Clinical categorization of anxiety disorders
According to the Diagnostic and Statistical Manual of Men- tal Disorders, 5th Edition,5 anxiety and stress disorders are characterized by an excessive fear response and/or worry that interferes with functioning or causes significant distress. This class of disorders includes panic disorder (PD), specific phobia (SP), social anxiety disorder (SAD), PTSD, and gen- eralized anxiety disorder (GAD).
Panic disorder
PD is characterized by sudden panic attacks, often occurring unexpectedly, followed by a month or more of worrying about having another attack or the consequence of the attack (eg, heart attack, stroke). Common symptoms during a panic attack include racing heart, shortness of breath, tightness in chest, paresthesia, gastrointestinal distress, sweating, hot/cold flashes, fear of dying, and fear of losing control. PD suffer- ers often develop agoraphobia, avoiding places or situations where they think they might have a panic attack.
Specific phobia
SP is characterized by excessive fear triggered by a specific object or situation. SP falls into four subtypes, including animal, natural environment (eg, heights, storms), blood- injection-injury, and other (choking, vomiting, illness, cos- tumed characters, etc). The excessive fear brought on by the phobic object or situation leads to intense distress, anxious anticipation, panic attacks, and/or avoidance of the feared object or situation.
According to the Diagnostic and Statistical Manual of Men- tal Disorders, 5th Edition,5 anxiety and stress disorders are characterized by an excessive fear response and/or worry that interferes with functioning or causes significant distress. This class of disorders includes panic disorder (PD), specific phobia (SP), social anxiety disorder (SAD), PTSD, and gen- eralized anxiety disorder (GAD).
Panic disorder
PD is characterized by sudden panic attacks, often occurring unexpectedly, followed by a month or more of worrying about having another attack or the consequence of the attack (eg, heart attack, stroke). Common symptoms during a panic attack include racing heart, shortness of breath, tightness in chest, paresthesia, gastrointestinal distress, sweating, hot/cold flashes, fear of dying, and fear of losing control. PD suffer- ers often develop agoraphobia, avoiding places or situations where they think they might have a panic attack.
Specific phobia
SP is characterized by excessive fear triggered by a specific object or situation. SP falls into four subtypes, including animal, natural environment (eg, heights, storms), blood- injection-injury, and other (choking, vomiting, illness, cos- tumed characters, etc). The excessive fear brought on by the phobic object or situation leads to intense distress, anxious anticipation, panic attacks, and/or avoidance of the feared object or situation.
Social anxiety disorder
SAD is characterized by persistent fear of social or perfor- mance situations resulting from the possibility of negative judgment, embarrassment, or humiliation. Cognitive distor- tions and self-monitoring in social situations, involving hyperawareness of internal cues and behaviors, are often associated with SAD. Feared social situations are avoided or tolerated with dread.
Posttraumatic stress disorder
PTSD can develop after exposure to serious injury, death, or a potential threat to the physical integrity of self or oth- ers. Symptom clusters include intrusive reexperiencing symptoms (memories of trauma, nightmares, flashbacks); avoidance of trauma-related thoughts, memories, contexts or cues; negative mood and cognition; and hyperarousal/ hypervigilance.
Generalized anxiety disorder
The core symptom in GAD is excessive and continuous worry, anxiety, and apprehensive expectation in multiple contexts. The ambiguity and diversity of the sources of stress and anxiety distinguishes this disorder from cue-related anxiety disorders such as PD, SP, SAD, and PTSD. There is a cognitive component to GAD that is characterized by worrisome thoughts and cognitive errors.
Despite the lack of concrete knowledge regarding the specific mechanisms underlying anxiety, both pharmacologic (selective serotonin reuptake inhibitors) and psychotherapeutic (cognitive behavioral therapy) treatments for anxiety management have been developed.
SAD is characterized by persistent fear of social or perfor- mance situations resulting from the possibility of negative judgment, embarrassment, or humiliation. Cognitive distor- tions and self-monitoring in social situations, involving hyperawareness of internal cues and behaviors, are often associated with SAD. Feared social situations are avoided or tolerated with dread.
Posttraumatic stress disorder
PTSD can develop after exposure to serious injury, death, or a potential threat to the physical integrity of self or oth- ers. Symptom clusters include intrusive reexperiencing symptoms (memories of trauma, nightmares, flashbacks); avoidance of trauma-related thoughts, memories, contexts or cues; negative mood and cognition; and hyperarousal/ hypervigilance.
