Sona Patel

Sensory contribution to vocal emotion deficit in Parkinson's disease after subthalamic stimulation

Subthalamic nucleus (STN) deep brain stimulation in Parkinsons disease induces modifications in the recognition of emotion from voices (or emotional prosody). Nevertheless, the underlying mechanisms are still only poorly understood, and the role of acoustic features in these deficits has yet to be elucidated. Our aim was to identify the influence of acoustic features on changes in emotional prosody recognition following STN stimulation in Parkinsons disease. To this end, we analysed the performances of patients on vocal emotion recognition in pre-versus post-operative groups, as well as of matched controls, entering the acoustic features of the stimuli into our statistical models. Analyses revealed that the post-operative biased ratings on the Fear scale when patients listened to happy stimuli were correlated with loudness, while the biased ratings on the Sadness scale when they listened to happiness were correlated with fundamental frequency (F0). Furthermore, disturbed ratings on the Happiness scale when the post-operative patients listened to sadness were found to be correlated with F0. These results suggest that inadequate use of acoustic features following subthalamic stimulation has a significant impact on emotional prosody recognition in patients with Parkinsons disease, affecting the extraction and integration of acoustic cues during emotion perception.

Talking in Fury: The Cortico-Subcortical Network Underlying Angry Vocalizations

Although the neural basis for the perception of vocal emotions has been described extensively, the neural basis for the expression of vocal emotions is almost unknown. Here, we asked participants both to repeat and to express high-arousing angry vocalizations to command (i.e., evoked expressions). First, repeated expressions elicited activity in the left middle superior temporal gyrus (STG), pointing to a short auditory memory trace for the repetition of vocal expressions. Evoked expressions activated the left hippocampus, suggesting the retrieval of long-term stored scripts. Secondly, angry compared with neutral expressions elicited activity in the inferior frontal cortex IFC and the dorsal basal ganglia (BG), specifically during evoked expressions. Angry expressions also activated the amygdala and anterior cingulate cortex (ACC), and the latter correlated with pupil size as an indicator of bodily arousal during emotional output behavior. Though uncorrelated, both ACC activity and pupil diameter were also increased during repetition trials indicating increased control demands during the more constraint production type of precisely repeating prosodic intonations. Finally, different acoustic measures of angry expressions were associated with activity in the left STG, bilateral inferior frontal gyrus, and dorsal BG.

Right Hemisphere Regions Critical for Expression of Emotion Through Prosody

Impaired expression of emotion through pitch, loudness, rate, and rhythm of speech (affective prosody) is common and disabling after right hemisphere (RH) stroke. These deficits impede all social interactions. Previous studies have identified cortical areas associated with impairments of expression, recognition, or repetition of affective prosody, but have not identified critical white matter tracts. We hypothesized that: (1) differences across patients in specific acoustic features correlate with listener judgment of affective prosody and (2) these differences are associated with infarcts of specific RH gray and white matter regions. To test these hypotheses, 41 acute ischemic RH stroke patients had MRI diffusion weighted imaging and described a picture. Affective prosody of picture descriptions was rated by 21 healthy volunteers. We identified percent damage (lesion load) to each of seven regions of interest previously associated with expression of affective prosody and two control areas that have been associated with recognition but not expression of prosody. We identified acoustic features that correlated with listener ratings of prosody (hereafter “prosody acoustic measures”) with Spearman correlations and linear regression. We then identified demographic variables and brain regions where lesion load independently predicted the lowest quartile of each of the “prosody acoustic measures” using logistic regression. We found that listener ratings of prosody positively correlated with four acoustic measures. Furthermore, the lowest quartile of each of these four “prosody acoustic measures” was predicted by sex, age, lesion volume, and percent damage to the seven regions of interest. Lesion load in pars opercularis, supramarginal gyrus, or associated white matter tracts (and not control regions) predicted lowest quartile of the four “prosody acoustic measures” in logistic regression. Results indicate that listener perception of reduced affective prosody after RH stroke is due to reduction in specific acoustic features caused by infarct in right pars opercularis or supramarginal gyrus, or associated white matter tracts.

Bioelectrical brain effects of one's own voice identification in pitch of voice auditory feedback

ABSTRACT Control of voice fundamental frequency (F0) relies in part on comparison of the intended F0 level and auditory feedback. This comparison impacts “sense of agency”, or SoA, commonly defined as being the agent of ones own actions and plays a key role for self‐awareness and social interactions. SoA is aberrant in several psychiatric disorders. Knowledge about brain activity reflecting SoA can be used in clinical practice for these disorders. It was shown that perception of voice feedback as ones own voice, reflecting the recognition of SoA, alters auditory sensory processing. Using a voice perturbation paradigm we contrasted vocal and bioelectrical brain responses to auditory stimuli that differed in magnitude: 100 and 400 cents. Results suggest the different magnitudes were perceived as a pitch error in self‐vocalization (100 cents) or as a pitch shift generated externally (400 cents). Vocalizations and neural responses to changes in pitch of self‐vocalization were defined as those made to small magnitude pitch‐shifts (100 cents) and which did not show differential neural responses to upward versus downward changes in voice pitch auditory feedback. Vocal responses to large magnitude pitch shifts (400 cents) were smaller than those made to small pitch shifts, and neural responses differed according to upwards versus downward changes in pitch. Our results suggest that the presence of SoA for self‐produced sounds may modify bioelectrical brain responses reflecting differences in auditory processing of the direction of a pitch shift. We suggest that this modification of bioelectrical response can be used as a biological index of SoA. Possible neuronal mechanisms of this modification of bioelectrical brain response are discussed. HIGHLIGHTSSense of agency.Voice control mechanisms.Voice perturbation paradigm.Event Related Potentials.Auditory processing of pitch change direction.

Event related potentials study of aberrations in voice control mechanisms in adults with attention deficit hyperactivity disorder

OBJECTIVE The present study was designed to test for neural signs of impulsivity related to voice motor control in young adults with ADHD using EEG recordings in a voice pitch perturbation paradigm. METHODS Two age-matched groups of young adults were presented with brief pitch shifts of auditory feedback during vocalization. Compensatory behavioral and corresponding bioelectrical brain responses were elicited by the pitch-shifted voice feedback. RESULTS The analysis of bioelectrical responses showed that the ADHD group had shorter peak latency and onset time of motor-related bioelectrical brain responses as compared to the controls. CONCLUSIONS These results were interpreted to suggest differences in executive functions between ADHD and control participants. SIGNIFICANCE We hypothesize that more rapid motor-related bioelectrical responses found in the present study may be a manifestation of impulsiveness in adults with ADHD at the involuntary level of voice control.

Effects of vocal training on involuntary responses to pitch-shifted voice auditory feedback

Control of voice fundamental frequency (F0) relies on the interaction between various forms of sensory feedback and neural motor control mechanisms. Previous research has shown that unexpected changes in pitch in the auditory feedback result in two components of the compensatory vocal responses, an early involuntary response and a later voluntary response. In an attempt to determine whether these responses can be modified due to training, we examined involuntary vocal responses to unpredictable perturbations in pitch auditory feedback following a vocal training task. Ten subjects were trained over a five-day period to change their voice F0 in the opposite direction to the pitch-shifted feedback (±100 cents, 1000ms) and 10 in the same direction as the feedback. Results showed that the involuntary response was not affected by training. These results have implications on our understanding of voice control.