Table 2.
Hypotheses Concerning Possible Neurobiological Mechanisms of SDs
| Phenomenological Domains of SDs (Early Heidelberg School) | Neurocognitive/Neurobiological Model | Brain Area/Function |
|---|---|---|
| Movements and mental processes are experienced as having independence from self11–13,16,17 | Dysfunctional self-monitoring mechanisms: | -Somatosensory-related cortices (postcentral gyrus, insula)35,45 |
| -Abnormal self-referential processing | -Hippocampus, parahippocampal cortex, and cingulate cortex23 | |
| -Sensorimotor integration dysfunction/ abnormal feed forward mechanism | ||
| (see table 1: 1.5, 1.7) | ||
| -Bilateral temporoparietal junction and neighboring areas | ||
| Although intensely experienced, there is increased passivity and nonparticipation in one’s own experience11–13,14–17 | ||
| -CMS, insula26–28 | ||
| -Dorsal ACC and lateral PFC29 | ||
| (see table 1: 1.4, 1.5, 1.7) | ||
| Thoughts, feelings, actions, volition come under foreign power which paralyzes the I11–13,14,15 | ||
| (see table 1: 1.6) | ||
| In the thought disturbances of the SDs (eg, thought insertion, thought withdrawal, thought broadcasting), thinking is experienced as sensory. The collapse between thinking and perceiving is a direct “perception.” | ||
| (see table 1: 1.7) | ||
| Possible shared mechanisms of SDs across modalities16,17 | ||
| (see table 1: 1.5, 1.6) | ||
| Self-other boundary confusion11–13 | ||
| (see table 1: 1.1 1.4) | ||
| Sense of being embodied subject | ||
| (see table 1: 1.7, 1.9) | ||
| “No temporal order prevails, each sensory impression is equally valued, replacing its predecessor”11–13,16 ,17 | Disrupted salience: | -Dysregulation of the dopamine system, due to the chaotic firing of midbrain neurons and increased striatal dopamine release, leads to dysregulation of the hippocampal- VTA loop38,40,42 |
| -Increased striatal dopaminergic transmission causes the aberrant attribution of salience to non- novel or unrewarding stimuli and the development of inappropriate associations that underlie SDs and psychotic symptoms such as delusions | ||
| (see table 1: 1.1, 1.3, 1.8) | ||
| -Corticostriatal network comprising the midbrain, basal ganglia, lateral medial temporal, and prefrontal cortex41,42 | ||
| Loss of “common sense” disrupts the on-line contribution from past experience (context) in shaping the inner continuity of consciousness, with attendant disturbances in time perception14–17 | Weakening of the “grounding” effect of context: | -Hippocampus, amygdala, and medial prefrontal cortex17 |
| -Alteration of the inner continuity of consciousness in terms of prediction from past experience | -Increased striatal dopamine release, leading to dysregulation of the hippocampal-VTA loop38,40,42 | |
| Aberrant novelty salience | ||
| -Reduced expectation (Bayesian priors) in prediction error signaling22 | ||
| (see table 1: 1.2, 1.3, 1.8) |
Note: ACC, anterior cingulate cortex; CMS, cortical midline structures; PFC, prefrontal cortex; SD, self-disorder; VTA, ventral tegmental area.