Risk Factors for Poststroke Shoulder Pain: A Systematic Review and Meta-Analysis.

OBJECTIVE: To identify the risk factors identified within 1-month poststroke that predict the onset of poststroke shoulder pain (PSSP) within the first year after stroke. METHODS: Five databases (AMED, CINAHL, EMBASE, Medline, and PubMed) were searched from inception to April 2019. Prospective cohort studies that measured a potential risk factor for PSSP within the first month after stroke were included. Two authors independently reviewed and selected articles for inclusion. Risk of bias was assessed using the Quality in Prognosis Studies tool. Data extracted included raw data for odds ratio (OR) calculations, definition and measurement of pain, study limitations, and baseline characteristics of participants. The review was conducted following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. RESULTS: Nine articles were retrieved that met the inclusion criteria, and 6 presented data to use in meta-analysis. Fifty-four different factors were identified as potential risk factors. Meta-analysis was possible for 4 factors; sex (OR .93, confidence interval [CI] .75-1.15), laterality (OR .78, CI .59-1.05), diabetes (OR 2.09, CI 1.16-3.78), and history of shoulder pain (OR 2.78, CI 1.29-5.97). Reduced motor function in the upper limb was also identified as a significant risk factor through qualitative synthesis. CONCLUSIONS: Reduced motor function in the upper limb, diabetes, and a history of shoulder pain were identified as significant risk factors for the development of PSSP within the first year after stroke. Recommendations to standardize future studies in this area have been made, and it is suggested that defining subtypes of PSSP may aid future interventional studies.

A survey of the current practice of intramuscular Botulinum toxin injections for hemiplegic shoulder pain in the UK.

PURPOSE: To describe the current UK practice for the use of intramuscular Botulinum Toxin type A injections to treat hemiplegic shoulder pain. METHOD: A UK-based cross-sectional study using an online survey. Participants (n = 68) were medical and non-medical practitioners recruited via the membership of the British Society for Rehabilitation Medicine and the British Neurotoxin Network. Data was analysed using descriptive statistics and content analysis. RESULTS: The majority of respondents would consider Botulinum Toxin type A for hemiplegic shoulder pain (86.8%), though most of these respondents inject for this goal infrequently (83.1%). Pectoralis major was most commonly selected to achieve this goal. Barriers to this intervention included difficulties determining the cause of pain (29.4%), difficulty isolating muscles (27.9%), and a lack of evidence (25%). The doses reported regularly deviated from guidelines and a substantial range in the volumes suggested was observed. Clinicians were mostly reliant on unstandardised measures to assess outcomes. CONCLUSIONS: Current UK practice of Botulinum Toxin type A injections for hemiplegic shoulder pain associated with spasticity is highly variable. There are large gaps between current practice and available evidence with regards to muscle selection and doses used. A number of areas for further investigation have been identified to progress current understanding of this intervention. Implications for rehabilitation There are wide variations in practice for this complex intervention and clinicians should consider that their individual decision-making could be based on their own beliefs rather than available evidence. Pectoralis major is most commonly injected to treat hemiplegic shoulder pain, but further evaluation is required to address whether it is the most effective. Clinicians most often use a limitation of shoulder abduction and external rotation, flexor patterning of the upper limb, and pain on passive movement to identify when hemiplegic shoulder pain is due to spasticity over other causes. Further research is needed to identify which patients are most likely to benefit from this intervention and at what stage post-stroke its use is most optimal.

Nanoscale surface modifications to control capillary flow characteristics in PMMA microfluidic devices.

