Onset Of Apnea Research Articles

The clinical and polysomnographic features in complex sleep apnea syndrome

Complex sleep apnea syndrome (CompSAS) is characterized by the onset of central apneas or a Cheyne-Stokes breathing pattern in some patients with obstructive sleep apnea syndrome (OSAS) who were treated with continuous positive airway pressure (CPAP). The etiology of CompSAS is unclear, but derangement of respiratory control has been proposed. We sought to compare clinical and polysomnography (PSG) features of patients with CompSAS and OSAS. Materials and methods: Records of PSG were evaluated in a total of 270 patients, retrospectively. CPAP titration was prescribed in patients with an apnea-hypopnea index (AHI) of >=15. Patients who developed a central AHI of >=5 following titration PSG were diagnosed with CompSAS. Results: There were 71 patients with OSAS and 12 with CompSAS. The mean ages and body mass indexes (BMIs) were similar between the 2 groups. The incidences of diagnostic AHI, congestive heart failure (CHF), and chronic renal failure (CRF) were higher in patients with CompSAS. The average and minimum oxygen saturation levels were lower in patients with CompSAS and those with diagnostic PSGs. Conclusion: According to our results, lower oxygen saturation may cause instability of respiratory control in these patients and may be responsible for the pathophysiology of CompSAS.

Estimation of heart rate from an apnoea detection device using matched filtering

Today, there are several respiration monitors available that are intended to detect the onset of apnoea in sleeping infants and adults. These monitors typically detect movement due to the respiration. This paper presents a method for the extraction of a subject's heart rate from a commercial apnoea monitor. The significance of the method lies in the fact that certain cases of apnoea cannot always be detected when only monitoring breathing, and the heart rate can serve as an additional diagnostic or warning tool. An adaptive heartbeat detection system, based on matched filtering, is proposed which detects individual heartbeats from subjects with different physiological features. Additionally, a heart rate estimation system is proposed which determines the heart rate by using the information obtained from the heartbeat detection system. Data was recorded from adults and infants, and the matched filtering heartbeat detection system was able to monitor the heart rate of adults to within less than 5% and infants within 13% of the actual heart rate as determined using an electrocardiogram (ECG).

Ictal apnea linked to contralateral spread of temporal lobe seizures: Intracranial EEG recordings in refractory temporal lobe epilepsy

Respiratory mechanisms are implicated in sudden unexpected death in epilepsy (SUDEP). We previously demonstrated a high incidence of ictal hypoxemia in temporal lobe seizures. We now report on the temporal relationship between ictal apnea and seizure onset and spread in patients undergoing video-EEG (electroencephalography) telemetry (VET) with intracranial electrodes. Ten patients with medically refractory temporal lobe epilepsy (TLE) undergoing VET were studied. Data from synchronously recorded digital pulse oximetry (SaO(2)), end-tidal CO(2) (ETCO(2)), nasal airflow, abdominal excursions, and electrocardiography were obtained. Sixty-one seizures were captured. SaO(2) in the ictal/postictal period was available for 52 seizures, apnea onset times for 27 seizures, and ETCO(2) for 16 seizures. Apneas occurred only when seizures spread to the contralateral temporal lobe. The mean delay to apnea onset was significantly shorter after contralateral seizure spread (2.87 s) than after seizure onset (58.4 s); p < 0.001. The mean SaO(2) nadir with partial seizures or partial seizures prior to secondary generalization was 89.4 +/- 8.6% (91.5, 69-100). Following generalized convulsions the mean oxygen saturation nadir was 75.8 +/- 10.6% (78.5, 58-90). ETCO(2) elevations occurred with each ictal desaturation below 85%. There is a close temporal relationship between spread of seizures to the contralateral hemisphere and the onset of seizure-associated apnea. Apnea onsets are more tightly linked to time of contralateral spread than to time of seizure onset. Patients with TLE in whom there is evidence of contralateral seizure spread may be at higher risk for ictal-related respiratory dysfunction than those in whom seizures remain unilateral.