Generalized anxiety disorder
The core symptom in GAD is excessive and continuous worry, anxiety, and apprehensive expectation in multiple contexts. The ambiguity and diversity of the sources of stress and anxiety distinguishes this disorder from cue-related anxiety disorders such as PD, SP, SAD, and PTSD. There is a cognitive component to GAD that is characterized by worrisome thoughts and cognitive errors.
Despite the lack of concrete knowledge regarding the specific mechanisms underlying anxiety, both pharmacologic (selective serotonin reuptake inhibitors) and psychotherapeutic (cognitive behavioral therapy) treatments for anxiety management have been developed.
Sensory processing regions
According to rodent models and human imaging studies, a number of regions responsible for taking in and processing sensory information, such as the occipital cortex, fusiform gyrus, and thalamus, have been implicated in anxiety disorder neurocircuitry.11,20 The main finding reported is increased activation in these regions in response to threatening stimuli in anxious patients compared to healthy controls.
Occipital cortex and fusiform gyrus
The occipital cortex, a region responsible for processing visual stimuli, is more active in response to threatening images in anxious patients, particularly those with SAD, compared with controls. In patients with SAD, greater acti- vation in occipitotemporal regions predicted D-cycloserine treatment response, with greater pretreatment activation associated with a greater decrease in symptoms posttreat- ment.21 The fusiform gyrus contains neurons specific to face perception, known as the fusiform face area,22 which is more active in response to threat faces in SAD compared with healthy controls.23
Thalamus
The thalamus is implicated in sensory integration, and functional imaging studies revealed increased activation in the thalamus in response to phobic-related and threat stimuli in patients with SAD,24,25 blood-injection-injury phobia,26 dental phobia,27 spider phobia,28 snake phobia,29 and PTSD.30 Contrary to these findings, one study reported that dental phobics did not demonstrate increased activation in thalamus to phobic images.29 Activation in the thalamus was correlated with the degree of anxiety and disgust in blood-injury-injection phobia,26 as well as autonomic arousal in snake phobia, but not in dental phobia.29 Treatment with paroxetine reduced activation in thalamus compared with placebo treatment in response to a recorded performance task in SAD.31
Emotion generating/processing regions
Ample evidence from basic and human imaging studies suggests that regions such as the striatum,32 amygdala,10,33,34
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According to rodent models and human imaging studies, a number of regions responsible for taking in and processing sensory information, such as the occipital cortex, fusiform gyrus, and thalamus, have been implicated in anxiety disorder neurocircuitry.11,20 The main finding reported is increased activation in these regions in response to threatening stimuli in anxious patients compared to healthy controls.
Occipital cortex and fusiform gyrus
The occipital cortex, a region responsible for processing visual stimuli, is more active in response to threatening images in anxious patients, particularly those with SAD, compared with controls. In patients with SAD, greater acti- vation in occipitotemporal regions predicted D-cycloserine treatment response, with greater pretreatment activation associated with a greater decrease in symptoms posttreat- ment.21 The fusiform gyrus contains neurons specific to face perception, known as the fusiform face area,22 which is more active in response to threat faces in SAD compared with healthy controls.23
Thalamus
The thalamus is implicated in sensory integration, and functional imaging studies revealed increased activation in the thalamus in response to phobic-related and threat stimuli in patients with SAD,24,25 blood-injection-injury phobia,26 dental phobia,27 spider phobia,28 snake phobia,29 and PTSD.30 Contrary to these findings, one study reported that dental phobics did not demonstrate increased activation in thalamus to phobic images.29 Activation in the thalamus was correlated with the degree of anxiety and disgust in blood-injury-injection phobia,26 as well as autonomic arousal in snake phobia, but not in dental phobia.29 Treatment with paroxetine reduced activation in thalamus compared with placebo treatment in response to a recorded performance task in SAD.31
Emotion generating/processing regions
Ample evidence from basic and human imaging studies suggests that regions such as the striatum,32 amygdala,10,33,34
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insula,11,14,15 and dACC35 play a large role in identifying fear stimuli and generating fear responses. These areas often have structural abnormalities and are hyperactive in anxiety compared to controls. Extensive prior evidence13 suggests hyperactivation in the amygdala across all anxiety disorders. Hyperactivation was also reported in insula in SP, SAD, PTSD, and GAD, whereas activation differences were less consistent in PD. Hyperactivation in dACC was reported in SP and PTSD, with mixed findings in PD and SAD and limited evidence in GAD.
