Massage Therapy as a Complementary Treatment for Stiffness and Numbness Post Cervical Spinal Cord Injury: a Case Study.

Introduction: Spinal Cord Injuries (SCI) commonly result in pain, stiffness, weakness and numbness. There are limitations in the ability of the standard medical approach to manage many symptoms of SCI. This case study examined the effects of massage therapy as a "complementary" therapy to treat post-operative numbness and stiffness after removal of a cavernous hemangioma intermeshed with a 26-year-old male patient's spinal cord. Methods: The patient received eight, one-hour therapeutic massage sessions over five months. Therapeutic massage techniques were performed by a Board-Certified Therapeutic Massage and Bodywork Therapist and consisted of cranial sacral, Swedish, myofascial release, trigger point therapy, and passive stretching. Symptom intensity was recorded prior to each session on a qualitative scale (1-10) and was trended over the course of the study. Results: There was a slight decrease over time in left-arm and back numbness, as well as neck and upper body stiffness. The patient viewed therapeutic massage to be a beneficial component to his recovery. Discussion/Conclusion: Massage therapy should be considered as an adjunct therapy as part of a rehabilitation plan to address numbness and stiffness post-SCI. Further research is needed to understand the effects of massage therapy on SCI numbness and stiffness.

Questionnaire and Portable Sleep Test Screening of Sleep Disordered Breathing in Acute Stroke and TIA.

Sleep disordered breathing (SDB) is highly prevalent, but frequently unrecognized among stroke patients. Polysomnography (PSG) is difficult to perform soon after a stroke. We evaluated the use of screening questionnaires and portable sleep testing (PST) for patients with acute stroke, subarachnoid hemorrhage, or transient ischemic attack to expedite SDB diagnosis and management. We performed a single-center retrospective analysis of a quality improvement study on SDB screening of consecutive daytime, weekday, adult admissions to a stroke unit. We excluded patients who were unable to communicate and lacked available family members. Patients were screened with the Epworth Sleepiness Scale, Berlin Questionnaire, and STOP-BANG Questionnaire and underwent overnight PST and/or outpatient PSG. The 4-item STOP Questionnaire was derived from STOP-BANG for a secondary analysis. We compared the sensitivity and specificity of the questionnaires for the diagnosis of at least mild SDB (apnea hypopnea index (AHI) ≥5) on PST and correlated AHI measurements between PST and PSG using the Spearman correlation. Out of sixty-eight patients included in the study, 54 (80%) were diagnosed with SDB. Only one (1.5%) had a previous SDB diagnosis. Thirty-three patients completed all questionnaires and a PST. The STOP-BANG questionnaire had the highest sensitivity for at least mild SDB (0.81, 95% CI (confidence interval): 0.65-0.92) but a low specificity (0.33, 95% CI 0.10, 0.65). The discrimination of all questionnaires was overall poor (C statistic range 0.502-0.640). There was a strong correlation (r = 0.71) between the AHI results estimated using PST and outpatient PSG among 28 patients. The 4-item STOP Questionnaire was the easiest to administer and had a comparable or better sensitivity than the other questionnaires. Inpatient PSTs were useful for screening in the acute setting to facilitate an early diagnosis of SDB and to establish further outpatient evaluations with sleep medicine.

Mortality Outcomes With Intensive Blood Pressure Targets in Chronic Kidney Disease Patients.

Hypertension is highly prevalent and morbid in the chronic kidney disease population, and blood pressure (BP) targets for this population are unclear. We aimed to compare all-cause mortality outcomes with intensively targeting systolic BP to <130 mm Hg versus a standard of <140 mm Hg. Individual patient data from 4983 chronic kidney disease patients with hypertension were pooled from 4 multicenter randomized control trials-AASK (African American Study of Kidney Disease and Hypertension), ACCORD (Action to Control Cardiovascular Risk in Diabetes), MDRD (Modification of Diet in Renal Disease), and the SPRINT (Systolic Blood Pressure Intervention Trial). Patients were assigned their trial-assigned randomized intervention group-standard (n=2474) versus intensive (n=2509) BP targets. Additional analyses included excluding patients with a glomerular filtration rate ≥60 mL/min per 1.73 m2 along with those undergoing intensive glycemic control. The primary outcome was all-cause mortality. Average achieved BP was 125.0 mm Hg in the intensive group and 136.9 mm Hg in the standard group. In the primary analysis, the all-cause mortality rate trended towards improved outcomes with intensive treatment but was not statistically significant (hazard ratio: 0.87 [0.69-1.08]; P=0.21). One hundred seventy-three of 2474 patients (1.95% per year) in the standard group and 153 of 2509 patients (1.71% per year) in the intensive group died. After excluding patients with higher glomerular filtration rate values and those undergoing intensive glycemic control, there was a statistically significant decrease in all-cause mortality rate (hazard ratio: 0.79 [0.63-1.00]; P=0.048). An intensive BP target of <130 mm Hg decreases all-cause mortality when compared with a standard target of <140 mm Hg in patients with chronic kidney disease stage 3 or greater who are not undergoing intensive glycemic therapy.

