An examination of the startle response during upper limb stretch perturbations

  • Christopher J Forgaard Kinesiology, UBC
  • Ian M Franks Kinesiology, UBC
  • Dana Maslovat Kinesiology, UBC
  • Nicolette J Gowan Kinesiology, UBC
  • Jonathan C Kim Kinesiology, UBC
  • Romeo Chua Kinesiology, UBC

Abstract

Unexpected presentation of a startling auditory stimulus (SAS >120 decibels) in a reaction time (RT) paradigm results in the startle reflex and an early release (<100 ms) of the preplanned motor response (StartReact effect). Mechanical perturbations applied to the upper limbs elicit short (M1) and long-latency (M2) stretch reflexes and have also been shown to initiate intended motor responses early (<100ms). It was recently proposed that unexpected delivery of a perturbation could also elicit a startle response and therefore the StartReact effect may be responsible for the early trigger of a preplanned response (Ravichandran, Honeycutt, Shemmell, & Perreault, 2013). To investigate this further, we examined startle incidence, RT, and stretch reflex modulation for both expected and unexpected perturbation conditions. In Experiment 1, participants performed active (ACT) and passive (DNI) conditions to an expected large perturbation (similar to previous studies examining M2). No incidence of the startle response was observed; however, the perturbation still elicited the voluntary response (for ACT conditions) at short latency (<100ms) and goal-dependent modulation of the M2 response was observed. In Experiment 2, participants performed ACT and DNI conditions to a weak auditory stimulus or a small wrist perturbation. On unexpected trials we probed startle circuitry with a large perturbation or SAS. The SAS consistently elicited a startle response in both ACT and DNI conditions, but startle-like activity was only observed on 11.6% of ACT perturbation trials. Our findings suggest that while unexpected upper limb perturbations can be startling, the StartReact effect is not the primary mechanism responsible for goal-dependent modulation of the M2 response.

Acknowledgments: NSERC