Striatum
Less activation in ventral striatum has been reported in SAD while anticipating giving a speech, with greater levels of anticipatory anxiety predicting less activation.36 Although striatal activation is typically modulated in response to social cooperation, this was not observed in SAD, suggesting abnormalities in reward circuitry related to the initiation and maintenance of social relationships.37
Amygdala
Studies examining structural differences in the amygdala in anxiety patients compared with healthy controls find decreased amygdala volume and density in PD,38–40 SP,41 and PTSD,42 with symptom severity predictive of smaller amygdala volume.41 In contrast, some studies reported larger amygdala volume in anxiety, specifically GAD43 and PTSD.44 The picture for SAD is more complex, with reports of reduced amygdala volume,45 no differences in amygdala volume,46 and larger amygdala volume47 in SAD compared with controls.
Recent functional imaging studies report amygdala hyperactivation in response to threatening stimuli in PD,39 SP,28,48,49 SAD,24,36,50–52 and PTSD53,54 compared with healthy controls. The degree of amygdala activation was positively correlated with symptom severity in SP48 and SAD.50 More- over, treatment with medication and psychotherapy often results in decreased amygdala hyperactivation to threat from pre- to posttreatment in SP,48 SAD,55–58 and PTSD.59 Patterns of amygdala activation in GAD are more complex, with studies reporting increased60,61 or no difference62 in activation in GAD compared with healthy controls. Null and opposing findings suggesting no difference or decreased amygdala activation in anxiety compared with controls have also been reported in PD,63,64 SP,49 and SAD,65 with some evidence that medication treatment (paroxetine) increases amygdala activation in SAD compared with healthy controls.31
Striatum
Less activation in ventral striatum has been reported in SAD while anticipating giving a speech, with greater levels of anticipatory anxiety predicting less activation.36 Although striatal activation is typically modulated in response to social cooperation, this was not observed in SAD, suggesting abnormalities in reward circuitry related to the initiation and maintenance of social relationships.37
Amygdala
Studies examining structural differences in the amygdala in anxiety patients compared with healthy controls find decreased amygdala volume and density in PD,38–40 SP,41 and PTSD,42 with symptom severity predictive of smaller amygdala volume.41 In contrast, some studies reported larger amygdala volume in anxiety, specifically GAD43 and PTSD.44 The picture for SAD is more complex, with reports of reduced amygdala volume,45 no differences in amygdala volume,46 and larger amygdala volume47 in SAD compared with controls.
Recent functional imaging studies report amygdala hyperactivation in response to threatening stimuli in PD,39 SP,28,48,49 SAD,24,36,50–52 and PTSD53,54 compared with healthy controls. The degree of amygdala activation was positively correlated with symptom severity in SP48 and SAD.50 More- over, treatment with medication and psychotherapy often results in decreased amygdala hyperactivation to threat from pre- to posttreatment in SP,48 SAD,55–58 and PTSD.59 Patterns of amygdala activation in GAD are more complex, with studies reporting increased60,61 or no difference62 in activation in GAD compared with healthy controls. Null and opposing findings suggesting no difference or decreased amygdala activation in anxiety compared with controls have also been reported in PD,63,64 SP,49 and SAD,65 with some evidence that medication treatment (paroxetine) increases amygdala activation in SAD compared with healthy controls.31
insula
Structural imaging results revealed conflicting reports of increased volume in SAD,66 no difference in SP,67 and decreased volume in SAD46 and PTSD68–70 compared with controls.
