First-pass extracted concept

amygdala pain plasticity

Candidate: concept label1 source documents3 linked claims

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Evidence Snippets

Impairment of these cortical control mechanisms allows the development of amygdala pain plasticity.

Evidence 1Source 1DOI PubMedprovenance

Supporting Sources

Source 1review2017Pain Research and ManagementDOI PubMed

1 evidence snippet 3 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1mechanistic modelsupports2017Source 1DOI PubMed

The review describes hyperactivity of basolateral amygdala neurons as generating enhanced feedforward inhibition and deactivation of the medial prefrontal cortex, linked to pain-related cognitive deficits.

Quoted textsource-backed

Hyperactivity of basolateral amygdala (BLA) neurons generates enhanced feedforward inhibition and deactivation of the medial prefrontal cortex (mPFC), resulting in pain-related cognitive deficits.

Claim 2mechanistic modelsupports2017Source 1DOI PubMed

The review states that impairment of cortical control mechanisms permits the development of amygdala pain plasticity.

Quoted textsource-backed

Impairment of these cortical control mechanisms allows the development of amygdala pain plasticity.

Claim 3review summarysupports2017Source 1DOI PubMed

The review states that amygdala hyperactivity and impaired cortical control mechanisms are associated with pain states.

Quoted textsource-backed

Preclinical and clinical studies have identified amygdala hyperactivity as well as impairment of cortical control mechanisms in pain states.