mental health

4 traits of anxiety

1. anticipation of future negative event

2. accompanied by feelings of unhappiness, physical tension,

3. innate (we do not learn this)

4. NORMAL response that prepares us for danger

pathological anxiety

• disproportionate fear of harm: tendency toward negative predication

• Fear of error / pathological perfectionism

• Intolerance of uncertainty

• Negative self-assessment

• Need for control

symptoms of anxiety disorder

Distressing thoughts / sensation

Cardiovascular: irregular heartbeat, hypertension, tachycardia

respiratory

gastrointestinal: butterflies

neuromuscular: tremors, tension, weakness

altered behaviors under anxiety

Agitation

Increase/decrease in appetite

Avoidance of specific situation

brain changes in anxiety (grey matter)

1. grey matter decreases. grey matter in the PFCX helps to calm you down, therefore the decrease in grey matter results in increased worrying

SPECIFICALLY IN PFCX

brain changes in anxiety (amygdala)

Amygdala is responsible for detecting emotionally relevant/salient stimuli.

Anxiety shows increased and damages to the amygdala. this results in overactivity, more worrying

• this also influences the hypothalamus (which regulates the HPA axis). amygdala triggers hypothalamus, which triggers stress response

what have rat studies shown in brain differences of anxiety

two rat strains (normal and anxiety-bred) do no differ in baseline responses.

anxious rats show larger stress response, greater ACTH and greater corticosterone

monoamine function in anxiety

reduced serotonin release and norepinephrine depletion

what 2 symptoms must be present for depression diagnosis

1. depressed mood: Loss of interest or pleasure in almost all activities—indicated by subjective report or observation by others

2. Loss of interest or pleasure in almost all activities—indicated by subjective report or observation by others

some other symptoms of depression and how many are needed for diagnosis

3

• sig. weight gain or loss

• sleep disturbance

• Tiredness, fatigue, or low energy

• A sense of worthlessness

• Impaired ability to think

• Recurrent thoughts of death

importantly, depressive symptoms are ….

• constant, impairing, life threatening distress '

• not due to substance use

• is not accompanied by any manic episodes

ventral system

bottom up response - stimulus triggers response

Recognizes emotionally salient stimuli

Generates emotional state

brain areas involved in the ventral system

1. amygdala

2. insula: monitors your internal states

3. anterior cingulate ventral & medial (recognizes things in env. and creates response)

dorsal system

top down: modifying your reaction to the input

voluntary regulation of emotional states

top down automatic processes

Processes that are done without awareness

Behavioral: altering the behavioral expression of emotion / a behavioral response

Attentional: engaging / disengaging with a stimulus

Cognitive: re-appraising a previously emotionally significant stimulus

top down voluntary efforts

Behavioral

Attentional

Cognitive

automatic behavioural responses

• extinction of behaviour

• inhibition of the stress response

brain areas involved in automatic behavioural responses

• ventromedial cortex

• ventral anterior cingulate cx

damages in automatic behavioural responses seen in depression

blunted activity in the VAC cx

• not as active as it should be

• impaired aparaisal of stimuli

  • normally it evaluates a stim and tells the amygdala to “quiet down”. in depression, stimuli is appraised more negatively

voluntary behavioural responses

inhibition of ongoing emotive-expressive behaviour - stopping yourself from making a face/expression

differences in voluntary behavioral responses in depression

increased activity (more conflict and stronger engagement with negative stim.) in the ventral dorsal cingulate cx

• this causes everything to feel more effortful and stronger engagement. its as if your brain cannot get used to regulating the normal stimuli

automatic attentional processes

involves the ability to overcome interference from emotional distracters (you don’t over-react to things in the env)

brain involved in automatic attentional processes

posterior (Back) dorsomedial prefrontal cx

differences in automatic attentional processes brain areas

more activity here in the posterior dorsomedial prefrontal cx. means they get engaged more and automatically orient to negative stimuli

• they have a bias to tend to negative stimuli in the env and they have to work a lot harder to disengage with it

voluntary attentional processes

effortful attempts to over-come emotional distraction

• when the person is aware of the emotional context, they use effortful strategies to overcome the distraction

brain areas involved in voluntary attentional processes

• dorsolateral pfcx

• ventrolateral pfcx

differences in voluntary emotional processes in depression

hyper activity in the dorsolateral pfcx, because more focus and effort is needed

• this is coupled with degraded connectivity in the amygdala which causes difficulty in sending signals to amygdala to disengage

automatic cognitive processes and brain areas

the anticipation of emotional stimuli

brain areas: dorsomedial pfcx

damages in automatic cognitive processing in depression

increased activity with an increased need for control, more conflict monitoring

voluntary cognitive processes and brain areas

voluntarily altering your perception of an emotional stimulus

brain areas: DLPFC, VLPFC

voluntary cognitive processes damages in depression

hyper active in attentional process; but in cognitive re-apprasial (modifying appraisal), there is hypo-activity (they cannot engage these areas). they cannot kick in to change the amygdala activity

• results in negative self referential appraisal

2 inflammatory markers of anxiety and depression

• interleukin : generate by white blood cells, normally to help fight infections and transmit NT

• tumor necrosis factor: boosts immune response and can cause the death of some cells, but it can also work against you as well

tryptophan

a building block for serotonin

most is degraded by the liver. both inflammatory markers activate the things that degrade tryptophan

result of inflammatory markers in anxiety/depression

there are too many inflamatory factors which cause acitvation of an enzyme to degrade tryptophan

too much tryptophan gets degraded, there is not enough to build serotonin

default mode network and brain areas

engaged in rest. rumination, daydreaming, etc.

involves posterior cingulate cx

midline brain structures (medial pfcx)

anxiety/depression alterations in DMN

in anxiety in depression, there is less DMN volume in the hippocampus.

executive network & brain areas

involved during focused attention and working memory tasks

dorsolateral pfx

superior parietal cortices

salience network

in between the two systems and is activated during tasks but joins both networks together.

also activated when someone is challenged or anxious

changes in the salience network in anx/depres

lower volume in the amygdala and anterior cingulate cx

effects of ANXIETY ONLY on the mode networks

damages connectivity between the executive network wit the salience network

• if we increase this connectivity, there is better cognitive control

effects of DEPRESSION ONLY on the mode networks

less connectivity between the executive and default mode

• increased connectivity leads to reduction in self-referential processing

rat studies and effects of exercise on inflammatory markers

sedentary mouses showed increased interleukin and increased tumor necrosis

active mouse: decreased interleukin and decreased tumor necrosis

exercise is associated with lower inflammatory markers

general studies of human studies on inflammatory markers

individuals did either HIT, moderate training, or no exercise control

results:

• control group had increase in perceived depression, anxiety, and perceived stress, and decreased in perceived depression for moderate and HIT

results of human studies on inflammatory markers

• less tumor necrosis factor aver exercise and no change for control group

• interleukin 6 is produced by contracting mucles, so is was higher in the HIT group (obviously)

  • interleukin 6 stimuklates anti-inflamatory cytokines. with this, you get less tumor necrosis and less interleukin 1

what other aspects of inflammatory markers does exercise impact?

1. obesity: associated with increased production of inflammatory cytokines. exercise reduces adipose tissue, which reduces inflammation

2. vagal tone: the vagal nerve regulate the inflmmation response

   • if it is weak, you see more inflammation. with exercise, you improve the vagal tone and decrease information