Study shows neurological link behind 'freezing up' response to anxiety

Findings presented at the European College of Neuropsychopharmacology Congress suggest that adolescents’ response to anxiety includes brain regions associated with emotions as well as movement control centers in the brain, which may be related to movement inhibition experienced during stress.

“We found that when presented with an angry face the brain of socially anxious adolescents showed increased activity in the amygdala, which is the brain area concerned with emotions, memory and how we respond to threats,” Laura Muzzarelli, MSc, of Vita-Salute San Raffaele University, Milan, Italy, said in a press release. “Surprisingly, we also found this produced inhibition of some motor areas of the brain, the premotor cortex. This is an area which ‘prepares the body for action’, and for specific movements.”

Laura Muzzarelli

To assess structural and functional connectivity underlying anger processing in typically healthy adolescents and those with social anxiety disorder (SAD), researchers followed 150 children from age 8-9 years to 14-15 years. The current sample included 19 adolescents with a mean age of 14.8 years. Study participants underwent DSM-IV diagnostic screening, functional MRI and Diffusion Tensor Imaging scans to determine SAD status, brain response to expressions of emotions and white matter anisotropy. Five participants had SAD, five had subthreshold SAD and nine had no SAD symptoms. Researchers conducted functional MRI BOLD-FA correlation and psychophysiological interaction analyses.

Structural and functional connectivity analyses showed the effect of amygdalar activity on various brain regions, including the prefrontal and premotor cortices, and white matter, mainly on dorsal projectional and commissural tracts.

Dynamic causal modeling analyses indicated that the premotor cortex was a functional hub within the expressions to emotions processing network and modulated activity of other nodes.

Anger processing was particularly affected by SAD. Diagnosed SAD was associated with increased feed-forward connectivity from the fusiform gyrus to the amygdala (P = .035). Further, individuals with SAD exhibited increased inhibition of the precentral gyrus by the amygdala (P = .046).

Experiencing greater harm avoidance in childhood led to stronger excitatory effects of fusiform gyrus on subgenual anterior cingulate cortex (P=0.038).

“This is the first hard proof that strong emotions produce a response in brain areas concerned with movement. Adolescents who don’t show social anxiety tend not to show the inhibition in the movement centers. We don’t yet know how this inhibition feeds into movement — it may be that this has something to do with why we sometimes ‘freeze’ when we are frightened or under strong emotional stress, this still has to be tested. What it does give us is a possible explanation for some motor inhibition associated with emotional stress,” Muzzarelli said in the release. “We need to acknowledge that there are some limitations to this work. We started this 6-year study with 150 children, but by the time we reached adolescence we had narrowed down the field to just five children with social anxiety, and five with less severe (subthreshold) social anxiety, so it’s a small sample.” – by Amanda Oldt

Reference:

Muzzarelli L, et al. The emotional processing network at the onset of social anxiety disorder: a combined diffusion tensor imaging and functional connectivity study. Presented at: European College of Neuropsychopharmacology Congress; September 17-20, 2016; Vienna.

Disclosure: The researchers report the study was supported by the National Alliance for Research in Schizophrenia and Depression 2006 Independent Investigator Award, awarded to study researcher Marco Battaglia, MD.