Laryngeal Response Research Articles

Laryngeal muscle response to phasic and tonic upper airway pressure and flow.

The hypothesis that respiratory modulation due to upper airway (UA) pressure and flow is dependent on stimulus modality and respiratory phase-specific activation was assessed in anesthetized, tracheotomized, spontaneously breathing piglets. Negative pressure and flow applied to the isolated UA at room or body temperature during inspiration only enhanced posterior cricoarytenoid muscle activity from that present without UA pressure and flow (baseline) by 15--20%. Time shifting the onset of UA flow relative to tracheal flow decreased this enhancement. The same enhancement was observed with oscillatory or constant airflow. UA positive pressure and flow at room or body temperature applied during expiration only enhanced thyroarytenoid muscle activity from baseline by 50--160%. The same enhancement was observed with oscillatory or constant airflow at body temperature. Constant positive pressure and flow enhanced thyroarytenoid muscle activity more than oscillatory pressure and flow at room temperature. We conclude that the respiratory modulation of UA afferents is processed in a phase-specific fashion and is dependent on stimulus modality (tonic vs. phasic).

Laryngospasm and diaphragmatic arrest in immature dogs after laryngeal acid exposure: a possible model for sudden infant death syndrome.

Laryngopharyngeal reflux has been proposed as a possible cause of sudden infant death syndrome (SIDS). We investigated the efferent laryngeal and diaphragmatic responses to acid exposure on the laryngeal mucosa using a neonatal canine model. Electromyographic (EMG) recordings from the thyroarytenoid muscle and the diaphragm were measured with hooked-wire electrodes. Reproducible laryngospasm responses occurred in all animals after laryngeal exposure to hydrochloric acid at pH 2.0 or less. Laryngospasm occurred in combination with tachypnea and increased diaphragmatic activity in most of the animals. Laryngospasm was associated with prolonged apnea and total cessation of diaphragmatic EMG activity in 1 animal, and in another, initial tachypnea was followed by erratic diaphragmatic activity and brief apnea. Laryngeal acid exposure (below pH 2.0) causes laryngospasm and may result in paradoxical apneic events in neonatal dogs. Acid-induced, laryngospasm-associated apnea may represent a potential cause of SIDS, and the immature dog appears to be an excellent model for further investigations.

Laryngeal reinnervation with the hypoglossal nerve. I. Physiology, histochemistry, electromyography, and retrograde labeling in a canine model.

This study was performed to determine whether the hypoglossal nerve (cranial nerve XI [XII]) would serve as a useful donor for laryngeal reinnervation by anastomosis to the recurrent laryngeal nerve (RLN). Twenty hemilarynges in 10 dogs were studied prospectively after XII-RLN anastomosis (group A; n = 5), split XII-RLN anastomosis (group B; n = 3), XII-RLN anastomosis with a 2-cm interposition graft (group C; n = 2), no treatment (group D; n = 5), RLN section (group E; n = 2), or ansa cervicalis-RLN anastomosis (group F; n = 3). Spontaneous activity was observed monthly by infraglottic examination through permanent tracheostomies and was recorded by electromyography. Laryngeal adductory pressure and induced phonation were obtained by stimulating the RLN while passing a pressure transducer balloon or humidified air through the glottis. At sacrifice, the laryngeal muscles were stained for adenosine triphosphatase to determine the ratio of type I to type II fibers. Retrograde labeling of the brain stem was performed with horseradish peroxidase. Infraglottic examination at 6 months showed a full range of adductory motion in groups A and B during the swallow reflex, comparable with that in group D. Groups C and F showed good bulk and tone, but little spontaneous motion. Group E remained paralyzed. Stimulation of the transferred nerves caused more activity in groups A and B than in the other groups; groups C and F partially adducted at high levels. The laryngeal adductory pressure responses of groups A and B were similar to those of group D. The XII-reinnervated larynges were capable of producing normal induced phonation. Retrograde labeling of the RLN showed that the reinnervating axons originated only in the hypoglossal nucleus. Electromyography of the reinnervated adductor muscles confirmed spontaneous activity in the dogs (awake). Histochemical analysis confirmed slow-to-fast transformation of both the posterior and lateral cricoarytenoid muscles, indicating that significant reinnervation occurred. We conclude that the hypoglossal nerve functions well as a donor for adductory reinnervation of the larynx.

