Hypersensitive Gag Reflex and Pediatric Feeding Delays By Donna Scarborough Ph.D., CCC-SLP, BCS-S Miami University, Oxford, OH scarbod@muohio.edu

Introduction

Historically, two clinical areas in speech pathology have tested the gag reflex response as part of a standard oral mechanism examination including:

a) assessment of maximum velopharyngeal excursion (Mason & Simon, 1977; Pannbacker, 1985)

 

b) bedside evaluations of swallowing (Daniels, McAdam & Brailey, 1997). 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. 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. 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).

 

So why does the gag reflex continue to require attention?

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. 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. 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. 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. complications resulting from fundoplications and NES), and 5) other gastrointestinal diseases (e.g. eosinophilic esophagitis). In complex cases, more than one pathogenesis may be involved.

 

Back to basics, defining a gag reflex

For 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). 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. 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). The glossopharyngeal nerve sends projection fibers or sensory information to the nucleus tractus solitarius (NTS) of the medulla. 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).

 

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). To date the underlying neurologic pathway to include the trigeminal nerve for some individuals is unknown.

 

Wide degree of variability in general population

Despite 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. 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). In addition to varied sensory input, a range of motor responses can be observed. 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). 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). Another description adds a vocalization component to the traditional view; thus blurring the separation between a gag re- flex and a ‘retch’ (Faigenblum, 1968). Concomitant responses such as vomiting, nausea and autonomic signs and symptoms (diaphoresis, lacrimation, etc.) have also been included when defining the motor component of the gag reflex (Bassi, et al., 2004). In addition to reports of different degrees of motor responses, the strength of the gag reflex is quite variable across individuals, from absent to ‘hyperactive’ (Chaffee, Zabara, and Tansy, 1970; Pannbacker, 1985; Perlman et al., 1989; Leder, 1996).

 

What exactly does a ‘hypersensitive’ gag reflex mean?

Surprisingly, a clear definition of a hypersensitive gag reflex does not exist. Instead, descriptions of a ‘hyper’ gag reflex may be divided into two categories: a) the force/type of the motor response, and b) the place of sensory stimulation. The most common descriptions involve the strength or type of observed motor response. Such descriptions include: “severe” pulling away to tactile stimulation (Leder, 1986), spasms of the pharynx (Bassi et al., 2004), or a combination of reflex responses with both gagging and some aspect of the emetic or vomit response (Kramer and Braham, 1977, Miller, 2002, Bassi et al., 2004). A less common means of describing a hypersensitive gag reflex pertains to the place that the gag reflex is triggered. Historical reports of ‘stubborn’ gaggers described individuals who trigger a gag reflex in the anterior or middle portions of the oral cavity (Landa, 1946). Similar reports have been noted in individuals who present with a hypersensitive gag reflex during tooth brushing and an inability to shave as a result of gagging to touch to the face (Murphy, 1979). Recently, gag reflex responses to non-oral body parts and regions within the anterior oral cavity have also been documented in a group of children 3-18 months of age who presented with persistent feeding delays (Scarborough et al., 2006). To date, a correlation between the strength of the response and place of response has not been established.

 

Causes of hypersensitive gag reflex

The specific neurologic cause of a hypersensitive gag reflex response is not known and is likely to be due to more than one basic neurologic mechanism. One way to evaluate the cause is through inspection of the population who exhibit the problem. Children who have a history of traumatic brain injury, specifically bilateral cotrico-bulbar tracts demonstrate a ‘hypersensitive’ gag reflex due to the loss of upper motor neuron inhibition (Schulze-Delrieu & Miller, 1997). In contrast, the hypersensitive gag reflex ob- served in NICU and full-term medically fragile infants who have a history of tube feedings has been pro- posed to be a result of abnormal autonomic nervous system development (Scarborough & Isaacson, 2006). Based on this theory, ‘transient’ tactile connections between the touch sensory fiber tracts and the nucleus tractus solitarius (NTS) are present at birth via an inhibitory interneuron. Further, the activity of the transient fibers diminishes shortly after birth as a result of swallowing during oral feedings. In the ab- errant or hypergag situation these transient fibers fail to retract and consequently result in continued stimulation of the NTS with touch to areas other than the posterior 1/3 of the oral cavity (Scarborough & Isaacson, 2006).

 

Other children are reported to have conditioned responses to oral feedings which may lead to feed- ing aversions (including hypersensitive gag reflexes). Typically, for children with feeding aversions, a hypersensitive gag reflex has been reported to be a result of maladaptive parent-child interactions (Byars, Burlow, Ferguson, O’Flaherty, Santoro & Kaul, 2003). For children with this type of feeding presentation, a hypersensitive gag reflex is a conditioned negative behavior. The exact neurologic mediation of a hyper- sensitive gag reflex that is the result of a conditioned response is not yet known.

