JADA Continuing Education
Altering the Gag Reflex Via a Palm Pressure Point
Donna Scarborough, PhD,
Michael Bailey-Van Kuren, PhD and
Michael Hughes, MS
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ABSTRACT
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Background. The gag reflex regularly interferes with dental procedures. The authors hypothesize that applying pressure to a specific point on the palm alters the gag reflex and that hypersensitive gag reflexes may be categorized according to oropharyngeal landmarks.
Methods. Thirty-six neurologically intact subjects underwent a series of gag reflex trials (baseline, sham and treatment). The authors developed a hand pressure device for subjects to wear, which provided a consistent force, and they described a gag trigger point index (GTPI) scale. On the basis of the GTPI, they divided subjects into a hypersensitive group and an expected-sensitivity (control) group.
Results. The trigger point of the gag reflex moved posteriorly in all subjects as a result of pressure to the palm point. Statistical results from repeated measures analysis of variance support the GTPI baseline data, and group assignments helped predict mean GTPI scores across conditions. The authors noted a significant treatment-group interaction effect, which indicated that the difference in mean GTPI responses between the hypersensitive and expected-sensitivity groups depended on the treatment being used.
Conclusions. The authors introduce a treatment involving the stimulation of a pressure point that consistently altered the gag reflex trigger. The results of the study show the need for a more detailed, systematic approach to studying the hypersensitive gag reflex.
Clinical Implications. The change in trigger point in the hypersensitive group represented a functional gain. Application of the pressure point during dental procedures would decrease the likelihood of triggering a gag reflex.
Key Words: Reflex; gag; acupressure; adultAbbreviations: GTPI: Gag trigger point index
The gag reflex is a highly variable protective reflex that frequently interferes with dental procedures. Typically, tactile stimulation within five trigger zones—the anterior and posterior faucial pillars, the base of the tongue, the palate, the uvula and the posterior pharyngeal wall—will elicit the gag reflex.1 For some people, however, tactile stimuli more anterior to the trigger zones, visual stimuli (such as impression trays and spoons), auditory stimuli, olfactory stimuli and psychic stimuli (thinking about a stimulus) also can trigger a gag reflex.2–4 In addition to the various sensory input that can trigger a gag reflex, the type and the strength of motor response can differ within the general population. The most rigorous description of the motor response of the gag reflex is that it is a constriction of the pharynx.5,6 A more traditional view of the gag reflex, however, is that it is a lowering of the mandible in a forward and downward trajectory, with velar and pharyngeal constriction.7 And yet another description adds a vocalization component to the traditional view, thus blurring the difference between a gag and a retch.8 Concomitant responses such as vomiting, nausea, and autonomic signs and symptoms (for example, diaphoresis, lacrimation) also have been included in definitions of the motor component of the gag reflex.1 In addition to reports of different degrees of motor responses, gag reflex strengths vary among people from absent to hyperactive.7,9,10
There is no clear definition of a hypersensitive gag reflex in a neurologically intact person. Instead, descriptions of a hyper gag reflex can be divided into two categories: the force of the motor response and the place of sensory stimulation. The most common descriptions involve the force of motor response. They include severely pulling away from tactile stimulation,7 spasms of the pharynx1 or a combination of reflex responses with both gagging and some aspect of the emetic response.1,3,6 A less common description of the hypersensitive gag reflex pertains to where the gag reflex is triggered. Historical reports of stubborn gaggers described people who triggered a gag reflex in the anterior or middle portions of the oral cavity during toothbrushing or while shaving as a result of gagging caused by touch to the face.2,4 Recently, gag reflex responses to nonoral body parts and regions within the anterior oral cavity have been documented in a group of children 3 to 18 months of age who had persistent feeding delays.11
Attempts have been made to diminish the gag reflex within clinical settings. Early interventions included swabbing patients’ mouths with diluted cocaine; using distraction techniques; asking patients to use willpower,2 excise their uvulas,3 voluntarily increase respiration9 and hold their breath3; hypnosis12; and relaxation with hypnosis.4 Behavior modification, suggestion, systematic desensitization, sensory flooding and medications also have been explored.1,3,13 Acupuncture points on the ear14 or forearm15 can control the gag reflex effectively during dental treatments. In two 2005 articles, combinations of acupuncture and hypnosis were recommended to treat a hypersensitive gag reflex during long-term therapy.16,17 Although this combination treatment may alleviate a hyperactive gag reflex, complications may arise, specialized training or teams would be needed and the invasive nature of the technique is undesirable for many patients. For most dentists and other medical practitioners, a less invasive approach such as acupressure would be an attractive alternative. To our knowledge, only one brief clinical report has indicated that a pressure point on the chin would be effective for diminishing the gag reflex.18
One unpublished clinical technique used to remediate the hypersensitive gag reflex, which was used in the study population but not reported, involved children with feeding delays (the population is described in detail in Scarborough and colleagues11). The technique involves the use of a pressure point in the palm of the hand. This technique was being used in the field, but there was no research to substantiate its efficacy, and it was not derived from a known pressure point that was adapted for clinical use.
