Lecture 9.2: Adolescence and Psychopathology Flashcards
What are “Mental Disorders’ by Definition?
A clinically significant disturbance in cognition, emotion regulation, or behaviour that indicate a dysfunction in mental functioning that is usually associated with significant distress or disability
in work, relationships, or other areas of functioning
Why is the risk of mental disorders high in adolescence? (3)
1) A changing social environment
2) Neural, hormonal and genetic factors
3) Biological risk factors interacting with a
changing environment
What part of the brain is more active in adolescence when passively viewing fearful faces?
Higher activation of the anterior cingulate cortex (ACC), left orbitofrontal cortex (OFC) and amygdala than adults
What do Adolescents’ amygdala’s respond to more than adults?
- Adolescents’ amygdala respond to threat cue
more than adults’ - But not to the safety cue
Warning Signs of Depression (12)
- Feeling hopeless/pessimistic
- Feeling worthless/guilty
- Thoughts of death/suicide
- Restlessness
- Lack of enjoyment in things you usually enjoy
- Decreased Energy
- Irregular Sleep/Insomnia
- Changes in Mood
- Appetite/Weight Loss
- Persistent Sad/Empty/Anxious Mood
- Difficulty Making Choices
- Tearfulness
Defining Depression: 5+ of any of the following symptoms for 2 weeks or more (9)
- Depressed Mood Everyday
- Diminished interest in daily activities
- Significant weight change
- Insomnia/hypersomina everyday
- Psychomotor agitation/retardation everyday
- Fatigue Everyday
- Feelings of worthlessness/ excessive guilt
- Decreased ability to concentrate
- Recurrent thoughts of death
What is the Serotonin Hypothesis of Depression?
Depression is caused by a ‘serotonin imbalance’/’serotonin deficiency’ in the brain
Antidepressants: Tricyclic Antidepressants (TCAs)
- First treatment for depression
- E.g. Imipramine
- Block the reuptake of serotonin and
norepinephrine in presynaptic terminals - Which leads to increased concentration of
these neurotransmitters in the synaptic cleft
Antidepressants: Selective Serotonin Reuptake Inhibitors (SSRIs)
- TCAs replaced with SSRIs
- E.g. Prozac
- Block reuptake of serotonin
- Meaning more serotonin is available to pass
further messages between nearby nerve cells - In the absence of SSRIs, 5-HT binds to SERT
and is recycled to the interior of the presynaptic
neurone - SSRIs down-regulate the activity of SERT and
increase the extracellular level of 5-HT
What are Antidepressants used for? (5)
- Moderate to severe depressive illness (Not mild
depression) - Severe anxiety and panic attacks
- Obsessive compulsive disorders
- Chronic pain
- Eating disorders
- Post-traumatic stress disorder.
How well do they work (after 3 months treatment)?
50% and 65% if given an antidepressant
compared with 25 - 30% if given an inactive placebo pill
What Effect does Acute Tryptophan Depletion have on patients taking SSRIs?
- Acute tryptophan depletion (ATD) lowers
serotonin (5-HT) neurotransmission/synthesis - This induces a transient depressed mood in 50-
60% of patients treated with a selective
serotonin re-uptake inhibitor (SSRI)
What Effect does Acute Tryptophan Depletion have on healthy individuals?
- No robust mood effects
- Mood effects limited to those who are
vulnerable
What differences can be found on Neuroimaging of Depressive Patients?
- A constellation of cerebral blood flow (CBF) and
glucose metabolic abnormalities are found in
limbic and prefrontal cortex (PFC) structures by
PET studies of major depressive disorder
(MDD) - Some abnormalities reverse during symptom
remission and likely reflect areas where
physiologic activity changes to mediate or
respond to the emotional, behavioural &
cognitive manifestations of MDEs
What is the ‘Role’ of the Prefrontal Cortex (PFC)? (2)
- Maintains representations of goals and means
to achieve them (range of ‘executive functions’) - Emotion-processing/regulation or control of
emotional responses
