Neurophysiological aspects of trait anxiety and possible links with sensory processing alterations and central sensitisation   January 1st, 2015

Trait anxiety is an enduring (i.e. relatively stable) personality trait, or characteristic, indicative of differences in an individual's proneness to reactions of state anxiety when faced with a perceived psychological threat. (Compare this with state anxiety which is transient, in the present.) 

Individuals with high trait anxiety exhibit CNS-related physiological and behavioural differences when compared with their low trait anxiety counterparts. These differences are interesting to us as pain researchers because we are increasingly interested in the circuitry involved in the development of central sensitisation and the associated sensory processing alterations observed in this pain population. Here I briefly outline some of the experimentally observed differences and highlight some possible links with sensory processing alterations and central sensitisation for consideration. 

Individuals with high trait anxiety exhibit alterations in executive functioning. Executive functioning is processed via the medial (mPFC), ventral and dorso-lateral (DLPFC) prefrontal cortices and includes: 

  • Planning of cognitive behaviour
  • Expression of personality
  • Decision making
  • Moderation of social behaviour (mPFC; Farmer et al., 2012)
  • Cognitive Function including attention and concentration
  • Working memory
  • Inhibition of unnecessary sensory input
  • Sensory processing including making meaning of sensory input. (DLPFC; Stein 1998; Ristic and Landry 2015)

The prefrontal cortex receives information through the ventral stream regarding the characteristics of sensory input and the dorsal stream regarding the required response to sensory input. Sensory processing involves the receiving, perception, and meaning making of sensory input and the organisation of a required response. These functions are altered in high trait anxious individuals and the responses have implications in central sensitisation.

When compared with low trait anxiety subjects, those with high trait anxiety exhibit the following sensory processing and behavioural response differences:

  1. Reduced inhibition of stimulus distraction. 
    It is a normal function of the CNS to filter out, or inhibit, the perception of sensory stimuli when these are not considered relevant, important or threatening. This inhibition function is reduced in the highly trait anxious rendering them much more susceptible to distraction by other stimuli. Compare this loss of inhibition with loss of inhibitory control in central sensitisation. This inhibitory function forms a significant part of the attentional control theory (the ability to cognitively maintain attention on a task) posited by Eysenck et al (2007). Inhibition dysfunction is associated with sensory and cognitive processing inefficiency. For example in the review of Berggren and Derakshan (2013) they consider the role of cognitive loading on attentional control function in the highly trait anxious. They suggest that working memory capacity can be exceeded by cognitive loading and this further decreases the ability to inhibit irrelevant information. Under conditions of high task demand, dilution of cognitive resources between the task and inhibition of distracting stimuli can "overload" the highly trait anxious more so than people who are not anxious. 

    Compare this with clinical observations when a patient with central sensitisation is overloaded with cognitive and/or sensory processing demands they can experience increased symptoms and/or feelings of anxiety, and report poor concentration and working memory.

  2. Reduced shifting function. 
    Shifting function is the ability to switch focus of attention between tasks or stimuli, inhibiting focus of attention on one task or stimulus in favour of another. Compare this loss of shifting function, coupled with distractibility above, with the hyper-vigilance of some chronic pain patients who are easily distracted by stimuli they may perceive as threatening and focus their attention therein.

  3. Reduced sensory and cognitive processing efficiency (despite the same performance outcome). 
    In connection with reduced inhibition and shifting functions, the high trait anxious individual has to work much harder to maintain concentration and focus of attention on the task in hand when required to filter out distractions by other stimuli. This is significantly moderated by levels of motivation. Some anxiety studies show greater compensatory strategies to maintain performance and the recruitment of additional cognitive resources to enhance attentional control in high trait anxious individuals, compared with their low anxious peers. This is despite the performance outcomes remaining the same between groups (see Ristic and Landry, 2015, for review). 

    Compare this processing inefficiency with the difficulty in concentration and working memory reported in those with central sensitisation. Also compare this with the "diligence" of highly sensitive people described by Aron and Aron (1997). 


  4. Reduced ability towards extinction. 
    Extinction is the ability to extinguish behavioural responses to stimuli that do not carry consequences or, in some cases, reward. For example, people in Christchurch, New Zealand, experienced devastating earthquakes in 2011 resulting in the widespread destruction of homes, businesses and many lives. For one of my patients it has taken over 3 years for her state anxiety response to be extinguished when a passing truck creates a vibration and rumble on the road near her home, resembling earth tremors. 

    Compare this with our neurophysiology pain education - when a patient perceives a bodily sensation or sensory stimulus, he needs to learn that it is not threatening before being able to extinguish the state anxiety response to it. This is more difficult in those with high trait anxiety. This may also relate to the increased levels of activity observed in the nucleus accumbens circuitry in chronic pain patients linked to reinforcement learning and reward (Farmer et al 2012). 

    State anxiety creates a stress response involving the autonomic nervous system. People with high trait anxiety are more prone to the stress response associated with state anxiety. Compare this with the increased level of activity found in chronic pain patients in the anterior cingulate cortex associated with autonomic responses, also reported by Farmer et al (2012). 

    Anxiety has been shown to be correlated with sensorimotor and cognitive function alterations involving everyday slips and errors. This has been measured using the Cognitive Failures Questionnaire (by Broadbent et al., 1982) in which daily errors such as dropping things, forgetting things etc. can be self-reported, reflecting daily sensorimotor and cognitive errors. Compare this with sensory processing alterations found in chronic pain patients. 

To summarise, high trait anxiety is associated with CNS circuitry activities and alterations that overlap with those found in chronic pain populations and include cognitive, behavioural and sensory processing alterations. "Trait" is indicative of a patient's own characteristic and understanding individual trait characteristics further in chronic pain populations with central sensitisation (CS) may lead us closer to identifying those at risk of developing CS pain. 

Jacqui Clark 

2015 Pain in Motion

References

Berggran N., Derakshan, N, 2013, Attentional Control Deficits in Trait Anxiety: Why you see them and why you don't.  Biological Psychology92,440-446. 

Eysenck M., Derakshan N., Santos R., Calvo M.G., 2007, Anxiety and Cognitive Performance: Attentional Control Theory. Emotion. 7, 336-353 

Farmer, MA., Baliki M, Apkarian AV, 2012, A dynamic network perspective of chronic pain Neuroscience Letters 520; 197– 203 

Ristic J., Landry M., 2015, Combining attention: a novel way of conceptualising the links between attention, sensory processing and behaviour. Atten Percept Psychophys 77:36-49. Stein, B., 1998, Neural mechanisms for synthesising sensory information and producing adaptive behaviours. Exp Brain Res 123; 124-135.