Maturation of spontaneous arousals in healthy infants.

OBJECTIVE: The propensity to arouse from sleep is an integrative part of the sleep structure and can have direct implications in various clinical conditions. This study was conducted to evaluate the maturation of spontaneous arousals during the first year of life in healthy infants. DESIGN: Nineteen infants were studied with nighttime polysomnography on 3 occasions: aged 2 to 3 months, 5 to 6 months, and 8 to 9 months. Ten infants with a median age of 3 weeks were added to the main study to assess the maturation of arousals from birth. The infants were born full-term, were healthy at the time of study, and had no history of apnea. Sleep-state and cardiorespiratory parameters were scored according to recommended criteria. Arousals were differentiated into subcortical activations or cortical arousals, according to the presence of autonomic and/or electroencephalographic changes. Frequencies of subcortical activations and cortical arousals were studied at different ages in both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. RESULTS: During sleep time, the frequency of total arousals, cortical arousals, and subcortical activations decreased with age. The maturation of the arousal events differed according to sleep states and types of arousals. With age, cortical arousals increased in REM sleep (P = 0.006) and decreased in NREM sleep (P = 0.01). Subcortical activations decreased with age in REM (P < 0.001) and NREM sleep (P < 0.001). CONCLUSIONS: During total sleep time, the frequency of cortical arousals and subcortical activations decreased with maturation. However, the maturation process was different between cortical arousals and subcortical activations. This finding suggests a difference in the maturational sequence of the different brain centers regulating arousals.

QT interval prolongation in future SIDS victims: a polysomnographic study.

OBJECTIVE: Previous data have suggested that a prolonged QTc interval during the first days of life can be associated with some cases of sudden infant death syndrome (SIDS). Analysis of heart rate variability during sleep in future SIDS victims has shown findings compatible with an imbalance in autonomic tone. We hypothesized that some future SIDS infants could have longer QTc intervals during sleep, compared with healthy control infants, and that this difference would correlate with the autonomic imbalance already found in these infants. METHODS: QTc intervals and a heart rate autoregressive power spectral analysis were calculated during the same periods in the polysomnographic sleep recordings of 18 infants who eventually died of SIDS and of 18 control infants. The control infants were matched for sex, gestational age, postnatal age, birth weight, and sleep position. The median postnatal age was 8 weeks. RESULTS: Compared with control infants, future SIDS victims were characterized by having longer QTc intervals during total sleep (P = 0.019), rapid eye movement sleep (P = 0.045) and non-rapid eye movement sleep (P = 0.029). When the night was divided into 3 equal parts, this difference was always present but was most marked during the last part of the night. There was, respectively, a negative and a positive correlation between parasympathetic activity and sympathovagal balance and median and maximum QTc interval values. CONCLUSION: Compared with QTc intervals in matched control infants, QTc intervals were increased in future SIDS victims. Such a prolongation could be related to the autonomic dysfunction already reported in these patients.

Spontaneous arousability in prone and supine position in healthy infants.

STUDY OBJECTIVE: Compared with control infants, those who will be future victims of sudden infant death syndrome (SIDS) show a decreased arousability during sleep, with fewer cortical arousals and more-frequent subcortical activations. These findings suggest an incomplete arousal process in victims of SIDS. Prone sleep position, a major risk factor for SIDS, has been reported to reduce arousal responses during sleep. The present study was undertaken to evaluate whether the prone sleep position impairs the arousal process in healthy infants. METHODS: Twenty-four healthy infants were studied polygraphically during 1 night; 12 infants regularly slept supine and 12 infants regularly slept prone. Infants were matched for sex, gestational age, and age at recording. Arousals were differentiated into subcortical activations or cortical arousals, according to the presence of autonomic and/or electroencephalographic changes. Frequencies of subcortical activations and cortical arousals were compared in the prone- and the supine-sleeping infants. RESULTS: Compared with supine sleepers, prone sleepers had significantly fewer cortical arousals during rapid eye movement (REM) sleep (p = .043). There were no significant differences in cortical arousals between the 2 groups during non-REM sleep. No significant differences were seen in the frequencies of subcortical activations during both REM and non-REM sleep between supine and prone sleepers. The ratio of cortical arousal to subcortical activation showed no significant differences between the prone and the supine sleepers. CONCLUSIONS: Prone sleep position decreased the frequency of cortical arousals but did not change the frequency of subcortical activations, as has been previously found in SIDS victims. These results suggest specific pathways for impairment of the arousal process in SIDS victims.

