Exercise therapy improves pain and mouth opening in temporomandibular disorders: A systematic review with meta-analysis.

OBJECTIVE: To analyse the effectiveness of exercise therapy in improving pain and active or passive maximum mouth opening in patients with temporomandibular disorders. DATA SOURCES: PubMed Medline, Web of Science, Scopus, CINAHL Complete and Physiotherapy Evidence Database, until April 2022, in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. REVIEW METHODS: We included randomized controlled trials evaluating the effect of exercise therapy on pain and on active and passive maximum mouth opening in patients with temporomandibular disorders. Effect size was calculated using Cohen's standardized mean difference (SMD) and their 95% confidence interval (95% CI) in a random-effects model. RESULTS: A total of 16 studies with 812 participants were included. Exercise therapy is effective in reducing pain (SMD: -0.58; 95% CI: -1.01 to -0.12) and increasing the pain pressure threshold (SMD: 0.45; 95% CI: 0.14-0.76), active and passive maximum mouth opening (SMD: 0.43; 95% CI: 0.14-0.71 and SMD: 0.4; 95% CI: 0.06-0.75, respectively). Subgroup analyses showed more effect of exercise therapy more splints versus splints on pain (SMD: -0.5; 95% CI: -0.73 to -0.26), active and passive maximum mouth opening (SMD: 1.14; 95% CI: 0.22-2.07 and SMD: 0.56; 95% CI: 0.06-1.06, respectively). On pain pressure threshold, exercise therapy was better than physiotherapy approach (manual therapy and electrotherapy) (SMD: 0.48; 95% CI: 0.09-0.87). CONCLUSIONS: Therapeutic exercise is an effective therapy to reduce pain and increase pain pressure threshold and active and passive maximum mouth opening in patients with temporomandibular disorders.

Calcified Neurocysticercosis and Headache in an Endemic Village: A Case-Control Study Nested to a Population-Based Cohort.

Headache in patients with calcified neurocysticercosis (NCC) is probably common but has been largely overlooked. We aimed to assess the presence, characteristics, and diagnosis of headache across patients with calcified NCC and their matched controls. In this case-control study nested to a population-based cohort, Atahualpa residents aged ≥ 20 years with calcified NCC were identified as case patients and paired 1:1 to age- and gender-matched randomly selected controls. A culturally adapted questionnaire was derived from the EUROLIGHT. Headache diagnosis was established according to the International Classification of Headache Disorders, 3rd edition. Conditional logistic regression models for matched paired data were fitted to assess the independent association between calcified NCC (as the exposure) and headache variables, after adjusting for education, alcohol intake, depression, and epilepsy. The selection process generated 106 case patients and their matched controls. Lifetime headache prevalence (odds ratio [OR]: 4.18; 95% Confidence Interval [CI]: 1.79-9.75; P = 0.001), current headaches (OR: 4.19; 95% CI: 1.92-9.16; P < 0.001), and intense headaches (OR: 9.47; 95% CI: 2.88-31.19; P < 0.001) were more frequent among cases than in controls. In addition, migraine (but not other forms of headache) was more frequent among subjects with calcified NCC (OR: 4.89; 95% CI: 2.36-11.39; P < 0.001). This study shows a robust epidemiological association between headache-particularly migraine-and calcified NCC.

Non-neural tyrosine hydroxylase, via modulation of endocrine pancreatic precursors, is required for normal development of beta cells in the mouse pancreas.

AIMS/HYPOTHESIS: Apart from transcription factors, little is known about the molecules that modulate the proliferation and differentiation of pancreatic endocrine cells. The early expression of tyrosine hydroxylase (TH) in a subset of glucagon(+) cells led us to investigate whether catecholamines have a role in beta cell development. METHODS: We studied the immunohistochemical characteristics of TH-expressing cells in wild-type (Th (+/+) ) mice during early pancreas development, and analysed the endocrine pancreas phenotype of TH-deficient (Th (-/-) ) mice. We also studied the effect of dopamine addition and TH-inhibition on insulin-producing cells in explant cultures. RESULTS: In the mouse pancreas at embryonic day (E)12.5-E13.5, the ∼10% of early glucagon(+) cells that co-expressed TH rarely proliferated and did not express the precursor marker neurogenin 3 at E13.5. The number of insulin(+) cells in the Th (-/-) embryonic pancreas was decreased as compared with wild-type embryos at E13.5. While no changes in pancreatic and duodenal homeobox 1 (PDX1)(+)-progenitor cell number were observed between groups at E12.5, the number of neurogenin 3 and NK2 homeobox 2 (NKX2.2)-expressing cells was reduced in Th (-/-) embryonic pancreas, an effect that occurred in parallel with increased expression of the transcriptional repressor Hes1. The potential role of dopamine as a pro-beta cell stimulus was tested by treating pancreas explants with this catecholamine, which resulted in an increase in total insulin content and insulin(+) cells relative to control explants. CONCLUSIONS/INTERPRETATION: A non-neural catecholaminergic pathway appears to modulate the pancreatic endocrine precursor and insulin producing cell neogenesis. This finding may have important implications for approaches seeking to promote the generation of beta cells to treat diabetes.