To better understand why this clinical technique was successful in this group of children, we developed an adult model. We conducted an informal pilot study in three women and two men who were reported to have a hypersensitive gag reflex and who had an intact neurological system. Four of the subjects were white, and one was African-American. We found normalization (that is, triggering the gag reflex in the posterior portion of the oral cavity) in all of the subjects except for the black man when pressure was applied to a point in the palm of the hand.
This informal pilot study led to a second pilot study of seven healthy white women who had a hypersensitive gag reflex. We conducted this second study to develop consistent methodological techniques to apply in a larger sample. The results of this study showed a normalization of the gag reflex (or movement of the gag behind the anterior faucial pillar) when we applied pressure to the palm of the right or left hand.
We conducted an exploratory study on the basis of information we gleaned during these pilot studies. The aims of this exploratory study, which we report here, were to establish that a hand pressure point alters the trigger of the gag reflex in two groups of healthy adults and to introduce a methodological approach to evaluate the gag reflex on the basis of the location of sensory stimulation in the oral cavity.
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SUBJECTS, MATERIALS AND METHODS
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Hand pressure device.
A hand pressure device was designed at Miami University, Oxford, Ohio, for this study, specifically to apply two pounds of force to a specific pressure point on the palm of the hand. The device was modified from a hand splint that provided stiff support to the palm side of the hand and equally spaced the digits. The hand pressure device was secured to the hand via straps. A hole was cut in the palm of the device to allow an actuating cylinder to press against the palm of the hand, and the design allowed the actuating cylinder to be removed easily. These hand pressure devices were fabricated for both the right and left hands. The force was applied by means of a voice coil actuator with a three-quarter-inch–diameter circular pad that contacted the palm of the hand. This device was powered by a bipolar operational power supply/amplifier, which allowed for manual and variable control of the force applied to the subject’s hand.
Gag response sensor probe.
A sensor probe with a bend sensor potentiometer was developed at Miami University to record the amount of pressure applied to the anatomical structures that elicited the gag response. As the probe contacts the inner surface of the oral cavity, the probe bends the flexible sensor and generates a change in the output voltage, which is recorded by a desktop computer. The probe sensor has a light attached to the end for more accurate identification of the structures that are stimulated, as well as a time stamp.
Subjects.
All of the subjects were college students who volunteered to respond to a flier recruiting people with a self-perceived normal or hypersensitive gag reflex. We scheduled subjects for a single session in late morning or during the afternoon to avoid any influence that time of day might have on the gag reflex.1 We screened all volunteers for overt neurological difficulties. We excluded them if we observed gait difficulties, tremors, physical asymmetries, abnormal voice qualities, or speech or language disturbances. We also excluded volunteers if they reported having a history of neurological difficulties.
Forty-one subjects initially participated in the study. All of the subjects but two were white. Subjects were placed into two groups according to baseline scores (Table 1
). The hypersensitive group consisted of four women and three men with a mean age of 18.8 years (standard deviation [SD] = 0.35). The expected-sensitivity (control) group consisted of 20 women and 14 men with a mean age of 20.0 years (SD = 2.65). Five subjects (four women and one man) in the expected-sensitivity group were unable to continue the study past the baseline data collection because we observed no motor response bilaterally with stimulation of the posterior pharyngeal wall. Descriptive statistics for GTPI scores excluding these five subjects across the experimental treatments appear in Table 2.
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TABLE 1 Description of baseline gag trigger point index (GTPI) score coded by location in oral cavity where gag reflex is elicited, with number of subjects in each category.
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TABLE 2 Comparison of gag trigger point index data between the hypersensitive group and the expected-sensitivity group.
