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.

Medium LDL levels improvement after 1 month was 71.7 ±41.2 mg/dL (Table 1). 17 patients (10.55%) did not have an analytic in the last year, and 10 patients (6.21%) had not had an appointment with their doctor in more than a year. 38 patients (23.6%) had LDL levels over the objective. According to guidelines and protocol, these patients were referred to the physician for revision. Conclusion and relevanceAlthough some patients do not reach the desired outcome and/or their monitoring may be improved, our data show that PCSK9i causes a great reduction of LDL levels that is maintained over time.

A 70-year-old male patient, who was diagnosed with human immunodeficiency virus (HIV) in 2001 and did not undergo antiretroviral therapy, was admitted two months after the onset of left cortical-subcortical ischemic stroke, with involvement of the corona radiata and the left thalamus. As a consequence of this vascular event, he suffered aphasia, severe dysarthria, dysphagia, and right hemiparesis. The patient took part in a rehabilitation program at a rehabilitation centre for neurological diseases with a specialised interdisciplinary rehabilitation team. He underwent speech therapy intervention with a frequency of 2-3 hours per day. Despite the intensity of the program, there was a decline in his clinical and functional status during hospitalisation, with decreased capacity to swallow and communicate (either because of the exacerbation of the aphasia, or due to the worsening of dysarthria and apraxic features). Due to this global deterioration, additional imaging, as well as serological and aetiological examination was performed, which led to a diagnosis of progressive multifocal leukoencephalopathy in the context of HIV1 infection. Antiretroviral therapy was administered to reverse the symptoms. This case illustrates the relevance of clinical disclosure for the establishment of appropriate functional prognoses and discharge planning. It also shows that the initial clinical features can be misleading and can lead to concealment of the real aetiology, as well as delays in appropriate treatment, especially in multipathology patients.