995 resultados para Peripheral Neurogenic Pain


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OBJECTIVE: Care related pain (CRP) is generally under-estimated and rarely studied in rehabilitation as well as in general medecine. Beliefs about pain influence psychological distress, adjustment to pain and physical disability. In this sense, perceptions of CRP could limit recovery. This exploratory study aims to understand patients' and caregivers' subjective perceptions and beliefs about CRP. PATIENTS AND METHODS: Questionnaires about CRP were submitted to members of the interdisciplinary team of a rehabilitation hospital and to patients with musculoskeletal complaints (cross-sectional design). Twenty patients were also individually interviewed (qualitative data). Four topics were addressed: frequency of CRP, situations and procedures causing CRP, beliefs about CRP and means used to deal with CRP. RESULTS: Seventy-five caregivers and 50 patients replied to the questionnaire. CRP is a very common experience in rehabilitation and it is recognized by both groups. Generally, the situations causing CRP reflect the specificity of rehabilitation (mobilization...) and are similarly perceived by patients and caregivers, with patients considering them as more painful. Beliefs about CRP are clearly different from those usually associated with pain. Both groups point out the utilitarian and the inevitable character of CRP. They differ on that, that patients had a more positive view about CRP. They associate it more often with progress and see it as acceptable at least until a certain limit. They are also able to perceive the richness of means used by physiotherapists to help them coping with CRP. CONCLUSION: Our data may suggest new keys to motivate patient to be active in rehabilitation for example in choosing carefully arguments or words which may fit theirs' beliefs about CRP, or in using various means to manage CRP. Promoting the use of relational competences with chronic pain patients and of a patient-centred approach may also be a concern in training caregivers.

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Monocarboxylates have been implicated in the control of energy homeostasis. Among them, the putative role of ketone bodies produced notably during high-fat diet (HFD) has not been thoroughly explored. In this study, we aimed to determine the impact of a specific rise in cerebral ketone bodies on food intake and energy homeostasis regulation. A carotid infusion of ketone bodies was performed on mice to stimulate sensitive brain areas for 6 or 12 h. At each time point, food intake and different markers of energy homeostasis were analyzed to reveal the consequences of cerebral increase in ketone body level detection. First, an increase in food intake appeared over a 12-h period of brain ketone body perfusion. This stimulated food intake was associated with an increased expression of the hypothalamic neuropeptides NPY and AgRP as well as phosphorylated AMPK and is due to ketone bodies sensed by the brain, as blood ketone body levels did not change at that time. In parallel, gluconeogenesis and insulin sensitivity were transiently altered. Indeed, a dysregulation of glucose production and insulin secretion was observed after 6 h of ketone body perfusion, which reversed to normal at 12 h of perfusion. Altogether, these results suggest that an increase in brain ketone body concentration leads to hyperphagia and a transient perturbation of peripheral metabolic homeostasis.

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The present report describes the case of a 43-year-old diabetic patient with facial pain, protruding eyes, nasal congestion and decreased right vision (involvement of the ipsilateral cranial nerves III, IV and V). Computed tomography showed diffuse sinusitis at right, cribriform plate erosion and presence of a hypodense collection in the frontal lobe with peripheral enhancement. Magnetic resonance imaging confirmed the presence of a cerebral abscess. Samples were collected from the lesion, confirming hyphae compatible with mucormycosis.

