5 Limitations
Several limitations must be considered when interpreting the results of
the current study.
First, this study only compared the comorbid patient group (MDD+AD) with
patients with MDD alone. Future research comparing comorbid patients
with patients with only anxiety disorders and no MDD would be essential
to gain further insight into the specific pathophysiology of this group
of disorders.
In addition, the close connection of the VAN to the amygdala plays a key
role in the interpretation of RSFC changes in patients with anxiety
disorders. Several studies have shown altered RSFC between the VAN and
the amygdala (Pisoni et al., 2021; Williams, 2016). The amygdala is
known to play a central role in the development and maintenance of
anxiety disorders (Rauch et al., 2003). One possibility from a network
perspective is that the amygdala functions by signalling saliency to the
insula, a key node of the VAN (Menon, 2011; Paulus & Stein, 2006).
Thus, disruptions in amygdala function and its connectivity to the VAN
are thought to alter the ability of the VAN to adequately switch between
the DMN and the ECN (Paulus & Stein, 2006). Because we utilized the
networks as defined by Yeo et al. (2011), the amygdala was not included
in our analysis. However, several authors, including Menon (2011),
consider the amygdala as part of the salience network, commonly
equalized with or seen as a part of the VAN (Yeo et al., 2011).
Therefore, we suggest this as an important issue for further research.
Medication was not found to have a significant effect on the results.
However, there are findings that antidepressant medication influences
RSFCs (Rolls et al., 2019) and in our study the effect of medication may
not have been detected since only 25 % of patients were unmedicated at
the time of the study. Thus, future studies should focus on
antidepressant-free patients