Chapter 8: Anxiety and Trauma Flashcards
which brain circuits may be malfunctioning in GAD
amygdala and CSTC
Anxiety and fear are regulated by which brain circuit
amygdala centered circuit
worry is regulated by which brain circuit
cortico-striatal-thalamic-cortical (CSTC)
the affect of fear is regulated by reciprocal connections between which two brain circuits
-amygdala and anterior cingulate cortex
-amygdala and orbitofrontal cortex
what regulates motor responses to fear
connections between the amygdala and periaqueductal gray area of the brain stem
what causes the endocrine output of fear
connections between amygdala and hypothalamus causing changes in the HPA axis to give a quick boost of cortisol to enhance survival instincts
what causes changes to breathing output during anxiety
connections between amygdala and parabrachial nucleus (PBN) in the brainstem
autonomic and cardio responses to fear are mediated by what connections
connections between the amygdala and the locus coeruleus
how is the hippocampus the internal fear monger
anxiety can be triggered by traumatic memories stored in the hippocampus and activated by connections to the amygdala
what is thought to cause worry/obsessions
worry may be d/t overactivation of the CSTC loop originating and terminating in the DLPFC
how do benzodiazepines work as medications for anxiety
act as PAMs on postsynaptic GABAA receptors in the amygdala where they blunt fear outputs and enhance the action of inhibitory GABA in the PFC
what is the key neurotransmitter that innervates the amygdala as well as elements of the CSTC circuits
serotonin
what action makes buspirone an effective anxiety treatment for GAD
5HT1A partial agonism
what disorder is treated by buspirone
GAD is the only anxiety disorder it works for
where in the brain does buspirone enhance serotonergic activity to reduce worry
in projections to the amygdala, PFC, striatum, and thalamus
how fast does buspirone work
delayed onset of action like SSRIs
where in the brain does norepinephrine have important regulatory input
amygdala, PFC, and thalamus CSTC circuits
what causes the peripheral manifestations of autonomic overdrive
excessive norepinephrine output from the locus coeruleus
anxiety symptoms caused by excessive norepinephrine output from the locus coeruleus
central symptoms
reduced information processing in the PFC and CSTC circuits
central symptoms of anxiety/fear
nightmares
hyperarousal states
flashbacks
panic attacks
what can happen to anxiety symptoms after SNRI initiation and why?
fear and worry can get worse initially until B1-adrenergic receptors are downregulated
how does the amygdala “remember” stimuli associated with a fearful situation
it increases the efficacy of glutamate neurotransmission in the lateral amygdala when fearful stimuli is received from the thalamus or sensory cortex. Input is then relayed to the central amygdala where neurotransmission of glutamate is further improved by fear conditioning
VMPFC role in fear conditioning
-if VMPFC cannot suppress fear response before it reaches the amygdala fear conditioning results
hippocampus role in fear conditioning
remembers the context of the fear conditioning so that fear is experienced when same or associated stimuli is encountered
what causes a fear response to be generated or suppressed
input from fearful experience is relayed to amygdala where it is integrated with input from the VMPFC and hippocampus to generate or suppress a fear response
what causes a fear response to be more efficiently triggered upon repeated exposure to anxiety-provoking situation
amygdala “remembers” associated stimuli by increasing efficiency of glutamate neurotransmission in response to it
what causes fear conditioning
when increased glutamate neurotransmission from the amygdala is not countered with input from the VMPFC to suppress the fear response, fear conditioning results
what is fear extinction
progressive reduction of fear response when stimuli is repeatedly presented without adverse consequences
how does fear extinction work
the VMPFC activates the amygdala over and over without fear being triggered then the hippocampus begins to remember the new context of the feared stimulus having no adverse consequences
how does fear extinction overrule fear conditioning
when the new circuit has stronger synaptic connections and long-term potentiation it is able to produce inhibitory GABAerbic drive that overcomes excitatory glutamatergic drive
what is reconsolidation
a memory becomes labile while being re-experienced and becomes malleable so that it can be modified
classifications of drugs used to treat GAD
SSRI
SNRI
benzodiazepines
buspirone
ligands (pregabalin, gabapentin)
off label txs for GAD
mirtazapine
trazadone
vilazodone
TCAs
sedating antihistamines (Vistaril)
medication categories for treatment of panic disorder
SSRI
SNRI
benzodiazepines
ligands (pregabalin, gabapentin)
off label treatments for panic attacks
mirtazapine
trazadone
medication categories of treatment options for social anxiety disorder
SSRI
SNRI
ligands
what is PTSD treatment often aimed at
comorbidities (depression, insomnia, substance abuse)
