Active clinical trials for "Back Pain"

This study aims to compare the outcomes of a traditional, exercise-based rehabilitation intervention for chronic low back pain with the outcomes achieved by combining a traditional intervention with adjunct therapy delivered using an interactive gaming-based system for home-based therapy.

This study was designed to answer 3 primary research questions: In adults with low back pain, reduced SLR ROM (Range of Motion) and a positive sensitized SLR (Straight leg raise) test, does neurodynamic mobilization result in greater SLR ROM, pain reduction and perceived improvement than muscle stretching? In adults with low back pain, reduced SLR ROM and a negative sensitized SLR test, does muscle stretching result in greater SLR ROM, pain reduction and perceived improvement than neurodynamic mobilization? In adults with low back and reduced SLR, does neurodynamic mobilization or muscle stretching result in greater SLR ROM, pain reduction and perceived improvement irrespective of the outcome of SLR sensitization? The research hypotheses are threefold: Subjects determined to have nerve-related pain and ROM restrictions by a positive sensitized SLR test would benefit more from neurodynamic mobilization than muscle stretching. Subjects determined to have muscle-related pain and ROM restrictions by a negative sensitized SLR test would benefit more from muscle stretching than neurodynamic mobilization. Subjects would benefit the same from muscle stretching and neurodynamic mobilization when not matched on the outcome of the SLR sensitization.

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The cluneal nerves are a group of pure sensory nerves that provide direct cutaneous innervation to the buttocks. In recent years, pain syndromes secondary to cluneal nerve pathology ,have been implicated as the cause of chronic pain that both arises directly from the buttocks and is referred from the lower back, pelvic area, or even lower extremity regions . Cluneal syndromes are the causes of neuropathic pain, often underdiagnosed and overlooked, and other anatomical sources are often cited as the cause of pain in the etiology.The cluneal nerve complex includes the superior cluneal nerves (SCN), the middle cluneal nerves (MCN), and the inferior cluneal nerves (ICN). These nerves are susceptible to entrapment neuropathy due to direct or indirect compression and cause different clinical symptoms depending on their location. The superior cluneal nerve(SCN) originates from the T11-L5 nerve roots and has at least 3 branches from medial to lateral; these are the medial, intermediate, and lateral branches. Anatomy studies have shown that the medial branch passes 6-7 cm lateral to the midline on the posterior iliac crest. Nerve branches pass through the osteofibrous tunnel formed by the thoracolumbar fascia and the superior edge of the iliac crest, where they can be trapped. Controversial data exist regarding the osteofibrous tunnel. It may not be present in all cases, and in some cases more than one nerve has been shown to pass through the osteofibrous tunnel. As a result, there are discussions about superior cluneal nerve anatomy and there is not enough information. In patients with superior cluneal nerve entrapment syndrome, low back pain radiates to the upper part of the hip and may cause leg pain that mimics radiculopathy. The diagnosis is clinical. Diagnostic criteria for superior cluneal nerve (SCN) entrapment; Low back pain involving the iliac crest and buttocks, symptoms aggravated by lumbar movement or posture, trigger point over the posterior iliac crest corresponding to the nerve compression zone, patients report numbness and radiating pain in the SCN area (Tinel sign) when the trigger point is compressed, symptom relief by SCN block at the trigger point. Prevalence studies of superior cluneal nerve entrapment syndrome are very few. Maigne et al reported superior cluneal nerve entrapment in 1.6% of 1,800 patients with low back pain. Kuniya et al showed that 14% of 834 patients with low back pain met the criteria for superior cluneal nerve entrapment. Superior cluneal nerve entrapment is not as rare as it is thought to be among the causes of low back pain. In Turkey, there is no study showing the prevalence of the superior cluneal nerve or its importance in patients with low back pain. The aim of this study is to examine the patients who applied to Cerrahpasa Faculty of Medicine, Department of Physical Medicine and Rehabilitation polyclinic with low back pain; To confirm the diagnosis with an ultrasound-guided diagnostic injection test, to determine the importance of superior cluneal nerve entrapment.

The overarching aim of this project is to conduct a randomized controlled study to determine whether Mindfulness-Oriented Recovery Enhancement (MORE) vs. a Support Group (SG) can improve pain regulation and hedonic functions (i.e., natural reward responsiveness) thought to be governed by the endogenous opioid system among opioid-treated, chronic, non-neuropathic back pain patients (CNBP) and thereby improve clinical pain, affect, and opioid use.

The most common chronic low back pain conditions are a consequence of disc disease as well as muscular and bony etiologies. The discs degenerate and weaken, bulge and are pushed into the space containing the spinal cord or a nerve root resulting in severe pain. A common treatment is then surgery. Whole-body vibration combined with un-weighting traction and specific manual mobilization plus active therapeutic exercise seems to treat chronic low back pain by non-invasively firing muscles of the lumbar spine. The investigators are seeking to show such therapy reduces the need for surgery and significantly out performs traditional physical as the preferred conservative treatment.