Physiology of apnoea and the benefits of preoxygenation

This article will concentrate on factors that accelerate or delay the onset of severe hypoxaemia during apnoea (Fig. 1). In the anaesthetized patient, the oxygen consumption (VO2) remains fairly constant at 250 ml min. This is delivered to the tissues by haemoglobin whose oxygen is then replenished, on return to the pulmonary circulation, by the diminishing store of oxygen within the lungs. The alveolar partial pressure of oxygen (PAO2) decreases steadily, not only because the oxygen is being removed from the lungs but also because this oxygen removal generates a substantial negative intrathoracic pressure if the airway is obstructed. Although the arterial partial pressure of oxygen (PaO2) decreases in direct relation to the PAO2, the arterial haemoglobin oxygen saturation (SaO2) remains .90% as long as the haemoglobin can be re-oxygenated in the lungs. The SaO2 only starts to decrease when the store of oxygen in the lungs is depleted and the PaO2 is of the order of 6–7 kPa. Its subsequent decline is of a constant and rapid nature, about 30% every minute. At the start of this rapid decline, the SaO2 is still 90–95%. This inflection point we will define as ‘critical hypoxia’. It is for this reason that oximetry is not a good tool for predicting impending severe hypoxaemia. However, because oximetry detects the decrease in SaO2 before any clinical signs are apparent, it has proved invaluable in detecting critical situations and has helped improve clinical practice to avoid these situations. Various factors significantly influence the time period from the onset of apnoea to critical hypoxia.

The Trigemino-cardiac Reflex

The trigemino-cardiac reflex (TCR) is clinically defined as the sudden onset of parasympathetic activity, sympathetic hypotension, apnea, or gastric hypermotility during central or peripheral stimulation of any of the sensory branches of the trigeminal nerve. Clinically, the TCR has been reported to occur during craniofacial surgery, manipulation of the trigeminal nerve/ganglion and during surgery for lesion in the cerebellopontine angle, cavernous sinus, and the pituitary fossa. Apart from the few clinical reports, the physiologic function of this brainstem reflex has not yet been fully explored. The manifestation of the TCR can vary from bradycardia and hypotension to asystole. From the experimental findings, the TCR represents an expression of a central reflex leading to rapid cerebrovascular vasodilatation generated from excitation of oxygen-sensitive neurons in the rostral ventro-lateral medulla oblongata. By this physiologic response, the systemic and cerebral circulations may be adjusted in a way that augments cerebral perfusion. This review summarizes the current state of knowledge about TCR.

The effects of airway closure in central apneas and obstructed respiratory efforts in mixed apneas in preterm infants

Airway closure during central apnea could allow for better gas exchange. However, the return of inspiratory efforts against a closed airway may cause greater desaturation and prolongation of apnea. To investigate the effect of patency of the airway and obstructed respiratory efforts on the length of apneas and the degree and slope of O(2) desaturation and bradycardia. All mixed apneas observed in 15 preterms were matched 1:2 with the longest central apneas in each infant. Central apneas were further classified using the amplified cardiac airflow oscillation in those with airway open and in those with airway closed. No differences were found in the length of apnea, slope of O(2) desaturation, delay between the onset of apnea and onset of desaturation, lowest post-apneic SpO(2), and time of recovery of SpO(2) between central apneas with and without airway closure. Although mixed apneas were significantly longer than central apneas, their initial central component was significantly shorter than the length of central apneas. In mixed apneas, the onset of O(2) desaturation occurred faster, SpO(2) decreased lower, and recovered slower compared with central apneas. The slope of O(2) desaturation after the obstructed respiratory efforts was significantly greater than before the obstructed respiratory efforts. In preterm infants: (1) airway closure during central apneas does not limit oxygen desaturation; (2) respiratory efforts against a closed airway prolong apnea and worsen the degree of desaturation and bradycardia. Although respiratory efforts are not necessary to induce airway closure, inspiratory efforts against a closed airway could trigger inhibitory cardio-respiratory responses causing significant desaturation, bradycardia, and prolongation of apnea.