The laryngeal, pharyngeal and hyoid muscle responses associated with swallowing, belching and vomiting

The laryngeal, pharyngeal and hyoid muscle responses associated with swallowing, belching and vomiting

The laryngeal, pharyngeal and hyoid muscle responses associated with swallowing, belching and vomiting+

The laryngeal, pharyngeal and hyoid muscle responses associated with swallowing, belching and vomiting+

Pediatric laryngopharyngeal sensory testing during flexible endoscopic evaluation of swallowing: feasible and correlative.

Laryngopharyngeal sensory testing can predict aspiration risk in adult patients. Its feasibility and potential role in the evaluation of pediatric swallowing is undetermined. The goals of this study were to determine the feasibility of performing laryngopharyngeal sensory testing in awake pediatric patients and to assess whether the sensory testing results correlated with aspiration during a feeding assessment or correlated with a history of pneumonia. Fiberoptic endoscopic evaluation of swallowing with sensory testing was performed in 100 pediatric patients who were evaluated for feeding and swallowing disorders. The swallowing function parameters evaluated were pooled secretions, laryngeal penetration, and aspiration. The laryngopharyngeal sensory tests were performed by delivering a pressure-controlled and duration-controlled air pulse to the aryepiglottic fold through a flexible laryngoscope to induce the laryngeal adductor response (LAR). The air pulse stimulus ranged in intensity from 3 to 10 mm Hg. The patients tested ranged from 1 month to 24 years of age, with a median age of 2.7 years. Sensory testing was completed in 92% of patients. Patients who had an LAR at less than 4 mm Hg rarely if ever had episodes of laryngeal penetration or aspiration. Those with an LAR at 4 to 10 mm Hg had variable amounts of aspiration and laryngeal penetration. The LAR could not be elicited at the maximum level of intensity (10 mm Hg) in 22 patients, who demonstrated severe laryngeal penetration and/or aspiration. Elevated laryngopharyngeal sensory thresholds correlated positively with previous clinical diagnoses of recurrent pneumonia, neurologic disorders, and gastroesophageal reflux, and correlated positively with findings of pooled secretions, laryngeal penetration, and aspiration. Laryngopharyngeal sensory testing in children is feasible and correlative.

Laryngeal reflexomyographic responses in rabbits: a neurolaryngological study of glottal movement.

The role of the laryngeal reflex in glottal movement has been reported, but its mechanism remains unclear. To further investigate the neurophysiological characteristics of glottal movement, we recorded the laryngeal reflexomyographic responses (LRMRs) to electrical stimulation of the superior laryngeal nerve (SLN) in rabbits. The procedure involved simultaneous recording of the LRMRs from the thyroarytenoid muscles by means of bipolar hooked wire electrodes after electrical stimulation to the SLN. The results demonstrated characteristic patterns of the responses, consisting of R1 and R2, similar to those found in humans. The R1 response was obtained with a latency of 10.7 +/- 0.78 ms. The ipsilateral R2 response was obtained with a latency of 43.76 +/- 4.67 ms in all rabbits, and the contralateral R2 response with a latency from 42.6 to 50.2 ms in 4 rabbits. It was concluded that LRMRs may serve as a potential central laryngeal function test in the investigation of glottal movement control.

Sound-induced laryngeal and respiratory reflexes originate from vestibular afferents.

To determine whether the auditory or vestibular system causes the sound-induced laryngeal reflex, which has been considered to participate in the auditory feedback control of vocalization, click-induced laryngeal responses were compared before and after sectioning of the cochlear and/or vestibular nerves in cats. The sound-induced reflex modulation of respiratory muscle activity was also investigated, because respiratory movement is important for vocal control. Sectioning of the cochlear nerves had little influence on these responses. In contrast, sectioning of the vestibular nerves abolished these responses. It was concluded that the sound-induced laryngeal and respiratory reflexes are attributed to the vestibular system.

Chemical control of laryngeal vascular resistance in anesthetized dogs.

