Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • 2024-05
  • 2024-06
  • Power in the delta frequency band

    2018-11-03

    Power in the delta frequency band of the EEG is the predominant frequency in early life as neural activity develops into its adult-like form (Bell, 1998; Stern et al., 2001). Delta oscillations are visible in primitive animal brains (González et al., 1999) and, in humans, have been linked to generators in subcortical areas and linked to motivational, reward, and emotional processes (Knyazev, 2007; Uhlhaas and Singer, 2006). In contrast, power in the beta frequency band of the EEG is associated with alertness, with greater beta power visible during periods of cognitive processing (Ray and Cole, 1985). Although their neural bases are not entirely clear, fast-wave oscillations such as beta are believed to reflect intra-cortical connections that are important for attention and higher cognitive functions (Engel et al., 2001; Ray and Cole, 1985) which exert an inhibitory influence on subcortical systems (Robinson, 1999). While the spatial resolution of EEG limits the degree to which real-time oscillations can be linked to specific neural structures, relations between slow (e.g., delta) and fast (e.g., beta) wave activity are believed to reflect functional interactions between cortical and subcortical circuitry (Knyazev and Slobodskaya, 2003; Knyazev, 2007). Indeed, physiological studies have suggested that the stimulation of brainstem and limbic areas of the histamine dihydrochloride result in increased slow-wave activity (Gray, 1982; Guyton, 1976) while fast-wave beta oscillations are associated with increased activity in cortico-cortical circuits (Knyazev and Slobodskaya, 2003). Greater positive associations between delta and beta power are believed reflect functional coherence between cortical (i.e., cerebral cortex) and subcortical (i.e., limbic) structures. Thus, it has been proposed that delta–beta coupling may reflect, in real time, efforts by cognitively-oriented, cortical systems to regulate reactivity in emotionally-oriented, subcortical systems (Knyazev, 2007; Knyazev et al., 2006), providing a proxy for emotion-regulation processes. Although these types of interpretations remain tentative, this theory is consistent with evidence that greater delta–beta coupling has been associated with greater anxiety in adults (Knyazev, 2011; Miskovic et al., 2010), greater trait-level inhibition (Putman, 2011; Van Peer et al., 2008), and heritable levels of risk for anxiety problems in children (Miskovic et al., 2011a). Furthermore, delta–beta coupling is reduced in concert with the remediation of symptoms following treatment for Social Anxiety Disorder (Miskovic et al., 2011b).
    Methods
    Results Similar to previous research, Pearson correlation coefficients served as estimates of delta–beta coupling (Miskovic et al., 2010, 2011a,b). We examined levels of coupling during baseline at frontal, central, and parietal electrodes and investigated associations between coupling and high- and low-threat contexts. Differences in coupling between high and low-fear groups in each episode were tested using Fisher\'s r-to-z transformation. We first examined differences in coupling associated with high versus low levels of fear in a low-threat context. High levels of fear in a low-threat context (i.e., dysregulated fear) were associated with significant delta–beta coupling at frontal (r=0.65, p<0.05), central (r=0.83, p<0.01), and parietal (r=0.78, p<0.01) electrodes. In contrast, low levels of fear in a low-threat context were associated with significant coupling only at parietal sites (frontal: r=0.19, p>0.10, central: r=0.43, p>0.10, parietal: r=0.74, p<0.01). Differences in coupling between dysregulated fear and low fear groups fear were observed at frontal (z=1.42, p<0.10) and central (z=1.81, p<0.05) sites. No group differences were observed at parietal (z=0.28, p>0.10) electrodes (Fig. 1A). Next, we examined differences in coupling associated with high versus low levels of fear in a high-threat context. Note that high levels of fear under conditions of high-threat reflect a match between contextual incentives and fear responses. Thus, while some children may show high levels of fear in leukocytes context, this type of response reflects high fear, but not dysregulated fear. High levels of fear in a high-threat context were associated with significant coupling at central (r=0.62, p<0.01), and parietal (r=0.73, p<0.01), but not frontal (r=0.41, p>0.10) sites. Low levels of fear in a high-threat context were associated with significant coupling only at parietal sites (frontal: r=0.25, p>0.10, central: r=0.54, p>0.10, parietal: r=0.78, p<0.05). Importantly, coupling did not differ between low and high fear children at frontal (z=0.43, p>0.10), central (z=0.28, p>0.10), or parietal sites (z=−0.28, p>0.10; Fig. 1B).