Selected examples from man and canine experiments with time series of reticular neurons, respiration, arterial blood pressure, and cutaneous forehead blood content fluctuations were analyzed using multiscaled Time-Frequency-Distribution (TFD), Post-Event-Scan (PES), and Pointwise Transinformation (PTI), resp.. We found in both experiments a "0.15 Hz rhythm" which exhibited periods of spindle wave epochs (increasing and decreasing amplitudes) to be phase synchronized with respiration at 1:2, 1:1 and 2:1 integer number ratios. At times of these wave-epochs and n:m phase-synchronization, the "0.15 Hz rhythm" appeared also in heart rate and arterial blood pressure fluctuations. If phase synchronization of the "0.15 Hz rhythm" with respiration was established at a 1:1 integer number ratio, it was maintained throughout and resulted in consensualization of all cardio-vascular-respiratory oscillations at 0.15 Hz. Analysis of a canine experiment supplied evidence that the emergence of the "0.15Hz rhythm" and n:m phase synchronization appears to result from a decline in the level of the general activity of the organism which was associated with a decline in the level of activity of reticular neurons in the lower brainstem network. These findings corroborate the notion of the "0.15 Hz rhythm" to be a state marker of the `trophotropic mode of operation` which was introduced by W.R. Hess.
Background: Post-traumatic stress disorder (PTSD) is characterized by deficits in the self-regulation of cognitions and emotions. Neural networks of emotion regulation may exhibit reduced control mediated by the anterior cingulate cortex (ACC), contributing to aberrant limbic responses in PTSD.Methods: Real-time fMRI neurofeedback (rt-fMRI NF) assessed self-regulation of the ACC in nine patients with PTSD after single trauma exposure and nine matched healthy controls. All participants were instructed to train ACC upregulation on three training days.Results: Both groups achieved regulation, which was associated with wide-spread brain activation encompassing the ACC. Compared to the controls, regulation amplitude and learning rate was lower in patients, correlating with symptom severity. In addition, a frontopolar activation cluster was associated with self-regulation efforts in patients.Conclusions: For the first time, we tested self-regulation of the ACC in patients with PTSD. The observed impairment supports models of ACC-mediated regulation deficits that may contribute to the psychopathology of PTSD. Controlled trials in a larger sample are needed to confirm our findings and to directly investigate whether training of central regulation mechanisms improves emotion regulation in PTSD.
Neurofunctional alterations in acute posttraumatic stress disorder (PTSD) and changes thereof during the course of the disease are not well investigated. We used functional magnetic resonance imaging to assess the functional neuroanatomy of emotional memory in surgical patients with acute PTSD. Traumatic (relative to non-traumatic) memories increased neural activity in the amygdala, hippocampus, lateral temporal, retrosplenial, and anterior cingulate cortices. These regions are all implicated in memory and emotion. A comparison of findings with data on chronic PTSD suggests that brain circuits affected by the acute disorder are extended and unstable while chronic disease is characterized by circumscribed and stable neurofunctional abnormalities.
Highlights
We found neurofeedback-specific attenuation of amygdala responses.
Trauma symptoms and the affective state improved in patients at one-month follow-up.
Reduced amygdala responses were associated with improved well-being at follow-up.
75% of individuals with PTSD used the learned strategies in daily life.
Left lateral prefrontal cortex responses were reduced during neurofeedback training.
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