Dysphagia is described as a highly relevant comorbidity of Alzheimer’s disease (AD). However, there is a scarcity of studies aiming at the characteristics and progression of dysphagia. Objective: The objective of this study was to identify the specific characteristics, progression, and prevalence of dysphagia in AD. Methods: Publications were searched in the PubMed (MEDLINE), EBSCO, ScienceDirect, and BASE databases. Critical appraisal and evidence-level analysis were conducted using the Joanna Briggs Institute and Effective Public Health Practice Project’s (EPHPP) tools. Results: A total of 26 studies were reviewed. Symptoms begin in the early stage of AD, as oral phase impairments, and progress to pharyngeal symptoms and swallowing apraxia in the later stages of AD. Dysphagia progresses, as AD, along a continuum, with severity depending on individual variability. There were no studies found on prevalence. Conclusions: Dysphagia is a complex and important comorbidity in AD that impacts the quality of life. No recent publications on prevalence may imply that is not being coded as a potential cause for pneumonia deaths in AD.

Background: Stroke is the leading cause of cortical deafness (CD), the most severe form of central hearing impairment. CD remains poorly characterized and perhaps underdiagnosed. We perform a systematic review to describe the clinical and radiological features of stroke-associated CD. Methods: PubMed and the Web of Science databases were used to identify relevant publications up to 30 June 2021 using the MeSH terms: “deafness” and “stroke”, or “hearing loss” and “stroke” or “auditory agnosia” and “stroke”. Results: We found 46 cases, caused by bilateral lesions within the central auditory pathway, mostly located within or surrounding the superior temporal lobe gyri and/or the Heschl’s gyri (30/81%). In five (13.51%) patients, CD was caused by the subcortical hemispheric and in two (0.05%) in brainstem lesions. Sensorineural hearing loss was universal. Occasionally, a misdiagnosis by peripheral or psychiatric disorders occurred. A few (20%) had clinical improvement, with a regained oral conversation or evolution to pure word deafness (36.6%). A persistent inability of oral communication occurred in 43.3%. A full recovery of conversation was restricted to patients with subcortical lesions. Conclusions: Stroke-associated CD is rare, severe and results from combinations of cortical and subcortical lesions within the central auditory pathway. The recovery of functional hearing occurs, essentially, when caused by subcortical lesions.

Facial palsies have multiple etiologies, but have in common the negative impact not only on the functions of the stomatognathic system but also on the self-image and emotional expression. This article aimed to describe a case study of unilateral peripheral facial palsy caused by the Guillain-Barré Syndrome. Hence, it shares assessment and intervention experiences related to this type of change and presents its functional results. It also highlights the important role of the interdisciplinary team (which comprised a physiatrist, physical therapist, speech-language-hearing therapist, occupational therapist, and nurses) to catalyze the patient’s evolution and the management of possible complications. Moreover, it is rather important to integrate the patients as members of the rehabilitation team, empowering them and giving them responsibility for the success of the intervention.

Background: Head motion and variability in scan quality remain major methodological challenges in autism neuroimaging. Large multi-site datasets such as ABIDE-II provide a unique opportunity to systematically quantify diagnostic differences in MRI data quality and assess the influence of site-level heterogeneity. Methods: Functional MRI Quality Assessment Protocol (QAP) metrics were combined with phenotypic data from ABIDE-II. Participants were classified as autistic (ASD) or typically developing (TD). Key quality metrics—including mean framewise displacement (mFD), proportion of volumes exceeding 0.20 mm (FD > 0.20), signal-to-noise ratio (SNR), and entropy focus criterion (EFC)—were analyzed alongside age, sex, IQ, and site. Group differences were evaluated using non-parametric tests and linear mixed-effects models with site as a random factor. Additional analyses examined site-level heterogeneity and the impact of quality-control (QC) thresholds on sample composition. Results: The final sample included 1277 participants (579 ASD; 698 TD) across 14 sites. ASD participants exhibited significantly greater head motion (median mFD = 0.101 vs. 0.081 mm; p < 1 × 10⁻¹⁰) and modest reductions in signal quality (lower SNR, higher EFC). Elevated motion in ASD was observed in 12 of 14 sites, although effect sizes varied substantially. Mixed-effects models confirmed that diagnosis remained a significant predictor of motion after adjusting for covariates. In contrast, signal-quality differences were small and largely explained by site effects. Simulated QC procedures disproportionately excluded ASD participants, with exclusion rates up to 31% compared to 18% in TD. Conclusions: ASD participants show consistently higher head motion, while signal-quality differences are minimal and largely site-driven. Standard QC procedures disproportionately exclude ASD individuals, highlighting the need for improved motion handling and more balanced quality-control strategies in multi-site studies.