Interoceptive cues: When ‘gut feelings’ point to anxiety
Exploring patients’ somatic experiences can help expose their unconscious fears.
Neurobiology of anxiety
The fear system. Dynamic changes in stimulus-specific physical sensations—anxious feelings—are linked to activity of the brain’s fear system. This system, which detects and rapidly learns to anticipate danger or distress, can exhibit low-level tonic activity (chronic, generalized anxiety), phasic high-amplitude reactivity (spikes of anxiety), and combinations of the 2.4,12
This precognitive, primary-process alarm system can generate:
- behaviors, often centered around avoidance—though other types (such as impulsive) can occur
- physiologic responses, which may or may not become conscious
- states of mind, including attention (hypervigilance, dissociation), cognitive contents (specific worries), and viscerosomatic awareness (“feelings”).
Through learning—and under the influence of temperamental/genetic predispositions—the fear system can be linked to internal and external stimuli, yielding a spectrum of clinical disorders that includes anxiety disorders.5
Consciously experiencing an emotion, attending to an emotionally arousing external stimulus, and remembering an emotionally arousing event all involve overlapping mental and neurobiologic processes in brain areas that process and regulate sensations from the body.2,7 Therefore, one does not need to remember “how one felt in the past” to elicit similar neurobiologic and physiologic responses in the present. These responses are recreated in the present when one consciously activates the memory. This understanding underlies the use of interoceptive cues.
Interoception is intentional, mindful awareness of the physiologic state of one’s body. Consciously directing attention to one’s internal state actively unifies the activity of the attending mind and brain with ongoing visceromotor sensations from the body.8,9 These body-based somatic markers often lie at the border of consciousness and can be brought into awareness via interoceptive cues.9 Awareness of and exposure to these often private, physiologic symptoms is an important part of many evidence-based therapies for anxiety disorders.10,11
Brain basis of fear. The amygdala and insula are 2 key components of the brain basis of fearful feelings.
The amygdala processes internal or external stimuli, alerts other brain areas that a threat is present, and triggers a fear or anxiety response (Table 1).13-16 Early, nonconscious threat detection by the amygdala may be a core component of the brain basis of many anxiety disorders.17
Amygdala activity has been associated with automatic fear perception, associative fear learning, trauma,18 and (on the treatment side) extinction of learned fears via active coping.19 The amygdala provides an extremely rapid response to fearful stimuli—within milliseconds—and can be active without conscious awareness of the stimuli (which may take several hundred milliseconds to develop).20,21
Inputs into the amygdala can come from:
- inside the brain (memories, images, emotions, predictions of the future)
- or outside (contemporary stimuli).
In treatment, the amygdala may be one site of activity of serotonergic medications.22 It is partially regulated by orbitofrontal and medial prefrontal areas that may be target sites of “top-down” psychotherapeutic interventions.23
The insula—a sector of cortex tucked beneath the fissure between the temporal and parietal lobes—is involved in interoception, modulation of emotional processing, and emotional learning, especially as related to aversive internal states.24,25
Paulus24 proposes that in anxiety-prone individuals the insula may create a negatively valenced, preattentive, body-centered warning of negative things to come—in a sense, a somatic semaphore that signals danger ahead. In a related study, Stein et al26 presented college students with emotion-provoking faces. Students prone to anxiety had elevated activity in the amygdala and insula compared with normal controls.
The insula also may respond to mindful mental exercise. Lazar et al27 found increased cortical thickness in prefrontal and anterior insula in 20 subjects with extensive experience in insight meditation, which involves focusing attention on internal states.
Table 1
Amygdala output pathways that result in anxiety symptoms
| Link to specific brain area | Clinically important responses |
|---|---|
| Hypothalamus | Sympathetic activation: increased heart rate, sweating, dilated pupils, striated muscle tension, strained breathing |
| Dorsal motor nucleus of vagus | Parasympathetic activation: slowed heart rate, bladder and bowel symptoms—frequent urination, diarrhea—via smooth muscle activity, gastric acid secretion |
| Parabrachial nucleus | Increased respiratory rate: sighing respirations |
| Ventral tegmental area/locus ceruleus | Generalized arousal, perceptual vigilance (excessive stimulation leads to disruption of attention/dissociation, via prefrontal cortical connections) |
| Nucleus reticularis pontis caudalis | Startle response, jumpiness |
| Periaqueductal gray matter | Automatic coping patterns, from passive (freeze, collapse) to active (confrontation, fight) |
| Trigeminal facial motor nuclei | Jaw tension, facial expressions of fear |
| Source: Adapted with permission from references 13 with additional information from references 14-16 | |
CASE CONTINUED: Using focused interoception
You help Ms. N become aware of her somatic symptoms of anxiety by using a series of questions to direct her attention to her physical responses in a “head-to-toe” approach: “Do you notice the tension in your jaw?” “Is your neck tense?” “How is your breathing now?” Though Ms. N had been unaware of these symptoms, she easily agrees: “Yes, now that you mention it, I am aware of that, but I never knew it was anxiety. I thought it was just stress.”