Epidemiology of dog bites: a Belgian experience of canine behaviour and public health concerns.

This paper reviews three studies that have been conducted in Belgium on dog bites on children. (1) A telephone study revealed that 22/1000 children <15 years of age were victims of dog bites annually. (2) Data on the characteristics of dog bites were collected prospectively over a period of 8.5 months in six hospital emergency departments. "Dangerous dogs" were not responsible for the majority of the accidents. In 67/100, incidents documented, the bites appeared to be triggered by an interaction of the child. Education appeared to be the preventive measure with the highest priority. (3) Among 22 child victims of dog bites, 12 had symptoms of post-traumatic stress disorders some seven months following the accident. Based on these local studies, several initiatives have been undertaken to favour both primary and secondary prevention measures. An appropriate psychological preventive intervention should be offered to all victims of dog bites.

Incongruent cerebral growth in sudden infant death syndrome.

Sudden infant death syndrome remains a leading cause of post-neonatal mortality in developed countries. Its etiopathogenic mechanisms are unknown. In this neuropathologic study, we noticed that the weights of the brains of infants who died from sudden infant death syndrome (n = 97) were invariably heavier in comparison with those of a group of age-matched controls (n = 23) issuing from the same local population. Brain edema was not a major element, and there were no significant microscopic or macroscopic cerebral anomalies in the brains from either of the study groups. Head circumference did not show a parallel increase in infants with sudden infant death syndrome. The excessive brain weight might reflect abnormal cerebral development and could be detrimental to vital neural control. In a previous study, we disclosed cytokine overexpression in the brains of these victims. Whether increased brain weight is linked to cytokine up-regulation remains, however, a moot case and merits further exploration.

Increased cardiac autonomic responses to auditory challenges in swaddled infants.

STUDY OBJECTIVES: When infants have been swaddled and sleep supine, their risk of dying from sudden infant death syndrome (SIDS) is reduced with an odds ratio of 0.64 to 0.69. Alternatively, the risk for SIDS in swaddled infants shows a 3-fold increase in the prone position. The protective role of swaddling during supine sleep has remained unexplained. This study was designed to evaluate the effects of swaddling on cardiac reactivity to auditory stimuli during sleep in both the prone and the supine position. DESIGN: Thirty healthy infants with a median age of 11 weeks (range 8 to 15 weeks) were studied polygraphically for 1 night while sleeping successively prone and supine, or vice versa. The infants were studied while swaddled and nonswaddled in both positions. Heart rates were studied during rapid eye movement sleep, before and after exposure to 90 dB(A) of white-noise. RESULTS: Ten infants were excluded from the study because they woke up during the position change or the auditory challenge. Before the administration of the noise stimulus, swaddling decreased values of basal heart rates in the supine position only (P = .049). Following swaddling, the values of basal heart rate were significantly lower in the supine than in the prone position (P = .003). Auditory challenges were followed by a greater increase in heart rate when the supine sleeping infants were swaddled than when not swaddled (P = .018). When swaddled, beat-to-beat heart-rate variability increased following auditory stimulation in the supine position only (P = .012). CONCLUSION: When sleeping supine, swaddled infants had greater cardiac autonomic changes in response to noise challenges than when they were not swaddled.

Cardiac changes during sleep in sleep-deprived infants.