Respiratory failure induced by acute organophosphate poisoning in rats: Effects of vagotomy

Acute organophosphate (OP) poisoning causes respiratory failure through two mechanisms: central apnea and pulmonary dysfunction. The vagus nerve is involved in both the central control of respiratory rhythm as well as the control of pulmonary vasculature, airways and secretions. We used a rat model of acute OP poisoning with and without a surgical vagotomy to explore the role of the vagus in OP-induced respiratory failure. Dichlorvos (2,2-dichlorovinyl dimethyl phosphate) injection (100 mg/kg subcutaneously, 3× LD50) resulted in progressive hypoventilation and apnea in all animals, irrespective of whether or not the vagi were intact. However, vagotomized animals exhibited a more rapidly progressive decline in ventilation and oxygenation. Artificial mechanical ventilation initiated at onset of apnea resulted in improvement in oxygenation and arterial pressure in poisoned animals with no difference between vagus intact or vagotomized animals. Our observations suggest that vagal mechanisms have a beneficial effect during the poisoning process. We speculate that vagally mediated feedback signals from the lung to the brainstem serve as a modest protective mechanism against central respiratory depressive effects of the poison and that bulbar-generated efferent vagal signals do not cause sufficient pulmonary dysfunction to impair pulmonary gas exchange.

Effects of Age and Stimulus on Submental Mechanomyography Signals During Swallowing

Mechanomyography (MMG) is the measurement of the vibrations associated with muscle contraction. As an indicator of muscle activity in swallowing, MMG has several potential advantages over conventional electromyography (EMG), including robustness to variations in sensor placement, perspiration, and food spillage. The objective of this study was to investigate the effects of participant age and stimulus on submental muscle activity as measured by MMG. Nasal airflow was utilized as a reference signal. Four liquid stimuli were investigated: water, nectar-thick and honey-thick apple juices, and a thin-liquid barium suspension. Each of 15 healthy adults completed nine swallowing sequences, each consisting of four discrete swallows via a self-administered cup-drinking task, with an MMG sensor at a midline submental location and a nasal cannula at the nares. Muscle activity and swallowing apneas in the signals were identified with pseudo-automatic segmentation algorithms. Various timing and amplitude features were extracted from each segmented swallow. Muscle activity onset preceded the onset of swallow apnea. Significant main effects of stimulus were found for the duration of muscle activity and for the time difference between the offsets of muscle activity and swallow apnea. No other main or interaction effects were significant. In general, the timing and amplitude variations of submental muscle activity revealed by MMG seem to agree with previously reported findings using EMG. The minor discrepancies between the results of this study and those of previous EMG studies are likely due to differences in experimental tasks. MMG may serve as an alternative measure of muscle activity during swallowing and further investigation is warranted.

Management of the trigeminocardiac reflex: Facts and own experience

The trigeminocardiac reflex (TCR) is defined as the sudden onset of parasympathetic dysrhythmia, sympathetic hypotension, apnea, or gastric hyper-motility during stimulation of any of the sensory branches of the trigeminal nerve. The proposed mechanism for the development of TCR is--the sensory nerve endings of the trigeminal nerve send neuronal signals via the Gasserian ganglion to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc. It has been demonstrated that the TCR may occur with mechanical stimulation of all the branches of the trigeminal nerve anywhere along its course (central or peripheral). The reaction subsides with cessation of the stimulus. But, some patients may develop severe bradycardia, asystole, and arterial hypotension which require intervention. The risk factors already known to increase the incidence of TCR include: Hypercapnia; hypoxemia; light general anesthesia; age (more pronounced in children); the nature of the provoking stimulus (stimulus strength and duration); and drugs: Potent narcotic agents (sufentanil and alfentanil); beta-blockers; and calcium channel blockers. Because of the lack of full understanding of the TCR physiology, the current treatment options for patients with TCR include: (i) risk factor identification and modification; (ii) prophylactic measures; and (iii) administration of vagolytic agents or sympathomimetics.