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The Institutional Review Board of Miami University approved this study. We used universal precautions for infection control in all subjects.
Once subjects signed an informed consent form, we explained the basic procedures to them and asked them to remove all watches, rings and bracelets. The subjects then underwent a series of gag reflex tests: baseline, sham and treatment.
Baseline trials.
We elicited one gag reflex from the left side of a subject’s oral cavity and one from the right side of the oral cavity in random order. We did not apply treatment. We provided subjects with breaks of at least one minute between the two trials. Throughout this study, the minimal acceptable motor response to input from the gag response sensor probe included constriction of the pharynx and velum.5,6 The point in the mouth (the anatomical marker) at which each subject gagged during these two trials was determined by means of a gag trigger point index (GTPI) and served as baseline data. The GTPI is an ordinal index in which the oropharyngeal regions are divided according to anatomical landmarks and assigned a score (an integer value from 0 to 8) (Figure 1 and Table 1
). All of the stimulation to elicit the gag reflexes began from a high GTPI area (the internal cheek) to a low GTPI area (the pharyngeal wall). Once a subject elicited a gag response, we stopped the trial and did not test any more-posterior positions. To differentiate responses that occurred at the posterior pharyngeal wall (gag response elicited versus no motor response), we assigned two potential values (1 or 0) to this point. If a subject scored a 0 for both sides of the intraoral cavity, we terminated the trial. We adapted this severity rating scale from our second pilot study.
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Figure 1. Photograph of oral cavity showing key landmarks of the gag trigger point index. Photograph courtesy of D.B. Fankhauser, University of Cincinnati.
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The sole determiner of group classification (expected-sensitivity or hypersensitive) for this study was the baseline data. We placed subjects who gagged at stimulation of structures in front of the anterior faucial pillar (GTPI score = 6) on at least one side during baseline data collection into the hypersensitive group. The other subjects were placed in the expected-sensitivity group.
Sham trials.
Once we completed the baseline trials, we elicited two gag responses as part of a sham condition. All subjects were told that the sham trials were related to over-the-counter antinausea bracelets that may be effective in minimizing the gag response. An adjustable bracelet was fastened lightly around a randomly selected wrist. We also randomized the order (right first or left first) in which the oral cavity was stimulated. We provided breaks of at least one minute between trials. The point in the mouth at which stimulation elicited a gag reflex during the two sham trials was scored according to the GTPI (Table 1).
Treatment trials.
The pressure point we used was located in the middle of the palm at the angle of intersection of the thumb and third digit (Figure 2). We marked the subjects’ hands at this intersection with a felt-tip marker. We placed the force actuator of the hand pressure device over the marked point on a randomly selected hand (right or left). Once the hand pressure device was secured, subjects were instructed not to resist the pressure applied to the hand while the primary investigator manually increased the force of the actuator to two pounds. This pressure threshold is based on methods used in our second pilot study in which pressure was applied to the palm.19 Unlike the sham trials in which the subjects were led to believe that the bracelet was effective, we gave them no information about the treatment trials. If a subject asked, we minimized the response (for example, stating "We’re just trying this out"). We then elicited gag responses, one on the right side of the intraoral cavity and one on the left side, in random order. We then used the hand pressure device on the alternate hand and followed the same procedures. We provided breaks of at least one minute between trials, and we provided a longer break if the subject requested it.
At completion of the study, we gave each subject a debriefing statement addressing the deception component of the sham trials in compliance with the Miami University Institutional Review Board guidelines.
Statistical analysis.
We analyzed the data by using repeated measures analysis of variance (ANOVA) of a mixed effect model fit to the experimental GTPI scores. This type of model allows for assessment of effects of between-subjects factors and within-subjects factors, and it accommodates potential correlation among measurements made in the same subject.20,21 Between-subjects factors were group (hypersensitive or expected-sensitivity, as determined from baseline trials) and sex (male or female). Within-subjects factors were experimental treatment (sham, left hand pressure device or right hand pressure device) and stimulus side (left or right). We constructed follow-up contrasts to assess group discrepancies in mean GTPI score between pairs of treatments. We checked and verified assumptions regarding normality of residual distributions. We performed all analyses by using statistical software (PROC MIXED, Version 9.1 for Windows, SAS, Cary, N.C.).