OBJECTIVE: To evaluate the influence of a brief period of sleep deprivation on cardiac autonomic controls during sleep in healthy infants. DESIGN: Twelve healthy infants with a median age of 8 weeks (range, 7 to 18 weeks) were recorded polygraphically during a morning and an afternoon nap in a sleep laboratory. They were sleep deprived for approximately 2 hours, either in the morning or in the afternoon, before being allowed to fall asleep. Six infants were sleep deprived before the morning nap, and 6 before the afternoon nap. During both naps, their sleep, breathing, and heart-rate characteristics were continuously recorded. Spectral analysis of heart rate was evaluated as a function of sleep stages. Two major peaks were recognizable: a low-frequency component related to sympathetic and parasympathetic activities and a high-frequency component reflecting parasympathetic tonus. The ratio of low-frequency to high-frequency powers was calculated as an index of sympathovagal interaction. RESULTS: When sleep deprived, the infants had an increase in basal heart rate during non-rapid eye movement sleep (P=.021). With sleep deprivation, the ratio of low-frequency to high-frequency powers increased in non-rapid eye movement sleep (P=.005). These findings were consistent with an increase in sympathetic tone. CONCLUSION: Infants exposed to short-term sleep deprivation manifest changes in cardiac autonomic controls during sleep. These findings could be relevant to mechanisms associated with the sudden infant death syndrome.

Sudden infant deaths: arousal as a survival mechanism.

The mechanisms responsible for sudden infant death syndrome (SIDS) are still largely unknown. To explain what factors contribute to the deaths, we suggest a model: the '3 S model for SIDS' that includes 'sicknesses', 'stages of development' and 'surroundings': (1) 'sicknesses' refers to infectious diseases or other medical condition. (2) 'Stages of development' relates to the maturation of vital systems including respiratory, neurovegetative or sleep-wake behavioral controls. (3) 'Surroundings' refers to environmental conditions that enhance the deficiency of cardiorespiratory, vegetative and/or arousal controls. Such conditions were identified by epidemiological studies and include the following main risk factors: the prone body position during sleep, high environmental temperature, maternal smoking or sleep deprivation. An infant could be at higher risk for SIDS because of a deficiency in breathing and cardiac autonomic controls during sleep, inducing repeated episodes of hypoxia and hypoxemia. The risk is increased when the infant has a lower propensity to arouse from sleep and so, to autoresuscitate. The accident has a greater probability to occur when an infection, or an unfavorable environmental factor aggravates the immature cardiorespiratory and sleep/wake behaviors of the infant. The clinical findings could be related to the changes reported in the brainstems of SIDS victims.

Physiological relationship between autonomic reactions and arousals in infancy.

OBJECTIVE: Changes in blood pressure (BP) were measured following auditory stimuli in the prone and the supine position to study the correlation between arousal from sleep and autonomic responses. METHOD: Two newborns born at term, two infants and four children were recorded polygraphically during one night, while sleeping in the prone and the supine position. They were exposed to white noises of increasing intensities during both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep in each position. BP changes were measured by Finapress in the children and by pulse transient time (PTT) in the infants and newborns. RESULTS: Basal systolic BP pressures were lower (P<0.001) and PTT were higher (P=0.008) in the prone than in the supine position in children and in infants. Following the auditory stimulations, the increases in systolic BP (P=0.024) and the decreases in PTT (P=0.006) were smaller in prone than in supine position. During cortical arousals, the same findings were found, independently of sleep stages. CONCLUSION: Compared with when they are sleeping supine, children and infants sleeping prone had lower basal BP and higher PTT and smaller changes in BP and PTT after auditory stimulation. Reduced BP changes to stimuli could be implicated in the increased arousal thresholds in prone position.

Arousal deficiency theory in sudden infant death syndrome with reference to neuronal plasticity.

OBJECTIVE: Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age (including 26 infant victims of sudden infant death syndrome (SIDS), five with congenital cardiac abnormalities, two from infected pulmonary dysplasia, two from septic shock with multi-organ failure, one with a prolonged seizure, one from prolonged neonatal hypoxemia and one from meningitis and brain infarction). METHOD: The frequency and duration of sleep apnea events recorded some 3-12 weeks before the infants' deaths were analyzed. Brainstem material from these 38 infants was studied in an attempt to elucidate the relationship between sleep apnea and neuronal pathological changes in the arousal pathway. The histochemical analyses included Bielschowsky staining and the immunohistochemical analyses included the evaluation of growth-associated phosphoprotein 43 (GAP43) and of synaptophysin as markers for synaptic plasticity. Neurofibrae with positive pathological reactions were quantitatively analyzed. Pathological and physiological data were linked for each infant. RESULTS: The correlation between sleep apnea and neuronal plasticity in the arousal pathway of the SIDS victims was not seen in the control infants and the correlation between sleep apnea and neuronal plasticity in the arousal pathway found in the control infants was not seen in the SIDS victims. CONCLUSION: These findings suggest that neuronal plasticity in the brainstem arousal pathway is related with SIDS.