Letters to the Editor

3 May 2008 Dear Editor, RE: AP-ROP IN AN INFANT WITH MINIMAL OXYGEN EXPOSURE Buksh et al. report development of severe retinopathy of prematurity (ROP) in a 700 gm preterm baby with minimal oxygen exposure.1 The patient reported in the case is an extremely low birthweight infant (weight less than 1000 gm). Extremely low birthweight is proven to be the most important risk factor for development of ROP in various studies.2,3 The ROP disease spectrum seen in these babies is entirely different from more mature low birthweight babies. Schulenburg et al. reported variable morphological pattern of ROP seen in these extremely low birthweight infants.4 In our experience also, we found that they do not follow the typical staging pattern seen in mature babies with ROP. The specific features of ROP seen in extremely low birthweight infants are no typical demarcation line or ridge is seen between vascular and avascular retina. The shunting vessels or demarcating vessels (communication between temporal arcade vessels) are commonly seen in these babies. The site of demarcating vessel is the site of future new vessel formation. The neovascularisation seen in these babies is usually seen as filiform tangles with reduced calibre than the mature new vessels seen with ROP in mature babies. Most of these babies present with zone 1 or posterior zone 2 ROP. Flynn et al. reported two distinct pathogenetic mechanisms lying under zone 1 and zone 2 ROP.5 They described zone 1 disease as more severe form occurring frequently in low birthweight infants and as relatively insensitive to laser photocoagulation. Diagnosis of plus disease is difficult as the retinal vascular calibre is less compared with mature babies. One may observe corkscrew pattern of retinal vessels in the entire retina. This is the usual sign of plus disease, we observe in these babies. Irrespective of gestational age, we prefer initial screening for ROP at 3–4 weeks of chronological age in these extremely low birthweight babies. From then we follow them at less than 1-week intervals (3 days–1 week). We perform immediate laser photocoagulation in these babies in the presence of demarcating vessels (can term as stage I), as this is the site of future new vessel formation. We do not wait until the frank signs of plus disease like haemorrhages to appear. They usually require multiple sessions of laser photocoagulation to ablate the large avascular retina. Multiple laser sessions are also required as these babies are more prone to apnoea attacks. To conclude, we feel frequent follow up (less than a week intervals), understanding the unique disease pattern of extremely low birthweight infants and timely laser photocoagulation (usually multiple sessions) within the crucial window period are necessary to avoid the avoidable blindness of ROP.

Apnea-Associated Reduction in Lower Esophageal Sphincter Tone in Premature Infants

To characterize esophageal motility during episodes of prolonged apnea in premature infants. We retrospectively reviewed combined manometric and physiological monitoring studies performed in tube-fed premature infants from 1994 to 2002. Apnea was defined as a respiratory pause of >20 seconds. For each apneic event, pharyngeal swallowing, esophageal motility, and lower esophageal sphincter (LES) pressure were assessed before, during, and after apneic episodes. Twelve episodes of apnea (duration, 20 to 120 seconds) were identified in 7 infants (34 to 37 weeks postmenstrual age (PMA); study weight, 1950 to 2380 g). During the apneic episodes, swallowing increased (median[interquartile range], 0[0,0], 5[4,7], and 1[0,2] swallows/minute before, during, and after apnea, respectively; P < .05), esophageal pressure wave sequences (PWS) increased (1[0,2], 5[3,6], and 2[1,3] PWS/minute before, during, and after apnea, respectively; P < .05) and LES pressure decreased (16[12,21], 6[5,8], and 27[12,32] mmHg before, during, and after apnea, respectively; P < .05). In premature infants, apnea is associated with reduced LES tone, potentially increasing the likelihood of reflux occurring after the onset of apnea.