Recent functional imaging studies revealed insula hyper- activation to threat in patients with SP,27–29,71 SAD,36,50,52,65,72,73 and PTSD30,54,74–77 compared with controls. The degree of insula hyperactivation was positively correlated with symp- tom severity in SAD.72 Both medication and psychotherapy have been shown to decrease insula hyperactivation from pre- to posttreatment in SAD.31,58,78 In contrast, one study found that patients with dental phobia did not show hyperactivation in insula during exposure to phobic stimuli compared with healthy controls.29
Dorsal anterior cingulate cortex
Literature suggests decreased dACC gray matter and white matter volume in PD,40 SP,79 and PTSD80–82 compared with healthy controls. In contrast, some studies have reported increased volume in dACC in SAD66 and GAD.43
Functional imaging studies reported dACC hyperac- tivation to threat in SP,26–29,71 SAD,24,50,83 and PTSD.30,84–86 Increased dACC activation was correlated with greater autonomic arousal29 and subjective anxiety levels26,71 in SP. Cognitive behavioral therapy was found to decrease ACC activation in SP,71 and pretreatment ACC activation pre- dicted positive treatment response in patients with GAD.61 Despite relatively consistent findings of hyperactivation in dACC, some idiosyncrasies exist in the literature. In contrast to other types of phobia, patients with dental phobia26 and blood-injection-injury phobia29 did not exhibit increased ACC activation to phobic stimuli relative to healthy controls, suggesting dACC may not be involved in threat processing in some anxiety symptom presentations. Moreover, one study reported that dACC was less active to threat in SAD compared with healthy controls.87
Emotion modulation regions
Regions involved in regulating threat responding are particu- larly important in anxiety, as they can decrease activation in threat-processing regions such as the amygdala, insula, and dACC. These have been identified using basic science models and human imaging studies. The mPFC, hippocampus, dorsolateral prefrontal cortex (dlPFC), and rACC have been implicated in modulating fear responding. Although the mPFC10,33,34,88 and rACC89 are primarily involved in modulating emotion, the dlPFC89 has been implicated in both emotion modulation and attention control. The hippocampus
Recent functional imaging studies revealed insula hyper- activation to threat in patients with SP,27–29,71 SAD,36,50,52,65,72,73 and PTSD30,54,74–77 compared with controls. The degree of insula hyperactivation was positively correlated with symp- tom severity in SAD.72 Both medication and psychotherapy have been shown to decrease insula hyperactivation from pre- to posttreatment in SAD.31,58,78 In contrast, one study found that patients with dental phobia did not show hyperactivation in insula during exposure to phobic stimuli compared with healthy controls.29
Dorsal anterior cingulate cortex
Literature suggests decreased dACC gray matter and white matter volume in PD,40 SP,79 and PTSD80–82 compared with healthy controls. In contrast, some studies have reported increased volume in dACC in SAD66 and GAD.43
Functional imaging studies reported dACC hyperac- tivation to threat in SP,26–29,71 SAD,24,50,83 and PTSD.30,84–86 Increased dACC activation was correlated with greater autonomic arousal29 and subjective anxiety levels26,71 in SP. Cognitive behavioral therapy was found to decrease ACC activation in SP,71 and pretreatment ACC activation pre- dicted positive treatment response in patients with GAD.61 Despite relatively consistent findings of hyperactivation in dACC, some idiosyncrasies exist in the literature. In contrast to other types of phobia, patients with dental phobia26 and blood-injection-injury phobia29 did not exhibit increased ACC activation to phobic stimuli relative to healthy controls, suggesting dACC may not be involved in threat processing in some anxiety symptom presentations. Moreover, one study reported that dACC was less active to threat in SAD compared with healthy controls.87
Emotion modulation regions
Regions involved in regulating threat responding are particu- larly important in anxiety, as they can decrease activation in threat-processing regions such as the amygdala, insula, and dACC. These have been identified using basic science models and human imaging studies. The mPFC, hippocampus, dorsolateral prefrontal cortex (dlPFC), and rACC have been implicated in modulating fear responding. Although the mPFC10,33,34,88 and rACC89 are primarily involved in modulating emotion, the dlPFC89 has been implicated in both emotion modulation and attention control. The hippocampus
is primarily involved in encoding contextual information and modulating fear responding within the context of threat and safety signals.11 As such, these regions underlie differ- ent functions that may work in concert to modulate threat response. Evidence reported before the scope of the current review13 suggests hyperactivation in the hippocampus in PD and PTSD but little evidence for hippocampus involvement in other anxiety disorders. Hypoactivation in the mPFC has been reported in PTSD and GAD, with less consistent results seen in PD, SP, and SAD. Evidence for dlPFC and rACC is less consistent and less studied, with both hyper- and hypo- activation reported in PD, SP, SAD, and PTSD.