 

In adults, a heightened motor response of the gag has been linked to metabolic disturbances such as carbohydrate starvation and dehydration with ketosis (Bassi, 2004); however, in children no such data has been reported. Another report on severe gagging within the geriatric population found an increase in gastrointestinal disorders, 36%, compared to 20% of an elderly ‘non-gagging’ population. Children with gastrointestinal disorders (e.g. reflux, chronic constipation, eosinphilic esophagitis) have also clinically been found to present with a hypergag reflex, although the specific pathophysiology is unknown. Similar clinical reports have been made in children who have undergone surgical procedures such as a fundoplication. One of the reported side effects is “gagging/retching” syndrome. Although the exact neurologic mechanism is not known at this time, the gut has direct connections with the NTS of the medulla and vagus nerve, both of which are involved with basic afferent/efferent loop of the gag reflex.

 

Clinical Implications

Like many other areas of pediatric treatment one of the challenges for the professional is making clinical judgments based on observed behaviors. A ‘hypersensitive’ gag reflex is one observed behavior which has major implications for our pediatric feeding population. By obtaining a thorough history of the child with a hypersensitive gag reflex, the clinician may better determine a potential cause of the abnormal response. Treatment techniques to remediate the hypersensitive gag reflex have been plentiful; but rarely does one technique work for all populations.

 

Interventions of a Hypersensitive Gag Reflex

A number of attempts over time have been made to remediate the hypersensitive gag reflex, particularly in the adult populations. Some early attempts noted in the dental literature included swabbing the mouth with diluted cocaine, using distraction by ‘disengaging the patient’s mind from its tangle of gagging stimuli’ and redirecting it towards some other interest, exercising maximum will power, and altering the dental appliance to minimize the amount of area stimulated when placed in the oral cavity (Landa, 1947). Early reports also found surgical resection of the uvula as successful for individuals with a stubborn gag (Kramer, 1977). Other less invasive approaches have suggested voluntarily increasing the respiratory rate (Chaffee, et al 1970), having the patient hold their breath (Kramer, 1977), hypnosis (Bartlett, 1973), re- laxation in conjunction with hypnosis (Murphy, 1979), behavior modification, suggestion, systematic de- sensitization, sensory flooding, and medications (Kramer, 1977; Bassi et al., 2004). Acupuncture to the upper part of the ear between the concha and triangular fossa has been found to normalize the gag reflex (Fiske & Dickinson, 2001). More recently, combinations of acupuncture and hypnosis have been recommended to treat a hypersensitive gag reflex in long-term therapy needs (Eitner, Wichmann and Holst, 2005a, b). One acupressure point on the chin (Cheng Jiang REN-24) has also been reported to success- fully control the gag reflex during maxillary impression procedures as noted in a brief clinical report (Vachiramon and Wang, 2002). A small region on the palm of the hand has been found to move the afferent limb of the gag reflex posteriorly in neurologically intact adults if at least 2 pounds of pressure are applied (Scarborough, Bailey-Van Kuren, and Hughes, 2008; unpublished data, Scarborough). At this time, individual variability is being explored to determine if the variability is related to the natural curvature of the hand using 3-D technology. None of these techniques have been reported with children although our lab will begin trials in pediatrics in the upcoming months.

 

Behavioral psychologists in the pediatric feeding arena have developed successful behavioral feed- ing programs which address feeding aversions (including a hypersensitive gag reflex) as a result of conditioning or a breakdown of the child-caregiver interactions. Specific behavior management techniques including reinforcement patterns (both positive and negative), shaping, discrimination training and extinction to name a few, are used to remediate feeding aversions (Burklow, McGrath & Kaul, 2002; Patel, Piazza, Martinez, Volkert & Santana, 2002). Professionals who run these programs have done an exceptional job in documenting the specifics related to their success. And although these programs have been successful with remediating a hypersensitive gag reflex in some children, not all children respond to this type of treatment.

 

Finally, in an attempt to begin to unravel the neurologic conundrum of the hypersensitive gag re- flex, animal research is currently underway in our lab. We have begun the process of utilizing c-fos immunohistochemistry and immunofluorescence to begin to map the gag reflex including the specific neuro- transmitters involved (Scarborough & Isaacson, 2007), in hopes that some day future feeding specialists might have answers to a complex and frustrating clinical problem. A research reporting our animal model findings are now available (Scarborough and Isaacson, 2014, in press).

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