Estudos publicados em periódicos indexados sobre decisões judiciais para acesso a medicamentos no Brasil: uma revisão sistemática Estudios publicados en revistas indexadas acerca de decisiones judiciales para el acceso a los medicamentos en Brasil: una revisión sistemática

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The cervical spine is considered a possible source of headaches, however there are still some controversies regarding the pathophysiology, clinical presentation, and treatment. Objective: To propose a physical therapy treatment protocol with multimodal approach for cervicogenic headache and evaluate the effects of manual therapy on such patients. Method: This was an uncontrolled experimental study in which 9 patients from the UNIFESO Physical Therapy Clinic (Teresópolis, RJ) diagnosed with cervicogenic headache underwent 10 physiotherapy interventions with manual therapy techniques. The experimental protocol included joint techniques, fascial release, and muscle recruitment. The Neck Disability Index (NDI) and a visual analogic scale (VAS) were used as measurement tools and the pain pattern was recorded. Results: Of the nine selected patients, all were female and had an average age of 43.3 years (± 15.5). Significant differences were observed between the average intensity of pain (VAS) before treatment (8.0 ± 1.3) and after (2.2 ± 0.9, p < 0.01). The NDI also showed improvement after intervention 63.9% (p < 0.01). Regarding crises frequency, a decrease of 70% was observed after the intervention (p < 0.01) and a reduction was also shown in the duration of such crises before (4 hours ± 1.5) and after treatment (1 hour ± 0.5; p < 0.01). Conclusion: A multimodal approach by manual therapy techniques was beneficial in the reduction of the patients' symptoms and it provided a decrease in cervical disability.

This report aims to inform on the progression of research into the genetic factors involved in the development of Alzheimer’s disease (AD). AD is a life-altering disease that affects millions of individuals from varying races and ethnic backgrounds1. According to the National Institute on Aging, a faculty of the U.S. Department of Health and Human Services, AD has been ranked as the third leading cause of death in the United States, only behind cancer and heart failure. It is predicted that by 2050, approximately one in 45 Americans will be afflicted with the disease5.            Distinctive physical indications of the onset of AD include neuron loss, amyloid plaques and neurofibrillary tangles5. Onset is not frequent prior to 60 years of age but can be caused by one of two reasons. The first is a mutation in the amyloid precursor protein (APP) gene on chromosome 21. This gene is responsible for the regulation of the production of amyloid beta (Aβ) proteins, which are known to be abundant in the brains of AD patients. A mutation in the gene leads to an inappropriate regulation of this protein. The second, and more common cause is a result of an unidentified gene on chromosome 14 in AD patients2. It has been confirmed that there is involvement of chromosome 19 in late onset AD (LOAD)  as well1. Most of the genes that are associated with the development of AD have yet to be identified, but the research is bringing society closer and closer to that goal everyday.Ce rapport vise à fournir de l’information sur la progression de la recherche au sujet des facteurs génétiques impliqués dans le développement de la maladie d'Alzheimer (MA). La MA est une maladie bouleversant la vie de la personne et qui affecte des millions d’individus de diverses races et ethnicité1. Selon l'Institut national sur le vieillissement, un corps professoral du département américain de la santé et des services sociaux, la MA a été classée comme la troisième cause de décès aux États-Unis, ne cédant le pas qu’au cancer et à l'insuffisance cardiaque. Il est prévu que d'ici l'an 2050, environ une personne sur 45 Américains sera affligée avec cette maladie5.Des indications visuelles distinctives de l'apparition de la MA comprennent la perte des neurones, les plaques amyloïdes et des enchevêtrements neurofibrillaires5. L'apparition précoce n’est pas fréquente avant 60 ans, mais peut être causée par l'une des deux raisons. La première raison est une mutation dans le gène de la protéine précurseur de l'amyloïde (PPA) sur le chromosome 21. Ce gène est responsable de la régulation de la production de protéines bêta-amyloïde (Aß), qui sont connues pour être abondant dans le cerveau des patients atteints de la MA. Une mutation dans le gène conduit à une régulation inappropriée de cette protéine. La seconde cause, et celle-là plus communes sont le résultat d'un gène inconnu sur le chromosome 142. Il a été confirmé qu'il y a aussi une participation du chromosome 19 dans l'apparition tardive de la MA (ATMA)1. La plupart des gènes qui sont associés avec le développement de la MA n’ont pas encore été identifiés, mais la recherche rapproche la société de cet objectif de plus en plus tous les jours.