Medial prefrontal cortex
Structural imaging studies report differences in mPFC, with increased volume in SAD,90 decreased volume in PTSD,77,80 and no difference in GAD,91 with decreased volume associ- ated with greater symptom severity in PTSD.92,93
Functional imaging studies, including two recent meta- analyses and a literature review,30,76,94 primarily report decreased mPFC activation in PTSD compared with healthy controls. Some other studies of PTSD patients reported increased mPFC activation in response to fearful faces.74,75,95 Similar findings are reported in SAD, with both increased96 and decreased97 mPFC activation in response to threat and social tasks. Results are somewhat more consistent in GAD, with the majority reporting decreased mPFC activation.62,98–100 It has been suggested that hyperactivation and hypoactiva- tion in mPFC may be associated with different symptom profiles.101 It is also possible that although hypoactivation indicates a deficit in emotion regulation, hyperactivation indi- cates an overcompensatory response in an effort to decrease excessive fear responding. Regardless of these discrepancies, the treatment literature is quite consistent, suggesting that both pharmacotherapy and psychotherapy produce increases in mPFC activation in SAD57,58,102,103 and PTSD,59 which is related to symptom improvements.
Hippocampus
Although the hippocampus is often considered part of the limbic system responsible for fear generation, the majority of evidence in rodent and human models examining hippocampal function suggests its primary role is in context learning and fear modulation in the presence of safety and threat contexts.11 Structural imaging studies of the hippocampus suggest decreased volume and density in PD,38,40 SAD,45,104,90, GAD,106 and PTSD. There is also evidence for increased hippocampal volume after treatment with selective serotonin reuptake inhibitors in PTSD.107 However, findings are somewhat mixed, with studies also reporting no differences46 and larger47,108 hippocampal volume in SAD compared with healthy controls.
Medial prefrontal cortex
Structural imaging studies report differences in mPFC, with increased volume in SAD,90 decreased volume in PTSD,77,80 and no difference in GAD,91 with decreased volume associ- ated with greater symptom severity in PTSD.92,93
Functional imaging studies, including two recent meta- analyses and a literature review,30,76,94 primarily report decreased mPFC activation in PTSD compared with healthy controls. Some other studies of PTSD patients reported increased mPFC activation in response to fearful faces.74,75,95 Similar findings are reported in SAD, with both increased96 and decreased97 mPFC activation in response to threat and social tasks. Results are somewhat more consistent in GAD, with the majority reporting decreased mPFC activation.62,98–100 It has been suggested that hyperactivation and hypoactiva- tion in mPFC may be associated with different symptom profiles.101 It is also possible that although hypoactivation indicates a deficit in emotion regulation, hyperactivation indi- cates an overcompensatory response in an effort to decrease excessive fear responding. Regardless of these discrepancies, the treatment literature is quite consistent, suggesting that both pharmacotherapy and psychotherapy produce increases in mPFC activation in SAD57,58,102,103 and PTSD,59 which is related to symptom improvements.
Hippocampus
Although the hippocampus is often considered part of the limbic system responsible for fear generation, the majority of evidence in rodent and human models examining hippocampal function suggests its primary role is in context learning and fear modulation in the presence of safety and threat contexts.11 Structural imaging studies of the hippocampus suggest decreased volume and density in PD,38,40 SAD,45,104,90, GAD,106 and PTSD. There is also evidence for increased hippocampal volume after treatment with selective serotonin reuptake inhibitors in PTSD.107 However, findings are somewhat mixed, with studies also reporting no differences46 and larger47,108 hippocampal volume in SAD compared with healthy controls.
Functional imaging studies report increased hippocampal activation to threat in SP,49 SAD,24 and PTSD30,75,95 compared with healthy controls. Increased hippocampal activation was related to defensive reactivity in response to threat stimuli in SP.49 Differences in hippocampus activation in PTSD during memory tasks53,109,110 and emotional activation tasks54 have been less consistent, with both increased and decreased activation reported.
Other modulatory regions
Evidence exists suggesting that other regions, including the dlPFC and subgenual/rACC, play a role in emotion modulation.89 Structural imaging studies report increased dlPFC volume and thickness in SP,111 with larger volume predicting more severe symptoms and arousal levels.
