Week 11- Neuroscience of Bipolar, Autism, and Schizophrenia Flashcards
AUTISM
mirror system
Portions of LS activated when someone is sad, also activated when see another person sad
Attachment theory and mirror neurons
Contagious yawning
The more severe the symptoms of autism, the less active the mirror neuron system seems to be. Studies have demonstrated that children with autism have difficulties understanding the intention of others on the basis of the action they observe. In order to decide what others are doing, they rely on object meaning or the context in which the action is performed. To them, a cup means “drinking” even when others would intuit that the intention is to clear it from the table.
AUTISM
Mesolimbic system and social reward
Anomalous mesolimbic responses to social and nonsocial rewards
AUTISM
Volumetric differences and pruning
Neuronal overgrowth
Lack of synaptic pruning
Areas such as prefrontal cortex (role in communication, social skills, executive functioning)
SCHIZOPHRENIA
Classes of symptoms
Positive- delusions, hallucinations
Negative- apathy, anhedonia, cognitive blunting, neuroleptic, dysphoria
Cognitive- impaired attention and information processing, executive dysfunction
Aggressive- overt hostility, assault, self-injury, arson
Affective- depression, anxiety, guilt, tension, irritability, worry
SCHIZOPHRENIA
Associated circuitry
Positive- Mesolimbic system (nucleus accumbens)
Negative and affective- Mesocortical and ventromedial PFC
Cognitive- Dorsolateral PFC (occur later in illness)
Aggressive- Orbitofrontal PFC (and connections with amygdala)
SCHIZOPHRENIA
The dopamine hypothesis (including pathways)
Schizophrenia related to not enough dopamine in cortex, too much in limbic structures
Arose because too much dopamine causes psychosis and medications that reduce dopamine reduce psychosis
SCHIZOPHRENIA
The glutamate hypothesis
Glutamate driving dopamine
Insufficient glutamate leads to not enough dopamine in cortex
Because of GABA interneurons (inhibitory), end up with dysregulation of dopamine in limbic structures
Hypofunction of glutamate receptors (NMDA receptors)
BIPOLAR
Monoamine hypothesis
Now know serotonin, norepinephrine, and dopamine are all involved (monoamines)
Deficiency = depression
Excess = mania
Evidence lacking for monoamines themselves, focus has shifted to their receptors
BIPOLAR
serotonin
Present in many tissues
Plays important role in transmission of other neurochemicals (the catecholamines)
Switches affecting various mood-states- regulation of mood
Role in sleep, eating, arousal
Regulation of pain
Ascending projections regulate mood, anxiety, sleep
Descending projections regulate pain
BIPOLAR
norepinephrine
“Noradrenergic” Synthesized from dopamine Increases arousal, vigilance Influences reward system Ascending projections regulate mood, arousal, cognition Descending projections regulate pain
BIPOLAR
hypothetical structures in mania
PFC- racing thoughts, grandiosity, distractibility, talkative/pressured, speech; (ACC?): risks, grandiosity, talkative/pressured speech, racing thoughts; mood
NAcc- racing thoughts, goal-directed, grandiosity
Striatum- motor/agitation
Thalamus- decreased sleep/arousal
Hypothalamus- decreased sleep/arousal
Amygdala- mood
Basal Forebrain- decreased sleep/arousal
BIPOLAR
hypothetical structures in depression
PFC- (DLCC): concentration, interest/pleasure; (MedCC): psychomotor fatigue; (ACC?): guilt, suicidality, worthlessness; mood
NA- pleasure, interests, fatigue/energy
S- psychomotor, fatigue (physical)
Hy- sleep/appetite
A- guilt, suicidality, worthlessness, mood
BIPOLAR
Extrapyramidal side effects
drowsiness tremors in your hands dry mouth, increased thirst or urination nausea, vomiting, loss of appetite, stomach pain changes in your skin or hair cold feeling or discoloration in your fingers or toes feeling uneasy impotence, loss of interest in sex
