Effectiveness of individualized physiotherapy on pain and functioning compared to a standard exercise protocol in patients presenting with clinical signs of subacromial impingement syndrome. A randomized controlled trial

<p>Abstract</p> <p>Background</p> <p>Shoulder impingement syndrome is a common musculoskeletal complaint leading to significant reduction of health and disability. Physiotherapy is often the first choice of treatment although its effectiveness is still under debate. Systematic reviews in this field highlight the need for more high quality trials to investigate the effectiveness of physiotherapy interventions in patients with subacromial impingement syndrome.</p> <p>Methods/Design</p> <p>This randomized controlled trial will investigate the effectiveness of individualized physiotherapy in patients presenting with clinical signs and symptoms of subacromial impingement, involving 90 participants aged 18-75. Participants are recruited from outpatient physiotherapy clinics, general practitioners, and orthopaedic surgeons in Germany. Eligible participants will be randomly allocated to either individualized physiotherapy or to a standard exercise protocol using central randomization.</p> <p>The control group will perform the standard exercise protocol aiming to restore muscular deficits in strength, mobility, and coordination of the rotator cuff and the shoulder girdle muscles to unload the subacromial space during active movements. Participants of the intervention group will perform the standard exercise protocol as a home program, and will additionally be treated with individualized physiotherapy based on clinical examination results, and guided by a decision tree. After the intervention phase both groups will continue their home program for another 7 weeks.</p> <p>Outcome will be measured at 5 weeks and at 3 and 12 months after inclusion using the shoulder pain and disability index and patients' global impression of change, the generic patient-specific scale, the average weekly pain score, and patient satisfaction with treatment. Additionally, the fear avoidance beliefs questionnaire, the pain catastrophizing scale, and patients' expectancies of treatment effect are assessed. Participants' adherence to the protocol, use of additional treatments for the shoulder, direct and indirect costs, and sick leave due to shoulder complaints will be recorded in a shoulder log-book.</p> <p>Discussion</p> <p>To our knowledge this is the first trial comparing individualized physiotherapy based on a defined decision making process to a standardized exercise protocol. Using high-quality methodologies, this trial will add evidence to the limited body of knowledge about the effect of physiotherapy in patients with SIS.</p> <p>Trial registration</p> <p>Current Controlled Trials ISRCTN86900354</p

Antidepressants and the risk of traumatic brain injury in the elderly: differences between individual agents

Federica Edith Pisa,1,2 Jonas Reinold,1 Bianca Kollhorst,3 Ulrike Haug,1,4 Tania Schink1 1Clinical Epidemiology, Leibniz Institute for Prevention Research and Epidemiology &ndash; BIPS, Bremen, Germany; 2Institute of Hygiene and Clinical Epidemiology, University Hospital of Udine, Udine, Italy; 3Biometry and Data Management, Leibniz Institute for Prevention Research and Epidemiology &ndash; BIPS, Bremen, Germany; 4Faculty of Human and Health Sciences, University of Bremen, Bremen, Germany Objective: To determine the association of individual antidepressants (ADs) with the risk of traumatic brain injury (TBI) in the elderly. Patients and methods: We conducted a case&ndash;control study nested in a cohort of new users of ADs aged &ge;65 years, identified in the German Pharmacoepidemiological Research Database during 2005&ndash;2014. Cases were patients first hospitalized for TBI. Up to 100 controls per case were selected using incidence density sampling. AD use was ascertained at the index date based on the supply of last dispensing (adding 150% of the defined daily doses [DDDs]; in sensitivity analysis, no additional DDDs were considered). We estimated adjusted ORs (aORs) and 95% CIs using conditional logistic regression. Results: Among 701,309 cohort members, 16,750 cases were identified and matched to 1,673,320 controls (in both groups: 70.4% women; median age 80 years). Compared with remote users of the same AD, current users had an aOR (95% CI) of 1.87 (1.56&ndash;2.24) for duloxetine, 1.74 (1.41&ndash;2.15) for escitalopram, 1.70 (1.58&ndash;1.83) for citalopram, 1.66 (1.40&ndash;1.97) for sertraline, 1.64 (1.24&ndash;2.15) for fluoxetine and 1.57 (1.20&ndash;2.06) for paroxetine. The aOR was lower for amitriptyline (1.45; 1.32&ndash;1.58), trimipramine (1.17; 0.99&ndash;1.38) and opipramol (1.11; 0.99&ndash;1.25). Mirtazapine had an aOR of 1.03 (0.94&ndash;1.12). Sensitivity analysis confirmed the findings. Conclusion: The large variability between individual ADs shows the importance of considering the safety of individual agents rather than focusing on class alone. Keywords: antidepressants, traumatic brain injury, elderly, health insurance claims databases, pharmacoepidemiolog