Functional imaging studies report dlPFC hyperactivation to threat in SP111 compared with controls. In addition, dlPFC mediated the influence of SAD on laughter perception, which was related to symptom severity.112 Hypoactivation in rACC has been reported in SAD,65 PTSD,94,113 and GAD.62,100,114However, treatment with computerized attention training58 and paroxetine31 reduced activation in subgenual ACC in SAD.
Connectivity between regions
More recent studies have begun to focus on connectivity between brain regions in anxiety patients. Results over- whelmingly suggest decreased connectivity between emo- tion processing (amygdala, insula) and emotion modulation (mPFC, rACC) regions. This finding is consistent both during rest and while performing a variety of cognitive and emo- tional tasks and is often interpreted as a deficit in regulating fear responding. Studies examining the structural connectiv- ity between medial-frontal and basal-limbic areas, including the amygdala, measured via volume of the uncinated fascicu- lus, revealed smaller volume in the left uncinated fasciculus in patients with SAD than in controls. This finding suggests communication deficits between emotion-generating and emotion-modulation regions in SAD.115
Functional connectivity analyses reveal less connectiv- ity between amygdala and mPFC in SAD,116 PTSD,94 and GAD.117–120 There is also evidence for reduced connectivity between the amygdala and ventrolateral prefrontal cortex (vlPFC) in GAD,60,121 and the amygdala and subgenual/rACC
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Other modulatory regions
Evidence exists suggesting that other regions, including the dlPFC and subgenual/rACC, play a role in emotion modulation.89 Structural imaging studies report increased dlPFC volume and thickness in SP,111 with larger volume predicting more severe symptoms and arousal levels.
Functional imaging studies report dlPFC hyperactivation to threat in SP111 compared with controls. In addition, dlPFC mediated the influence of SAD on laughter perception, which was related to symptom severity.112 Hypoactivation in rACC has been reported in SAD,65 PTSD,94,113 and GAD.62,100,114However, treatment with computerized attention training58 and paroxetine31 reduced activation in subgenual ACC in SAD.
Connectivity between regions
More recent studies have begun to focus on connectivity between brain regions in anxiety patients. Results over- whelmingly suggest decreased connectivity between emo- tion processing (amygdala, insula) and emotion modulation (mPFC, rACC) regions. This finding is consistent both during rest and while performing a variety of cognitive and emo- tional tasks and is often interpreted as a deficit in regulating fear responding. Studies examining the structural connectiv- ity between medial-frontal and basal-limbic areas, including the amygdala, measured via volume of the uncinated fascicu- lus, revealed smaller volume in the left uncinated fasciculus in patients with SAD than in controls. This finding suggests communication deficits between emotion-generating and emotion-modulation regions in SAD.115
Functional connectivity analyses reveal less connectiv- ity between amygdala and mPFC in SAD,116 PTSD,94 and GAD.117–120 There is also evidence for reduced connectivity between the amygdala and ventrolateral prefrontal cortex (vlPFC) in GAD,60,121 and the amygdala and subgenual/rACC
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in SAD122 and GAD.98,114,117 Connectivity improves after treat- ment for GAD60,123 and SAD.116 Some conflicting findings do exist, however, with reports of increased connectivity between dorsomedial prefrontal cortex (dmPFC) and amygdala103 and between mPFC and amygdala124 in patients with SAD com- pared with controls.
Differences in connectivity within emotion-processing regions are also reported in anxiety compared with controls in a small number of studies, with the majority reporting decreased connectivity. Specifically, reports show decreased connectivity between insula and dACC in SAD73 and between amygdala and insula in GAD.120,125 However, increased connectivity between amygdala and insula was reported in PTSD.126
More global differences in connectivity have been observed in SAD, with differences in gray matter volume across the whole brain127 and deficits in global brain networks including the default mode network and the central-executive network compared with healthy controls.104 Deficits in con- nectivity were also observed in and between regions involved in general arousal and attention.25
Differences in connectivity within emotion-processing regions are also reported in anxiety compared with controls in a small number of studies, with the majority reporting decreased connectivity. Specifically, reports show decreased connectivity between insula and dACC in SAD73 and between amygdala and insula in GAD.120,125 However, increased connectivity between amygdala and insula was reported in PTSD.126
More global differences in connectivity have been observed in SAD, with differences in gray matter volume across the whole brain127 and deficits in global brain networks including the default mode network and the central-executive network compared with healthy controls.104 Deficits in con- nectivity were also observed in and between regions involved in general arousal and attention.25
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