Figures from Chapter 4

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Figure 4.1 (A) Amygdala hyperactivity is present in MDD, in both depressed and remitted
individuals. (B) This hyperactivity distinguishes an MDE and predicts the severity of symptoms
Figure 4.2 In MDD, there is (A) hyperactivity of the amygdala (1), dACC (2), and anterior insula (3),
as well as (B) in the pulvinar nucleus of the thalamus (1, 2), which relays visual information
Figure 4.3 Increased severity of depressive symptoms in MDD is related to weaker functional
connectivity between the amygdala and the mPFC
Figure 4.4 The risk of developing MDD in response to stress is greater in individuals with higher
levels of negative affect and anxiety, as indexed by the trait of neuroticism
Figure 4.5 (A) Treatment of MDD with SSRIs appears to increase functional connectivity between
the amygdala and mPFC and decrease amygdala hyperactivity. (B) CBT treatment of MDD resulted
in decreased amygdala hyperactivity
Figure 4.5 (A) Treatment of MDD with SSRIs appears to increase functional connectivity between
the amygdala and mPFC and decrease amygdala hyperactivity. (B) CBT treatment of MDD resulted
in decreased amygdala hyperactivity (Part 1)
Figure 4.5 (A) Treatment of MDD with SSRIs appears to increase functional connectivity between
the amygdala and mPFC and decrease amygdala hyperactivity. (B) CBT treatment of MDD resulted
in decreased amygdala hyperactivity (Part 2)
Figure 4.6 (A) Amygdyla activity in BD shows state-dependent differences: hyperactivity during
mania, hypoactivity during depression, and activity equivalent to healthy during euthymia. (B) In
contrast, vlPFC hypoactivity in BD is state-independent and unchanging
Figure 4.7 A panic attack captured on fMRI. Initial increase in insula activity was related to feelings
of discomfort (A) and followed by increased amygdala activity (B) just before the patient
discontinued the scan
Figure 4.7 A panic attack captured on fMRI. Initial increase in insula activity was related to feelings
of discomfort (A) and followed by increased amygdala activity (B) just before the patient
discontinued the scan
Figure 4.8 Amygdala (A) and insula (B) hyperactivity is more pronounced in social anxiety disorder
and specific phobia than in PTSD
Figure 4.9 (A,B) Exposure therapy significantly decreased amygdala hyperactivity in individuals
with spider phobia. (C) These decreases in amygdala hyperactivity likely reflect increases in
regulatory activity of the prefrontal cortex, including the vmPFC
Figure 4.9 (A,B) Exposure therapy significantly decreased amygdala hyperactivity in individuals
with spider phobia. (C) These decreases in amygdala hyperactivity likely reflect increases in
regulatory activity of the prefrontal cortex, including the vmPFC (Part 1)
Figure 4.9 (A,B) Exposure therapy significantly decreased amygdala hyperactivity in individuals
with spider phobia. (C) These decreases in amygdala hyperactivity likely reflect increases in
regulatory activity of the prefrontal cortex, including the vmPFC (Part 2)
Figure 4.9 (A,B) Exposure therapy significantly decreased amygdala hyperactivity in individuals
with spider phobia. (C) These decreases in amygdala hyperactivity likely reflect increases in
regulatory activity of the prefrontal cortex, including the vmPFC (Part 3)
Figure 4.10 (A) Hyperactivity of the amygdala and dorsal ACC (yellow); and hypoactivity of the
vmPFC and vlPFC (blue) in PTSD. (B) Amygdala hyperactivity to negative trauma-related imagery
predicts symptom severity
Figure 4.11 (A) Activity of the dmPFC is associated with decreased PTSD symptom severity
measured with the CAPS. (B) Activity of the HF is also associated with decreased symptoms
Figure 4.12 Individuals with PTSD exhibit impaired fear extinction and associated abnormal
corticolimbic circuit function
Figure 4.12 Individuals with PTSD exhibit impaired fear extinction and associated abnormal
corticolimbic circuit function (Part 1)
Figure 4.12 Individuals with PTSD exhibit impaired fear extinction and associated abnormal
corticolimbic circuit function (Part 2)
Figure 4.13 Studies with military personnel reveal that amygdala hyperactivity prior to combat
exposure predicts increased sensitivity to combat-related stress
Figure 4.14 (A) During processing of emotional facial expressions, there is amygdala hyperactivity
