Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2023 Oct-Dec;23(4):100385.
doi: 10.1016/j.ijchp.2023.100385. Epub 2023 Mar 22.

Role of the intraparietal sulcus (IPS) in anxiety and cognition: Opportunities for intervention for anxiety-related disorders

Lily Brown  1 , Lauren K White  2 , Walid Makhoul  3 , Marta Teferi  3 , Yvette I Sheline  3 , Nicholas L Balderston  3
Affiliations

Role of the intraparietal sulcus (IPS) in anxiety and cognition: Opportunities for intervention for anxiety-related disorders

Lily Brown et al. Int J Clin Health Psychol. 2023 Oct-Dec.

Abstract

Our objective was to review the literature on the parietal cortex and intraparietal sulcus (IPS) in anxiety-related disorders, as well as opportunities for using neuromodulation to target this region and reduce anxiety. We provide an overview of prior research demonstrating: 1) the importance of the IPS in attention, vigilance, and anxious arousal, 2) the potential for neuromodulation of the IPS to reduce unnecessary attention toward threat and anxious arousal as demonstrated in healthy samples; and 3) limited data on the potential for neuromodulation of the IPS to reduce hyper-attention toward threat and anxious arousal among clinical samples with anxiety-related disorders. Future research should evaluate the efficacy of IPS neuromodulation in fully powered clinical trials, as well as the value in augmenting evidence-based treatments for anxiety with IPS neuromodulation.

Keywords: Anxiety; Neuromodulation; Parietal cortex; Threat; Working memory.

PubMed Disclaimer

Conflict of interest statement

The authors report no biomedical financial interests or potential conflicts of interest.

Figures

Fig 1
Fig. 1
Potential model showing how the IPS may mediate hyperarousal and hypervigilance symptoms in anxiety disorders. A) Strong connectivity between the IPS and the dlPFC facilitates bottom-up processing of threat-related stimuli leading to hypervigilance (Blue arrows). Strong connectivity between subcortical regions like the amygdala and locus coeruleus and the IPS elevate arousal (Orange arrows). B) Inhibitory TMS protocols may alleviate hypervigilance and hyperarousal symptoms in PTSD and anxiety by weakening the connections between the IPS and the cortical/sub-cortical regions involved in these symptoms.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Admon R., Pizzagalli D.A. Dysfunctional reward processing in depression. Current Opinion in Psychology. 2015;4:114–118. doi: 10.1016/j.copsyc.2014.12.011. - DOI - PMC - PubMed
    1. Amaral D.G., Behniea H., Kelly J.L. Topographic organization of projections from the amygdala to the visual cortex in the macaque monkey. Neuroscience. 2003;118(4):1099–1120. - PubMed
    1. Amaral, D. G., Price, J. L., Pitkänen, A., & Carmichael, T. (1992). Anatomical organization of the primate amygdaloid complex. In Aggleton, J. (Ed.), The Amygdala: Neurobiological Aspects of Emotion, Memory, and Mental Dysfunction (pp. 1-66). New York: Wiley-Liss.
    1. Anderson B.A. Reward processing in the value-driven attention network: Reward signals tracking cue identity and location. Social Cognitive and Affective Neuroscience. 2017;12(3):461–467. doi: 10.1093/scan/nsw141. - DOI - PMC - PubMed
    1. Baeken C., De Raedt R., Van Schuerbeek P., Vanderhasselt M.a, De Mey J., Bossuyt a, et al. Right prefrontal HF-rTMS attenuates right amygdala processing of negatively valenced emotional stimuli in healthy females. Behavioural Brain Research. 2010;214(2):450–455. doi: 10.1016/j.bbr.2010.06.029. - DOI - PubMed