Intensive Blood Pressure Targets for Diabetic and Other High-Risk Populations: A Pooled Individual Patient Data Analysis.

Optimal blood pressure (BP) targets for different populations, especially diabetics, remain uncertain after conflicting data on intensive management. We assessed whether a <120 mm Hg systolic target is beneficial and whether certain patient populations differ in response. Individual patient data of 14 094 patients from 2 randomized control trials was pooled. Seven thousand forty patients were assigned to an intensive target of <120 mm Hg and 7054 patients to a standard target of <140 mm Hg in an intention-to-treat analysis. The primary outcome was a composite of myocardial infarction, other acute coronary syndromes, stroke, heart failure, and cardiovascular mortality. Interactions between treatment and baseline characteristics were assessed. Secondary outcomes included nonfatal myocardial infarction, stroke, heart failure, cardiovascular mortality, and overall mortality. Intensive management significantly lowered primary outcome rate (hazard ratio, 0.83; 95% confidence interval, 0.74-0.92; P<0.001). No significant interaction was observed between treatment effect and diabetes mellitus status (P=0.16). Significantly reduced secondary outcomes included stroke (hazard ratio, 0.75; P=0.033) and heart failure (hazard ratio, 0.76; P=0.014). No significant interactions were observed between treatment effect and baseline age, sex, race, cardiovascular disease history, systolic BP, or diastolic BP (P values: 0.40, 0.95, 0.54, 0.18, 0.86, and 0.67, respectively). BP targets of <120 mm Hg improved cardiovascular outcomes. Diabetic patients responded similarly to this intervention, as did those with different age, sex, cardiovascular disease history, baseline BPs, and race. The intensive group had increased risk of intervention-related adverse outcomes (3.97% versus 1.53%; P<0.001). Clinicians should consider <120 mm Hg systolic targets for a variety of patients, including diabetics.

Mechanisms of Intestinal Barrier Dysfunction in Sepsis.

Intestinal barrier dysfunction is thought to contribute to the development of multiple organ dysfunction syndrome in sepsis. Although there are similarities in clinical course following sepsis, there are significant differences in the host response depending on the initiating organism and time course of the disease, and pathways of gut injury vary widely in different preclinical models of sepsis. The purpose of this study was to determine whether the timecourse and mechanisms of intestinal barrier dysfunction are similar in disparate mouse models of sepsis with similar mortalities. FVB/N mice were randomized to receive cecal ligation and puncture (CLP) or sham laparotomy, and permeability was measured to fluoresceinisothiocyanate conjugated-dextran (FD-4) six to 48 h later. Intestinal permeability was elevated following CLP at all timepoints measured, peaking at 6 to 12 h. Tight junction proteins claudin 1, 2, 3, 4, 5, 7, 8, 13, and 15, Junctional Adhesion Molecule-A (JAM-A), occludin, and ZO-1 were than assayed by Western blot, real-time polymerase chain reaction, and immunohistochemistry 12 h after CLP to determine potential mechanisms underlying increases in intestinal permeability. Claudin 2 and JAM-A were increased by sepsis, whereas claudin-5 and occludin were decreased by sepsis. All other tight junction proteins were unchanged. A further timecourse experiment demonstrated that alterations in claudin-2 and occludin were detectable as early as 1 h after the onset of sepsis. Similar experiments were then performed in a different group of mice subjected to Pseudomonas aeruginosa pneumonia. Mice with pneumonia had an increase in intestinal permeability similar in timecourse and magnitude to that seen in CLP. Similar changes in tight junction proteins were seen in both models of sepsis although mice subjected to pneumonia also had a marked decrease in ZO-1 not seen in CLP. These results indicate that two disparate, clinically relevant models of sepsis induce a significant increase in intestinal permeability mediated through a common pathway involving alterations in claudin 2, claudin 5, JAM-A, and occludin although model-specific differences in ZO-1 were also identified.

