Another description adds a vocalization component to the traditional view thus blurring the separation between a gag re- flex and a ‘retch’ (Faigenblum, 1968). However, a more traditional view of the gag reflex involves lowering of the mandible in a forward and downward trajectory, with velar and pharyngeal constriction (Leder, 1996). The most rigorous description of the motor response of the gag reflex is characterized as constriction of the pharynx (Martin and Jessell, 1996 Miller, 2002). In addition to varied sensory input, a range of motor responses can be observed. For some, tactile stimuli presented more anterior to the ‘trigger zones’, visual stimuli (such as spoons, etc.), auditory stimuli, olfactory stimuli, and ‘psychic’ stimuli can also trigger a gag reflex (Landa, 1947 Kramer and Braham, 1977 Murphy, 1979 Scarborough, Bailey-Van Kuren, Hughes, 2008). Wide degree of variability in general populationĭespite this rudimentary pathway description of the gag reflex, the specific neurologic underpinnings are poorly understood and the pathway does not explain the large variability, both sensory and motor, observed across individuals. To date the underlying neurologic pathway to include the trigeminal nerve for some individuals is unknown. Variability of the trigger of the gag reflex has been reported in neurologically intact adults to include the trigeminal nerve in as many as 17% of the population tested (Scarborough, Bailey Van Kuren, Hughes, 2008). Information from the NTS then sends signals to the nucleus ambiguus (NA) (also in the medulla) which in turn activates the vagal (CN X) efferent fibers to produce the specific motor response (Logemann, 1983 Nolte, 1993: Martin and Jessell, 1996). The glossopharyngeal nerve sends projection fibers or sensory information to the nucleus tractus solitarius (NTS) of the medulla. The posterior 1/3 of the oral cavity is innervated by the glossopharyngeal nerve (CN IX) or ninth cranial nerve which has been clearly documented as the afferent limb of this complex reflex (Martin, 1996 Zemlin, 1998). Upon closer inspection these “trigger zones” are all located within the posterior 1/3 of the mouth, thus from a neurologic perspective these “trigger zones” are not surprising. In complex cases, more than one pathogenesis may be involved.įor most individuals, tactile stimulation within five ‘trigger zones’ will elicit the gag reflex, including: the anterior and posterior faucil pillars, base of tongue, palate, uvula and posterior pharyngeal wall (Bassi, Humphris, and Longman, 2004). complications resulting from fundoplications and NES), and 5) other gastrointestinal diseases (e.g. NICU babies and other full-term medically fragile populations), 3) conditioned responses (behavioral food aversions, etc), 4) surgical alterations of the gastrointestinal system (e.g. Children may present with a hypersensitive gag reflex for a number of reasons including: 1) bilateral lesions of the corticobulbar tracts (observed in TBI populations, etc.), 2) interruption of autonomic nervous system development (e.g. Yet, a hypersensitive gag reflex is an abnormal clinical sign which should alert the feeding specialist to pursue a complete medical history and provide medical referrals when appropriate. In the pediatric feeding arena, a hypersensitive gag reflex is a relatively common phenomenon which frequently interferes with the ability to complete a thorough oral assessment, limits food advancement, and restricts treatment options. So why does the gag reflex continue to require attention? More importantly, research has shown that the presence or absence of the gag reflex response does not correlate to dysphagia or the ability of an individual to adequately protect the airway (Davies, 1995 Leder, 1996 Irwin, 1999). Testing of the gag reflex response during bedside evaluations should only be part of a complete cranial nerve battery, not as an independent criterion, because individual variance is so great. However, due to the complexity of velar movement and the inability to view the posterior pharyngeal region adequately, the gag reflex is not a good indicator of velopharyngeal movement. Historically, two clinical areas in speech pathology have tested the gag reflex response as part of a standard oral mechanism examination including:Ī) assessment of maximum velopharyngeal excursion (Mason & Simon, 1977 Pannbacker, 1985)ī) bedside evaluations of swallowing (Daniels, McAdam & Brailey, 1997).
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |