View clinical trials related to Central Sensitisation.
Filter by:Familial Mediterranean Fever (FMF) is an autosomal recessive inherited disease with a course of autoinflammation, which is characterized by the episodes of fever and serositis. Central sensitization (CS) is defined as increased response to normal or sub-threshold stimuli of central nervous system and its close relationship with many rheumatological diseases has been demonstrated in several studies. However, there are no data on the frequency of CS in FMF patients.
In this study, the effect of sensory discrimination training on cortical reorganization, pain and functionality in chronic nonspecific low back pain in which central sensitization is dominant will be investigated.
Nowadays migraine is conceptualized as a continuum, with at the one hand episodic migraine (EM) and at the other hand chronic migraine (CM) (1). The general aim of the study is to determine where exactly in this continuum central sensitization (CS) appears. Recent studies support the presence of CS in migraine patients (2,3), but controversial evidence exists about where in the continuum exactly CS appears. Some studies determined no differences in sings of CS between EM and CM (4,5), whether other research indicate a clear difference between EM and CM (6-8). However a significant difference in CS parameters could be determined between a patient group (EM or CM) and a healthy control group (3,4,8). In addition, CS appears to be present during the migraine attack (2). In this research, the presence of signs of CS will be determined in between headache phases. The primary outcome measure is identification of CS by PPT, QST, TS, CPM and CSI. Secondary outcome measures are the outcome of the MIDAS, HADS and EUROLIGHT.
Central sensitization (CS) is a common feature in chronic musculoskeletal pain conditions including rheumatoid arthritis, chronic whiplash syndrome, fibromyalgia, temporomandibular joint disorders, low back pain and lateral elbow pain. CS is defined as "an amplification of neural signaling within the central nervous system that elicits pain hypersensitivity". Clinical signs are allodynia, hyperalgesia and widespread pain, originating from the enhanced activity of central nervous system to peripheral afferent input from unimodal and polymodal receptors. CS not only induces abnormal pain processing, it may also lead to motor performance dysfunction in chronic pain population. CS induce cortical reorganization including changes in gray matter, cortical representation and cortical excitability both in motor and somatosensory cortex. This process ultimately generates sensorimotor conflict that described as a mismatch between motor intention and sensory feedback, and may directly effect on motor performance. The structural changes in basal ganglia and reduced GABAergic activity in the motor cortex contribute to the alteration of the motor performance. It has been known that CS and fatigue, another indicator of the motor performance, has a bidirectional effect and fatigue is predicted by CS, independently of the presence of pain. CS affect fatigue via causing disrupted reward process, increased effort and pain expactation. The increased cervical spine hypersensitivity in patients with LEP even if there is no accompanied neck or upper limb pain may also indicate of the fatigue as pain does not always suggest an injury and biomechanical damage to a tissue does not always suggest that an individual will experience pain. If neck muscle fatigue is effected by central sensitization in patients with LEP, it can be important to develop therapeutic strategies to prevent neck muscle fatigue as there is a relationship between fatigue and increased risk of injury. Despite the fact that central sensitization effect on neck pain has been well documented in patients with LEP, its role on fatigue had not gain enough clinical and research attention. To know about central sensitization effect on motor performance can also be useful for determine subgroup of population who have central sensitization. However, it is unknown whether remote body endurance alteration occur in lateral elbow pain or not.
In the literature there is still debate about the concept of central sensitization, as a pain mechanism that can support a neuromusculoskeletal pathology and which for Woolf corresponds to an amplification of neural signaling within the Central Nervous System causing hypersensitivity to pain. This mechanism is often confused with the concept of chronic pain, as in many conditions such as fibromyalgia, traumatic neck pain, low back pain or osteoarthritis, central sensitization supports its maintenance beyond 6 months. We believe it is important to investigate among Italian physiotherapists the management of the patient in which the presence of a central pain sensitization phenomenon is suspected, in order to provide consistent data to direct the education of health professionals towards more effective management of this problem. To achieve this goal we aim to: - Conduct a Delphi study in order to reach consensus, into a panel of experts, on the methods useful for the management, in each phase of the physiotherapy process, of the patient with neuromusculoskeletal problems with pain underlying central sensitization mechanism - Investigate, through a survey among Italian physiotherapists, their clinical approach to the patient in question - Develop a free online course available to clinical professionals and/or students who wish to deepen this issue.
Many chronic pain conditions show clear differences between between men and women, such as reported pain intensities or treatment effects, with chronic pain conditions being generally more frequent in women. Yet, the underlying mechanisms causing these differences are poorly understood. Central sensitization (CS) is considered one important mechanism in pain patients which differs between female and male patients. The central hypothesis is that already in the healthy population CS processes are more pronounced in women than in men.
Lumbar discectomy (i.e. surgically removing a hernia) is frequently performed in Belgium to treat lumbar radiculopathy. Every year >12,000 interventions are performed with variable long-term results. The treatment success of this procedure varies and up to 41% of the patients report post-operative persistent pain complaints, and consequently suffer from failed back surgery syndrome (FBSS). Chronic complaints in FBSS following lumbar discectomy are usually treated with symptomatic interventions (including painkillers, neuromodulation, etc), rather than from a biopsychosocial perspective. In order to develop a focused and effective treatment strategy, it is crucial to first gain insight into how persons with persistent complaints after lumbar discectomy differ from those without persistent symptoms. Different known contributing factors entail type of surgery, muscle and psychosocial impairments. Although in scientific and clinical literature it is assumed that dysfunctional pain processing also plays an important mechanistic role in FBSS, there is a lack of research to support this. However, this knowledge is crucial to depict the full mechanistic picture of pain generators and potentiators in FBSS. Therefore, we will examine whether residual complaints persisting following lumbar discectomy can be accounted for by underlying dysfunctional pain processing and whether a clinical classification algorithm can be used to identify the predominant pain mechanism in these patients.
Axial spondyloarthritis is one of the most common rheumatic diseases and chronic pain and morning stiffness are the main complaints of these patients. Central sensitization is defined as increased response to normal or sub-threshold stimuli of central nervous system and its close relationship with many rheumatological diseases has been demonstrated in several studies. There is no method for the diagnosis of central sensitization is accepted as a gold standard. The clinical scales and quantitative sensory testing (QST) widely is used for this purpose widely. The most commonly used QST types include pressure pain threshold (PPT), temporal summation (TS) and conditioned pain modulation (CPM). The well-known scale used for the evaluation of central sensitization is the Central Sensitization Inventory (CSI) , developed in 2011 for detect central sensitization in chronic pain patients. In this study, it was aimed to investigate the relationship between QST and CSI and sacroiliac MRI changes.
Central sensitization (CS) is as increased response to normal or sub-threshold stimuli of central nervous system and its close relationship with fibromyalgia has been demonstrated in several studies. However, the effect of initial CS severity on treatment response in these patients is not fully known. In this study, it was aimed to investigate the severity of CS and its effect on treatment response in patients with fibromyalgia.
A longitudinal observational cohort study to investigate the value of prognostic factors, here sensory profiles , and others, in the development of central sensitization in the low back pain population. A type 2 prognostic factor research following the PROGRESS framework. Sensory profiles are identified a prognostic factors which can predict the development of central sensitization in the low back pain population.