Dysphagia in Older Adults.

Dysphagia, which is a geriatric syndrome affecting 10% to 33% of older adults, is commonly seen in older adults who have experienced a stroke or neurodegenerative diseases such as Alzheimer or Parkinson disease. Patients diagnosed as having dysphagia can experience malnutrition, pneumonia, and dehydration. Patients can also experience increased rates of mortality and long-term care admission. Providers can identify the specific type of dysphagia for treatment in approximately 80% of patients by asking 5 questions in the patient's history: What happens when you try to swallow? Do you have trouble chewing? Do you have difficulty swallowing solids, liquids, or both? Describe the symptom onset, duration, and frequency? What are the associated symptoms? Providers can then request a videofluoroscopic swallow study or a fiberoptic endoscopic evaluation of swallowing for further evaluation of oropharyngeal dysphagia. If providers are diagnosing esophageal dysphagia, barium esophagraphy or esophagogastroduodenoscopy (EGD) can be used as part of the assessment. Patients can be treated for oropharyngeal dysphagia by using compensatory interventions, including behavioral changes, oral care, dietary modification, or rehabilitative interventions such as exercises and therapeutic oral trials. Providers often address treatment of esophageal dysphagia by managing the underlying etiology, which could include removal of caustic medications or using EGD as a therapeutic modality for esophageal rings. High-quality, large research studies are necessary to further manage the diagnosis and appropriate treatment of this growing geriatric syndrome.

The extent of intrauterine growth restriction determines the severity of cerebral injury and neurobehavioural deficits in rodents.

BACKGROUND: Cerebral Palsy (CP) is the most common physical pediatric neurodevelopmental disorder and spastic diplegic injury is its most frequent subtype. CP results in substantial neuromotor and cognitive impairments that have significant socioeconomic impact. Despite this, its underlying pathophysiological mechanisms and etiology remain incompletely understood. Furthermore, there is a need for clinically relevant injury models, which a) reflect the heterogeneity of the condition and b) can be used to evaluate new translational therapies. To address these key knowledge gaps, we characterized a chronic placental insufficiency (PI) model, using bilateral uterine artery ligation (BUAL) of dams. This injury model results in intrauterine growth restriction (IUGR) in pups, and animals recapitulate the human phenotype both in terms of neurobehavioural and anatomical deficits. METHODS: Effects of BUAL were studied using luxol fast blue (LFB)/hematoxylin & eosin (H&E) staining, immunohistochemistry, quantitative Magnetic Resonance Imaging (MRI), and Catwalk neurobehavioural tests. RESULTS: Neuroanatomical analysis revealed regional ventricular enlargement and corpus callosum thinning in IUGR animals, which was correlated with the extent of growth restriction. Olig2 staining revealed reductions in oligodendrocyte density in white and grey matter structures, including the corpus callosum, optic chiasm, and nucleus accumbens. The caudate nucleus, along with other brain structures such as the optic chiasm, internal capsule, septofimbrial and lateral septal nuclei, exhibited reduced size in animals with IUGR. The size of the pretectal nucleus was reduced only in moderately injured animals. MAG/NF200 staining demonstrated reduced myelination and axonal counts in the corpus callosum of IUGR animals. NeuN staining revealed changes in neuronal density in the hippocampus and in the thickness of hippocampal CA2 and CA3 regions. Diffusion weighted imaging (DWI) revealed regional white and grey matter changes at 3 weeks of age. Furthermore, neurobehavioural testing demonstrated neuromotor impairments in animals with IUGR in paw intensities, swing speed, relative print positions, and phase dispersions. CONCLUSIONS: We have characterized a rodent model of IUGR and have demonstrated that the neuroanatomical and neurobehavioural deficits mirror the severity of the IUGR injury. This model has the potential to be applied to examine the pathobiology of and potential therapeutic strategies for IUGR-related brain injury. Thus, this work has potential translational relevance for the study of CP.