Our findings have contributed to a better understanding of the pathophysiology of this condition. We identified abnormalities in rectal sensitivity, anorectal pressure dynamics, and defecation-related anorectal dyscoordination in FARP. Additionally, We explored the psychological characteristics of patients with FARP and found that comorbid mood disorders are common in patients with FARP. Our findings provide a basis for the diagnosis and treatment of FARP.
Changes in the properties of the rectal wall and abnormalities in neural afferent pathways and central processing may all cause changes in rectal sensation. In terms of rectal sensory function, we found that when compared with controls, patients with FARP had significantly reduced sensation thresholds for desire to defecate, urgency to defecate and maximum tolerable sensation, indicating rectal hypersensitivity. Visceral hypersensitivity is a hallmark of IBS and manifests as reduced pain thresholds as a result of rectal distension and enhanced perception of bowel lumen distension, and studies have demonstrated a correlation between pain thresholds and the severity and frequency of pain symptoms [23]. FARP and irritable bowel syndrome are both centrally mediated FGIDs, and the mechanisms via pain that occur in these conditions may be similar. Several studies have shown that patients with IBS have lower initial sensation and initial pain thresholds and that visceral hypersensitivity to intestinal dilatation correlates with symptom severity [24,25,26]. Our findings suggest that visceral hypersensitivity is an important pathophysiological mechanism of FARP. Although the findings regarding first sensation were not statistically significant, patients with FARP showed an overall trend toward reduced sensation threshold, which might be related to the material in the expanded balloon used in our examination to assess rectal sensation. Rectal sensory thresholds are influenced by the stiffness of the rectal balloon. This balloon was mounted on a manometry catheter, and its tension might directly affect rectal compliance [27]. In future studies, we plan to investigate rectal sensory thresholds in patients with FARP further by using non-compliant polyethylene balloons and constant pressure or by means of electrical stimulation.
In this study, resting anal pressure and maximum anal squeeze pressure were significantly lower in the patients with FARP than in the controls, and the pelvic floor muscles were predominantly flaccid, which is consistent with previous findings [28]. Some investigators have focused on FARP associated with abnormal anorectal pressure. The correlation between abnormal anorectal pressure and anal pain is controversial, with few relevant reports in the literature. However, it is generally believed that anal levator ani syndrome is mostly caused by spasm of the pelvic floor muscles and elevated annal resting pressure and that an overactive anal sphincter muscle causes chronic pain. Grimaud et al. have suggested that chronic idiopathic anal pain may be caused by persistent abnormal contraction of the external anal sphincter and that this pain can be relieved by biofeedback treatment to relax the external anal sphincter and reduce muscle spasm and neuropsychological stress [23, 29]. We found that the anal resting pressure was lower in patients with FARP, which was the opposite of previous findings and might reflect the epidemiological characteristics of FARP. In our study, 72.14% of FARP patients were female, mainly perimenopausal patients, which is consistent with the characteristics of FARP patients in the study of Atkin GK et al. [30]. Most of these women had a history of pregnancy and childbirth, with obstetric damage to the anal sphincter and pubic nerves, damage to the tissues supporting the pelvic floor muscles, decreased muscle function, decreased hormone levels, and loss of elastin, manifesting as reduced pelvic floor muscle strength and decreased muscle tone [31, 32]. Weakness or spasm of the pelvic floor muscles is thought to be one of the pathophysiological bases for chronic pelvic pain [33].
During testing, we identified paroxysmal, transient, periodic sphincter spasms with elevated pressure in some patients with FARP, which might explain the spasm-related pain that occurs in these patients. Proctalgia fugax is short and episodic and is usually considered to be pain caused by abnormal smooth muscle contractions [34, 35, 36]. Some studies have shown that botulinum toxin injections relax the anal sphincter or levator ani muscle, but their therapeutic effect is inconsistent. The mechanism underlying anal sphincter or levator ani muscle tension in FARP remains unclear.
Some studies reported that the majority of patients with functional defecation disorders had anal levator muscle pressure pain and that their defecation disorders were improved with biofeedback treatment, suggesting that rectoanal incoordination of defecation is the pathophysiology of levator ani syndrome [37]. Interestingly, this hypothesis was consistent with our finding of paradoxical contraction of the anal sphincter during defecation in 76.92% of men with FARP. Defecation coordination disorders are manifested by insufficient rectal impulsion or abnormal anal canal relaxation during defecation. Chronic pain over time may cause the patient to fear defecation, which further increases pelvic floor muscle coordination disorders. Therefore, pelvic floor muscle dysfunction may be one of the causes of FARP.
Our findings indicate that anal resting pressure is positively correlated with sensory thresholds. The anal resting pressure mainly reflects the pressure of the internal anal sphincter (smooth muscle), so it is inferred that there may be a correlation between rectal sensitivity and smooth muscle pressure, but the mechanism of action needs to be investigated further. In contrast, the pathogenesis of FARP in patients with high anal resting pressure may be pain caused by smooth muscle spasms.
In our study, most patients with FARP exhibited symptoms of anxiety and depression. Although no significant gender differences were observed in anxiety and depression scores, female patients tended to report higher levels of these symptoms than males. Currently, Gut-brain interaction disorder is the most widely accepted theory regarding the pathogenesis of FGIDs. These disorders are often associated with psychiatric comorbidities, such as depression and anxiety, and these mood disorders cause gastrointestinal symptoms [38]. Anxiety states are widespread in patients with irritable bowel syndrome, and psychological factors may influence the persistence and perceived severity of these symptoms, which are significantly associated with pain levels and physical symptoms. Women’s anxiety, depression, and somatization are more obvious [39, 40]. Pain intensity is closely related to emotional symptoms. Pain has been shown to cause emotional disorders, and emotional disorders can exacerbate pain [41]. Whether pain is a somatic manifestation of psychological disorders and whether chronic pain is the main cause of emotional problems requires further research. Although our study did not find a correlation between mood and pain, it provides a basis for guidelines for the management of mood disorders in patients with FARP, which may include central neuromodulators, such as antidepressants, antipsychotics, and other central nervous system-targeted agents.
There were several imitations in our study. First, as a retrospective study, we were unable to obtain complete data on VAS scores, HAM-A scores, and HAM-D scores. A prospective study is needed to further investigate the anorectal physiological characteristics of FARP. Second, we did not assess the structure and function of the pelvic floor muscles in patients with FARP using a combination of pelvic floor ultrasound and defecography. Although HARM can aid in understanding the physiological features of the anus and rectum, it is better to be combined with other examinations to improve the diagnostic system for FARP, clarify its etiology and pathogenesis.