Clinical determinants and neural correlates of presbyphagia in community-dwelling older adults

Background“Presbyphagia” refers to characteristic age-related changes in the complex neuromuscular swallowing mechanism. It has been hypothesized that cumulative impairments in multiple domains affect functional reserve of swallowing with age, but the multifactorial etiology and postulated compensatory strategies of the brain are incompletely understood. This study investigates presbyphagia and its neural correlates, focusing on the clinical determinants associated with adaptive neuroplasticity.Materials and methods64 subjects over 70 years of age free of typical diseases explaining dysphagia received comprehensive workup including flexible endoscopic evaluation of swallowing (FEES), magnetoencephalography (MEG) during swallowing and pharyngeal stimulation, volumetry of swallowing muscles, laboratory analyzes, and assessment of hand-grip-strength, nutritional status, frailty, olfaction, cognition and mental health. Neural MEG activation was compared between participants with and without presbyphagia in FEES, and associated clinical influencing factors were analyzed. Presbyphagia was defined as the presence of oropharyngeal swallowing alterations e.g., penetration, aspiration, pharyngeal residue pooling or premature bolus spillage into the piriform sinus and/or laryngeal vestibule.Results32 of 64 participants showed swallowing alterations, mainly characterized by pharyngeal residue, whereas the airway was rarely compromised. In the MEG analysis, participants with presbyphagia activated an increased cortical sensorimotor network during swallowing. As major clinical determinant, participants with swallowing alterations exhibited reduced pharyngeal sensation. Presbyphagia was an independent predictor of a reduced nutritional status in a linear regression model.ConclusionsSwallowing alterations frequently occur in otherwise healthy older adults and are associated with decreased nutritional status. Increased sensorimotor cortical activation may constitute a compensation attempt to uphold swallowing function due to sensory decline. Further studies are needed to clarify whether the swallowing alterations observed can be considered physiological per se or whether the concept of presbyphagia may need to be extended to a theory with a continuous transition between presbyphagia and dysphagia

Effect of Intestinal Levodopa-Carbidopa Infusion on Pharyngeal Dysphagia: Results from a Retrospective Pilot Study in Patients with Parkinson’s Disease

Background. Pharyngeal dysphagia is a common symptom of Parkinson’s disease (PD) leading to severe complications. PD-related pharyngeal dysphagia (PDrPD) may significantly improve in up to half of patients following acute oral levodopa challenge. Objective. The aim of this study was to investigate the effects of levodopa-carbidopa intestinal gel (LCIG) on PDrPD. Methods. Forty-five PD patients under LCIG treatment were available for retrospective analysis. In all patients with PDrPD who underwent flexible endoscopic evaluation of swallowing (FEES) in the clinical “on-state” both before and after implementation of LCIG treatment, FEES videos were systematically reassessed. PDrPD was characterized using a PD-specific FEES score evaluating premature bolus spillage, penetration/aspiration, and pharyngeal residue. Further, the duration of white-out was assessed, as a parameter for pharyngeal bradykinesia. Results. Eleven patients with PDrPD (mean age 74.6 ± 4.4 years; mean Hoehn and Yahr stage 3.8 ± 0.6) received FEES both before and after the onset of LCIG treatment. The mean swallowing score improved from 14.9 ± 7.3 to 13.0 ± 6.9 after implementation of LCIG; however, this difference was not significant (p=0.312). Premature bolus spillage decreased significantly (p=0.002) from 5.4 ± 1.1 to 3.6 ± 1.0, and white-out duration decreased significantly (p=0.002) from 984 ± 228 ms to 699 ± 131 ms after implementation of LCIG. Conclusions. LCIG may affect PDrPD and reduce premature bolus spillage and pharyngeal bradykinesia. Future studies with larger sample sizes are required to follow-up on these pilot results and identify which factors predict a good response of PDrPD to LCIG treatment

Mind the gap: acute bilateral vocal cord palsy in CIDP after extending the IVIG treatment interval?

Cranial nerve involvement is rarely seen in chronic inflammatory demyelinating polyneuropathy (CIDP). We present a patient diagnosed with CIDP who was in a stable medical condition under long-term treatment with intravenous immunoglobulin (IVIG) every five weeks for more than seven years. Following a 12-day delay in the patient’s regular IVIG therapy, he developed acute bilateral vocal cord palsy. The patient had to be intubated and tracheostomized because of acute respiratory distress. Weaning from mechanical ventilation was complicated due to pneumonia. After antibiotic treatment and restarting IVIG therapy vocal cord palsy rapidly improved allowing for subsequent decannulation. Although coincidence between treatment delay and symptom development does not prove definitive causality this case report may serve as a reminder how time critical IVIG therapy can be for sufficient symptom control. Moreover, it provides evidence that IVIG therapy may be effective for the treatment of cranial nerve symptoms in CIDP

Sarcopenic Dysphagia Revisited: A Cross-Sectional Study in Hospitalized Geriatric Patients

Oropharyngeal dysphagia (OD) is a frequent finding in older patients with potentially lethal complications such as aspiration pneumonia, malnutrition, and dehydration. Recent studies describe sarcopenia as a causative factor for OD, which is occasionally referred to as “sarcopenic dysphagia” in the absence of a neurogenic etiology. In most of the previous studies on sarcopenic dysphagia, the diagnosis was based only on clinical assessment. In this study, flexible endoscopic evaluation of swallowing (FEES) was used as an objective method to evaluate the presence of OD, its association with sarcopenia, and the presence of pure sarcopenic dysphagia. In this retrospective cross-sectional study, 109 acute care geriatric hospital patients with suspected OD received FEES examination and bioimpedance analysis (BIA) in clinical routine. 95% of patients had at least one neurological disease, 70% fulfilled the criteria for sarcopenia, and 45% displayed moderate or severe OD. Although the prevalence of sarcopenia and OD was high, there was no significant association between OD and sarcopenia. Considering these results, both the association between sarcopenia and OD and pure sarcopenic dysphagia appear questionable. Further prospective studies are needed to elucidate if sarcopenia is merely an epiphenomenon of severe disease or whether it plays a causative role in the development of OD

Oropharyngeal Dysphagia and Impaired Motility of the Upper Gastrointestinal Tract—Is There a Clinical Link in Neurocritical Care?

