Sensory Gating in Cerebral Palsy

What's the science?

Around the time of birth, brain injury can result in cerebral palsy. Children with cerebral palsy have deficits in motor function, and these deficits are known to be due in part to sensory deficits. Further, the neural responses (‘event-related potentials’) and oscillations in the somatosensory cortex at alpha, theta and beta frequency ranges have been linked to the severity of both perceptual and motor deficits. Sensory gating’ is when two sensory stimuli are presented in a row and the second stimulus results in a smaller neural response. This phenomenon occurs normally and may be due to the fact that the second sensory stimulus is somewhat redundant and not novel in the environment. How sensory gating manifests in children with cerebral palsy is not known. This week in Cerebral Cortex, Kurz and colleagues performed a sensory gating task and magnetoencephalography (MEG) to understand more about the sensory deficits in children with cerebral palsy.

How did they do it?

Fifteen children with cerebral palsy and nineteen healthy children participated. The mean age for both groups was 14 years old. Children were seated while MEG data was recorded – this type of brain scan measures magnetic fields that are generated due to the brain’s electrical activity (e.g. neuron firing). Electrical stimulation was applied to a nerve (tibial nerve) on the leg. The non-dominant leg in healthy children and the most affected leg in children with cerebral palsy was used. 120 trials consisting of two electrical pulses each (500ms between pulses) were administered. Each participant also completed an MRI scan to map their brain structure, and the MEG data was mapped to their brain structure. Power at different frequency bands across sensors in the MEG scanner was calculated. Next beamforming (a technique which uses data from sensors in the MEG scanner to estimate activity at specific locations in the brain) was performed. Locations of peak activity within the somatosensory cortex (during nerve stimulation) were noted for participants who had their right leg and those who had their left leg stimulated separately. A mixed model was used to assess differences between children with and without cerebral palsy. Sensory gating was calculated as a ratio (higher/closer to one is less gating).

What did they find?

When they looked at the sensor data from the MEG system, they found synchronization across several frequency bands (10-75Hz) at central and frontal parietal electrodes (approximately over the somatosensory cortex) in the first 100 ms following each stimulus. After beamforming, the peak activation was found to be near the paracentral lobule of the somatosensory cortex (this area of the somatosensory cortex is typically activated when sensory stimulation is applied to the leg). Main effects for group and for stimulus were found; responses were weaker for the cerebral palsy group, and for the second stimulus compared to the first. An interaction was also noted; there was greater attenuation of the response to the second stimuli in children with cerebral palsy. There was also a stronger somatosensory gating response in children with cerebral palsy (0.45 versus 0.75 in healthy children), indicating that this response was unusually strong in the group with cerebral palsy.

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What's the impact?

This is the first study to assess sensory gating (a dampened neural response to a second stimulus when two are presented) in children with cerebral palsy. Children with cerebral palsy demonstrated more sensory gating and weaker activity in the somatosensory cortex following application of a sensory stimulus. Neurophysiological abnormalities in sensory gating may be an underlying cause of sensory and motor deficits. Future studies should assess the link between structural and functional damage to the central nervous system in cerebral palsy.


Kurz et al., Children with Cerebral Palsy Hyper-Gate Somatosensory Stimulations of the Foot. Cerebral Cortex (2018). Access the original scientific publication here.