Anxiety & Panic Disorders

Question 1

What is Lazarus’ definition of anxious mood?

Answer 1

An anxious mood is the affective and physiological state associated with the appraisal:

“I am facing uncertain, existential threat.”

This means the person feels under threat from something unclear, vague, or unavoidable.

Question 2

What is cognitive appraisal, and how does it contribute to anxious mood?

Answer 2

(1) Cognitive appraisal = how you interpret a situation.

• Example: A parent panicking about a falling toddler or a perfectionist being overly self-critical.
• CBT (Cognitive Behavioral Therapy) focuses on changing these appraisals to reduce anxiety.

Question 3

Why does Lazarus say anxiety is not caused by a single process?

Answer 3

Anxiety is not due to just one brain region or process.
It’s caused by multiple overlapping processes, including:

• Cognitive appraisal
• Sensory responses
• Autonomic nervous system
  activity
• Memory
• Coping ability, etc.

Question 4

What are unconditioned responses, and how do they contribute to anxiety?

Answer 4

• Unconditioned responses = automatic, hardwired reactions to sensory input (like pleasure or pain).
• Example: Pain signals triggering fear.
• Emphasized these basic emotional responses as building blocks of anxiety.

Question 5

What is the role of the physiological/autonomic state in anxious mood?

Answer 5

1) Acute responses: Immediate physical reactions (e.g., fight-or-flight).

2) Persistent traits: Long-term patterns (e.g., chronic stress reactivity).

3) These bodily reactions shape how anxiety feels and how easily it’s triggered.

Question 6

What does affect mean, and how does it contribute to anxious mood?

Answer 6

Affect = The personal, subjective feeling of anxiety.

It’s how anxiety feels from the inside, including emotional distress, tension, and discomfort.

Question 7

How does motivational state contribute to anxious mood?

Answer 7

Motivational state = Whether anxiety drives you to approach or avoid a situation.

Question 7

How does learning & memory contribute to anxious mood?

Answer 7

Past experiences with threats shape how threatening a new situation feels.

If you’ve been hurt in the past, you’re more likely to feel anxious in a similar situation.

Question 7

How does coping ability affect anxious mood?

Answer 7

Your perceived ability to handle the threat influences anxiety.

If you feel capable of handling it, anxiety decreases.
If you feel powerless, anxiety increases.

Question 8

What does shared environment mean in the context of anxiety and psychopathology?

Answer 8

Shared environment refers to environmental factors that make family members (like twins or siblings) more similar to each other in terms of traits, behaviors, or disorders.

Question 8

What’s the big picture summary of anxious mood according to Lazarus?

Answer 8

Anxious mood is a multi-dimensional state blending:

• Cognitive appraisals (how you interpret the situation)
• Physiological responses (fight-or-flight)
• Unconditioned sensory responses (pain/pleasure)
• Motivation (approach/avoid)
• Affect (subjective feeling)
• Memory of past threats
• Coping ability (how capable you feel)

Question 9

What do twin studies reveal about shared genetics and anxiety?

Answer 9

(1) Twin studies compare identical twins (100% genetic overlap) to fraternal twins (50% genetic overlap).

(a) If identical twins are more similar in anxiety levels than fraternal twins, this supports a genetic contribution to anxiety.

(b) Twin studies help separate genetic influences from shared environment influences.

Question 10

What is HiTOP, and why is it important for understanding anxiety and psychopathology?

Answer 10

• HiTOP = Hierarchical Taxonomy of Psychopathology.
• It’s a dimensional model (instead of categories like DSM-5).
• It sees mental disorders as continuous traits rather than “you have it or you don’t.”
• HiTOP groups disorders based on shared symptoms and causes, instead of treating them as totally separate conditions.
• Example: Anxiety disorders, depression, and OCD might cluster together under a higher-order internalizing factor.

Question 11

What are the key levels in HiTOP? (Explain the hierarchy.)

