Autonomic System

Neurobehavioral mechanisms in tic suppression

Principal Investigator:

Christine Conelea, PhD (Department of Psychiatry)

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Collaborators:

Kathryn Cullen, MD (Department of Psychiatry), Kelvin Lim, MD (Department of Psychiatry)

Abstract:

The overall research objective of this project is to examine neurobehavioral mechanisms underlying tic suppression using an innovative methodology that integrates repetitive transcranial magnetic stimulation (rTMS) with an established behavioral tic suppression paradigm. TMS is a non-invasive procedure that temporarily increases or decreases cortical activity, which allows researchers to make inferences about the neurobiological underpinnings of a disorder. TMS has been used to examine the pathophysiology of tics by targeting the motor cortex node of the CSTC, which is involved in voluntary suppression of movement (primary motor cortex, M1) and involuntary urges to move (supplementary motor cortex, SMA). This work has primarily compared M1 and SMA functioning across discrete diagnostic categories (e.g., Tourette Syndrome (TS) vs. controls; TS vs. TS+ADHD) but has yet to focus on the relationship between motor cortex functioning and tics themselves. Direct examination of tics and urges after rTMS can be accomplished using an established behavioral paradigm developed to study the effects of context on tic suppression. The proposed study will examine the effect of 1hz active versus sham rTMS over SMA on tic frequency, suppressability, and urges in youth with chronic tics. Research linking this behavioral tic suppression paradigm with targeted examination of SMA activation will help clarify the neurobehavioral mechanisms underlying tic suppression.

Pubertal stress recalibration hypothesis

Principal Investigator:

Megan R Gunnar, Ph.D. (Institute of Child Development)

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Collaborators:

Bradley Miller, M.D./Ph.D. (Department of Pediatrics)

Abstract:

Youth with severely adverse early life histories are at double the risk of increased emotional problems as they transition from childhood into adolescence. This risk may reflect the calibration of stress-mediating systems to harsh conditions during sensitive periods early in life. Yet, not all youth with such histories are affected. The proposed study tests the novel pubertal stress recalibration hypothesis; specifically puberty opens a second sensitive period for calibration of stress-mediating systems to current life conditions at the approach of sexual maturity. For youth who experienced adverse early care, pubertal development allows a shifting of stress-system activity to that seen among youth without such histories if concurrent stressors are low and a hyper-sensitization of stress activity if current life conditions are stressful. Our target participants will be youth adopted internationally from orphanages (post-institutionalied, PI) youth, compared to youth reared in their families of origin (non-adopted,NA). We will follow 368 youth examining them annually over 3 time points (0, 1 and 2 yrs). The use of an accelerated longitudinal design (4 grps: 7-8, 9-10, 11-12, 13-14 yrs) and growth curve modeling allows examination of a broad range of the pubertal period (7 through 16 yrs). Annual measures will be made of the HPA axis (salivary cortisol), the ANS (salivary alpha amylase) for PI and NA youth in relation to current life stress (Youth Life Stress Interview completed annually) and pubertal stage (annual nurse-conducted Tanner Staging). Measures of stress-mediating systems activity will be obtained using the Trier Social Stress Test for Children and home assessment of the cortisol awakening response (CAR). Our prior research with PI youth showed a normalization of the CAR by Tanner stage 3-5, compared to same aged youth at stages 1-2. This proposal is a logical extension of that work that will also test the hypothesis that shifts in stress-system activity mediates the increase in emotional problem symptoms in adolescence. The results of this study should help determine whether the peripubertal period is a critical time to intervene with children exposed to early life adversity.

