11-12 Neuroscience of Anxiety and Depression Flashcards Preview

2911 Brain and Behaviour > 11-12 Neuroscience of Anxiety and Depression > Flashcards

Flashcards in 11-12 Neuroscience of Anxiety and Depression Deck (45):
1

What's the difference between fear and anxiety?

Fear is the response to threat; anxiety is anticipation of perceived threat - could be real or imagined. Anxiety tends to be longer-lasting than fear response.

2

What are the five types of anxiety disorder?

1. Generalised Anxiety Disorder
2. Phobia
3. Obsessive Compulsive Disorder (OCD)
4. Post-Traumatic Stress Disorder (PTSD)
5. Panic Disorder

3

What is the incidence of anxiety disorders in Australia?

One in seven in any one year; one in four in lifetime

4

Why did benzodiazepines replace barbiturates as anxiety treatments?

Barbiturates have very poor therapeutic index (window between beneficial effect and dangerous side effects). Benzos better TI.

5

What were two misconceptions about the long-term effects of benzodiazepines?

1. That they were not addictive
2. That the sedative effects would decrease with tolerance and anxiolytic effects would remain

6

How do benzodiazepines act on GABA receptors?

They have binding sites on GABA-A (ionotropic) receptors and facilitate activation

7

Why are benzodiazepines dangerous to use with alcohol?

Both are GABA agonists - too much GABA, everything slows down

8

What withdrawal profile do benzodiazepines have?

Similar to that of alcohol - anxiety, jitters...

9

What class of drugs is the first-line treatment for anxiety disorders today?

SSRIs and SNRIs

10

How can adrenergic antagonists be used to reduce anxiety disorders?

Beta-blockers such as Propranolol can be used to reduce physiological symptoms of anxiety.

11

What do beta-blockers do?

Block noradrenergic activity

12

How can beta-blockers affect memory of emotional events?

We tend to remember more emotionally charged events, because arousal facilitates memory. Ability of emotion to affect memory performance relies on noradrenaline.

13

What did Cahill et al. show in their 1994 study of beta-blockers and memory?

It was shown that beta-blockers prevent memory enhancement for emotional part of a story. Pps remembered the emotionally charged part of narrative no better than neutral part. In control group, emotional part of story remembered in drastically more detail.

14

What are the DSM criteria for major depression?

For the last 2 weeks have you had:
1. Depressed mood
2. Loss of interest or pleasure?

If you answered 'YES' have you experienced:
1. Depressed mood most of the day 2. Less interest or pleasure in all activities
3. Weight loss or gain (when not dieting) 4. Sleeping difficulties
5. Slowed or fastened movements
6. Tiredness or loss of energy
7. Feeling worthless
8. Difficulty concentrating
9. Thoughts of death

15

What are the DSM criteria for bipolar?

Behaviour associated with mania includes:

increased energy
irritability
overactivity
being reckless or taking unnecessary risks increased spending
increased sex drive
racing thoughts
rapid speech
decreased sleep
grandiose ideas
hallucinations and/or delusions.

16

By 2020 depression will be...

...the second most common disease in the world

17

What is the incidence of clinical depression among Australians?

1 in 5 Australians

18

What percent of Australians have depression at any given time?

7%

19

How often is depression treated by GPs?

It's the second most common ailment after hypertension

20

What percentage of all mental health prescriptions are antidepressants?

50%

21

How do MAO inhibitors work?

They prevent the breakdown of monoamines DA, NE and 5-HT, thus increasing the levels of these neurotransmitter in the brain

22

In which cases are MAOIs and tricyclics used today?

When patients don't respond to SSRIs

23

What drugs superseded MAOIs?

Tricyclic - more specific than MAOIs, but not by much.

24

How do tricyclics work?

They stop NT reuptake by blocking reuptake pump. Still have wide side effect profile, and overdose can be lethal

25

What are some SSRIs?

Fluoxetine - Prozac; Sertraline - Zoloft

26

How are SSRIs different from MAOIs and tricyclics?

They block reuptake only of 5-HT - more specific

27

How many subclasses of 5-HT receptors are there?

At least 9

28

What are side effects of SSRIs?

•  Anxiety + jitteriness in first few days of use •  Insomnia, or more rarely, sedation
•  Headache
•  Sexual side effects
•  Nausea and diarrhea
•  Withdrawal (discontinuation syndrome)

29

Which of the serotonin receptors has been most closely linked to reducing anxiety?

5-HT1A has been implicated in anxiety reduction and antidepressant action.

30

What is the most popular antidepressant in Australia? And what type of drug is it?

As of 2007, Efexor. It's a SNRI and SSRI.

31

What are the typical side effects of SNRIs?

Tremor, agitation, blood pressure, cardiac effects, tachycardia.

32

What is tachycardia?

Tachycardia is a heart rate that exceeds the normal range. A heart rate over 100 beats per minute is generally accepted as tachycardia.

33

Why does it take two weeks for SSRIs and SNRIs to work?

It may take time for autoreceptors to become downregulated - with continual stimulation they may gradually become less sensitive.

34

What are autoreceptors and what do they do?

Autoreceptors are receptors on the presynaptic neuron that bind the neurotransmitter and generate negative feedback. This inhibits further release - tells cell there is too much NT in synapse.

35

What unlikely disorders are SSRIs being prescribed for?

Premenstrual dysphoric syndrome; bulimia; hot flashes, premature ejaculation

36

What drugs appear most effective in treating bipolar?

Mood stabilisers such as lithium carbonate

37

Why are SSRIs often not recommended for children and babies?

Increased risk of suicidal ideation (fluoxetine may be exception) among kids and adolescents. Babies have increased risk of cardiac malformations and neonatal pulmonary hypertension

38

What is the efficacy rate of SSRIs?

65% response rate (in favourable studies) vs. 40% placebo

39

What does electroconvulsive therapy change in the brain?

Enhances inhibitory neurotransmitter systems (GABA), serotonergic receptor function, notably 5-HT1A-receptor sensitization, enhances striatal dopamine receptor binding, and produces an acute surge in plasma catecholamines, growth hormone, oxytocin, and prolactin and induces neurogenesis.

40

What are the theoretical problems with ECT?

No one knows how it works - which of the biochemical changes it induces are associated with efficacy

41

What is the main side effect of ECT?

Amnesia

42

What is deep brain stimulation (DBS)?

Deep brain stimulation (DBS) is a surgical treatment involving the implantation of a medical device called a brain pacemaker which sends electrical impulses to specific parts of the brain. Basically, it's more specific, milder ECT.

43

What happens in depression patients with stimulation of nucleus accumbens (rich in DA neurons)?

They want to go bowling and see the Cologne Cathedral. Weird, huh? OK, sudden increase in reward-seeking behaviours whose absence characterises depression. No euphoria - patient can't tell if stimulation is on or off.

44

What are one-year follow-up scores after deep-brain stimulation?

Some don't respond. For those who do, significant increase in positive activities.

45

How can beta-blockers help PTSD sufferers?

Can also help reduce PTSD if administered immediately following traumatic event – doesn't change memory, but reduces emotional intensity. Has also been proven effective when used before discussion of traumatic event to reduce emotional distress.