Answer 11

1. Higher levels (broad dimensions) – e.g., Internalizing (which includes anxiety, depression, OCD, etc.).
2. Middle levels – e.g., Distress disorders or Fear disorders.
3. Lower levels (specific symptoms) – e.g., panic attacks, avoidance, rumination.

• Biological factors (like brain function, genetics, hormones) linked to higher HiTOP levels (broad traits) affect a wider range of behaviors.
• Factors linked to lower HiTOP levels (specific symptoms) only affect narrower, more specific behaviors.
• erotonin system might influence general anxiety-proneness (high level), while heart rate response to stress might only influence panic attacks (low level).

Question 12

What are the three main steps in Latzman’s HiTOP research process?

Answer 12

(1) Identify relevant HiTOP constructs and appropriate measures.

• Pick the right levels (broad or narrow) and use tools to measure them (questionnaires, interviews, etc.).

(2) Assess in representative population, possibly oversampling clinical cases.

• Include a wide range of people, but especially those with high anxiety or other disorders.

(3) Test hypotheses about associations between HiTOP dimensions and neurobiological variables.

• Check how brain function, genetics, hormones correlate with different HiTOP traits.

Question 13

Why does HiTOP help improve anxiety research compared to older diagnostic systems?

Answer 13

1) Old systems (like DSM-5) treat disorders as separate, all-or-none categories.

2) HiTOP recognizes that anxiety overlaps with other disorders (like depression).

3) HiTOP focuses on underlying dimensions, which fits better with how symptoms actually cluster in real life.

4) This allows researchers to link brain and genetic factors to broad patterns, not just single disorders.

Question 14

What does amygdala reactivity to negative faces tell us about anxiety risk?

Answer 14

• When people see negative or threatening faces (angry, disgusted), the amygdala (a brain region involved in detecting threat) becomes more active.
• High amygdala reactivity to negative faces is associated with higher anxiety risk.
• Moderate amygdala reactivity is average.
• Low amygdala reactivity is linked to lower anxiety risk.
• The more reactive your amygdala, the more likely you are to develop anxiety symptoms.

Question 15

How does early life adversity (ELA) affect brain reactivity to emotional and cognitive challenges?

Answer 15

• Early life adversity (like neglect, abuse, family instability) changes how the brain responds to stress later in life.
• Higher amygdala reactivity (more sensitive to threat).
• Lower prefrontal cortex (PFC) reactivity (less control over emotions and responses).
• This imbalance (overactive amygdala + underactive PFC) is linked to higher risk for anxiety and depression.

Question 16

What does amygdala reactivity + stressful life events predict over time?

Answer 16

• If someone has high amygdala reactivity and experiences many stressful life events, they are more likely to develop internalizing symptoms (anxiety and depression).
• This predictive effect can last up to 4 years.
• The combination of a sensitive threat system + life stress = higher future anxiety risk.

Question 17

How does amygdala reactivity predict high vs. low anxiety risk?

Answer 17

(1) High-risk individuals (more likely to develop anxiety):
- Show high amygdala response to threats.

(2) Low-risk individuals (less likely to develop anxiety):
- Show low amygdala response to threats

Question 18

What is the difference between reappraisal and suppression in emotional regulation? (with example)

Answer 18

(1) Reappraisal:
- Changing how you think about an image or situation to reduce its emotional impact.
- Example: Looking at a sad image and thinking, “This is just an actor; no one is really hurt.”

(2) Suppression:
- Trying to hold your facial expression still and hide your emotional reaction, without changing how you think.
- Example: Seeing a sad image but keeping your face neutral.

Reappraisal is healthier and more effective for anxiety regulation than suppression.

Question 19

What is tDCS and how is it used to study anxiety?

Answer 19

• tDCS = Transcranial Direct Current Stimulation.
• It applies a weak electrical current to the scalp to increase or decrease brain activity.
• When applied to the DLPFC (Dorsolateral Prefrontal Cortex), anodal tDCS (positive stimulation) increases DLPFC activity.
• This allows researchers to test causality — they can see if directly increasing DLPFC activity reduces anxiety symptoms.