The branch of the cranial superior thyroid artery that supplies the larynx was perfused unilaterally at a constant flow rate in dogs anesthetized with pentobarbitone sodium (30 mg.kg-1, i.v.). Laryngeal vascular resistance (RLv) was calculated. Intraluminal laryngeal pressure (PL) was determined. Asphyxia caused a diminution in PL (-27.7 +/- 4.2%) (p < 0.01) and an initial decrease followed by an increase in RLv (-10.9 +/- 2.3% and +12.8 + 2.8%) (p < 0.001). Following vagotomy, asphyxia decreased PL (-17.1 +/- 4.2%) and increased RLv (+45.5 +/- 11.0%). Systemic hypoxia induced by breathing 8% O2-N2 increased RLv (+8.4 +/- 1.3%) (p < 0.001) and decreased PL (-24.9 +/- 3.7%) (p < 0.001). In chemodenervated dogs, the response of PL to hypoxia was abolished while that of RLv was similar to that in intact animals. Breathing of 7% CO2 in air caused an increase in RLv (+6.1 +/- 1.6%) (p < 0.001) and a decrease in PL (-20.9 +/- 3.2%) (p < 0.001). Following chemodenervation, hypercapnia still increased RLv (+11.3 +/- 3.2%) (p < 0.01) and diminished PL (-29.9 +/- 2.5%). Bilateral vagotomy reduced the response of PL to hypercapnia (-13.3 +/- 6.9%) (p < 0.05). Local intra-arterial injection of KCN produced an increase in RLv and PL (+7.0 +/- 1.2%, +9.0 +/- 1.0%). After peripheral chemodenervation KCN injection slightly increased PL (+2.0 +/- 0.9%). The response of RLv was almost abolished. In conclusion, laryngeal vasoconstriction in response to systemic hypoxia after chemodenervation is probably mediated by increased sympathetic discharge to the larynx due to hypoxia of the CNS. Laryngeal responses to hypercapnia may be due to the action of central chemoreceptors.

Effect of intravenous calcitonin gene-related peptide antagonist on the laryngeal chemoreflex in piglets

The laryngeal chemoreflex (LCR) is characterized by mixed apnea and cardiovascular instability and is elicited by applying water to the laryngeal mucosa of developing animals. The LCR may be fatal in very young animals, and the reflex has been postulated as a possible mechanism of sudden infant death syndrome. Several antagonists have been found to alter the severity of the LCR, but the primary neurotransmitters involved in mediating the reflex response are not yet well understood. This study investigates the effect, on the LCR, of the pharmacologic antagonism of calcitonin gene-related peptide (αCGRP), a neurochemical found in abundance in the mammalian laryngeal mucosa and its innervating system. The LCR was elicited in 10 mixed breed piglets, 17.7 days of age (12 to 22 days), before and during infusion of αCGRP 8-37, a pharmacologic inhibitor of αCGRP, and cardiorespiratory and laryngeal responses were compared. The duration of obstructive apnea decreased from 17.9 to 9.8 seconds ( P < 0.03) in the presence of αCGRP 8-37. Mean central apnea did not change for the group ( P > 0.05), although it was completely inhibited in 2 animals. Cardiovascular changes were not significantly altered by the αCGRP inhibitor. αCGRP appears to play a regulatory role in the apneic response of the LCR, particularly its obstructive component, but not the cardiovascular response. Otolaryngol Head Neck Surg 1999;121:1-6.)

IL-6 Cerebrospinal Fluid Levels Are Related to Laryngeal IgA and Epithelial HLA-DR Response in Sudden Infant Death Syndrome

The objective was to investigate whether there is any correlation between signs of central and peripheral immune stimulation in victims of sudden infant death syndrome (SIDS), the former expressed by IL-6 in cerebrospinal fluid (CSF), the latter by IgA, IgG, and IgM immunocytes, T lymphocytes, and HLA-DR expression in laryngeal mucosa. Seventeen SIDS cases with low CSF IL-6 levels (< or =5 pg/mL) and 20 cases with high CSF IL-6 levels (> or =30 pg/mL) were subjected to immunohistochemical quantitation of IgA, IgG, and IgM immunocytes; semiquantitative scoring of T lymphocytes in the mucosa of epiglottis and larynx, and semiquantitative evaluation of HLA-DR expression. SIDS cases with IL-6 levels > or =30 pg/mL had a significantly higher number of IgA immunocytes in laryngeal mucosa (p = 0.007) and in epiglottis (p = 0.03) than cases with IL-6 levels < or =5 pg/mL. Furthermore, laryngeal HLA-DR expression was significantly more extensive in SIDS cases with IL-6 levels > or =30 pg/mL than in those with levels < or =5 pg/mL (p = 0.05). No differences were found for IgG and IgM immunocytes or for T cells. In addition, babies found prone more often had symptoms of slight infection before death and had a higher number of IgA immunocytes in the larynx (p = 0.02) than babies sleeping on their side or back. Because IL-6 levels > or =30 pg/mL correspond to the levels found in infants who die from infectious diseases such as meningitis/septicemia and pneumonia, the findings favor the hypothesis that many SIDS cases may be caused by an "overreaction" of the immune system to an otherwise harmless infection.