Blood flow and metabolic regulation in seal muscle during apnea

In order to examine myoglobin (Mb) function and metabolic responses of seal muscle during progressive ischemia and hypoxemia, Mb saturation and high-energy phosphate levels were monitored with NMR spectroscopy during sleep apnea in elephant seals (Mirounga angustirostris). Muscle blood flow (MBF) was measured with laser-Doppler flowmetry (LDF). During six, spontaneous, 8-12 min apneas of an unrestrained juvenile seal, apneic MBF decreased to 46+/-10% of the mean eupneic MBF. By the end of apnea, MBF reached 31+/-8% of the eupneic value. The t(1/2) for 90% decline in apneic MBF was 1.9+/-1.2 min. The initial post-apneic peak in MBF occurred within 0.20+/-0.04 min after the start of eupnea. NMR measurements revealed that Mb desaturated rapidly from its eupenic resting level to a lower steady state value within 4 min after the onset of apnea at rates between 1.7+/-1.0 and 3.8+/-1.5% min(-1), which corresponded to a muscle O(2) depletion rate of 1-2.3 ml O(2) kg(-1) min(-1). High-energy phosphate levels did not change with apnea. During the transition from apnea to eupnea, Mb resaturated to 95% of its resting level within the first minute. Despite the high Mb concentration in seal muscle, experiments detected Mb diffusing with a translational diffusion coefficient of 4.5 x 10(-7) cm(2) s(-1), consistent with the value observed in rat myocardium. Equipoise P(O(2)) analysis revealed that Mb is the predominant intracellular O(2) transporter in elephant seals during eupnea and apnea.

Differential diagnosis of apneas in preterm infants

Clinically relevant apneas, which are common in preterm infants, may adversely affect later neuropsychological condition in this group of patients. Pharmacotherapy to stimulate respiratory functions may be unsuccessful. Polygraphic recording may help in the differential diagnosis of these clinically relevant events. Twenty-nine preterm neonates born before 36 weeks of gestational age were examined using polygraphic recording (respiration--two channels, perioral electromyography, oxygen saturation, heart rate, electroencephalography, electrocardiography, electrooculography). The examination was ordered by the attending physician after an unsuccessful treatment of apnea by Aminophylline, and it should contribute to the clarification of the causes of these events. In the course of the polygraphic examinations, altogether 63 episodes were recorded during which the pulse oximeter alarm signal was set off. In 42 cases, the alarm signal was set off in events during which SaO(2) fell below 85%. In the remaining 21 cases, the alarm signal was set off in episodes during which early bradycardia below 90/min occurred. The onset of apnea was very often associated with the phasic increase of the perioral electromyography and with electroencephalography arousal reaction. Because of suspicion that these apneas may be triggered by episodes of gastroesophageal reflux, the interruption of the Aminophylline treatment and setting up an antireflux regimen were recommended. These therapeutic measures had a positive effect: The frequency of alarm signals decreased within 48 h by a statistically significant 50%. In cases where the pharmacotherapy of apnea by stimulation of respiratory functions is not successful, differential diagnostic analysis should be performed. Polygraphy may contribute to the clarification of the causes underlying clinically relevant apneas in a view of newly described polygraphic signs. It is feasible to suspect, based on these signs, that gastroesophageal reflux is the cause for clinically significant apneas in that case.

Nasal continuous positive airway pressure (nCPAP) therapy in obstructive sleep breathing disorders

The therapeutic efficacy and the incidence of significant side effects of nasal continuous positive airway pressure (nCPAP) treatment was investigated in 1140 patients with sleep-related apnoea (1089 men, 51 women; mean age 53.2 +/- 9.2 [16-84] years). All had been treated for the condition with nCPAP at the Marburg University Medical Polyclinic between 1986 and 1992. The mean number of attacks of apnoea and/or hypopnoea per hour of sleep ("respiratory disturbance index", RDI) was 45.8 +/- 25.6 before treatment and 3.5 +/- 4.8 under nCPAP. 21.1% of patients had an apnoea index of no more than 10/h. 11.6% an RDI of no more than 15/h. The average airway pressure was 8.7 (3-18) cm H2O. The treatment was successful in 1023 patients and these decided to continue the treatment long-term. The RDI could not be lowered under 10/h in 63 patients, while 4 patients declined ambulant treatment despite the demonstrated efficacy of nCPAP. Three patients developed acute left ventricular failure in the initial phase of the treatment, while in another 16 patients long-persisting central hypoventilation was shown to occur. These data show that treatment with nCPAP can be employed for all degrees of severity of obstructive sleep apnoea. However, because of the potentially life-threatening side effects, the introduction of the treatment must be undertaken in the sleep laboratory under continuous monitoring.

