3. Ulrich-Lai, Yvonne M., & Herman, James P. (2009). Neural regulation of endocrine and autonomic stress responses. Nat Rev Neurosci, 10(6), 39
4. Engelmann, Mario, Landgraf, Rainer, & Wotjak, Carsten T. (2004). The hypothalamic–neurohypophysial system regulates the hypothalamic–pituitary–adrenal
axis under stress: An old concept revisited. Frontiers in Neuroendocrinology, 25(3–4), 132-149.
12. Gordon, I, Carina, M., Feldm
an, F, & Leckman, J. (2011).
Oxytocin and Social
Motivation. Development
and cognitive
science, 1(4), 471-493.
13. Gordon, I, Carina, M., Feldm
an, F, & Leckman, J. (2011).
Oxytocin and Social
Motivation. Development
and cognitive
science, 1(4), 471-493.
TEND AND BEFRIEND VS FIGHT AND FLIGHT
14. Stress and ASD: social corollaries
• Reduced response to soothing because
reduced oxytocin
• Reduced access to peers and social
solutions
• Social interaction as a source of threat
• Failure of social sanctions
• Challenging behaviour and not assault, or
criminal damage, or threatening behaviour
• Perceived lack of planned impact on others
15. Parents stressedEstes, A., Olson, E., Sullivan, K., Greenson, J., Winter, J., Dawson, G., & Munson, J. (2012). Parenting-related stress and
psychological distress in mothers of toddlers with autism spectrum disorders. Brain & Development. doi:
10.1016/j.braindev.2012.10.004
• Mothers of 18-30 month old infants with
autism, intellectual disability, or infants who
are normally developing
• Mothers did not differ on anxiety or
depression
• Parenting stress greater for mothers of
children with autism
• Anxiety or depression and parenting stress
correlated with child’s problematic behaviour
16. People with an ASD are stressed and
this contributes to challenging behaviour
• Anxiety contributes to challenging behaviour
(Pruijssers, van Meijel, Maaskant, Nijssen, & van Achterberg, 2013)
especially in children with ASD where poor sleep is also a factor
(Rzepecka, McKenzie, McClure, & Murphy, 2011)
• People with ASD have chronic stress states (Kushki et al., 2013)
• Displacement (e.g. rituals) relieves stress (Mohiyeddini & Semple, 2013)
Kushki, A., Drumm, E., Pla Mobarak, M., Tanel, N., Dupuis, A., Chau, T., et al. (2013). Investigating the autonomic nervous
system response to anxiety in children with autism spectrum disorders. PLoS One, 8(4), e59730, Mohiyeddini, C., &
Semple, S. (2013). Displacement behaviour regulates the experience of stress in men. Stress, 16(2), 163-171, Pruijssers, A.
C., van Meijel, B., Maaskant, M., Nijssen, W., & van Achterberg, T. (2013). The relationship between challenging behaviour
and anxiety in adults with intellectual disabilities: a literature review. J Intellect Disabil
Res, Rzepecka, H., McKenzie, K., McClure, I., & Murphy, S. (2011). Sleep, anxiety and challenging behaviour in children with
intellectual disability and/or autism spectrum disorder. Res Dev Disabil, 32(6), 2758-2766.
17. Catastrophes and stress
• Life-threatening stressor
• Integrity threatening stressor
• Social integrity: shame
• Control: outrage at broken rules or coercion
• Inner integrity: catastrophic reaction/ meltdown
18. Catastrophic reaction in dementiaYeom, H.-A., & Watson, N. M. (2009). Patterns of Antecedents of Catastrophic Reactions in Nursing Home Residents
With Dementia in the United States. Asian Nursing Research, 3(3), 99-110.
• Fight: extreme anger
or hostility
• Perhaps influenced
by modelling
• Flight: extreme
sorrow or withdrawal
• Combination of fight
and flight: agitation
19. Meltdowns in ASD are a kind of catastrophic
reaction, supervening on chronic stress, with an expression that is
shaped by modelling, with one trigger being cognitive overload
• Executive function
• What have I forgotten?
• There’s not enough time…
• Nonverbal interpretation task
• Was that a joke?
• What’s going on in this group?
• Language task
• What does that mean?
20. Implications
• Track an increase in ‘stress’
• Be aware of shame and humiliation as
contributory factors
• Can sensory factors be a trigger—perhaps
especially olfaction
• Reduce complex cognitive demands
• Take fatigue into account
Notas do Editor
The sympatho-adrenomedullary (see the left-hand side of the figure) and hypothalamic-pituitary-adrenocortical (HPA) (see the right-hand side of the figure) axes are the primary systems for maintaining or reinstating homeostasis during stress. Stressor exposure results in activation of preganglionic sympathetic neurons in the intermediolateral cell column of the thoracolumbar (T and L, respectively) spinal cord (shown in blue). These preganglionic neurons project to pre- or paravertebral ganglia that in turn project to end organs and to chromaffin cells of the adrenal medulla. This sympathetic activation represents the classic 'fight or flight' response that was first characterized by Walter Cannon and colleagues in the early twentieth century152; it generally increases circulating levels of adrenaline (primarily from the adrenal medulla) and noradrenaline (primarily from sympathetic nerves), heart rate and force of contraction, peripheral vasoconstriction, and energy mobilization. Parasympathetic tone can also be modulated during stress. In the parasympathetic system (shown in red), activation of craniosacral preganglionic nuclei activates postganglionic nuclei located in or near the end organs that they innervate; parasympathetic actions are generally opposite to those of the sympathetic system.For the HPA axis, stressor exposure activates hypophysiotrophic neurons in the paraventricular nucleus of the hypothalamus that secrete releasing hormones, such as corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP), into the portal circulation of the median eminence. These releasing hormones act on the anterior pituitary to promote the secretion of adrenocorticotropic hormone (ACTH), which in turn acts on the inner adrenal cortex (that is, the zonafasciculata) to initiate the synthesis and release of glucocorticoid hormones (for example, corticosterone in rats and cortisol in humans). Circulating glucocorticoids then promote the mobilization of stored energy and potentiate numerous sympathetically mediated effects, such as peripheral vasoconstriction. Moreover, the adrenal cortex is directly innervated by the sympathetic nervous system, which can regulate corticosteroid release153. Thus, the HPA axis and sympathetic system have largely complementary actions throughout the body, including energy mobilization and maintenance of blood pressure during stress.