in GAD only, MDD only, or comorbid for both GAD and MDD. (B) The opposite pattern of hypo- and
hyperactivity is observed for the vmPFC
Figure 4.14 (A) During processing of emotional facial expressions, there is amygdala hyperactivity
in GAD only, MDD only, or comorbid for both GAD and MDD. (B) The opposite pattern of hypo- and
hyperactivity is observed for the vmPFC (Part 1)
Figure 4.14 (A) During processing of emotional facial expressions, there is amygdala hyperactivity
in GAD only, MDD only, or comorbid for both GAD and MDD. (B) The opposite pattern of hypo- and
hyperactivity is observed for the vmPFC (Part 2)
Figure 4.15 Individuals with GAD exhibit amygdala hyperactivity during the anticipation but not the
actual viewing of either aversive or neutral pictures
Figure 4.16 Activity in the BNST increases as healthy participants track the probability of receiving
a mild electric shock in the future
Figure 4.17 In men, the propensity to experience more or less anger in contexts of reasonable
provocation is predicted by the magnitude of amygdala activity to angry but not fearful facial
expressions
Figure 4.18 Unlike healthy individuals, who focus their attention on the eyes of a face, individuals
with ASD focus their attention on the mouth
Figure 4.19 (A) Amygdala activity is greater in individuals with ASD when they attend to the eyes of
face stimuli. (B) The magnitude of amygdala activity is positively correlated with the amount of time
attended to the eyes
Figure 4.20 (A) Amygdala activity to faces habituates on repeated exposure in healthy participants
but not individuals with ASD. (B) Lack of amygdala habituation in ASD is associated with social
deficits
Figure 4.21 Individuals with MDD exhibited relative amygdala hypoactivity to happy facial
expressions but hyperactivity to sad facial expressions. The opposite pattern was found in healthy
participants
Figure 4.22 (A) Boys with certain traits exhibit decreased amygdala activity to fearful faces. (B)
Decreased connectivity between the amygdala and vmPFC and CU traits. (C) Adolescent boys with
high levels of CU traits spend significantly time attending to the eyes of fearful expressions
Figure 4.22 (A) Boys with certain traits exhibit decreased amygdala activity to fearful faces. (B)
Decreased connectivity between the amygdala and vmPFC and CU traits. (C) Adolescent boys with
high levels of CU traits spend significantly time attending to the eyes of fearful expressions (Part 1)
Figure 4.22 (A) Boys with certain traits exhibit decreased amygdala activity to fearful faces. (B)
Decreased connectivity between the amygdala and vmPFC and CU traits. (C) Adolescent boys with
high levels of CU traits spend significantly time attending to the eyes of fearful expressions (Part 2)
Figure 4.22 (A) Boys with certain traits exhibit decreased amygdala activity to fearful faces. (B)
Decreased connectivity between the amygdala and vmPFC and CU traits. (C) Adolescent boys with
high levels of CU traits spend significantly time attending to the eyes of fearful expressions (Part 3)
Figure 4.23 (A) Psychopaths were conscious of which stimulus was paired with pain (the CS) and
perceived the CS as aversive. (B) Psychopaths showed decreased activity in amygdala, mPFC,
and insula, which is consistent with failure to acquire conditioned fear response
Figure 4.23 (A) Psychopaths were conscious of which stimulus was paired with pain (the CS) and
perceived the CS as aversive. (B) Psychopaths showed decreased activity in amygdala, mPFC,
and insula, which is consistent with failure to acquire conditioned fear response (Part 1)
Figure 4.23 (A) Psychopaths were conscious of which stimulus was paired with pain (the CS) and
perceived the CS as aversive. (B) Psychopaths showed decreased activity in amygdala, mPFC,
and insula, which is consistent with failure to acquire conditioned fear response (Part 2)
Figure 4.24 (A) Amygdala hypoactivity to fearful faces is associated with greater levels of
remorseless and callous exploitation of others. (B) Amygdala hyperactivity to angry faces is
associated with dangerous activities and reckless behavior
Figure 4.25 Individuals with Williams syndrome exhibit amygdala hyperactivity to happy facial
expressions but hypoactivity to fearful facial expressions
Figure 4.26 Individuals with Williams syndrome exhibit amygdala hypoactivity to social threat but
hyperactivity to nonsocial threat

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