Patients in the neurological ICU are at risk of suffering from disorders of the upper gastrointestinal tract. Oropharyngeal dysphagia (OD) can be caused by the underlying neurological disease and/or ICU treatment itself. The latter was also identified as a risk factor for gastrointestinal dysmotility. However, its association with OD and the impact of the neurological condition is unclear. Here, we investigated a possible link between OD and gastric residual volume (GRV) in patients in the neurological ICU. In this retrospective single-center study, patients with an episode of mechanical ventilation (MV) admitted to the neurological ICU due to an acute neurological disease or acute deterioration of a chronic neurological condition from 2011–2017 were included. The patients were submitted to an endoscopic swallowing evaluation within 72 h of the completion of MV. Their GRV was assessed daily. Patients with ≥1 d of GRV ≥500 mL were compared to all the other patients. Regression analysis was performed to identify the predictors of GRV ≥500 mL/d. With respect to GRV, the groups were compared depending on their FEES scores (0–3). A total of 976 patients were included in this study. A total of 35% demonstrated a GRV of ≥500 mL/d at least once. The significant predictors of relevant GRV were age, male gender, infratentorial or hemorrhagic stroke, prolonged MV and poor swallowing function. The patients with the poorest swallowing function presented a GRV of ≥500 mL/d significantly more often than the patients who scored the best. Conclusions: Our findings indicate an association between dysphagia severity and delayed gastric emptying in critically ill neurologic patients. This may partly be due to lesions in the swallowing and gastric network

Assessment of dysphagia after stroke -state of the art and future directions

After a stroke, most patients have dysphagia, which can lead to aspiration pneumonia, malnutrition, and adverse functional outcomes. Protective interventions aimed at reducing these complications remain the cornerstone of treatment. Dietary adjustments and oral hygiene help mitigate the risk of aspiration pneumonia, and nutritional supplementation, including tube feeding, might be needed to prevent malnutrition. Rehabilitative interventions aim to enhance swallowing function, with different behavioural strategies showing promise in small studies. Investigations have explored the use of pharmaceutical agents such as capsaicin and other Transient-Receptor-Potential-Vanilloid-1 (TRPV-1) sensory receptor agonists, which alter sensory perception in the pharynx. Neurostimulation techniques, such as transcranial direct current stimulation, repetitive transcranial magnetic stimulation, and pharyngeal electrical stimulation, might promote neuroplasticity within the sensorimotor swallowing network. Further advancements in the understanding of central and peripheral sensorimotor mechanisms in patients with dysphagia after a stroke, and during their recovery, will contribute to optimising treatment protocols

Effects of cognitive and motor dual‑tasks on oropharyngeal swallowing assessed with FEES in healthy individuals

Dysphagia is frequent in many neurological diseases and gives rise to severe complications such as malnutrition, dehydration and aspiration pneumonia. Therefore, early detection and management of dysphagia is essential and can reduce mortality. This study investigated the effect of cognitive and motor dual-task interference on swallowing in healthy participants, as dual-task effects are reported for other motor tasks such as gait and speech. 27 participants (17 females; 29.2 ± 4.1 years) were included in this prospective study and examined using flexible endoscopic evaluation of swallowing (FEES). Using a previously established FEES-based score, the paradigms "baseline swallowing", "cognitive dual-task" and "motor dual-task" were assessed. Scores of the three paradigms were compared using a repetitive measures ANOVA and post-hoc analysis. Mean baseline swallowing score in single task was 5 ± 3. It worsened to 6 ± 5 in the cognitive (p = 0.118), and to 8 ± 5 in the motor dualtask condition (p < 0.001). This change was driven by subclinical worsening of premature bolus spillage and pharyngeal residue. Oropharyngeal swallowing is not exclusively reflexive in nature but requires attention, which leads to motor dual-task interference. This has potential diagnostic and therapeutic implications, e.g. in the early screening for dysphagia or in avoiding dual-task situations while eating

Dysphagia as Isolated Manifestation of Jo-1 Associated Myositis?

Dysphagia can be predominant or sole symptom of myositis. However, diagnostic evaluation is difficult in such cases. Here, we present evidence for dysphagia as sole manifestation of Jo-1 associated myositis. A 77-year-old patient suffering from isolated dysphagia was assessed by flexible endoscopic evaluation of swallowing, videofluoroscopy, high resolution esophageal manometry, whole body muscle MRI, electroneurographic and electromyographic examination, cerebrospinal fluid analysis, screening for autoantibodies, and body plethysmography. We detected isolated oropharyngeal dysphagia including a decreased pressure of the upper esophageal sphincter leading to cachexia in an anti-Jo-1 positive patient without any abnormalities in the other diagnostics. Immunosuppressive therapy with cortisone and azathioprine led to long-term improvement of dysphagia. This is the first report of isolated dysphagia as manifestation of Jo-1 associated myositis. Therefore, Jo-1 associated myositis should be considered as a possible differential diagnosis for isolated dysphagia. Typical signs for myositis in instrumental dysphagia assessment are presented