Neuronal Correlates of Cognitive Control Are Altered in Women With Endometriosis and Chronic Pelvic Pain

Abstract

Endometriosis is a debilitating women's health condition and is the most common cause of chronic pelvic pain. Impaired cognitive control is common in chronic pain conditions, however, it has not yet been investigated in endometriosis. The aim of this study was to explore the neuronal correlates of cognitive control in women with endometriosis. Using a cross-sectional study design with data collected at a single time-point, event-related potentials were elicited during a cued continuous performance test from 20 women with endometriosis (mean age = 28.5 ± 5.2 years) and 20 age- and gender-matched controls (mean age = 28.5 ± 5.2 years). Event-related potential components were extracted and P3 component amplitudes were derived with temporal principal components analysis. Behavioral and ERP outcomes were compared between groups and subjective pain severity was correlated with ERP component amplitudes. No significant behavioral differences were seen in task performance between the groups (all p > 0.094). Target P3b (all p < 0.034) and SW (all p < 0.040), and non-target early P3a (eP3a; all p < 0.023) and late P3a (lP3a; all p < 0.035) amplitudes were smaller for the endometriosis compared to the healthy control group. Lower non-target eP3a (p < 0.001), lP3a (p = 0.013), and SW (p = 0.019) amplitudes were correlated with higher pain severity scores. Findings suggest that endometriosis-associated chronic pelvic pain is linked to alterations in stimulus-response processing and inhibitory control networks, but not impaired behavioral performance, due to compensatory neuroplastic changes in overlapping cognitive control and pain networks.

Effect of dry needling on pain and central sensitization in women with chronic pelvic pain: A randomized parallel-group controlled clinical trial

“…Chronic pain, regardless of the cause, is associated with changes in brain function, especially in pain processing centers and other sensory information [ 11 , 12 ]. Changes in brain electroencephalography (EEG) activity have been observed in some chronic pain diseases, such as patients with neuropathic pain [ 13 , 14 ], chronic back pain [ 15 ], and endometriosis [ 16 ]. Besides, because that chronic pain is considered a frequent stress physiologically and psychologically, dysfunction of the hypothalamic-pituitary-adrenal axis (HPA), the primary regulator of the stress response under normal conditions, is regarded as an almost main finding in chronic pain conditions [ 17 ].…”

“…Cortisol is the main component for the phenomenon of stress-induced analgesia [ 18 ], and therefore, a decrease in cortisol levels secondary to HPA dysfunction may exacerbate pain. The altered function of the HPA axis has been reported in some CPPS, although it appears to depend mainly on the type of syndrome in terms of hypocortisolism [ 16 , 19 ] or hypercortisolism [ 20 , 21 ]. The endogenous central pain modulation system includes a network linking multiple brain areas (prefrontal cortex, cingulate cortex and insula), the periaqueductal gray (PAG) and the rostral ventromedial medulla with the spinal cord, modulate pain through the facilitatory and inhibitory mechanisms [ 22 ].…”

Implicit Motor Imagery for Chronic Pelvic Pain: A Cross-Sectional Case–Control Study

“…According to the International Classification of Diseases [7], although its origin could be a documented nociceptive pain, it becomes chronic when it has been continuous or recurrent for at least three months [3] or, in the case of cyclic pain, over six months. Several studies have shown that, during such time, a cortical reorganisation takes place, causing structural, morphological, and functional changes in the central nervous system (CNS) [4][5][6][8][9][10][11][12][13][14][15][16][17][18], specifically in the pain modulation areas, which can maintain the perception of pain in the absence of acute injuries, with alteration of the sensory processing and greater emotional/cognitive processing of pain [12,19]. Such cortical reorganisation is characterised by an increase in the excitatory neural activity, along with a decrease in the inhibitory neural activity, in addition to alterations in the amount of grey matter in the anterior insula, amygdala [20], primary somatosensory cortex (S1), and hippocampus.…”

“…Such cortical reorganisation is characterised by an increase in the excitatory neural activity, along with a decrease in the inhibitory neural activity, in addition to alterations in the amount of grey matter in the anterior insula, amygdala [20], primary somatosensory cortex (S1), and hippocampus. These changes generate and maintain situations such as: increase in pain perception [13,17,21], changes in the integration of the viscerosomatic and motor process [22,23], and the appearance of maladaptive cognitive and emotional components (catastrophising, kinesiophobia, depression and alteration of attention and decision making in external tasks) [11,24]. All these characteristics are pathognomonic and representative in patients with CPP.…”