Effect of intravenous substance P on laryngeal adductor activity in young dogs.

Reflex laryngeal adduction is a component of both the laryngeal chemoreflex and the esophagolaryngeal adductor reflex, two life-threatening reflexes that occur in immature animals. These two reflex responses are also thought to exist in infants and may play a role in causing life-threatening laryngospastic events and perhaps sudden infant death syndrome. Identifying neurotransmitters that mediate laryngeal adduction is important to understanding the mechanism of reflex laryngeal responses and to identifying potential means of pharmacologic prevention. Substance P (SP), a tachykinin, putatively functions as a sensory neurotransmitter and may play a role in mediating laryngeal reflexes. Substance P-immunoreactive-like fibers and receptors are present in the subepithelial tissues of the larynx, the vagus nerves, the nodose and jugular ganglia, and the vagal brain stem nuclei. In this investigation, the effect of SP infusion on laryngeal motor activity in an in vivo model is reported. Substance P was infused intravenously into 8 puppies (20 to 133 days of age, mean 81.2), on a mean of 3.0 occasions (range 1 to 6). Cardiovascular, respiratory, arterial blood gas, and cricothyroid (CT), thyroarytenoid (TA), and genioglossus electromyographic (EMG) responses to infusion of the tachykinin were recorded and subsequently analyzed. The SP infusion induced a marked increase in CT or TA EMG activity in 23 of 24 studies, and the increase was typically apparent within 60 seconds of the infusion. An increase in genioglossus EMG activity did not occur. An immediate, profound decrease in mean arterial pressure and an increase in respiratory rate and depth of chest wall excursion accompanied the laryngeal response. Arterial blood gas values remained unchanged (p > .05). The laryngeal adductor response to SP infusion was blocked when animals were pretreated with a systemic SP antagonist (Pfizer CP-96,345). This study demonstrates that peripheral infusion of the tachykinin SP induces a marked increase in laryngeal adductor activity. The response may be blocked by pretreatment of animals with a systemic SP antagonist. Because SP is thought to act primarily as a sensory neurotransmitter, these findings may be important in understanding the mechanism of reflex laryngeal adductor responses.

Upper Airway Reflexes during a Combination of Propofol and Fentanyl Anesthesia

The effects of intravenous anesthetics on airway protective reflexes have not been fully explored. The purpose of the present study was to characterize respiratory and laryngeal responses to laryngeal irritation during increasing doses of fentanyl under propofol anesthesia. Twenty-two female patients anesthetized with propofol and breathing through the laryngeal mask airway were randomly allocated to three groups: (1) eight patients who received cumulative total doses of 200 microg fentanyl given in the form of two doses of 50 microg and one dose of 100 microg spaced 6 min under mechanical controlled ventilation while end-tidal carbon dioxide tension (PCO2) was maintained at 38 mmHg (fentanyl-controlled ventilation group), (2) eight patients who received cumulative total doses of 200 microg fentanyl while breathing spontaneously while end-tidal PCO2 was allowed to increase spontaneously (fentanyl-spontaneous ventilation group), and (3) six spontaneously breathing patients who were anesthetized with propofol alone (propofol group). The laryngeal mucosa of each patient was stimulated by spraying the cord with distilled water, and the evoked responses were assessed by analyzing the respiratory variables and endoscopic images. Before administration of fentanyl, laryngeal stimulation caused vigorous reflex responses, such as expiration reflex spasmodic panting, cough reflex, and apnea with laryngospasm. Increasing doses of fentanyl reduced the incidences of all these responses, except for apnea with laryngospasm, in a dose-related manner in both the fentanyl-controlled ventilation and the fentanyl-spontaneous ventilation groups. Detailed analysis of endoscopic images revealed several characteristics of laryngeal behavior during the airway reflex responses. Incremental doses of fentanyl depress airway reflex responses in a dose-related manner, except for apnea with laryngospasm.

