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Arousal Theories (Measuring arousal (Startle Response:
has short &…
Arousal Theories
Measuring arousal
Startle Response:
- has short & precise onset latency
- protective reflex elicited by intense & unexpected sensory stimuli eg. flash of light or loud noise
- eg. Eye blink reflex, which helps to protect the eye from unexpected noxious stimuli
- influenced by attention: while attending to visual stimuli, startle responses to auditory stimuli are attenuated
- positive emotions/moods reduce startle amplitude
Other:
- Physiological: EEG, Heart rate
- Neurochemical: neurotransmitter activity (norepinephrine), single cell recordings (LC activity)
- Vigilance: Mackworth Clock Task
Skin Conductance Response:
- index of electrodermal activity
- taken from electrodes placed on palmar surface of hands & feet (high concentration of sweat glands)
- activity of sweat glands during emotional arousal eg. public speaking, increases electrical conductance
- good indicator of arousal levels associated with specific emotions
- average SCR over time = measure of tonic level of arousal
- spontaneous fluctuations of the baseline level = measure of anxiety/contextual fear (absence of particular sensory stimulus)
- phasic SCRs = time-locked to the onset of sensory stimulus
- similar temporal profile to fMRI (good to combine the two methods
- to identify arousal responses that arise unconsciously eg. prosopagnosia patients
Issues with mentioned measurements:
- confounded by extraneous factors -> complicated interpretations eg. during polygraph test
- SCR is modulated by emotions & novel stimuli -> it isnt necessarily lying on polygraph
- not specific enough, very sensitive to multiple factors (hard to disentangle)
-> we always need to incorporate knowledge about the context
-
Arousal Theory:
- based on Yerkes-Dodson Law
- Assumptions: 1) performance is related to arousal in the form of an inverted U (best at intermediate level), 2)The optimum value of arousal level is inversely related to the difficulty of the task (if easy-> high arousal, if hard -> low arousal)
Problems:
- early findings hard to replicate
- many physiological indices of arousal but they often don't correlate -> are there more types of arousal?
- Paradoxical REM: asleep but measures show high arousal levels
- Effect on arousal often can't be defined independently of effects on performance eg. what if noise is boring & decreases arousal?
- What does task difficulty mean?
- Does difficulty affect arousal by itself?
- theory is hard to falsify
- the task content matters, not the task difficulty (2nd assumption falsified)
- detrimental effects of noise get larger during a long work period but the Y-D would predict a smaller effect & stronger effect at the beginning
- inverted U pattern only seen in repetitive/monotonous tasks eg. vigilance
- methodology of studies: manipulations that increase arousal are also distracting attention from the task
Evidence:
- Sleep loss + noise both degrade performance. But after sleep loss, noise improves performance
- effect of one stressor doesnt depend on the level of the other stressor -> effects are additive eg. opening eyes leads to higher SCR but to decrease in EEG alpha
- Early support from Andreassi (induced Muscle Tension): performance measures eg. verbal learning had inverted U relation with muscle tension
Cumulative Depletion: the more stressors, the worse performance (application of General Adaptation Syndrome)
- the effect of one stressor may be slight (still on safety margin). But if you add another stressor, the performance will suffer. -> the combined impairment by 2 stressors is larger than the sum of their separate effects
PRO:
- effects of practically any stressor increase over time during task
- noise + time on task: effects of noise increase during the task
- sleeploss + time on task: in the beginning of a long task, the sleep loss effect is small & later on it is big
-
Easterbrook: Increases in arousal restrict the range of stimuli that could be processed (narrowing)
- at low arousal: main problem is distractability/ competing irrelevant cues -> blurred discrimination between relevant & irrelevant
- at high arousal: the issue is the insufficient task relevant information
- a more complex task will suffer more from high arousal
CON:
- speculative if tasks are composed of cues from which only a certain number is processed
- attentional narrowing can also be strategical
- high anxiety people are not more narrowed/less distractible
What is arousal?
- state of being awoken, active, attentive, ready to respons
- involves activation of the ARAS (release of ACh, NE, DA) -> increase in cortical activity
Cannon's concept of homeostasis:
- maintenance several physiological variables (eg. core temperature) within acceptable ranges
- sensors recognize discrepancies & effectors try to reduce them
- psychosocial threats could also disturb homeostasis
Negative feedback regulation in Homeostasis
- Homeostats are bodies' homeostatic comparators. They compare information supplied by a sensor with a setpoint for responding (setpoint determined by a regulator)
- Effectors try to reduce any too large discrepancy
- odd number of negative relationships in the loop
- good for our bodies because it is constantly updating & optimizing bodily systems. It changes the variable back to its ideal state
Selye's concept of stress:
- Doctrine if Nonspecificity: there is an uniform response pattern, regardless of the type of stressor
- prolonged stress can produce physical disease & mental issues
- General Adaptation Syndrome: universal stages of coping with stress
- Alarm: nonspecific/acute mobilization, analogous to flight/fight
2: Resistance: chronic: the body resists & compensates as the PNS tries to return physiological functions to normal levels while body remains alert & copes with the stressor
- Exhaustion: if the stressor continues beyond body's capacity, the resources become exhausted & body is susceptible to disease & death
Allostatic load: cumulative adverse effects of prolonged/continuous or intermittent activation of effectors involved in allostasis
- provides a basis for studying longterm health consequences of stress
What is allostasis?
- stability occurring by natural alterations in acceptable ranges of variables, fluctuations that are still acceptable
- "maintain stability through change"
- because levels of activity to re-establish homeostasis differ depending on changing conditions eg. standing vs. walking -> the states are maintained by multiple effectors
- allostatic settings can change dynamically
Positive feedback mechanisms:
- the output enhances the original stimulus, it accelerates the changes in levels of the variable -> threatens homeostasis, there is no switch off
- distress could be a part of it: cognitive recognition of an aversive condition, requires consciousness/interpretation of how to cope with the situation
Relative intensities of activation of HPA, Adrenomedullary hormonal system & SNS during exposure to different stressors:
- Cold Exposure: HPA (0), AHS (+), SNS (+++)
- Active Escape: HPA (+), AHS (+), SNS (++)
- Exercise: HPA (+), AHS (++0, SNS (+++)
- Social Stress: HPA(++), AHS (++), SNS (++)
- Passive/immobile fear: HPA (++), AHS (+++), SNS (+)
- Pain: HPA (++), AHS (+++), SNS (++)
- Exercise to exhaustion:HPA (++), AHS (+++), SNS (++++)
- Fainting: HPA (++), AHS (++++), SNS (0)
Sympathetic NS:
- flight/fight system, quick response mobilizing system
- arousal & energy generation, digestion inhibited, enhanced blood flow to skeletal muscles & lungs, increased Heart rate
- preganglion: ACh, postganglion: NE
Parasympathetic NS:
- rest & digest system, slowly activated dampening system
- calming nerves, enhanced digestion
-pre & post ganglion: ACh
HPA:
- paraventricular nucleus of hypothalamus contains neurons that synthesise & secrete Vasopressin & Corticotropin-releasing hormone
- The two peptides regulate the anterior lobe of pituitary gland
- CRH & Vasopressin stimulate the secretion of ACTH
- ACTH acts on the adrenal cortex, which produces glucocorticoid hormones ie. cortisol
- Glucocorticoids act back on the hypothalamus & pituitary to suppress the CRH & vasopressin -> negative feedback cycle