<p>Understanding the pathophysiology of endometriosis-associated pain is absolutely essential in order to effectively treat the condition. In addition to cyclical nociceptive pain, neuropathic and, above all, nociceptive pain often develop as the condition progresses. If the condition is initially cyclical in nature, the progression of the lesions also leads to inflammation and fibrosis. Newly ingrown nerve fibers in the endometriotic tissue secrete pro-inflammatory neurotransmitters, resulting in neurogenic inflammation, which can also cause acyclic, hormone-independent pain. Moreover, years of untreated pain also triggers peripheral and central sensitisation, leading to an expansion of the nociceptive field and a&#xa0;lowering of the pain threshold. Visceral–visceral cross-sensitisation increasingly leads to visceral pain, including in neighbouring organs (the bowel and bladder). In response to severe pain, secondary imbalances in the pelvic floor muscles and activation of myofascial trigger points occur, resulting in the addition of exertion-related pain, which is also acyclic and originates from the pelvic floor muscles. Endometriosis must be understood as a&#xa0;chronic, inflammatory pain disorder characterised by direct oestrogen dependence. It is not uncommon for patients with complex endometriosis-related pain to also suffer from other overlapping pain disorders such as migraine, fibromyalgia and vulvodynia, which are likewise underpinned by a&#xa0;disturbance in the central nervous system’s processing of stimuli. The incidence of psychological comorbidities such as depression and anxiety disorders increases significantly with persistent pain.</p>