神経喉頭科学のフィールド

The larynx is a small organ innervated by two branches of the vagus nerve. On first glance the study of this organ may appear to be simple but the field of neurolaryngology covers a vast range of research topics. The major areas are anatomy and physiology of the motor system, sensory system, proprioception, autonomic nervous system, laryngeal reflex, mechanism of neuronal transmission, laryngeal responses against the feedback system, voluntary motor activities, and neuromuscular pathologies. This paper describes the scope of these areas and presents the major results of basic and clinical investigations conducted by the author and colleagues at Kurume University over the past 35 years.

Effects of stimulus intensity on laryngeal long latency responses in awake humans

Percutaneous electrical stimulation applied to the internal branch of the superior laryngeal nerve (ISLN) results in two long latency laryngeal adductor responses in awake humans: an ipsilateral thyroarytenoid (TA) R1 muscle response at 16 ms, and later bilateral TA R2 muscle responses at 60 ms. The purpose of this study was to determine whether a functional relationship existed between the R1 and R2 responses by gradually increasing the level of electrical stimulation from threshold to supramaximal levels. R1 amplitude increased linearly with stimulation intensity in 9 of the 11 subjects, whereas R2 only had a positive linear relationship in 3 subjects and a negative relationship with stimulation intensity in 1 subject. Significant negative relationships were found between response latency and stimulation intensity in 3 subjects for the R1 responses and 3 other subjects for the R2 responses. Overall, R1 amplitudes increased systematically, whereas R2 responses varied in latency and amplitude with increasing stimulus intensity. Neither the latencies nor the amplitudes of the two responses were related after adjusting for stimulation intensity within subjects by using partial correlation coefficients. The R1 and R2 responses were functionally unrelated and most likely have different neural components. (Otolaryngol Head Neck Surg 1997;117:521-9.)

Effects of stimulus intensity on laryngeal long latency responses in awake humans.

Percutaneous electrical stimulation applied to the internal branch of the superior laryngeal nerve (ISLN) results in two long latency laryngeal adductor responses in awake humans: an ipsilateral thyroarytenoid (TA) R1 muscle response at 16 ms, and later bilateral TA R2 muscle responses at 60 ms. The purpose of this study was to determine whether a functional relationship existed between the R1 and R2 responses by gradually increasing the level of electrical stimulation from threshold to supramaximal levels. R1 amplitude increased linearly with stimulation intensity in 9 of the 11 subjects, whereas R2 only had a positive linear relationship in 3 subjects and a negative relationship with stimulation intensity in 1 subject. Significant negative relationships were found between response latency and stimulation intensity in 3 subjects for the R1 responses and 3 other subjects for the R2 responses. Overall, R1 amplitudes increased systematically, whereas R2 responses varied in latency and amplitude with increasing stimulus intensity. Neither the latencies nor the amplitudes of the two responses were related after adjusting for stimulation intensity within subjects by using partial correlation coefficients. The R1 and R2 responses were functionally unrelated and most likely have different neural components.

Characteristics of laryngeal late responses to superior laryngeal nerve stimulation in rabbits

Characteristics of laryngeal late responses to superior laryngeal nerve stimulation in rabbits

Influence of sleep states on laryngeal and abdominal muscle response to upper airway occlusion in lambs.

This study was aimed at describing abdominal and laryngeal muscle responses to upper airway occlusion (UAO) in early life and the effect of sleep states on these responses. Twelve nonsedated, 9-26-d-old lambs were studied. We simultaneously recorded 1) airflow (pneumotachograph + face mask); 2) sleep states (electrocorticogram and electrooculogram); 3) abdominal muscle (external obliquus) electromyogram (EMG); and 4) glottic constrictor (thyroarytenoid) and dilator (posterior cricoarytenoid and cricothyroid) muscle EMGs. The pneumotachograph was repeatedly occluded for 15-30 s in wakefulness and natural sleep. We analyzed 90 occlusions during wakefulness (11 lambs), 28 during non-rapid eye movement (nREM) sleep (six lambs), and 23 during rapid eye movement (REM) sleep (five lambs). A phasic expiratory external obliquus EMG was present during baseline and progressively increased throughout UAO in wakefulness and nREM sleep, but not in REM sleep. Phasic thyroarytenoid EMG progressively increased during inspiratory efforts throughout UAO in wakefulness and nREM sleep, paralleling the increase in glottic dilator (posterior cricoarytenoid and cricothyroid) EMG. In contrast, glottic muscle response to UAO in REM sleep was severely blunted or disorganized by frequent swallowing movements. We conclude that UAO triggers complex and coordinated laryngeal and abdominal muscle responses during wakefulness and nREM sleep in lambs; these responses are largely absent, however, in REM sleep. These unique results, together with the defective arousal response in REM sleep, suggest that vulnerability to airway occlusion could be increased during REM sleep in early life. Possible implications for understanding severe postnatal apneas are discussed.

