Iliopsoas impingement refers to the painful contact between the iliopsoas tendon and the anterior acetabular rim of the hip joint. This mechanism can occur in the native hip as part of an internal snapping hip syndrome and, in particular, following total hip arthroplasty, leading to chronic groin pain and a substantial reduction in the quality of life. This review article outlines the diagnostic approaches for identifying iliopsoas impingement and presents both established open procedures and innovative minimally invasive arthroscopic techniques for iliopsoas tendon release, in order to facilitate precise treatment planning and avoid potential complications.

Pain is the leading cause of disease burden and disability worldwide. Physiotherapy plays a major role in the treatment of people with pain; however, there appears to be a lack of knowledge in this area.

Negatively experienced emotions, especially anger, influence pain-related variables and impair the quality of life. Although a variety of treatment approaches exist there is still no comprehensive overview of anger-related interventions for chronic pain and which effects with respect to anger-specific and pain-specific variables can be detected.

Patients with chronic widespread pain (CWP) and/or fibromyalgia syndrome (FMS) are considered difficult to treat. Various disease models and treatment preferences exist.

Fatigue and chronic pain show a high level of comorbidity and are both not only frequent symptoms of chronic diseases without known somatic structural causes (e.g. irritable bowel syndrome or nonspecific low back pain) but also as leading symptoms of diseases with a specific etiology (e.g., cancer, rheumatoid arthritis or multiple sclerosis). Fatigue and pain also often co-occur for months or years after overcoming an acute organic illness, such as an acute bacterial or viral infection. In all cases, fatigue and pain can be accompanied by increased anxiety or depression. Moreover, research indicates that psychosocial factors, such as emotional distress, dysfunctional behavioral responses to fatigue or pain or social stigmatizing, can be involved in the perpetuation of the complaints and also independent of the etiology of the underlying disease. Physiological processes, such as autonomic dysregulation, an altered activation of adrenocortical activity as well as altered brain activity are increasingly being discussed as biological mechanisms. These common factors suggest a transdiagnostic approach investigating overlapping features in terms of biopsychosocial mechanisms that may play a role not only in the maintenance of pain but also of fatigue. As a consequence, both the diagnostics and management can be provided in a more individualized and resource-efficient way. The present narrative review gives a preliminary summary of the transdiagnostic mechanisms and possible clinical approaches for fatigue and chronic pain.

A high percentage of the world's population suffers from diabetes mellitus (DM). The disease leads to considerable DM-related pathological consequences and aggravates disease processes and pain as a comorbidity. This has a significant impact on the quality of life of these patients. This article describes DM-induced mechanisms that may contribute to increased pain. Diabetic patients exhibit low-grade systemic inflammation, high levels of blood glucose, and increased formation and accumulation of advanced glycation end products (AGEs). These factors can activate intracellular inflammatory signaling pathways and induce reactive oxygen species (ROS) formation, which can lead to the release of cytokines, oxidative stress, and mitochondrial dysfunction. These processes lead to increased local inflammation and damage to blood vessels and nerve fibers, which are considered to be causes of many diabetic complications. The increased release of pro-inflammatory mediators contributes to peripheral and central sensitization and thus to increased acute and chronic pain in diabetic patients. About 50% of people with DM develop diabetic neuropathy, which can cause numbness, discomfort, or severe pain. In addition, diabetic patients have an increased incidence of musculoskeletal disorders, which can cause additional pain.

Migraine is the most frequent neurological disorder and has a prevalence of 10-14% of the population. In addition to the frequency and the fact that it is usually manifested in adolescence, the frequent comorbid illnesses are also the cause of the high burden associated with migraine. Diseases from very different functional areas are associated with the presence of migraine. In general, this increased risk is more pronounced in the presence of migraine with aura and in women. For example, migraine is associated with a higher risk of developing stroke, heart attack, arterial hypertension, depression, anxiety disorder and probably dementia syndromes. The article presents the most important epidemiological studies on a number of these comorbid diseases. It is unclear what the neurobiological basis is for this accumulation of comorbid diseases in migraine. In addition to the purely coincidental cooccurrence in individual cases, other factors can be responsible for the increased risk: a shared genetic background, e.g. in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) or epileptic seizures, or treatment of a primary independent chronic disease (e.g. treatment with phosphodiesterase inhibitors, hormone substitution therapy or beta-interferon therapy). Another cause, which is discussed more broadly here, is inflammatory mechanisms, which are found in both the triggering of migraine and in a variety of comorbid diseases. This applies primarily to all chronic inflammatory diseases such as rheumatoid arthritis but also to depression and cardiovascular diseases. So far, these findings have not had any influence on the treatment of migraine but this may change in the future with a better understanding of the molecular mechanisms (e.g. activation of microglia).

Antibodies against CGRP or its receptor (eptinezumab, erenumab, fremanezumab, galcanezumab, from here on: "CGRP(R) antibodies") are modern migraine preventives. German statutory health insurance covers CGRP(R) antibodies only for patients refractory to other preventive therapies. Thus, the effect of this regulation on patient selection was investigated, as well as the effect of a change of insurance coverage for erenumab in October 2022.