Dysphagia Knowledge Hub — 吞嚥困難知識庫

Multiple Sclerosis and Dysphagia: A Comprehensive Guide

Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease of the central nervous system characterised by demyelination and axonal damage. With an estimated global prevalence of 2.8 million people (Wallin et al., 2019), it is one of the leading causes of neurological disability in young adults. Dysphagia in MS is more prevalent than widely recognised — epidemiological studies report swallowing difficulties in 30–45% of MS patients across all subtypes (Calcagno et al., 2002), rising to over 60% in progressive MS. Despite this, dysphagia assessment and intervention remain inconsistently integrated into MS care pathways in Hong Kong and internationally.

MS Lesion Locations Causing Dysphagia

The swallowing network in the central nervous system is distributed across the cortex, subcortex, brainstem, and cerebellum. Demyelinating plaques at any of these levels can disrupt swallowing function, but certain locations carry particularly high dysphagia risk.

Brainstem lesions are the strongest predictor of dysphagia in MS. The brainstem contains the central pattern generator for swallowing — the nucleus tractus solitarius (NTS) and nucleus ambiguus — as well as motor and sensory nuclei of cranial nerves V, VII, IX, X, and XII, all of which are critical to oropharyngeal swallowing. Plaques at the medulla oblongata, pons, or lower midbrain can impair pharyngeal constriction, laryngeal elevation, hyoid displacement, cricopharyngeal relaxation, and bolus propulsion (Calcagno et al., 2002; Prosiegel et al., 2004).

Cerebellar lesions contribute to dysphagia through disruption of the fine temporal coordination of the swallowing sequence. The cerebellum modulates the timing and sequencing of swallowing muscle contractions; cerebellar demyelination produces dyscoordinated, poorly timed swallows with premature bolus spillage and residue.

Cortical and subcortical lesions contribute to oral-phase dysfunction (reduced bolus formation, tongue control, and oral transit), as well as higher-level difficulties including reduced swallowing frequency, hypersalivation management, and integration of eating with breathing.

Total lesion burden and disease duration are stronger predictors of dysphagia than any single lesion location; patients with EDSS (Expanded Disability Status Scale) scores above 6.0 have markedly elevated dysphagia prevalence.

Fatigue Impact on Swallowing Function

Fatigue is the most commonly reported symptom in MS, affecting approximately 80% of patients. Central MS fatigue — distinct from general tiredness — is a pathological symptom linked to demyelination, impaired axonal conduction velocity, and altered central motor drive. Its impact on swallowing is clinically significant and often underestimated.

Swallowing is a high-frequency motor activity: adults typically swallow 500–1,000 times per day, with each meal requiring sustained oropharyngeal muscle activation over 20–30 minutes. In MS patients with significant fatigue, swallowing efficiency may be adequate at the beginning of a meal but deteriorate progressively as the session continues. This meal-dependent deterioration is distinct from the pattern seen in most other neurological dysphagia conditions and requires specific assessment and management.

Diastolic oral transit time, pharyngeal constriction amplitude, and hyoid displacement have all been documented to worsen with sustained swallowing effort in fatigued MS patients on VFSS (Prosiegel et al., 2004). Clinically, patients may report that food “feels harder to swallow” near the end of meals, or that evening meals are more difficult than breakfast — consistent with central fatigue accumulation across the day.

Relapse vs. Progressive MS: Management Differences

MS presents in several clinical subtypes with distinct dysphagia trajectories:

Relapsing-Remitting MS (RRMS): Dysphagia typically presents acutely during relapses affecting brainstem or cortical swallowing networks, with partial or complete recovery during remission. SLT intervention should begin promptly during relapse to: (1) establish safe feeding during the acute period with appropriate dietary texture modification; (2) monitor recovery; and (3) implement rehabilitation exercises as function recovers. Compensatory strategies may be needed temporarily but should be reassessed as relapse resolves.

Secondary and Primary Progressive MS (SPMS/PPMS): Dysphagia in progressive MS follows a slower but continuous trajectory without remission. Management emphasis shifts toward: maintaining safe oral nutrition as long as possible with sustainable compensatory strategies and dietary adaptation; advance care planning including gastrostomy discussion at an appropriate stage; and ongoing monitoring to detect clinically meaningful deterioration.

Disease-modifying therapies (DMTs) — including interferon-beta, glatiramer acetate, natalizumab, and ocrelizumab — reduce relapse frequency and may slow progression in RRMS and PPMS, potentially moderating dysphagia progression. SLTs should be aware of these treatments and communicate with the neurologist regarding disease activity when making management recommendations.

Adapted Exercises for Fatigue

Standard dysphagia rehabilitation exercises — including tongue strengthening, Mendelsohn manoeuvre, effortful swallow, and shaker/CTAR exercises — require adaptation for MS patients with significant fatigue. Key adaptations:

Cooling Strategies

Core body temperature elevation markedly worsens MS neurological function through impaired axonal conduction in demyelinated pathways (Uhthoff’s phenomenon). Swallowing function may transiently deteriorate during fever, exercise, hot weather, or hot showers. Conversely, cooling strategies can temporarily improve function.

Pre-meal cooling:

Temperature-modified food and drinks:

These strategies are particularly relevant in Hong Kong’s hot, humid summer months, when Uhthoff’s phenomenon is commonly triggered and MS patients may experience seasonal worsening of all neurological symptoms including swallowing.

MS Society HK Resources

The Multiple Sclerosis Society of Hong Kong (MSSHK) provides peer support, information, and welfare referral for MS patients and families. The MSSHK can be contacted via the Hong Kong Neurological Society referral pathway. Support groups offer practical advice on daily living adaptations including mealtime management, and experienced patient educators can provide peer guidance on managing MS fatigue during meals.

For clinical management, MS specialist neurologists at Queen Mary Hospital (HKU Department of Medicine), Prince of Wales Hospital (CUHK), and private neurological practices manage MS cases in HK. SLTs embedded in hospital neurology teams typically manage the dysphagia component; community SLT referral via the HA Community Rehabilitation Network is available for stable outpatients.

Summary

MS-related dysphagia requires a nuanced, adaptive approach that accounts for brainstem and cerebellar lesion distribution, the profound impact of central fatigue on swallowing performance, and the fundamentally different trajectories of relapsing-remitting versus progressive subtypes. Fatigue-adapted exercise protocols, cooling strategies, and appropriately timed sessions are essential practical adaptations for this population.

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