Spinal prostaglandin E receptors of the EP2 subtype and the glycine receptor alpha3 subunit, which mediate central inflammatory hyperalgesia, do not contribute to pain after peripheral nerve injury or formalin injection

Inflammation, peripheral nerve injury and chemical irritants can cause central sensitization in pain pathways. Prostaglandins produced in the CNS induce central sensitization during inflammation mainly by relieving nociceptive neurons from glycinergic inhibition. We have recently identified spinal prostaglandin E receptors of the EP2 subtype (EP2 receptors) and the glycine receptor alpha3 subunit (GlyR alpha3) as signal transduction elements involved in the generation of central inflammatory hyperalgesia. It is however still unknown to what extent inhibition of glycine receptors by PGE2 contributes to neuropathic or chemically induced pain. To address this question, we have analyzed mice deficient in the EP2 receptor (EP2-/- mice) or in the GlyR alpha3 subunit (GlyR alpha3-/- mice) using the chronic constriction injury (CCI) model of neuropathic pain and the formalin test. We found that EP2-/- mice and GlyR alpha3-/- mice develop thermal and mechanical hyperalgesia in the CCI model indistinguishable from that seen in wild-type mice. In the formalin test, EP2-/- mice, but not GlyR alpha3-/- mice, exhibited reduced nocifensive behavior. The lack of a phenotype in GlyR alpha3-/- mice together with the absence of a facilitating effect of intrathecal PGE2 on formalin-induced nociception in wild-type mice suggests that peripheral rather than spinal EP2 receptors are involved. These results indicate that inhibition of glycinergic neurotransmission by EP2 receptor activation does not contribute to pain following peripheral nerve injury or chemical irritation with formalin. Our results thus provide further evidence that inflammatory hyperalgesia and neuropathic pain involve different mechanisms of central sensitization

Reversal of pathological pain through specific spinal GABAA receptor subtypes

Inflammatory diseases and neuropathic insults are frequently accompanied by severe and debilitating pain, which can become chronic and often unresponsive to conventional analgesic treatment. A loss of synaptic inhibition in the spinal dorsal horn is considered to contribute significantly to this pain pathology. Facilitation of spinal gamma-aminobutyric acid (GABA)ergic neurotransmission through modulation of GABA(A) receptors should be able to compensate for this loss. With the use of GABA(A)-receptor point-mutated knock-in mice in which specific GABA(A) receptor subtypes have been selectively rendered insensitive to benzodiazepine-site ligands, we show here that pronounced analgesia can be achieved by specifically targeting spinal GABA(A) receptors containing the alpha2 and/or alpha3 subunits. We show that their selective activation by the non-sedative ('alpha1-sparing') benzodiazepine-site ligand L-838,417 (ref. 13) is highly effective against inflammatory and neuropathic pain yet devoid of unwanted sedation, motor impairment and tolerance development. L-838,417 not only diminished the nociceptive input to the brain but also reduced the activity of brain areas related to the associative-emotional components of pain, as shown by functional magnetic resonance imaging in rats. These results provide a rational basis for the development of subtype-selective GABAergic drugs for the treatment of chronic pain, which is often refractory to classical analgesics

GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization

Prostaglandin E2 (PGE2) is a crucial mediator of inflammatory pain sensitization. Here, we demonstrate that inhibition of a specific glycine receptor subtype (GlyR alpha3) by PGE2-induced receptor phosphorylation underlies central inflammatory pain sensitization. We show that GlyR alpha3 is distinctly expressed in superficial layers of the spinal cord dorsal horn. Mice deficient in GlyR alpha3 not only lack the inhibition of glycinergic neurotransmission by PGE2 seen in wild-type mice but also show a reduction in pain sensitization induced by spinal PGE2 injection or peripheral inflammation. Thus, GlyR alpha3 may provide a previously unrecognized molecular target in pain therapy

Resisting the Pressures of Globalisation: The Repeated Failure of Elite Sport Reforms in Re-United Germany

During the German divide, the two Germanys developed quite different elite sport systems. After reunification, the expensive and compromised East German state sport system was dismantled and the West German neo-corporatist policy approach to elite sport prevailed. The neo-corporatist approach is characterised by a large number of veto players which constantly bargain over influence and scarce resources. Globalisation and the diffusion of East German policy approaches have increased the competitive intensity in international sport and made the neo-corporatist approach increasingly anachronistic. Declining competitiveness has inspired several initiatives of the federal government to reform elite sport policymaking. So far, German elite sport seems to represent a policy domain where neo-corporatism resists the pressures of globalisation