RESUMEN
PURPOSE: Dysphagia is most prevalent among post stroke aging adults. This systematic review was conducted to collect evidence-based data regarding assessment and therapeutic techniques used to rehabilitate post stroke dysphagia patients. METHODS: Four major databases including PubMed, Cochrane Library, Science direct and Google scholar were searched systematically using the defined search strategy to target Randomized Controlled Trials conducted from January 2018 to 2023 using the pre-defined search strategy by three independent reviewers. RESULTS: After following PRISMA guidelines, fifteen articles matched the inclusion criteria. Several evidence based therapies like Neuromuscular Electrical Stimulation Therapy, Effortful Swallowing Training, Tongue Pressure Strength and Accuracy Training, Electrical Stimulation of Hyoid Muscles, Modified Chin Tuck Against Resistance exercise, Oral Neuromuscular Training, and Conventional Speech Therapy with Functional Electrical Stimulation were used frequently for the treatment of old age post stroke dysphagia in different rehabilitation centers. Along with this, a list of different assessment methodologies and tools was made that were used including Functional Oral Intake Scale, Fiber optic Endoscopic Evaluation of Swallowing, Penetration Aspiration Scale, Pooling Scale, Video fluoroscopic Dysphagia Scale, Iowa Oral Performance Instrument, Mann Assessment of Swallowing Ability, and Repetitive Saliva Swallowing Test. CONCLUSION: Dysphagia is known to be serious complication of stroke. This systematic review shows a significant impact of therapeutic techniques on post stroke dysphagia patients and demonstrates that neuromuscular electrical stimulation therapy is one of the most effective therapeutic techniques used to rehabilitate post stroke dysphagia patients.
RESUMEN
EAT-26 questionnaire is used globally to screen people for the risk of eating disorders. In addition to this, the EAT-26 is being used in its original English version in research and clinical settings due to unavailability of the Urdu version. Therefore, the aim of this study was to introduce the Urdu version of EAT-26 to clinicians and academicians in Pakistan, interested in the assessment of population at risk of eating disorders. After getting the formal permission for translation by Dr. D. M. Garner, WHO guidelines were followed for the translation and adaptation process. Two independent translators with psychological background worked under the supervision of a lead to produce the definitive version following six steps of translation and adaptation. Cognitive interviews and focused group discussions helped in the assessment process for the understanding level of translated Urdu version. The pre-final version showed comprehension and acceptability during initial pilot testing.â¢The final translated version of EAT-26 in Urdu will be available on Internet to use. It is expected that the use of EAT-26 will be widespread in Pakistan, aiming at the assessment of eating disorders.â¢The Urdu version of EAT-26 is finalized, and ready to use by researchers and clinicians in Pakistan.
RESUMEN
The execution of agricultural activities on an industrial scale has led to indiscriminate deposition of toxic xenobiotics, including organophosphates, in the biome. This has led to intoxication characterized by deleterious oxidative and neuronal changes. This study investigated the consequences of oxidative and neurogenic disruptions that follow exposure to a combination of two organophosphates, chlorpyrifos (CPF) and dichlorvos (DDVP), on neuro-cognitive performance and anxiety-like behaviors in rats. Thirty-two adult male Wistar rats (150â»170 g) were randomly divided into four groups, orally exposed to normal saline (NS), DDVP (8.8 mg/kg), CPF (14.9 mg/kg), and DDVP + CPF for 14 consecutive days. On day 10 of exposure, anxiety-like behavior and amygdala-dependent fear learning were assessed using open field and elevated plus maze paradigms, respectively, while spatial working memory was assessed on day 14 in the Morris water maze paradigm, following three training trials on days 11, 12, and 13. On day 15, the rats were euthanized, and their brains excised, with the hippocampus and amygdala removed. Five of these samples were homogenized and centrifuged to analyze nitric oxide (NO) metabolites, total reactive oxygen species (ROS), and acetylcholinesterase (AChE) activity, and the other three were processed for histology (cresyl violet stain) and proliferative markers (Ki67 immunohistochemistry). Marked (p ≤0.05) loss in body weight, AChE depletion, and overproduction of both NO and ROS were observed after repeated exposure to individual and combined doses of CPF and DDVP. Insults from DDVP exposure appeared more severe owing to the observed greater losses in the body weights of exposed rats. There was also a significant (p ≤0.05) effect on the cognitive behaviors recorded from the exposed rats, and these deficits were related to the oxidative damage and neurogenic cell loss in the hippocampus and the amygdala of the exposed rats. Taken together, these results provided an insight that oxidative and neurogenic damage are central to the severity of neuro-cognitive dysfunction and increased anxiety-like behaviors that follow organophosphate poisoning.