Lecture 7: Disorders Flashcards
Positive symptoms of schizophrenia
- delusions
- hallucinations
- though disorders
Negative symptoms of schizophrenia
- apathy
- lack of emotion
- anhedonia
- asociality
Cognitive symptoms of schizophrenia
- attention
- learning/memory
- problem solving
- abstract thinking
Family studies
Fisher
-looked at the prevalence rate of schizophrenia in children of MZ twins where one parent had schizophrenia
-prevalence rate is similar and greater then general pop
Adoption studies
*eliminates effects of shared environment
Heston
- followed people born of parent in mental hospital
- 50 control children
-16.6% of children who’s mother had schizophrenia were also diagnosed with it
Diathesis-stress model
=that genetics underpin however needs an environmental trigger
The dopamine hypothesis
=believed that positive symptoms of dopamine related to increased levels of dopamine
-Antipsychotic drugs reduce levels of dopamine (antagonists as block receptors)
•Amphetamines results in paranoid schizophrenic symptoms
- cause dopamine and norepinephrine release and prevents breakdown
- act as dopamine agonists
Dopamine hypothesis currently
- The levels of the dopamine metabolite, HVA, is not increased in patients with schizophrenia
- Increased number of dopamine receptors or increased sensitivity of receptors are what is important-increased sensitivity of receptors/number of receptors not increase of dopamine
Negative/cognitive: brain damage
• Enlarged ventricles
• Prefrontal cortex
-Goal-directed behaviour, speech, decision making
-Poor performance on studies designed to tap prefrontal cortex performance
-Reduced grey matter
-Low metabolic rate in prefrontal cortex
What causes brain damage (schizophrenia)
*use of epidemiological studies
- Season of birth
- Viral epidemics
- Population density
- Substance abuse
Relationship between positive and negative symptoms
Genetic and/or environmental causes results in:
- Abnormalities in DA transmission and prefrontal cortex
- Abnormalities in DA transmission cause prefrontal abnormalities
- Abnormalities in Prefrontal cause abnormal DA transmission
PCP and ketamine
- cause all 3 types of symptoms
- caused by reduced metabolic activity in the frontal lobes
- indirect antagonists of NMDA receptors which decrease activity in the prefrontal cortex
- also decrease the level of DA utilisation
Traditional treatments
Schizophrenia
- decrease DA transmission in mesolithic pathway
- reduce positive but increase negative and cognitive symptoms
New treatments
Schizophrenia
- Decrease activity in the mesolimbic system
- Increase DA activity in the prefrontal cortex
- Partial agonist*= compete with dopamine with the brain for the receptor, have high affinity for receptors, act to a lesser extent that dopamine, bind more regularly, activate much less, so in mesolimbic pathway activity is decrease, positive symptoms decreased
- still get net increases in activity than what you’d get from dopamine itself
- Major depressive disorder
* Bipolar disorder
• Major depressive disorder
- Depressed mood
- Loss of interest/pleasure
- Changes in sleep, appetite, attention, suicidal thoughts
• Bipolar depression
- Symptoms of depression
- Episodes of mania – intense elation, flight of ideas
Etiology
- Heritable
- Sullivan et al., (2000): meta-analysis 37 % heritability for MDD
- Kelsoe (1997): Bipolar disorder 70 % concordance rate between MZ twins, 25 % for DZ
- Genetic predisposition to developing but need an environmental trigger
Monoamine oxidase (MAO) inhibitors
- destroys excess monoamine transmitter in terminal boutons
- inhibitors inhibit this breakdown
-increases availability of DA, serotonin and norepinephrine
Tricyclic antidepressants
- Inhibit the reuptake of serotonin and norepinephrine into terminal buttons
- Increase post-synaptic potentials
Biological treatments: ECT
- Used to treat seizures and found improved mood
- Decreases brain activity
- TMS: stimulate very specific areas of the brain, target regions of the brain involved in depression
Monoamine hypotheses
• What do we know from the treatments?
-Preventing the reuptake of monoamines = decreases in depression
• Depression results from decreased activity of monoaminergic neurons
-Serotonin and norepinephrine: believed underpinned by decreases in availability of these
• However, too simple
-Drugs take several weeks to have an effect
-lag between metal health improvement and when drug took its initial effect
-No increase in metabolites
Neuroimaging
• MDD associated with brain regions activated by emotions
-Amygdala
-Prefrontal cortex
-Anterior cingulate cortex
• Treatment : reduce ACC activity and increase PFC activity
-The ACC connects to the amygdala
-The ACC connects to the PFC which connects to the amygdala
-Decreased activity in the amygdala (involved in what emotions people have, fight and flight)
-by decreasing activity in amydala, decrease attention to negative stimuli
OCD
- Obsessive: persistent, uncontrollable, irrational thoughts
- Compulsions: repetitive and excessive acts that reduce anxiety
- Causes marked distress and impairs functioning
OCD ethology
- Genetic: Higher concordance rate in MZ vs. DZ twins
- Infections: basal ganglia-injury triggers OCD
- Brain injury: basal ganglia; prefrontal cortex; cingulate gyrus-all regions altered neural functioning which relates to OCD
- Neural activity: frontal lobes, prefrontal cortex, cingulate cortex, caudate nucleus
- Involved in emotional reactions
- Cause vs. Effect?-altered neural causes OCD or other way around?
Treatment OCD
• Decrease in symptoms associated with decrease neural activity in caudate nucleus and prefrontal cortex
• Destroy fibre bundles:
-Prefrontal and cingulate cortices with the limbic system
-Basal ganglia and prefrontal cortex
• Drugs
-SSRIs
-Serotonin has an inhibitory effect on behaviour
-Prefrontal cortex and basal ganglia are influenced by serotonin