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OBJECTIVE: There is currently no guideline regarding the management of neurogenic detrusor overactivity (NDO) refractory to intra-detrusor botulinum toxin injections. The primary objective of the present study was to find a consensus definition of failure of botulinum toxin intra-detrusor injections for NDO. The secondary objective was to report current trends in the managment of NDO refractory to botulinum toxin. METHODS: A survey was created, based on data drawn from current literature, and sent via e-mail to all the experts form the Group for research in neurourology in french language (GENULF) and from the comittee of neurourology of the French urological association (AFU). The experts who did not answer to the first e-mail were contacted again twice. Main results from the survey are presented and expressed as numbers and proportions. RESULTS: Out of the 42 experts contacted, 21 responded to the survey. Nineteen participants considered that the definition of failure should be a combination of clinical and urodynamics criteria. Among the urodynamics criteria, the persistence of a maximum detrusor pressure>40cm H2O was the most supported by the experts (18/21, 85%). According to the vast majority of participants (19/21, 90.5%), the impact of injections on urinary incontinence should be included in the definition of failure. Regarding the management, most experts considered that the first line treatment in case of failure of a first intra-detrusor injection of Botox(®) 200 U should be a repeat injection of Botox(®) at a higher dosage (300 U) (15/20, 75%), regardless of the presence or not of urodynamics risk factors of upper tract damage (16/20, 80%). CONCLUSION: This work has provided a first overview of the definition of failure of intra-detrusor injections of botulinum toxin in the management of NDO. For 90.5% of the experts involved, the definition of failure should be clinical and urodynamic and most participants (75%) considered that, in case of failure of a first injection of Botox(®) 200 U, repeat injection of Botox(®) 300 U should be the first line treatment. Level of proof 4.

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BACKGROUND: Most peripheral T-cell lymphoma (PTCL) patients have a poor outcome and the identification of prognostic factors at diagnosis is needed. PATIENTS AND METHODS: The prognostic impact of total metabolic tumor volume (TMTV0), measured on baseline [(18)F]2-fluoro-2-deoxy-d-glucose positron emission tomography/computed tomography, was evaluated in a retrospective study including 108 PTCL patients (27 PTCL not otherwise specified, 43 angioimmunoblastic T-cell lymphomas and 38 anaplastic large-cell lymphomas). All received anthracycline-based chemotherapy. TMTV0 was computed with the 41% maximum standardized uptake value threshold method and an optimal cut-off point for binary outcomes was determined and compared with others prognostic factors. RESULTS: With a median follow-up of 23 months, 2-year progression-free survival (PFS) was 49% and 2-year overall survival (OS) was 67%. High TMTV0 was significantly associated with a worse prognosis. At 2 years, PFS was 26% in patients with a high TMTV0 (>230 cm(3), n = 53) versus 71% for those with a low TMTV0, [P < 0.0001, hazard ratio (HR) = 4], whereas OS was 50% versus 80%, respectively, (P = 0.0005, HR = 3.1). In multivariate analysis, TMTV0 was the only significant independent parameter for both PFS and OS. TMTV0, combined with PIT, discriminated even better than TMTV0 alone, patients with an adverse outcome (TMTV0 >230 cm(3) and PIT >1, n = 33,) from those with good prognosis (TMTV0 ≤230 cm(3) and PIT ≤1, n = 40): 19% versus 73% 2-year PFS (P < 0.0001) and 43% versus 81% 2-year OS, respectively (P = 0.0002). Thirty-one patients (other TMTV0-PIT combinations) had an intermediate outcome, 50% 2-year PFS and 68% 2-year OS. CONCLUSION: TMTV0 appears as an independent predictor of PTCL outcome. Combined with PIT, it could identify different risk categories at diagnosis and warrants further validation as a prognostic marker.