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RESULTS
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For all subjects in both groups, the gag reflex moved posteriorly toward the pharyngeal wall after application of pressure to this point. We conducted a preliminary assessment that confirmed that there were no significant changes in mean GTPI score differences between the baseline and sham trials after adjusting for sex and stimulus side (F = 0.81, numerator degrees of freedom = 1, denominator df = 33, P = .3741). We then performed repeated-measures ANOVA on the treatment trial data to investigate the effect of the treatments on mean GTPI scores. We tested the high-order interactions between experimental factors iteratively, and we found that they were not significant, resulting in the reduced model results presented in Table 2. We checked and verified assumptions of residual normality and constant variance.
ANOVA results revealed a significant sex-group interaction in determining mean GTPI scores regardless of treatment (Table 3). In the hypersensitive group, women had an overall mean GTPI score of 2.58 (SD = 2.12), and men had an overall mean GTPI score of 4.17 (SD = 1.50). In the expected-sensitivity group, women had an overall mean GTPI score of 1.46 (SD = 1.38), and men had an overall mean GTPI score of 1.52 (SD = 1.31).
The analysis supports the finding that the GTPI baseline data and group assignments can be used to predict mean GTPI scores across conditions. We noted a significant treatment-group interaction effect, indicating that the difference between mean GTPI responses for the hypersensitive group and expected-sensitivity group depended on the treatment being used. Because of this interaction, we determined that assessments of group effects must be made according to treatment, and that the stimulus side was not a significant factor in determining mean GTPI.
To further investigate the treatment effect in both groups of subjects, we constructed statistical contrasts to compare group discrepancy in mean GTPI between all pairs of trials. These results appear in Table 4, and Bonferroni-adjusted P values are provided. Discrepancies between the groups were statistically similar in left hand pressure device and right hand pressure device trials. The pairwise trial contrasts that compared group discrepancy in mean GTPI between the sham trial and a treatment trial (left hand pressure device or right hand pressure device) produced statistically lower GTPI scores for treatment trial (P < .05).
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DISCUSSION
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To our knowledge, this study was the first of its kind to document that the application of pressure to the center of the palm moves the trigger point of the gag reflex. For all subjects in both groups, the gag reflex moved posteriorly toward the pharyngeal wall after application of pressure to this point. Although all subjects demonstrated a change in the trigger of the gag reflex, the subjects in the hypersensitive group demonstrated a statistically significant degree of movement according to the GTPI areas compared with the subjects in the expected-sensitivity group. The change in trigger point in the subjects in the hypersensitive group represents a functional gain. Application of pressure to the center of the palm during dental procedures would make triggering a gag reflex less likely (Figure 3).
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Figure 3. Mean hypersensitive and expected-sensitivity group gag trigger point index scores, by order of application. Error bars represent plus or minus one standard error of the mean.
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The trigger points in the expected-sensitivity group also moved to the posterior pharyngeal wall for at least one of the treatment trials. This finding was important because nine subjects in the expected-sensitivity group reported a self-perceived heightened gag reflex sensitivity during the initial interview, and the palm pressure point was effective in this group.
Finally, we found a statistically significant sex-group interaction in the hypersensitive group that we did not see in the expected-sensitivity group, and it does not appear to be the result of a small sample size. We found that gag reflexes in the men in the hypersensitive group were stimulated significantly more anteriorly than were gag reflexes in women in the hypersensitive group. It is not clear at this time why males in the hypersensitive group tend to react to more anterior stimulation and why this same sex difference is not seen in the expected-sensitivity group.
To our knowledge, our study also was the first to categorize subjects with a hypersensitive gag reflex on the basis of the location of the trigger of the gag reflex rather than on the strength of muscle contraction. We divided subjects into the two groups according to our understanding of the afferent component of the gag reflex. Previous study results indicated that a typical gag response is triggered in the posterior one-third of the oral cavity within one of five trigger zones.1 This region is innervated by the glossopharyngeal nerve, which is the afferent limb for the gag reflex. In our study, however, subjects in the hypersensitive group gagged when they received stimulation in more anterior regions. Thus, the seven subjects in the hypersensitive group represented a neurologically abnormal or unexpected group. Furthermore, our choice of the criteria used to distinguish the two groups was supported statistically (Tables 3 and 4).
The subjects in the hypersensitive group came from the general population and were otherwise neurologically intact. However, it seems unlikely that the observed differences in the location of the trigger of the gag reflex relate to anatomical variations of the glossopharyngeal nerve. Considering that the hypersensitive group constituted 17 percent of the subjects recruited for our study, we expected to find literature regarding this possibility. To our knowledge, however, no literature in neurosurgery, otolaryngology, anatomical review or dentistry supports this idea.