[Interruption of antifungal secondary prophylaxis in AIDS-related histoplasmosis]. / Interrupción de la profilaxis secundaria antifúngica en la histoplasmosis asociada al sida.

The clinical data of 21 patients, suffering AIDS-related histoplasmosis, who were able to interrupt antifungal secondary prophylaxis, after achieving a partial restoration of the cell mediated immunity by HAART administration, are presented. They were 16 males and five females, whose ages varied between 32 and 54 years (mean = 38.5 years). All of them presented disseminated progressive forms of histoplasmosis, with multiple locations (skin, mucous membranes, liver, spleen, lymph nodes and lungs). The majority of the cases suffered other concomitant diseases (specially tuberculosis and Kaposi sarcoma), 66.6 % of the patients had less than 50 CD4+ cells/microl at the start of treatment and the average viral burden was 278,385 RNA copies/ml. The initial treatment consisted in 400 mg/day of itraconazole, by oral route, in 14 cases and the remaining seven patients were treated with amphotericin B, intravenously, at a daily dose of 0.7 mg/kg of body weight. One patient who did not tolerate amphotericin B and presented a partial response to itraconazole, was treated with posaconazole orally at a daily dose of 800 mg. Fourteen patients received oral itraconazole at a daily dose of 200 mg as a secondary prophylaxis, the remaining three patients were treated with intravenous amphotericin B, 50 mg twice a week. After HAART for an average lapse of 16.7 months (10 to 32 months), five cases showed CD4+ cells counts above 150 cells/microl and the remaining 16 presented more than 200 cells/microl; 18 of them had undetectable viral burden and all cases were asymptomatic. The follow up after secondary prophylaxis discontinuation varied between six months and six years (mean= 33.6 months). Twenty out of 21 patients (95 %) were clinically stable, without any manifestation of relapses, including two patients who abandoned HAART. One patient, who discontinued HAART, contracted a fatal bacterial pneumonia. Even though the limited number of cases, the data presented in this study seem to suggest that it is possible to interrupt antifungal secondary prophylaxis of histoplasmosis, when the patient is clinically asymptomatic and the CD4+ cells counts are above 150 cells/microl.

Re-HEDP : pharmacokinetic characterization, clinical and dosimetric evaluation in osseous metastatic patients with two levels of radiopharmaceutical dose.

BACKGROUND: A study for pain relief therapy with 188Re-HEDP was done in patients with bone metastases secondary to breast and prostate cancer. MATERIALS AND METHODS: Patients received 1.3 or 2.2 GBq, in single or multiple doses. Platelets, white and red cells were evaluated during 11 weeks. Pharmacokinetic characterization was done from blood and urine samples for 5 patients along 24 hours. Urinary excretion was evaluated in other 16 patients during 6 hours. Bone uptake was estimated as remaining activity in whole body. Scintigraphic images were acquired at 2 and 24 hs post-administration. Absorbed dose in bone marrow was estimated with Mirdose3. Analgesics intake and pain score were daily recorded. Tumour markers (PSA, and Tn-structure) were monitored in 9 patients during 4 to 6 months. Single doses of low activity (1.3 GBq) were given to twelve patients. Nine patients received multiple doses. RESULTS: All except one patient had normal levels of platelets, white and red cells. Remaining dose in blood at 2 hours was 9%. Urinary elimination was 58%. Bone uptake at 24 hours was 43% (mean value; n = 5). No changes of the haematological parameters were detected along follow-up period. Pain relief was evidenced by decrease or supression of opioid analgesic and by subjective index. PSA showed a decrease in prostate cancer patients (n = 4). Tn-structure showed a significant increase after 4 to 8 months. CONCLUSION: Single or multiple dose scheme could be safely used, with administered activity of 188Re-HEDP up to 60 mCi, with low bone marrow absorbed doses.