Neurophysiological strategies for the diagnosis of disorders of the neuromuscular junction in children

The disorders of the neuromuscular junction seen in children, the congenital myasthenic syndromes and autoimmune myasthenia gravis, are very rare. Their clinical symptoms and signs may be variable, most notably in the neonate and infant. They should enter the differential diagnosis of many different clinical presentations, such as 'floppy infant' or attacks of episodic apnoea. Many molecular genetic abnormalities have been discovered in congenital myasthenic syndromes, but screening for these is impracticable without confirmation of a disorder of the neuromuscular junction. In this review, the different neurophysiological tests that can be used are discussed, with their merits and contraindications in children. After consideration of the acceptability of the different techniques, it has been found that stimulation single-fibre electromyography (stimSFEMG) of orbicularis oculi seems to be the best choice in children. In most instances it can be performed on the conscious child and it has a good specificity and high sensitivity. A protocol for using stimSFEMG is described.

A case of Commotio cordis in a young child caused by a fall

Commotio cordis or ventricular fibrillation caused by a blow to the chest is a rare cause of cardiac arrest in a well child. We report a case of a young child falling from a low height landing chest first with rapid onset of unconsciousness, apnoea and cyanosis. Cardiopulmonary resuscitation was given by parents under telephone instruction from an ambulance dispatch centre. On arrival of officers, 7 min after the fall, ventricular fibrillation was present but responded to defibrillation (biphasic 3 J/kg). No clinical or CT evidence of chest or brain trauma was present and investigations (ECGs, cardiac MRI, echocardiography, viral tests, metabolic tests, drug tests, serum electrolytes) did not reveal any cardiac illness or abnormal cardiac anatomy. Specifically, a long QT was absent and a Flecainide challenge for Brugada syndrome was negative. There was no family history of sudden death. No further dysrrhythmia occurred and the child recovered neurologically well after 3 days of therapeutic hypothermia (for cerebral ischaemia) and 7 days of mechanical ventilation.

A novel form of lethal microcephaly with simplified gyral pattern and brain stem hypoplasia

We report on four patients from the same family affected by a lethal form of autosomal recessive microcephaly of prenatal onset. Symptoms include low birth-weight and length with disproportionately small head, fetal distress, apnea, seizures and facial features reminiscent of Amish microcephaly and Bowen-Conradi syndrome. Brain imaging revealed a simplified gyral pattern with normal to slightly thinned cortical gray matter, thin corpus callosum, mild brainstem and cerebellar hypoplasia. No abnormalities of the internal organs, eye, or skeleton, and no striking dysmorphic facial features were found to be associated with this syndrome. All patients died within hours to weeks after birth following severe apnea attacks and central hypoventilation. Recessive primary microcephaly with lethality in early infancy is rarely reported. The patients described here do not resemble any other published cases of such clinical severity and the locus for the only reported early lethal microcephaly gene found in Amish families was excluded. Therefore, this appears to be a distinct genetic cause of lethal microcephaly.

