https://journal.chestnet.org/article/S0012-3692(15)36028-1/pdf

Aspiration pneumonia and dysphagia in the elderly.

A sensitive immunohistochemical method for phosphorylated α-synuclein was used to stain sets of sections of spinal cord and tissue from 41 different sites in the bodies of 92 subjects, including 23 normal elderly, 7 with incidental Lewy body disease (ILBD), 17 with Parkinson’s disease (PD), 9 with dementia with Lewy bodies (DLB), 19 with Alzheimer’s disease with Lewy bodies (ADLB) and 17 with Alzheimer’s disease with no Lewy bodies (ADNLB). The relative densities and frequencies of occurrence of phosphorylated α-synuclein histopathology (PASH) were tabulated and correlated with diagnostic category. The greatest densities and frequencies of PASH occurred in the spinal cord, followed by the paraspinal sympathetic ganglia, the vagus nerve, the gastrointestinal tract and endocrine organs. The frequency of PASH within other organs and tissue types was much lower. Spinal cord and peripheral PASH was most common in subjects with PD and DLB, where it appears likely that it is universally widespread. Subjects with ILBD had lesser densities of PASH within all regions, but had frequent involvement of the spinal cord and paraspinal sympathetic ganglia, with less-frequent involvement of end-organs. Subjects with ADLB had infrequent involvement of the spinal cord and paraspinal sympathetic ganglia with rare involvement of end-organs. Within the gastrointestinal tract, there was a rostrocaudal gradient of decreasing PASH frequency and density, with the lower esophagus and submandibular gland having the greatest involvement and the colon and rectum the lowest.

Multi-organ distribution of phosphorylated α-synuclein histopathology in subjects with Lewy body disorders

There is growing recognition that gastrointestinal dysfunction is common in Parkinson's disease (PD). Virtually all parts of the gastrointestinal tract can be affected, in some cases early in the disease course. Weight loss is common but poorly understood in people with PD. Dysphagia can result from dysfunction at the mouth, pharynx, and oesophagus and may predispose individuals to aspiration (accidental inhalation of food or liquid). Gastroparesis can produce various symptoms in patients with PD and may cause erratic absorption of drugs given to treat the disorder. Bowel dysfunction can consist of both slowed colonic transit with consequent reduced bowel-movement frequency, and difficulty with the act of defecation itself with excessive straining and incomplete emptying. Recognition of these gastrointestinal complications can lead to earlier and potentially more effective therapeutic intervention.

Gastrointestinal dysfunction in Parkinson's disease.

Gastrointestinal dysfunction is a frequent and occasionally dominating symptom of Parkinson's disease (PD). Features of gastrointestinal dysfunction include disordered control of saliva, dysphagia, gastroparesis, constipation in the sense of decreased bowel movement frequency, and defecatory dysfunction necessitating increased straining and resulting in incomplete evacuation. Excess saliva accumulates in the mouth because of decreased swallowing frequency. Dysphagia develops in approximately 50% of patients and may be a reflection of both central nervous system and enteric nervous system derangement. Gastroparesis may produce a variety of symptoms, including nausea, and also may be responsible for some of the motor fluctuations seen with levodopa therapy. Bowel dysfunction in PD may be the result of both delayed colon transit and impaired anorectal muscle coordination.

AGA technical review on management of oropharyngeal dysphagia

The radiologic characteristics of pharyngoesophageal (PE) dysfunction in Parkinson's disease (PD) are not well established, partly because most previous studies have examined only small numbers of patients. We administered a dynamic videofluoroscopic swallowing function study to 71 patients with idiopathic PD. Using the Hoehn and Yahr disease severity scale, patients were subdivided into those with mild/moderate disease, subgroup I (n = 38), and advanced PD disease, subgroup II (n = 33). From pharyngeal ingestion to gastric emptying, bolus transport was normal in only 2 patients. The most common abnormalities occurring during pharyngeal ingestion included impaired motility, vallecular and pyriform sinus stasis, supraglottic and glottic aspiration, and deficient epiglottic positioning and range of motion. Esophageal abnormalities were multiple but most commonly included delayed transport, stasis, bolus redirection, and tertiary contractions. Typical aberrations of lower esophageal sphincter (LES) function included an open or delayed opening of the LES and gastro-esophageal reflux. A pathogenesis linking PE with the pathology of PD is proposed.

Pharyngo-esophageal dysphagia in Parkinson's disease.