Another explanation may be derived from a hypothetical model that has been proposed to explain similar response patterns in a group of orally deprived infants.22 On the basis of this theory, transient tactile connections between the touch sensory fiber tracts and the nucleus tractus solitarius are present at birth via an inhibitory connection. Furthermore, the activity of the transient fibers diminishes shortly after birth. In the aberrant or hypersensitive gag situation, these transient fibers fail to retract and consequently result in continued stimulation of the nucleus tractus solitarius with touch to areas other than the posterior one-third of the oral cavity.22 We do not know if this model can apply to the neurologically intact subjects in the hypersensitive group, nor do we understand the exact neurological mechanism of the hand pressure point’s influencing the gag reflex. Animal research is being conducted to identify and map the specific pathway of the gag reflex, and it includes discovering the underlying neurochemical substrates involved23 and understanding the neurological mechanisms and anatomical regions involved with the hand pressure point.
Another facet we targeted specifically for this study involved the purposeful use of light touch for the sham trials and firm pressure for the treatment trials. We carefully selected these two methods because in many people light touch follows a different neurological pathway than does firm pressure. Furthermore, at the skin level, different sensory receptors are responsible for transmitting light touch versus firm pressure. Research is being conducted in rats to determine the exact neurological mechanisms within the brain stem for these two tactile sensory systems.
Another aspect of the study that needs further discussion is a potential order effect (Figure 3). Some may argue that with repeated stimulation of the gag reflex in a person, the gag reflex would become extinct or fatigued. The results in our study were solely manifestations of an order effect. However, we provided subjects with breaks of at least one minute between the trials, which should have been sufficient time for the strength of the contraction to return to the baseline state.24
Another argument regarding our findings may be related to distraction. One might argue that application of pressure to the palm of the hand would cause a person to be distracted from the gag reflex trials. However, we conducted and manipulated the sham trials in a way that convinced subjects that a change in the gag reflex would occur. We did not observe significant changes in the gag trigger point with the sham trial. Also, if distraction were the underlying phenomenon that reduced the gag reflex, one would predict the gag reflex would return to baseline values across the four trials—baseline, sham, left hand pressure device and right hand pressure device—as the subjects became accustomed to the procedures.
In future studies, we will randomize the order of the sham and treatment trials to enhance the methodology of the study. For this preliminary study, however, we tried to design a study that would give subjects every opportunity to cognitively control the gag reflex, and we led them to believe that the sham trial would be effective. We also designed the study so we could begin exploring the premise that with increased subject expectation we would have an increased ability to cognitively manipulate or alter the gag reflex. Thus, we made every effort during the sham trials to compare the antinausea bracelet used in our study to over-the-counter antinausea wristbands with which many subjects were familiar. We wanted the subjects to believe that this light touch technique worked because we thought that subjects’ expectation was an important idea to build into the study.
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CONCLUSIONS
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The results of our study are preliminary and imply that a larger, randomized study is needed to statistically analyze any trends that affect direct clinical applications. Basic characteristics such as sex, age, handedness, ethnicity and associated behaviors or patterns require further exploration. Future study should investigate subjects’ self-perceptions about the gag reflex and include the development of a severity scale. In our study, nine subjects in the expected-sensitivity group and the seven subjects in the hypersensitive group had a self-perceived hypersensitive gag reflex, but we did not explore the strength of the motor response of the gag reflex. A better understanding of subjects’ perceptions and a detailed severity rating scale may help us better understand the trigger zones and the strength of the motor response.
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FOOTNOTES
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Dr. Scarborough is an assistant professor, Department of Speech Pathology and Audiology, Miami University, 26 Bachelor Hall, Oxford, Ohio 45056, e-mail "scarbod{at}muohio.edu". Address reprint requests to Dr. Scarborough.
Dr. Bailey-Van Kuren is an associate professor, Mechanical and Manufacturing Engineering, Miami University, Oxford, Ohio.
Mr. Hughes is the manager, Statistical Consulting Center, and instructor, Department of Mathematics and Statistics, College of Arts and Science, Miami University, Oxford, Ohio.
Disclosures. None of the authors reported any disclosures.
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ABSTRACT
SUBJECTS, MATERIALS AND METHODS
