Brain structural correlates of sensory phenomena in patients with obsessive–compulsive disorder

Background

Sensory phenomena (SP) are uncomfortable feelings, including bodily sensations, sense of inner tension, “just-right” perceptions, feelings of incompleteness, or “urge-only” phenomena, which have been described to precede, trigger or accompany repetitive behaviours in individuals with obsessive–compulsive disorder (OCD). Sensory phenomena are also observed in individuals with tic disorders, and previous research suggests that sensorimotor cortex abnormalities underpin the presence of SP in such patients. However, to our knowledge, no studies have assessed the neural correlates of SP in patients with OCD.

Methods

We assessed the presence of SP using the University of São Paulo Sensory Phenomena Scale in patients with OCD and healthy controls from specialized units in São Paulo, Brazil, and Barcelona, Spain. All participants underwent a structural magnetic resonance examination, and brain images were examined using DARTEL voxel-based morphometry. We evaluated grey matter volume differences between patients with and without SP and healthy controls within the sensorimotor and premotor cortices.

Results

We included 106 patients with OCD and 87 controls in our study. Patients with SP (67% of the sample) showed grey matter volume increases in the left sensorimotor cortex in comparison to patients without SP and bilateral sensorimotor cortex grey matter volume increases in comparison to controls. No differences were observed between patients without SP and controls.

Limitations

Most patients were medicated. Participant recruitment and image acquisition were performed in 2 different centres.

Conclusion

We have identified a structural correlate of SP in patients with OCD involving grey matter volume increases within the sensorimotor cortex; this finding is in agreement with those of tic disorder studies showing that abnormal activity and volume increases within this region are associated with the urges preceding tic onset.     

Current considerations for the management of musculoskeletal pain in Asian countries: a special focus on cyclooxygenase-2 inhibitors and non-steroid anti-inflammation drugs

Chronic pain is a complex problem that eludes precise definition and can be clinically difficult to diagnose and challenging to treat. In the Asia-Pacific region, prevalence estimates that chronic pain ranges from 12% to 45% of the population, with musculoskeletal, rheumatic or osteoarthritis pain making up the majority of the disease burden. Implementation of current management guidelines into routine clinical practice has been challenging and as a result, patients with musculoskeletal pain are often poorly managed. For these reasons, a multidisciplinary Chronic Pain Advisory Board of leading physicians from various Asian countries was convened to explore ways to improve treatment and compliance, especially among patients with osteoarthritis and rheumatoid arthritis. We have identified a number of unmet therapeutic needs and prioritized initiatives with the potential to contribute toward a more integrated approach to chronic pain management. Key priorities included using evidence-based interventions as recommended by current guidelines, particularly those aspects pertinent to addressing treatment priorities in Asia (e.g., patient compliance), and the incorporation of cyclooxygenase-2 inhibitors and non-steroid anti-inflammation drugs into the management algorithms for osteoarthritis and rheumatoid arthritis. Treatment must be individualized for each patient based on efficacy, side-effect profile and drug accessibility. Further studies are required to examine head-to-head comparisons among analgesics, combinations of analgesics and long-term efficacy outcomes. Our increasing understanding of the problem combined with the promise of new therapy options offers hope for improved management of musculoskeletal pain in Asian countries.     

Increased in vitro glial fibrillary acidic protein expression,telomerase activity,and telomere length after productive human immunodeficiency virus‐1 infection in murine astrocytes

Although HIV‐associated neurocognitive disorders (HAND) result from injury and loss of neurons, productive infection routinely takes place in cells of macrophage lineage. In such a complex context, astrocytosis induced by local chemokines/cytokines is one of the hallmarks of HIV neuropathology. Whether this sustained astrocyte activation is able to alter telomere‐aging process is unknown. We hypothesized that interaction of HIV with astrocytes may impact astrocyte telomerase activity (TA) and telomere length in a scenario of astrocytic activation measured by expression of glial fibrillary acidic protein (GFAP). To test this hypothesis, cultured murine astrocytes were challenged with pseudotyped HIV/vesicular stomatitis virus (HIV/VSV) to circumvent the absence of viral receptors; and GFAP, telomerase activity, and telomere length were quantified. As an early and transient event after HIV infection, both TA activity and telomere length were significantly augmented (P < 0.001). Later, a strong negative correlation (?0.8616, P < 0.0001) between virus production and telomerase activity was demonstrated. Once HIV production had reached a peak (7 dpi), the TA decreased, showing levels similar to those of noninfected cells. In contrast, the astrocyte became activated, exhibiting significantly increased levels of GFAP expression directly related to the level of HIV/VSV replication (P < 0.0001). Our results suggest that HIV‐infected astrocytes exhibit early disturbance in their cellular functions, such as telomerase activity and telomere length, that may attenuate cell proliferation and enhance the astrocyte dysregulation, contributing to HIV neuropathogenesis. Understanding the mechanisms involved in HIV‐mediated persistence by altering the telomere‐related aging processes could aid in the development of therapeutic modalities for neurological complications of HIV infection. © 2013 Wiley Periodicals, Inc.     

‘The Problem of the Color Line’: Faculty approaches to teaching Social Justice in Baccalaureate Nursing Programs

Social justice is put forth as a core professional nursing value, although conceptualizations within foundational documents and among nurse educators remain inconsistent and contradictory. The purpose of this study was to explore how faculty teach social justice in theory courses in Baccalaureate programs. This qualitative study utilized constructivist grounded theory methods to examine processes informing participants' teaching. Participants utilize four overarching approaches: fostering engaging classroom climates, utilizing various naming strategies, framing diversity and culture as social justice, and role modeling a critical stance. They deploy specific strategies, varying largely by race, educational background, and nursing specialty. A background in social sciences supports pedagogy that interrogates health inequities rather than merely raising awareness about disparities. Findings also reveal that faculty of color navigate institutional structures predicated upon colorblind racism and problematic views of culture, which many white faculty teaching non‐Community Health Nursing courses described doing. To enact social justice and be answerable to our communities, concerted anti‐oppression efforts are needed across education, research, practice, and policy. This includes sustained commitment to address colonialism and whiteness in every institution that defines, promotes, and claims to advance nursing so that we can fulfill our responsibility to address unjust systems and structures to serve our communities.     

Age-related burden and characteristics of embolic stroke of undetermined source in the real world clinical practice

Journal of Thrombosis and Thrombolysis - Few data are available on age-related burden and characteristics of embolic stroke of undetermined source (ESUS) in the real world clinical practice. The...     

Promoter hypermethylation of the phosphatase DUSP22 mediates PKA‐dependent TAU phosphorylation and CREB activation in Alzheimer's disease

Genetic screening in Alzheimer's disease (AD) has identified only a handful of genes that are mutated in the disorder. Thus, for a very large proportion of patients, the biology of their disease is poorly understood. Epigenetic alterations may provide an explanation in these cases. Using DNA methylation profiles of human hippocampus from controls and patients, we have identified the presence of promoter hypermethylation of the dual‐specificity phosphatase 22 (DUSP22) gene in AD. DUSP22 is a likely candidate gene for involvement in the pathogenesis of the disorder since, as we demonstrate here, it inhibits PKA activity and thereby determines TAU phosphorylation status and CREB signaling. © 2014 The Authors. Hippocampus Published by Wiley Periodicals, Inc.