Dysphagia in patients with Parkinson's disease (PD) is most often atributed to pharyngeoesophageal motor abnormalities. In our study of patients with idiopathic PD, attention was focused on prepharyngeal symptoms and motor functions. Using the Hoehn and Yahr disease severity scale, patients were grouped into those with mild/moderate disease [subgroup I (n=38)] and those with advanced disease [subgroup II (n=34)]. Dysphagia symptoms were present in 82% of all patients, but subgroup I patients voiced significantly more complaints. Conversely, many prepharyngeal abnormalities of ingestion, including jaw rigidity, impaired head and neck posture during meals, upper extremity dysmotility, impulsive feeding behavior, impaired amount regulation, and lingual transfer movements were statistically more frequent in subgroup II patients. Impaired mastication and oral preparatory lingual movements were the most common aberrations observed during dynamic videofluoroscopy (48/71), with most patients being concordant for both. The motor disturbances of ingestion reported herein reflect the disintegration of volitional and automatic movements caused by PD-related akinesia, bradykinesia, and rigidity.

Prepharyngeal dysphagia in Parkinson's disease.

Degenerative diseases of the basal ganglia are commonly complicated by dysphagia. In 35 patients with Huntington's disease (HD), a hereditary neurodegenerative basal ganglia disease characterized by chorea, dementia, and emotional changes, an extensive battery of clinical and radiologic procedures helped to identify numerous abnormalities of deglutition. The results permitted the classification of our patients with HD into hyperkinetic (HD-h) or rigid-bradykinetic (HD-rb) groups. Although the two groups share multiple abnormalities, statistically significant intergroup differences were observed. Clincial assessmen of the HD-h cohort (30 patients) demonstrated rapid lingual chorea, swallow incoordination repetitive swallows, prolonged laryngeal elevation, inability to stop respiration and frequent eructations. In the HD-rb group (five patients), frequently observed abnormalities included mandibular rigidity, slow lingual chorea, coughing on foods, and choking on liquids. Videofluoroscopic swallowing studies (VFSS) using a variety of barium-impregnated, foods and liquids confirmed the abnormalities noted on the clinical assessment. Respiratory and laryngeal chorea, pharyngeal space retention, and aspiration were also identified. Numerous compensatory techniques introduced during videofluoroscopy benefited all patients.

Dysphagi in Huntington's disease: A 16-year retrospective

The current classifications of dysphagia are based on local structural or central nervous system pathology causing dysfunction of the aerodigestive tract. The result is a clinical science grounded in the analysis of the swallow with its lingual, pharyngeal, and esophageal stages. Adding bolus preparation to the swallowing paradigm improves but still constrains the study of dysphagia and treatment of the dysphagic patient. Those pre-oral facets of mealtime behavior that may evoke or exacerbate dysphagia remain beyond the existing classification boundaries imposed by the conceptual swallow and anatomic aerodigestive tract. We offer a more inclusive strategy for investigating dysphagia based on a five-stage process of ingestion: pre-oral (anticipatory), preparatory, lingual, pharyngeal, and esophageal. The first stage considers the interaction of pre-oral motor, cognitive, psychosocial, and somataesthetic elements engendered by the meal. The limited literature regarding the interaction of the pre-oral stage with other ingestion stages, in both normal subjects and patients with cortical, basal ganglia, and psychogenic diseases, is reviewed. The neurophysiologic and clinical justifications for embracing a pre-oral stage, and thus for the paradigm shift from deglutition to ingestion, are presented.

Dysphagia--ingestion or deglutition?: a proposed paradigm.

Dysphagia is a common complication of Huntington's disease (HD) that is frequently responsible for the potentially lethal respiratory events of aspiration or asphyxiation. Twelve patients who had HD and a history of dysphagia underwent extensive multidisciplinary clinical examinations. All of the patients, regardless of the clinical severity of their disease, demonstrated impaired control of many voluntary aspects of food intake that affected swallowing efficiency. Abnormalities of the rate of food consumption, mastication, bolus transfer, respiration, and swallow initiation seem to be responsible for most dysphagic symptoms in HD. Less prominent abnormalities of the pharyngoesophageal phases of ingestion were also noted. Dysphagia therapy was initiated in 11 of 12 patients. All of the patients' conditions improved; a majority (8/11) of the patients returned to an unrestricted diet. This improvement persisted for as long as three years, while other clinical features of HD intensified.

Marion C. Kagel

Papers

Pharyngo-esophageal dysphagia in Parkinson's disease.

Prepharyngeal dysphagia in Parkinson's disease.

Dysphagi in Huntington's disease: A 16-year retrospective

Dysphagia--ingestion or deglutition?: a proposed paradigm.

Dysphagia in Huntington's disease.