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BACKGROUND: Chronic postsurgical pain (CPSP) is an important clinical problem. Prospective studies of the incidence, characteristics and risk factors of CPSP are needed. OBJECTIVES: The objective of this study is to evaluate the incidence and risk factors of CPSP. DESIGN: A multicentre, prospective, observational trial. SETTING: Twenty-one hospitals in 11 European countries. PATIENTS: Three thousand one hundred and twenty patients undergoing surgery and enrolled in the European registry PAIN OUT. MAIN OUTCOME MEASURES: Pain-related outcome was evaluated on the first postoperative day (D1) using a standardised pain outcome questionnaire. Review at 6 and 12 months via e-mail or telephonic interview used the Brief Pain Inventory (BPI) and the DN4 (Douleur Neuropathique four questions). Primary endpoint was the incidence of moderate to severe CPSP (numeric rating scale, NRS ≥3/10) at 12 months. RESULTS: For 1044 and 889 patients, complete data were available at 6 and 12 months. At 12 months, the incidence of moderate to severe CPSP was 11.8% (95% CI 9.7 to 13.9) and of severe pain (NRS ≥6) 2.2% (95% CI 1.2 to 3.3). Signs of neuropathic pain were recorded in 35.4% (95% CI 23.9 to 48.3) and 57.1% (95% CI 30.7 to 83.4) of patients with moderate and severe CPSP, respectively. Functional impairment (BPI) at 6 and 12 months increased with the severity of CPSP (P < 0.01) and presence of neuropathic characteristics (P < 0.001). Multivariate analysis identified orthopaedic surgery, preoperative chronic pain and percentage of time in severe pain on D1 as risk factors. A 10% increase in percentage of time in severe pain was associated with a 30% increase of CPSP incidence at 12 months. CONCLUSION: The collection of data on CPSP was feasible within the European registry PAIN OUT. The incidence of moderate to severe CPSP at 12 months was 11.8%. Functional impairment was associated with CPSP severity and neuropathic characteristics. Risk factors for CPSP in the present study were chronic preoperative pain, orthopaedic surgery and percentage of time in severe pain on D1. TRIAL REGISTRATION: Clinicaltrials.gov identifier: NCT01467102.

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The immune system is involved in the development of neuropathic pain. In particular, the infiltration of T-lymphocytes into the spinal cord following peripheral nerve injury has been described as a contributor to sensory hypersensitivity. We used the spared nerve injury (SNI) model of neuropathic pain in Sprague Dawley adult male rats to assess proliferation, and/or protein/gene expression levels for microglia (Iba1), T-lymphocytes (CD2) and cytotoxic T-lymphocytes (CD8). In the dorsal horn ipsilateral to SNI, Iba1 and BrdU stainings revealed microglial reactivity and proliferation, respectively, with different durations. Iba1 expression peaked at D4 and D7 at the mRNA and protein level, respectively, and was long-lasting. Proliferation occurred almost exclusively in Iba1 positive cells and peaked at D2. Gene expression observation by RT-qPCR array suggested that T-lymphocytes attracting chemokines were upregulated after SNI in rat spinal cord but only a few CD2/CD8 positive cells were found. A pronounced infiltration of CD2/CD8 positive T-cells was seen in the spinal cord injury (SCI) model used as a positive control for lymphocyte infiltration. Under these experimental conditions, we show early and long-lasting microglia reactivity in the spinal cord after SNI, but no lymphocyte infiltration was found.

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The purpose of this study was to clarify the concept of advocacy in context of procedural pain care and to investigate the implementation of advocacy in that context. First, the concept of advocacy was described on the basis of a literature review (n = 89 empirical studies from 1990 to 2003). Then, the concept was described in the context of procedural pain care on the basis of interview data (n = 22 patients, 21 nurses) in a medical and surgical context. In the second phase, an instrument exploring the content of advocacy and the implementation of advocacy in context of procedural pain care was developed and validated. Then, the content of advocacy and implementation of it was explored in a sample of otolaryngeal patients (n = 405) and nurses (n = 118) in 12 hospitals. In the third phase, an update literature review (n = 35 empirical studies from 2003 to 2007) was conducted, and all data from phases one and two were reviewed in order to refine the elements the concept of advocacy, and the relationships between these elements. As a result of this study, advocacy in context of procedural pain care was defined as consisting of the dual aspects of patient advocacy and professional advocacy, and called nursing advocacy. It was divided into dimensions and subdimensions in which patient and nurse empowerment seems to play a vital role. All the data obtained lend support to this definition of nursing advocacy. Patients and nurses felt that nearly all of the activities that they considered as advocacy were implemented.