Social Buffering over the Pubertal Transition

Principal Investigator:

Megan Gunnar, PhD (Institute of Child Development), Kathleen Thomas, PhD (Institute of Child Development)

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Collaborators:
Abstract:

The effectiveness of social buffering in regulating stress appears to wane for a period with puberty at the same time that stress-reactivity increases and young adolescents become more vulnerable to stress-related affective pathology. However, there is a dearth of knowledge regarding the neural underpinnings of social buffering in children and the changes in neural responses to potential social buffers with puberty. In addition, to date, the loss of social buffering effectiveness with puberty has primarily been examined using activity of the hypothalamic-pituitary-adrenocortical (HPA) axis as the stress measure. Our proposed experiments will examine the pervasiveness of the effect by examining sympathetic and parasympathetic responses, in addition to salivary cortisol. They will determine whether the loss of social buffering also extends to threat stimuli as it does in adults and to situations in which two friends are both experiencing the stressful event together. Finally, they will explore whether puberty is associated with an emergence of sex differences in social buffering by parents and friends. Our prior research uncovered the waning of the effectiveness of parents to serve as social buffers of the HPA axis over the pubertal transition and the concomitant failure of friends to “step in” as stress buffers. The proposed experiments are the logical extension of this work. The results will have the potential to drive significant attention to the role of developmental disruptions in social stress buffering as possible contributing factors in the rise of affective problems in the early teen years.

Toddler and Parent Play Study

Principal Investigator:

Megan Gunnar, PhD (Institute of Child Development)

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Collaborators:

Emily Reilly, PhD candidate (Institute of Child Development)

Abstract:

Sensitive caregiving in the first years of life helps children manage their own emotions and arousal, promoting healthy development and a decreased risk of psychopathology-related symptoms later in childhood. This sensitive care can be derailed by parent trauma histories and depression, which is why sensitivity has become a target of many parenting interventions. Still, these interventions are not successful with some parents, challenging researchers to instead focus on the capacities necessary for sensitive responding. Compassion, we argue, is a principal capacity for sensitivity.

Compassion involves both an understanding of another’s distress and the motivation to act on this understanding to help alleviate their distress — abilities necessary to enact a sensitive response to a child. Encouragingly, compassion is malleable and can be induced with loving kindness meditations, which involve sending thoughts of loving kindness to yourself and a series of people. Biological measures, such as respiratory sinus arrhythmia (RSA), can be used to capture compassionate responding because another’s distress activates our physiological arousal. Employing heart rate variability methods provides an opportunity to measure effects of an LKM intervention at the biological level. Intervening to improve sensitivity by targeting compassion with an LKM could provide a cost-effective, efficient, and possibly more successful method for empowering parents to respond sensitively to their child, thereby preventing the development of mental illness in the next generation. However, it is first necessary to ensure the association between compassion and sensitivity.

Utilizing eye-tracking to study the normative trajectory of social information processing

Principal Investigator:

Suma Jacob, M.D., Ph.D. (Department of Psychiatry)

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Collaborators:

Sunday Francis, PhD (Department of Psychiatry), Amy Esler, PhD (Department of Pediatrics)

Abstract:

Social information processing includes many behaviors, deficits in some of these behaviors have been observed in autism spectrum disorder (ASD) individuals through behavioral and neuroimaging studies. These impairments emerge early in development and persist over time, and may in part be related to atypical eye movements during assessment of visual stimuli containing social information.

We propose to examine the normal distribution of social information processing and how these capacities differ in our existing cohort of ASD individuals. The developmental trajectories of social information processing change over time, and need to be thoroughly characterized across a broad age of NTs and ASD individuals. Our clinical research team is currently studying novel drug treatments that improve social functioning throughout development. However, treatment outcome measures that reliability document changes in social information processing are limited in ASD. Studies of novel pharmacological and non-pharmacological interventions would benefit from a non-invasive, easily measured, and accessible outcome measure that would provide a measurement of treatment efficacy. By collecting eye tracking and physiological data in typically developing individuals as they perform electronic visual tasks we aim to map the trajectory of social information processing in NTs. Improved characterization of the distribution of social information processing capacities in a neuro-typical cohort will provide a unique platform with which to compare individuals with neurodevelopmental disorders (NDDs).

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