Lactobacillus rhamnosus GG and Bifidobacterium longum attenuate lung injury and inflammatory response in experimental sepsis.

INTRODUCTION: Probiotic use to prevent nosocomial gastrointestinal and potentially respiratory tract infections in critical care has shown great promise in recent clinical trials of adult and pediatric patients. Despite well-documented benefits of probiotic use in intestinal disorders, the potential for probiotic treatment to reduce lung injury following infection and shock has not been well explored. OBJECTIVE: Evaluate if Lactobacillus rhamnosus GG (LGG) or Bifidobacterium longum (BL) treatment in a weanling mouse model of cecal ligation and puncture (CLP) peritonitis will protect against lung injury. METHODS: 3 week-old FVB/N mice were orally gavaged with 200 µl of either LGG, BL or sterile water (vehicle) immediately prior to CLP. Mice were euthanized at 24 h. Lung injury was evaluated via histology and lung neutrophil infiltration was evaluated by myeloperoxidase (MPO) staining. mRNA levels of IL-6, TNF-α, MyD88, TLR-4, TLR-2, NFΚB (p50/p105) and Cox-2 in the lung analyzed via real-time PCR. TNF-α and IL-6 in lung was analyzed via ELISA. RESULTS: LGG and BL treatment significantly improved lung injury following experimental infection and sepsis and lung neutrophil infiltration was significantly lower than in untreated septic mice. Lung mRNA and protein levels of IL-6 and TNF-α and gene expression of Cox-2 were also significantly reduced in mice receiving LGG or BL treatment. Gene expression of TLR-2, MyD88 and NFΚB (p50/p105) was significantly increased in septic mice compared to shams and decreased in the lung of mice receiving LGG or BL while TLR-4 levels remained unchanged. CONCLUSIONS: Treatment with LGG and BL can reduce lung injury following experimental infection and sepsis and is associated with reduced lung inflammatory cell infiltrate and decreased markers of lung inflammatory response. Probiotic therapy may be a promising intervention to improve clinical lung injury following systemic infection and sepsis.

Epidermal growth factor receptor expression and signaling are essential in glutamine's cytoprotective mechanism in heat-stressed intestinal epithelial-6 cells.

Epidermal growth factor receptor (EGFR) expression and signaling can induce cellular protection after intestinal inflammation. L-Glutamine (GLN) is known to prevent apoptosis after intestinal injury by activating MAPK and phosphatidylinositol 3-kinase (PI3-K)/Akt pathways. However, the role of EGFR expression and signaling in GLN-mediated cellular protection in intestinal epithelial-6 (IEC-6) cells after heat stress (HS) is unknown. To address the role of EGFR in GLN-mediated protection, IEC-6 cells were treated with GLN in the presence or absence of EGFR small interfering RNA, the EGFR tyrosine kinase inhibitor AG1478, the ERK1/2 inhibitor PD98059, the p38MAPK inhibitor SB203580, or the PI3-K/Akt inhibitor LY294002 under basal and HS conditions. GLN-mediated cell survival was measured using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Phosphorylated and/or total levels of EGFR, cleaved caspase-3, poly(ADP-ribose) polymerase-1, ERK1/2, p38MAPK, and Akt were assessed by Western blotting. We showed that HS induced a decrease in total, cytoplasmic, and nuclear EGFR levels in IEC-6 cells, which was prevented by GLN supplementation, leading to attenuated apoptosis via EGFR small interfering RNA. Furthermore, the protective effect of GLN was lessened by AG1478, PD98059, and LY294002 but was not affected by SB203580. AG1478 attenuated GLN-mediated increases in ERK1/2 and decreases in p38MAPK phosphorylation. However, AG1478 had no effect on GLN-mediated augmentations in Akt phosphorylation. In summary, EGFR expression was important in the protective mechanism of GLN, as well as GLN-mediated activation of EGFR tyrosine kinase activity. GLN-mediated EGFR signaling activated ERK1/2 and decreased p38MAPK signaling. However, GLN-mediated Akt phosphorylation after HS seems to be independent of EGFR signaling.