Hypothetical anatomical model to describe the aberrant gag reflex observed in a clinical population of orally deprived children

Abstract

In this 'clinical conundrum', we propose a hypothetical anatomical model to explain the abnormal gag reflex that is consistently observed in a clinical population of children experiencing feeding delays. This model is based on the presence of 'transient' connections formed during the normal development of autonomic brainstem circuitry involving the nucleus tractus solitarius (NTS). We propose that, as a result of normal feeding and swallowing, the activity of these transient fibers typically diminishes shortly after birth. In children who are orally deprived during infancy, these transient connections persist and the aberrant gag reflex is maintained into childhood. The most critical feature of the proposed model is the idea that swallowing during feeding initiates the retraction of the tactile 'transient' input to NTS. In the NICU feeding clinics, it has been suggested that triggering the gag reflex in neonates by tactile stimulation of non-oral body areas and anterior portions of the mouth directly or indirectly may contribute to oral feeding delays. To the contrary, we propose an anatomical model to suggest that oral feeding delays and lack of swallowing food, when experienced by neonates, actually contribute to the development of the aberrant gag reflex observed in later developmental stages.

The Significance of Gastric Juice Analysis for a Positive Challenge by a Standard Oral Challenge Test in Typical Cow's Milk Protein-Induced Enterocolitis

“…Symptoms of typical CMPIE commonly start before 2 months of age and thus this disorder mainly occur in neonate or early infancy (1, 5, 11). Based on our clinical experience, we think that oro-gastric tube insertion may be less invasive in neonate or early infancy than in children, because of the relatively fine tube, decreased gag reflex (13), and short oro-gastric distance.…”

Strategies and dental care in the treatment of patients with myelomeningocele

“…Patients with MMC may present exacerbation of gag reflex due to dysphagia as a result of cranial nerve injury related to the nonclosure of the neural tube . Another explanation for the gag reflex is that people with poor hygiene do not stimulate mouth desensitization, which contributes to the recurrence of reflexes during the dental treatment. In this case, the patient's reflexes were caused by physical stimuli and handling of the oral cavity, use of saliva ejector, and three‐way syringe and even saliva accumulation.…”

Activation of Neurons in the Rat Medulla Following a Gag Reflex Stimulus

“…The majority of vagal and glossopharyngeal afferent information from the posterior pharyngeal wall is carried to the NTS [17][18][19][20][21]. The NTS, in turn, excites neurons in the nucleus ambiguus (NA) which then activates the pharyngeal and velar muscles (CN X) and the muscles of the tongue (via CN XII) [14].…”

“…For example, SolVL has been linked to cessation of breathing [27], Sol M to baroreceptor reflexes with a decrease in parasympathetic innervations of the heart [28], and SolIM to laryngeal and pharyngeal sensation [21,29]. These are activities that take place during the gag motor response [1,[7][8][9]14].…”

“…*Address correspondence to this author at the Department of Speech Pathology and Audiology, Miami University, Oxford, OH 45056, USA; Tel: (513) 529-2506; Fax: (513) 529-2502; E-mail: scarbod@miamioh.edu Indeed, despite the fact that a hypersensitive gag reflex affects a number of individuals in the general and clinical populations, there is little known regarding the neurological mechanisms underlying this aberrant reflex. We recently developed a theoretical model that involves changes in the brainstem region, nucleus tractus solitarius (NTS), during development, to explain the existence of a hypersensitive gag reflex within a special population of children [14]. Yet in order to understand the underlying mechanisms in an altered gag reflex, we must first determine the basic processes involved following a pharyngeal stimulus.…”