Question 20

What did Heeren et al. (2017) find about DLPFC tDCS and Social Anxiety Disorder (SAD)?

Answer 20

• Participants received anodal tDCS to the DLPFC, which increased DLPFC activity.
• It reduced attentional bias toward negative faces (they were quicker to respond when a neutral stimulus replaced a negative face).
• This shows that increasing DLPFC activity can directly reduce negative attention bias in social anxiety.

Question 21

What is the attentional bias score in anxiety research?

Answer 21

1) The attentional bias score measures how much faster or slower someone responds to a probe (like a dot or colon) when it appears in the same place as a threatening face.

2) tDCS to the DLPFC reduces this bias in people with social anxiety disorder.

Question 22

How does increasing DLPFC activity (via tDCS) affect amygdala reactivity and anxiety?

Answer 22

1) Increased DLPFC activity (through anodal tDCS) helps the prefrontal cortex better regulate the amygdala. 2) This leads to lower amygdala reactivity to threats, which reduces anxiety symptoms.

Question 23

How does optogenetic dissection of brain circuits help us understand anxiety disorders?

Answer 23

- A neuroscience tool that uses light to turn specific neurons on or off. - Different symptoms of anxiety (freezing, avoidance, fast breathing, high heart rate) come from different brain circuits. - Optogenetics lets researchers map these circuits by activating or silencing specific connections. - This helps us understand how the amygdala, BNST, prefrontal cortex, hypothalamus, and brainstem all work together to create: 1) Fear responses 2) Chronic anxiety 3) Physical symptoms (breathing, heart rate) - Anxiety disorders happen when these circuits become overactive or imbalanced, especially the amygdala and BNST circuits.

Question 24

What role does serotonin (5-HT) play in anxiety and mood disorders?

Answer 24

1) Serotonin (5-HT) is a neurotransmitter involved in mood regulation, threat processing, and emotional responses. 2) Low serotonin is linked to increased anxiety and depression. 3) SSRIs (Selective Serotonin Reuptake Inhibitors), like citalopram, increase serotonin levels by blocking its reuptake. 4) Increased serotonin reduces overactivation of the amygdala (threat detector) and improves communication with mPFC (which regulates fear responses).

Question 25

How are serotonin and the amygdala related in healthy people?

Answer 25

- In healthy people, one week of SSRI treatment (citalopram): Decreased amygdala and mPFC response to preconscious threat images (threat cues presented too fast for conscious awareness). - This suggests serotonin dampens automatic threat processing. - It shows that SSRIs directly change how the brain processes threat, even in people without anxiety or depression. - This suggests SSRIs target basic brain circuits (amygdala, mPFC) — they don’t just treat symptoms, they change how the brain reacts to threat signals. - Supports the idea that serotonin dysfunction contributes to excessive threat processing in anxiety disorders.

Question 26

What role does norepinephrine (NE) play in anxiety?

Answer 26

- Norepinephrine is a neurotransmitter involved in the fight-or-flight response. - It increases alertness, arousal, and attention to threats. - High norepinephrine activity can exaggerate fear responses and is linked to hypervigilance and excessive threat sensitivity in anxiety disorders.

Question 27

What did the study with reboxetine show about norepinephrine and the amygdala?

Answer 27

(1) In healthy controls, a single dose of reboxetine (a norepinephrine reuptake inhibitor): Increased amygdala responses to threat stimuli. (2) This suggests norepinephrine enhances threat detection. (3) In people with anxiety disorders, overactive norepinephrine systems may exaggerate threat responses, contributing to hypervigilance.

Question 28

How does dopamine (DA) relate to anxiety and depression?

Answer 28

Low dopamine activity contributes to: - Reduced ability to experience pleasure (anhedonia) — seen in depression and some anxiety disorders. - Reduced motivation to engage with the environment, increasing avoidance.