Ovine Fetal Laryngeal Chemoreflex Thresholds and Respiratory Effects

In newborn infants, laryngeal contact with solutions of low chloride concentration or pH evokes swallowing, laryngeal adduction, and respiratory inhibition (laryngeal chemoreflex). To determine whether the laryngeal chemoreflex is present during fetal life and its effect on fetal respiratory activity, eight time-bred ewes (128 ± 2 days) were prepared with fetal electrocortical diaphragm and esophageal electrodes and a nasopharyngeal catheter. After a 60-minute control period, increasing volumes (0.1 to 1.0 ml/kg) of 0.15 mol/L NaCl or distilled water (0.05 to 1.0 ml/kg) and decreasing concentrations of NaCl (0.15 to 0.02 mol/L) at a fixed volume (0.3 ml/kg) were sequentially administered through the nasopharyngeal catheter (38° C). The minimum water volume that stimulated swallowing was significantly less than the minimum 0.15 mol/L NaCl volume (0.10 ± 0.02 vs. 0.70 ± 0.05 ml/kg). The maximum NaCl concentration that stimulated swallowing was 0.04 ± 0.01 mol/L. During the control period, respiratory activity averaged 14.6 ± 0.7 breaths/minute and did not change during absent swallow responses or isotonic saline-induced swallows. However, respiratory activity significantly decreased during water (4.7 ± 0.6 breaths/minute) and hypotonic saline-induced swallow responses (3.7 ± 0.7 breaths/minute). Fetal electrocortical activity did not change during absent or stimulated swallows. We conclude that laryngeal water or hypotonic saline solution may stimulate fetal swallowing and suppress fetal respiratory activity, similar to the newborn laryngeal chemoreflex. We speculate that an exaggeration of the laryngeal chemoreflex apnea response in the newborn may predispose to sudden infant death syndrome.

Ovine fetal laryngeal chemoreflex thresholds and respiratory effects

In newborn infants, laryngeal contact with solutions of low chloride concentration or pH evokes swallowing, laryngeal adduction, and respiratory inhibition (laryngeal chemoreflex). To determine whether the laryngeal chemoreflex is present during fetal life and its effect on fetal respiratory activity, eight time-bred ewes (128 ± 2 days) were prepared with fetal electrocortical diaphragm and esophageal electrodes and a nasopharyngeal catheter. After a 60-minute control period, increasing volumes (0.1 to 1.0 ml/kg) of 0.15 mol/L NaCl or distilled water (0.05 to 1.0 ml/kg) and decreasing concentrations of NaCl (0.15 to 0.02 mol/L) at a fixed volume (0.3 ml/kg) were sequentially administered through the nasopharyngeal catheter (38° C). The minimum water volume that stimulated swallowing was significantly less than the minimum 0.15 mol/L NaCl volume (0.10 ± 0.02 vs. 0.70 ± 0.05 ml/kg). The maximum NaCl concentration that stimulated swallowing was 0.04 ± 0.01 mol/L. During the control period, respiratory activity averaged 14.6 ± 0.7 breaths/minute and did not change during absent swallow responses or isotonic saline-induced swallows. However, respiratory activity significantly decreased during water (4.7 ± 0.6 breaths/minute) and hypotonic saline-induced swallow responses (3.7 ± 0.7 breaths/minute). Fetal electrocortical activity did not change during absent or stimulated swallows. We conclude that laryngeal water or hypotonic saline solution may stimulate fetal swallowing and suppress fetal respiratory activity, similar to the newborn laryngeal chemoreflex. We speculate that an exaggeration of the laryngeal chemoreflex apnea response in the newborn may predispose to sudden infant death syndrome. (Otolaryngol Head Neck Surg 1997;116:91-6.)