Supplementation of pre‐oxygenation in morbidly obese patients using nasopharyngeal oxygen insufflation

During apnoea following induction of anaesthesia, morbidly obese patients may suffer a rapid decrease in oxygen saturation. This study compares pre-oxygenation alone with pre-oxygenation followed by nasopharyngeal oxygen insufflation on the onset of desaturation occurring during the subsequent apnoea. A randomised controlled trial was performed in 34 morbidly obese patients undergoing gastric bypass or gastric band surgery. Seventeen patients received nasopharyngeal oxygen supplementation following pre-oxygenation (Study group, body mass index = 41.8 (6.9) kg.m(-2)), and the other 17 patients received pre-oxygenation alone (Control group, body mass index = 42.7 (5.4) kg.m(-2)). Time from the onset of apnoea until S(p)o(2) fell to 95% was compared between the two groups with a cut-off of 4 min. In the control group, the S(p)o(2) fell from 100% to 95% during the subsequent apnoea in 145 (27) s, with a significantly negative correlation (r(2) = 0.66, p < 0.05) between the time to desaturation to 95% and the body mass index. In the study group, the S(p)o(2) was maintained in 16 of 17 patients at 100% for 4 min when apnoea was terminated. In conclusion, nasopharyngeal oxygen insufflation following pre-oxygenation in morbidly obese patients delays the onset of oxyhaemoglobin desaturation during the subsequent apnoea.

Cervical Auscultation Synchronized with Images from Endoscopy Swallow Evaluations

Cervical auscultation is the use of a listening device, typically a stethoscope in clinical practice, to assess swallow sounds and by some definitions airway sounds. Judgments are then made on the normality or degree of impairment of the sounds. Listeners interpret the sounds and suggest what might be happening with the swallow or causing impairment. A major criticism of cervical auscultation is that there is no evidence on what causes the sounds or whether the sounds correspond to physiologically important, health-threatening events. We sought to determine in healthy volunteers (1) if a definitive set of swallow sounds could be identified, (2) the order in which swallow sounds and physiologic events occur, and (3) if swallow sounds could be matched to the observed physiologic events. Swallow sounds were computer recorded via a Littmann stethoscope from 19 healthy volunteers (8 males, 11 females, age range = 18-73 years) during simultaneous fiberoptic laryngoscopy and respiration monitoring. Six sound components could be distinguished but none of these occurred in all swallows. There was a wide spread and a large degree of overlap of the timings of swallow sounds and physiologic events. No individual sound component was consistently associated with a physiologic event, which is a clinically significant finding. Comparisons of groups of sounds and events suggest associations between the preclick and the onset of apnea; the preclick and the start of epiglottic excursion; the click and the epiglottis returning to rest; the click and the end of the swallow apnea. There is no evidence of a causal link. The absence of a swallow sound in itself is not a definite sign of pathologic swallowing, but a repeated abnormal pattern may indicate impairment. At present there is no robust evidence that cervical auscultation of swallow sounds should be adopted in routine clinical practice. There are no data to support the inclusion of the technique into clinical guidelines or management protocols. More evaluation using imaging methods such as videofluoroscopy is required before this subjective technique is validated for clinical use by those assessing swallowing outside of a research context.

Delayed Initiation of the Pharyngeal Swallow: Normal Variability in Adult Swallows

The purpose of this investigation was to determine bolus head timing and location relations with the onset of hyoid movement at the initiation of the pharyngeal swallow and at the onset of swallow-related apnea. Bolus head timing and location and the timing of swallow-related apnea were recorded from frame-by-frame analyses of 5-ml single liquid swallows using dual-modality videofluoroscopy and nasal airflow recordings in 82 consecutive, healthy volunteers. The presence, depth, and response to airway entry were also recorded and related to the bolus head location and the onset of hyoid movement. The majority of participants-80% on at least 1 trial-produced the onset of hyoid movement at pharyngeal swallow initiation after the bolus head passed the posterior angle of the mandible. There was a trend in older participants for later onset of hyoid movement and onset of apnea relative to bolus head arrival at the posterior angle of the mandible. Although entry of the bolus head into the pharynx prior to hyoid movement may result in a threat to the laryngeal airway, these data demonstrate that a "delay" by itself cannot be assumed to indicate a disordered swallow without coexisting impairments of swallowing physiology.