Pain Catastrophizing: An Updated Review.

Pain catastrophizing: an updated review.

Indian J Psychol Med. 2012 Jul; 34(3): 204-17
Leung L

Pain catastrophizing has been described for more than half a century which adversely affects the pain coping behavior and overall prognosis in susceptible individuals when challenged by painful conditions. It is a distinct phenomenon which is characterized by feelings of helplessness, active rumination and excessive magnification of cognitions and feelings toward the painful situation. Susceptible subjects may have certain demographic or psychological predisposition. Various models of pain catastrophizing have been proposed which include attention-bias, schema-activation, communal-coping and appraisal models. Nevertheless, consensus is still lacking as to the true nature and mechanisms for pain catastrophizing. Recent advances in population genomics and noninvasive neuroimaging have helped elucidate the known determinants and neurophysiological correlates behind this potentially disabling behavior. HubMed – rehab


Radixin expression in microglia after cortical stroke lesion.

Glia. 2013 Feb 26;
Persson A, Osman A, Bolouri H, Mallard C, Kuhn HG

Stroke induces extensive tissue remodeling, resulting in the activation of several cell types in the brain as well as recruitment of blood-borne leucocytes. Radixin is part of a cytoskeleton linker protein family with the ability to connect transmembrane proteins to the actin cytoskeleton, promoting cell functions involving a dynamic cytoskeleton such as morphological changes, cell division and migration which are common events of different cell types after stroke. In the healthy adult brain radixin is expressed in Olig2(+) cells throughout the brain and in neural progenitor cells in the subventricular zone. In the current study, we detected a 2.5 fold increase in the number of radixin positive cells in the peri-infarct cortex two weeks after the induction of cortical stroke by photothrombosis. Similarly, the number of Olig2(+) cells increased in the peri-infarct area after stroke; however, the number of radixin(+) /Olig2(+) cells was unchanged. Neural progenitor cells maintained radixin expression on their route to the infarct. More surprising however, was the expression of radixin in activated microglia in the peri-infarct cortex. Seventy percent of Iba1(+) cells expressed radixin after stroke, a population which was not present in the control brain. Furthermore, activation of radixin was predominantly detected in the peri-infarct region of oligodendrocyte progenitors and microglia. The specific location of radixin(+) cells in the peri-infarct region and in microglia suggests a role for radixin in microglial activation after stroke. HubMed – rehab


Multidisciplinary rehabilitation after primary brain tumour treatment.

Cochrane Database Syst Rev. 2013; 1: CD009509
Khan F, Amatya B, Ng L, Drummond K, Olver J

Brain tumours can cause significant disability, which may be amenable to multidisciplinary rehabilitation. However, the evidence base for this is unclear.To assess the effectiveness of multidisciplinary rehabilitation in adults after primary brain tumour treatment, especially the types of approaches that are effective (settings, intensity) and the outcomes that are affected.We searched the Cochrane Neuromuscular Disease Group Specialized Register (March week 2, 2012), The Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library Issue 3, 2012), MEDLINE (1966 to March week 2, 2012), EMBASE (1980 to March week 2, 2012), PEDro (1982 to March 2012) and LILACS (1982 to March week 2, 2012). We checked the bibliographies of papers identified and contacted the authors and known experts in the field to seek published and unpublished trials.Controlled clinical trials (randomised and non-randomised clinical trials) that compared multidisciplinary rehabilitation in primary brain tumour with either routinely available local services or lower levels of intervention, or studies that compared multidisciplinary rehabilitation in different settings or at different levels of intensity.Three review authors independently assessed study quality, extracted data and performed a ‘best evidence’ synthesis based on methodological quality.No randomised controlled trials (RCTs) or controlled clinical trials (CCTs) were identified.No RCTs or CCTs were available for synthesis of ‘best evidence’ for multidisciplinary rehabilitation after treatment for brain tumour patients. However, this does not suggest the ineffectiveness of multidisciplinary rehabilitation but rather highlights the challenges in trial design and rigour, outcome measurement and complexities of care in this population. For completeness of literature, 12 observational studies (with high risk of bias) involving patients with brain tumours were included. These studies provided ‘very low level’ evidence suggesting that multidisciplinary rehabilitation (inpatient, home-based) may improve functional outcomes, and ambulatory programmes (outpatient and home-based) may improve vocation and quality of life. These conclusions are tentative at best, given gaps in current research in this area. Further research is needed into appropriate and robust study designs, outcome measurement, caregiver needs, evaluation of optimal settings, type, intensity, duration of therapy, and cost-effectiveness of multidisciplinary rehabilitation in the brain tumour population. HubMed – rehab



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