Post-Movement Beta Rebound Is Decreased in Children with ASD

Thursday, May 14, 2015: 3:04 PM
Grand Ballroom D (Grand America Hotel)
W. C. Gaetz1, L. Blaskey2, E. S. Kuschner2, L. Bloy2, R. Murray3, C. Fisk4, M. Ku4, D. Chudnovskaya4, J. W. Dell5, R. Golembski4, P. Lam4, S. E. Levy6 and T. P. Roberts2, (1)The Children's Hospital of Philadelphia, Bala Cynwyd, PA, (2)Children's Hospital of Philadelphia, Philadelphia, PA, (3)Radiology, The Children's Hospital of Philadelphia, Philadelphia, PA, (4)The Children's Hospital of Philadelphia, Philadelphia, PA, (5)CHOP MEG Lab, The Children's Hospital of Philadelphia, Philadelphia, PA, (6)Developmental & Behavioral Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA

A variety of motor impairments have consistently been associated with ASD, such as low muscle tone, coordination/balance and imitation impairments, dyspraxia and motor stereotypies. However, the neurophysiological mechanisms underlying these motor impairments remain obscure. Movement-induced cortical rhythms have been investigated recently in ASD during tasks involving motor imitation and observation. These studies indicate a deficiency in beta (15 to 30 Hz) rhythm function associated with the imitation and observation of movement. It remains unclear however, whether these deficiencies are also evident when performing simple motor responses.


To compare movement-related cortical oscillations in TD and ASD children performing a simple button-press task.


Neuromagnetic activity was recorded in 12 children with ASD (mean 12.4 years) and 12 TD children (mean 12.2 years), during a task requiring a right index finger response. A visual contrast grating stimulus was presented adjacent to a central fixation cue once every 4 s. Subjects were required to maintain fixation and press a button at the disappearance of the grating stimulus (1.75 s duration; +- 0.25 s). 100 responses were collected over a 400 s MEG recording period. Movement related oscillatory changes for beta (15 to 30 Hz) and gamma (60 to 90 Hz) frequency bands were then assessed using beamformer spatial filter analysis. Beta ERD (event-related desynchronization), a decrease in movement-related resting beta band power was assessed at movement onset (active window; -0.3 to 0.2 s, with the button press at time 0 s) compared to a pre-movement baseline (-1.8 to -1.3 s) time period. Following movement, the expected re-synchronization of beta-band power (post-movement beta-rebound; PMBR) was assessed using a 0.5 to 1.0 s active time window compared to the pre-movement baseline (-1.8 to -1.3 s). Movement-related gamma-band synchrony (MRGS) was also assessed at the time of the button-press response using an active window of -0.1 to 0.2 s compared to the pre-movement baseline.


Right index finger movement was associated with strong contralateral modulations in beta band power as expected. In the contralateral left hemisphere, beta ERD power was observed maximally from primary motor cortex (MI), and was of similar magnitude for both TD and ASD (N.S.). Similarly, MRGS was observed maximally in contralateral MI and was not significantly different for both ASD and TD groups. In contrast, PMBR was significantly reduced or absent in ASD subjects compared to TD control children (p=0.04). 


These results provide physiological evidence for a distinct functional deficit in motor cortical responses for children with autism. These results may be important for interpreting related studies using more complex tasks such as action/observation methods to investigate “mirror-neuron” function from autistic children and adults.  PMBR is generally associated with motor deactivation or inhibition and PMBR power has been shown to correlate directly with GABA concentration in TD adults (more GABA results in stronger beta rebound). Reduced PMBR in autism is also interesting in light of a recent study from our group showing decreased GABA level in the motor cortex in ASD.