Chronic low back pain may be associated with active discopathy. This subset of individuals are defined by a clinical and radiological syndrome with specific MRI signals, known as MODIC changes. Three types (I, II and III) of MODIC changes are described. Type I refers to the inflammatory reaction regarding the intervertebral-disc subchondral bone and adjacent vertebral-endplate subchondral bone. The natural evolution of this active discopathy will lead to sclerosis (type III) supposedly less painful. So far the underlying mechanism remains unclear and debated (mechanical, local infection, genetic). In the absence of international guidelines on the management on chronic low back pain with MC type 1, different therapeutic strategies have been described. The main goal is to accelerate the transition to MC type 2, which is supposedly less painful. The estimated time to expect a transition from type 1 to type 2 is at least 1 year. The mechanical hypothesis found its origin in the Modic et al. initial study, linking Modic changes (MC) types 1 and 2 to degenerative disc disease. The Histological analysis of patient suffering from active discopathy has shown signs of micro fractures regarding vertebral endplates. The local inflammatory reaction may be part of a repair process following the micro fracture. Based on this mechanical explanation an orthopaedic treatment with a lumbar brace may accelerate the healing, thus the transition from modic I to type II. This approach has been studied in a retrospective analysis on 62 patients suffering from active discopathy (modic type I) who were prescribed a custom lumbar rigid brace for 3 months, at endpoint 80% of the patients treated described a reduction of at least 30% of their initial pain. This study aims to confirm the previous hypothesis, that lumbar immobilisation by custom rigid brace can reduce the pain after being worn for 3 months. Secondary objective will be to assess the pain reduction at 6 months along with functional outcome, fears and beliefs, mood and medical costs at short (3 months) and mid (6months) term.

Recently, it has been reported that the thoracolumbar fascia may play a role in the pathophysiology of chronic low back pain.There is still no standard method for imaging and analyzing the thoracolumbar fascia.The aim of this study is to advance the understanding of the role of the thoracolumbar fascia in chronic low back pain as well as to advance the analysis methods.

Chronic low back pain (CLBP) is established by the persistence of low back pain beyond 3 months of symptom initiation . The overwhelming element of treatment is physical exercise . Other methods of treatment like cognitive therapy, behavioural therapy and multidisciplinary rehabilitation can also lead to significant improvements 1. Prevalenc of CLBP increases linearly from the third decade of life on, until the 60 years of age, being more prevalent in women.2 CLBP is a common condition affecting many individuals at some point in their lives.3 The estimation is that between 5.0% and 10.0% of cases will develop CLBP, which is responsible for high treatment costs, sick leave, and individual suffering, in addition to being one of the main reasons for people to seek health care services.4 CLBP and related disorders represent a wide spectrum of syndromes that are associated with changes in the pain processing pathways of the central nervous system .5 Those syndromes affect many systems in the body, and the associated plasticity changes in the CNS can lead to augmentation of pain transmission and processing circuits. 6,7 The pain in patients with CLBP occurs as a result of a process called central sensitization (CS), which refers to increased excitability of the neurons in the dorsal horn of the spinal cord. This increased excitability is associated with increased spontaneous neuronal activity, expanded receptive fields, and enhanced responses to the impulses transmitted by both large and small-fiber sensory afferents.8 The Hoffman reflex , F-wave and Somatosensory evoked potential (SSEP) are often used to measure spinal excitability in various physiological and pathological states.9-10 The H-reflex is elicited by stimulation of type Ia afferent sensory fibers. These fibers synapse directly onto the alpha motor neurons in the anterior horn of the spinal cord, forming a monosynaptic reflex arc. Submaximal stimulation of this reflex arc elicits a compound muscle action potential (CMAP) known as the H wave. This reflex arc appears to depend on the balance between excitatory and inhibitory neurons in the spinal cord . F wave is a late response that follows the motor response (M) and is elicited by supramaximal electrical stimulation of a mixed or a motor nerve.11 The study of the F waves is particularly useful for the diagnosis of proximal nerve lesions that would be otherwise inaccessible to other routine NCSs.12 SSEPs are also important complementary diagnostic methods in the electrophysiologic evaluation of CLBP. SSEPs are a very sensitive measure of the functional integrity of the neuroaxis, including peripheral and central structures. When used in diagnostic mode they can provide additional information regarding the probable areas of dysfunction. Since a change in spinal excitability is one of the main mechanisms underlying the hypothesis of CS in CLBP, performing these tests might be an easy, widely available, cheap, and objective method for assessing spinal excitability in patients with CLBP.

The purpose of this study is to assess the benefits of Percutaneous Neuromodulation Therapy when compared to a reference sham treatment in the treatment of patients who have undergone surgical intervention for chronic low back pain with or without a radiating lower extremity pain component.