Polymethylmethacrylate (PMMA) microfluidic devices have been fabricated using a hot embossing technique to incorporate micro-pillar features on the bottom wall of the device which when combined with either a plasma treatment or the coating of a diamond-like carbon (DLC) film presents a range of surface modification profiles. Experimental results presented in detail the surface modifications in the form of distinct changes in the static water contact angle across a range from 44.3 to 81.2 when compared to pristine PMMA surfaces. Additionally, capillary flow of water (dyed to aid visualization) through the microfluidic devices was recorded and analyzed to provide comparison data between filling time of a microfluidic chamber and surface modification characteristics, including the effects of surface energy and surface roughness on the microfluidic flow. We have experimentally demonstrated that fluid flow and thus filling time for the microfluidic device was significantly faster for the device with surface modifications that resulted in a lower static contact angle, and also that the incorporation of micro-pillars into a fluidic device increases the filling time when compared to comparative devices.

Toward a microfluidic-based rapid amylase assay system.

This article describes work into a prototype system for the assay of amylase, using microfludic technologies. The new system has a significantly shorter cycle time than the current laboratory methods, which generally use microtitre plates, yet is capable of generating significantly superior results. As such, we have shown that sensitivity is enhanced by a factor of 10 in the standard assay trials, and by a factor of 2 in the real-sample lab trials. In both assays, the use of a microreactor system reduced the reaction time by a factor of 6.2, from 20 min incubation to 3.2 min. Basing the conclusion on the Megazyme Cerealpha Standard Method, and using the Cerealpha units as a measure of assay efficiency, the typical response for the microfluidic assay was shown to be 1.0 x 10(-3) CU/mL (standard deviation [SD] 2.5 x 10(-4) CU/mL), compared to 2.56 x 10(-4) CU/mL (SD 5.94 x 10(-5) CU/mL) for the standard macroassay. It is believed that this improvement in the reaction schematics is due to the inherent advantages of microfluidic devices such as superior mixing, higher thermal efficiency, and enhanced reaction kinetics.

Mismatch repair gene expression defects contribute to microsatellite instability in ovarian carcinoma.

BACKGROUND: hMLH1, the human MutL homologue, has been linked to microsatellite instability (MSI) in gastrointestinal tumors. However, to the authors' knowledge, the role of hMLH1, the other mismatch repair genes (MMR), and MSI in ovarian carcinoma has not been well defined. The purpose of the current study was to determine the relation between MSI of ovarian carcinoma and MMR gene expression, hMLH1 and hMSH2 hypermethylation, and hMLH1 and hMSH2 null mutations. METHODS: hMLH1 mRNA was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and amplification of cDNA using a housekeeping gene (glycerol 3-phosphate dehydrogenase) as a control for mRNA quality and quantity. Methylation-specific PCR (MS-PCR) was used to correlate methylation of the hMLH1 and hMSH2 CpG islands with mRNA expression status. Similar techniques were used to evaluate the concomitant expression of five other MMR: hMSH2, hMSH3, hMSH6, PMS1, and PMS2. Microsatellite instability was studied using the National Cancer Institute consensus markers (D2S123, D5S346, D17S250, BAT25, and BAT26) and NM23 as described previously. RESULTS: One hundred twenty-five primary tumors were analyzed. High-frequency MSI (MSI-H) was found in 21 tumors (16.8%). hMLH1 mRNA was absent in 10 of these 21 tumors (47.6%). In each case, coordinated hypermethylation of both regions A and C of the promoter was identified. Microsatellite stable and low-frequency MSI tumors all were found to express not only hMLH1 but the other MMR genes as well (P < 0.001). Absence of expression of hMSH2 and the four other MMRs occurred in tumors with absent hMLH1 mRNA expression because of CpG island hypermethylation. No absence of expression of hMSH2, hMSH3, hMSH6, PMS1, or PMS2 was found to occur in tumors expressing hMLH1. None of the 11 MSI-H tumors without promoter hypermethylation demonstrated a null mutation in hMLH1 or hMSH2. CONCLUSIONS: A molecular mechanism to explain > 50% of the MSI-H phenotype in ovarian carcinoma cases was demonstrated. MSI-H may occur because of MMR defects, especially hMLH1 promoter hypermethylation. Additional mechanisms are required to explain the balance between the cases of MSI-H as well as the phenomenon of MSI-L tumors.