Question 29

What happens when you overexpress D2 dopamine receptors (DRD2) in the striatum in mice?

Answer 29

1. Deficits in reward-related behavior (less interested in rewards). 2. Increased susceptibility to depression-like behavior, especially after social defeat stress (a model for social anxiety/depression). 3. This suggests dopamine dysfunction (too much D2 signaling) can contribute to reduced reward sensitivity and higher stress vulnerability.

Question 30

How does VTA-NAc dopamine firing relate to stress and depression in mice?

Answer 30

- VTA (ventral tegmental area) to NAc (nucleus accumbens) is the main reward circuit. - In mice, optogenetically increasing DA firing in this pathway can: Rescue depression-like behavior after social defeat stress. - This supports the idea that dopamine is needed for resilience to stress, and when dopamine is low, vulnerability to depression and anxiety increases.

Question 31

What is working memory, and why does it matter in anxiety?

Answer 31

- Working memory = the ability to hold and manipulate information in mind over short periods. - It’s controlled by the prefrontal cortex (PFC). - Anxiety can impair working memory by: a) Overloading the PFC with threat-related information. b) Reducing available cognitive resources for non-threat-related tasks. This leads to difficulty concentrating, poor decision-making, and increased rumination — all common in anxiety disorders.

Question 32

How does anxiety disrupt prefrontal cortex (PFC) function?

Answer 32

a) Anxiety increases amygdala activity (threat detector). b) The overactive amygdala sends too many threat signals to the PFC. c) The PFC struggles to filter out irrelevant threat information. d) This causes working memory deficits, poor attention control, and difficulty switching focus — contributing to the cognitive symptoms of anxiety.

Question 33

What is the relationship between the PFC, amygdala, and working memory in anxiety?

Answer 33

- Normally, the PFC regulates the amygdala, controlling emotional responses. - In anxiety, the amygdala is hyperactive and overwhelms the PFC. - This reduces the PFC’s ability to: Focus on non-threatening information. Hold and process working memory tasks. Suppress excessive worry and rumination. Cognitive dysfunction + increased avoidance behavior.

Question 34

How do serotonin, norepinephrine, and dopamine all contribute to anxiety and cognitive symptoms?

Answer 34

(1) Serotonin (5-HT) Regulates amygdala threat response, low serotonin = increased threat sensitivity & worry (2) Norepinephrine (NE) Increases alertness and threat detection, too much = hypervigilance & exaggerated threat responses (3) Dopamine (DA) Drives reward & motivation, low dopamine = anhedonia, avoidance, & poor stress resilience Anxiety involves hyperactive threat detection (amygdala), reduced prefrontal control, and dampened reward processing. This combo creates: Excessive avoidance Rumination & worry Working memory problems Reduced ability to experience pleasure or approach rewards

Question 35

What is the Biopsychosocial Diathesis-Stress Model for anxiety disorders?

Answer 35

This model explains how a combination of biological, psychological, and social factors (the "diathesis") interact with stressful life events to increase the risk of psychiatric disorders, including anxiety disorders. - Some people have a biological vulnerability (low DA autoreceptors, emotional dysregulation, etc.). - If they also experience high early life adversity (trauma, neglect), this stress can trigger the onset of anxiety or other disorders.

Question 36

What three factors make up the Three-Factor Model that predicts early onset DSM-5 disorders (like anxiety)?

Answer 36

1. High early life adversity (abuse, neglect) 2. High externalizing behaviors (poor emotional regulation, impulsivity). 3. Low midbrain dopamine (DA) autoreceptors.

Question 37

What is early life adversity? How does it contribute to anxiety?

Answer 37

- Early life adversity includes experiences like abuse, neglect, poverty, family conflict, or trauma in childhood. - These stressors can "program" stress response systems (like the HPA axis) and increase sensitivity to threat cues in adulthood. - This contributes to dysregulated emotion processing and greater risk for anxiety and depression.