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Objectives: To evaluate the intensity and location of musculoskeletal pain suffered by students and professors from different postgraduate programs of the School of Dentistry of the University of Barcelona (Spain), to identify the variables related to the occurrence of musculoskeletal symptoms and signs, and to establish possible preventive measures for such disorders. Materials and Methods: A cross-sectional study was made among students and faculty members from different postgraduate courses of the School of Dentistry at the University of Barcelona between May and June 2007. A total of 74 dentists (54 postgraduate students and 20 faculty members) completed an anonymous questionnaire containing 19 questions. The variables were divided into three main groups: sociodemographic information, ergonomic features and musculoskeletal pain arising from professional practice. Results: Most of the dentists (79.8%) had experienced some kind of musculoskeletal pain in the last 6 months. On comparing the different locations of pain (lumbar, cervical, dorsal, wrist, shoulder and others), the neck was found to be the most commonly affected location (58% of all subjects), and only 34% of the respondents took some preventive measures against musculoskeletal disorders. Women showed a higher frequency of intense pain involving the cervical, lumbar, dorsal and wrist areas (p<0.05). A higher incidence of wrist pain was recorded in professionals exclusively dedicated to oral surgery (p<0.05). No statistically significant correlation was found between the workload (hours) and pain in the different anatomical locations (p>0.05). Conclusions: An important incidence of pain symptoms secondary to musculoskeletal disorders was observed, particularly in the cervical region. Females and younger dentists showed a higher frequency of such symptoms. The implementation of preventive measures is necessary, in view of the high incidence of these disorders

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The autophagic process is a lysosomal degradation pathway, which is activated during stress conditions, such as starvation or exercise. Regular exercise has beneficial effects on human health, including neuroprotection. However, the cellular mechanisms underlying these effects are incompletely understood. Endurance and a single bout of exercise induce autophagy not only in brain but also in peripheral tissues. However, little is known whether autophagy could be modulated in brain and peripheral tissues by long-term moderate exercise. Here, we examined the effects on macroautophagy process of long-term moderate treadmill training (36 weeks) in adult rats both in brain (hippocampus and cerebral cortex) and peripheral tissues (skeletal muscle, liver and heart). We assessed mTOR activation and the autophagic proteins Beclin 1, p62, LC3B (LC3B-II/LC3B-I ratio) and the lysosomal protein LAMP1, as well as the ubiquitinated proteins. Our results showed in the cortex of exercised rats an inactivation of mTOR, greater autophagy flux (increased LC3-II/LC3-I ratio and reduced p62) besides increased LAMP1. Related with these effects a reduction in the ubiquitinated proteins was observed. No significant changes in the autophagic pathway were found either in hippocampus or in skeletal and cardiac muscle by exercise. Only in the liver of exercised rats mTOR phosphorylation and p62 levels increased, which could be related with beneficial metabolic effects in this organ induced by exercise. Thus, our findings suggest that long-term moderate exercise induces autophagy specifically in the cortex

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The autophagic process is a lysosomal degradation pathway, which is activated during stress conditions, such as starvation or exercise. Regular exercise has beneficial effects on human health, including neuroprotection. However, the cellular mechanisms underlying these effects are incompletely understood. Endurance and a single bout of exercise induce autophagy not only in brain but also in peripheral tissues. However, little is known whether autophagy could be modulated in brain and peripheral tissues by long-term moderate exercise. Here, we examined the effects on macroautophagy process of long-term moderate treadmill training (36 weeks) in adult rats both in brain (hippocampus and cerebral cortex) and peripheral tissues (skeletal muscle, liver and heart). We assessed mTOR activation and the autophagic proteins Beclin 1, p62, LC3B (LC3B-II/LC3B-I ratio) and the lysosomal protein LAMP1, as well as the ubiquitinated proteins. Our results showed in the cortex of exercised rats an inactivation of mTOR, greater autophagy flux (increased LC3-II/LC3-I ratio and reduced p62) besides increased LAMP1. Related with these effects a reduction in the ubiquitinated proteins was observed. No significant changes in the autophagic pathway were found either in hippocampus or in skeletal and cardiac muscle by exercise. Only in the liver of exercised rats mTOR phosphorylation and p62 levels increased, which could be related with beneficial metabolic effects in this organ induced by exercise. Thus, our findings suggest that long-term moderate exercise induces autophagy specifically in the cortex