recent findings concerning perception and evaluation of socioemotional information, social knowledge storage and access, advanced information processing mechanisms, and behavioral response selection and regulation across various neurodegenerative diseases.

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The impairment of emotion recognition in Huntington’s disease extends to positive emotions

Cited by 39 publications

References 24 publications

Emotion perception and electrophysiological correlates in Huntington’s disease

Emotion perception and electrophysiological correlates in Huntington’s disease

Altered brain mechanisms of emotion processing in pre-manifest Huntington's disease

Personality and social cognition in neurodegenerative disease

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