What exercises can I use with a patient who presents with a moderate dysphagia due to epiglottic inversion secondary to Guillian-Bare syndrome?
There are several issues that must be addressed before getting to the question of therapeutic intervention. These are the phenomenon of epiglottic activity during swallow, the impairments to be expected from Guillane-Barre' syndrome (GBS), and what the literature says about therapeutic intervention for individuals with GBS related swallowing impairments.
Regarding the phenomenon of epiglottic inversion, Curtis and Sepulveda (1968), consider epiglottic movement, what they call tilt, to be a neuromuscular event, in that there are extrinsic muscles, the geniohyoid and thyrohyoid, innervated by the Trigeminal cranial nerve (CNV) and Ansa Cervicalis, and intrinsic muscles, the thyroepiglotticus and aryepiglotticus, innervated by the Vagus cranial nerve (CNX). Impairment of epiglottic tilt, however, can be due to restrictive (masses or tissue changes) and neuromuscular reasons. It is also best to keep in mind that there is a passive element to epiglottic activity during swallow. This 'trap door-like' activity is do to the epiglottis being approximated to the laryngeal additus by the back and downward movement of the tongue base and up and forward elevation of laryngeal excursion.
Regarding GBS, an acute immune polyneuropathy, is known to be a virally based ascending and descending paralytic disease with neuromuscular manifestations and is thought to be the result of immune sensitization to components of myelin. Primarily transient nature, GBS can have permanent manifestations in 5-10% of patients (Leech and Shuman, 1992). Peripheral nerve involvement can be unilateral or bilateral.
Regarding the swallowing manifestations of GBS, it has been shown the larynx is positioned lower and that the width of the pharynx is maximally expanded in affected subjects. Also, tongue base movement and laryngeal elevation are not the same in GBS subjects. Further, there appears to be a consensus (Leonard, et al., 2004, Pearlman, et al., 1992, IA, Bleier, et al, 2006, Daniels and Foundas, 2001, and Smith, et al., 2000) that epiglottic dysmotility can result from several factors, with neuromuscular impairment being one of them. For example incomplete epiglottic close may be due to a primary oral impairment, pharyngeal motility variability, respiratory support impairments, autonomic nervous system impairments, or even aging. So, when diagnosing patient swallowing with GBS these factors must be taken into account.
In all likelihood, then, epiglottic inversion may be more the result of impaired neuromuscular oral and pharyngeal events surrounding epiglottic movements during swallowing. Hence, any focused intervention on epiglottic inversion will not be as effective as would work with the patient on improving oral and pharyngeal function. Medical literature appears to indicate that between five weeks to three months after onset of GBS symptoms is required before any swallowing therapy be initiated, depending on initial severity and residual fatigue (Peake, et al., 2003). Of course aspiration is a chief concern in this case. Kulemeier, et al. (2000) suggest that utilizing thin, thick, and ultrathick liquids and delivery by cup and spoon during a video fluoroscopic swallowing study of a patient with mild or moderate dysphagia can increase the chances of identifying a consistency that the patient can swallow without aspirating and without pharyngeal retention after swallowing. Once it is established that the patient has a modicum of control over the airway, including sufficient tongue, laryngeal and epiglottic movements, therapy might consist of strength and endurance exercises, the use of Vital Stim