Question 38

What are externalizing behaviors, and why do they predict anxiety and related disorders?

Answer 38

Impulsivity (acting without thinking). Poor emotion regulation (inability to manage anger, frustration, or distress). Aggression or rule-breaking These behaviors reflect poor self-control and difficulty managing stress, making individuals more vulnerable to developing anxiety when faced with adversity.

Question 39

What role do midbrain dopamine (DA) autoreceptors play in anxiety?

Answer 39

1. DA autoreceptors are inhibitory receptors located on dopamine neurons. 2. They regulate dopamine release. 3. Low DA autoreceptors = less control over dopamine release, meaning the system could be hyper- or hypo-responsive depending on the situation. 4. In the context of anxiety, low DA autoreceptors may reduce the brain’s ability to properly process rewards or regulate responses to stress.

Question 40

What was the Monetary Incentive Delay (MID) task, and how was it used to study anxiety risk?

Answer 40

- The MID task measures anticipation of monetary reward. - Participants see a cue that signals they could win money if they respond fast enough. - Brain responses to these reward cues were measured with fMRI. - In people with high early life adversity and dysregulated emotions, the reward system (mesocorticolimbic system) showed blunted responses during reward anticipation. - This blunted reward response is associated with higher anxiety and depression risk.

Question 41

What did the Mediation Analysis show about childhood trauma, externalizing behaviors, and psychiatric disorders?

Answer 41

- Childhood trauma increased risk for externalizing behaviors. - These externalizing behaviors (like impulsivity and emotional dysregulation) directly increased the risk for developing psychiatric disorders, including anxiety. - This shows that trauma doesn’t directly cause disorders — it increases externalizing traits, which then increase risk.

Question 42

What did the Moderation Analysis show about childhood trauma, fMRI brain response, and psychiatric disorders?

Answer 42

- The effect of childhood trauma on psychiatric disorders was moderated by brain responses to reward cues. - Specifically, trauma-exposed individuals with blunted reward system responses were at higher risk for psychiatric disorders, including anxiety. - This shows that brain response patterns shape how trauma leads to disorders.

Question 43

Why do PET and fMRI data seem to contradict each other in studies of dopamine and anxiety?

Answer 43

1. PET data (which measures DA receptors directly) suggests that anxiety risk is linked to low DA autoreceptors (less DA neuron inhibition) 2. fMRI data (which measures overall brain activity, not just DA) often shows blunted BOLD responses in reward systems. This isn’t a true contradiction because: a) fMRI BOLD reflects activity from multiple neurotransmitters, not just dopamine (e.g., GABA, glutamate, serotonin). b) Depending on the environment (presence/absence of stress or threat), DA system responses could increase or decrease.

Question 44

What is the Hierarchical Diathesis-Stress Model for anxiety and related disorders?

Answer 44

1. Combines biological vulnerabilities (low DA autoreceptors, poor emotion regulation) with environmental stressors (childhood trauma). 2. This combination increases general risk for many disorders — not just anxiety, but also depression, psychosis, compulsions, substance use, and rumination. 3. Specific triggers (like threat cues, drug cues, or obsessions) determine which disorder emerges.

Question 45

How do mesocorticolimbic (MCL) pathway responses differ in people at risk for psychiatric disorders?

Answer 45

Low DA autoreceptors lead to: 1. Low MCL activity to neutral/reward cues (disease-independent cues). 2. High MCL activity to stress/disease-relevant cues (like threat cues in anxiety). Explains why: People with anxiety may show low reward anticipation (in fMRI) but hyperactive threat detection (in amygdala).

Question 46

How does childhood adversity and dysregulation contribute to general psychopathology?

Answer 46

Depression (negative mood, hopelessness). Anxiety (hypervigilance, fear). Substance use (self-medication). Rumination (repetitive negative thinking). Compulsions (repetitive behaviors to relieve anxiety). Psychosis (severe thought disturbance).