Autonomic responses to sighs in healthy infants and in victims of sudden infant death.

OBJECTIVE: Sigh, defined as an isolated breath with an increased tidal volume, can be associated with abrupt changes in heart rate (HR) or blood oxygenation. Sigh may be followed by a central apnea. As impairment of autonomic control was postulated in future SIDS victims, we hypothesized that their autonomic responses to sighs were different from those of healthy control infants. METHODS: Sighs followed by central apnea were studied in the sleep recordings of 18 infants who eventually died of SIDS and of 18 control infants. The infants of the two groups were matched for sex, gestational age, postnatal age, weight at birth and sleep position during sleep recording. HR autoregressive power spectral analysis was performed on RR intervals preceding and following sighs. RESULTS: In all infants, most sighs followed by an apnea were found in NREM sleep. Compared to the control infants, the future SIDS victims were characterized by a greater sympathovagal balance and a lower parasympathetic tonus before the sighs. Following the sighs, no more differences were found in NREM sleep. CONCLUSION: Based on the present findings, it can be postulated that sighs contribute to reset autonomic tonus during NREM sleep.

Partial arousal deficiency in SIDS victims and noradrenergic neuronal plasticity.

Sudden infant death syndrome (SIDS) victims had exhibited during sleep a reduction in cortical arousals despite an increase in subcortical activation. Arousal deficiency in SIDS victims was partial. We could suggest the latent existence of inadequate noradrenergic neuronal plasticity as the background of this partial arousal deficiency of SIDS victims.

Pacifier use modifies infant's cardiac autonomic controls during sleep.

OBJECTIVE: The risk for sudden infant death (SIDS) was postulated to decrease with the use of a pacifier and by conditions increasing parasympathetic tonus during sleep. We evaluated the influence of a pacifier on cardiac autonomic controls in healthy infants. STUDY DESIGN: Thirty-four healthy infants were studied polygraphically during one night: 17 infants regularly used a pacifier during sleep and 17 never used a pacifier. Thumb users or occasional pacifier users were not included in the study. The infants were recorded at a median age of 10 weeks (range 6-18 weeks). Autonomic nervous system (ANS) was evaluated by spectral analysis of the heart rate (HR). The high frequency component of HR spectral analysis reflected parasympathetic tonus and the low frequency on high frequency ratio corresponded to the sympathovagal balance. RESULTS: Most infants (63.6%) lost their pacifier within 30 min of falling asleep. Sucking periods were associated with increases in cardiac sympathovagal balance. During non-sucking periods, in both REM and NREM sleep, infants using a pacifier were characterized by lower sympathetic activity and higher parasympathetic tonus compared with non-pacifier users. CONCLUSIONS: The use of pacifiers modifies cardiac autonomic controls during both sucking and non-sucking sleep periods. Non-nutritive sucking could regulate autonomic control in infants. These findings could be relevant to mechanisms implicated in the occurrence of sudden infant deaths during sleep.

Clinicopathological correlation between brainstem gliosis using GFAP as a marker and sleep apnea in the sudden infant death syndrome.

BACKGROUND: Chronic hypoxia, leading to brainstem gliosis, has been postulated as a factor in the sudden infant death syndrome (SIDS), which is still the main cause of postneonatal infant death. Gliosis detected by immunohistochemistry of glial fibrillary acidic protein (GFAP) is a marker of apoptosis. The correlation between GFAP-positive reactive astrocytes in the brainstem and sleep apnea in SIDS was investigated. MATERIALS AND METHODS: Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age, including 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected and immunohistochemistry of GFAP carried out. The density of GFAP-positive reactive astrocytes was measured quantitatively. Correlation analyses were carried out between the data on gliosis and the physiological data of sleep apnea. RESULTS: A SIDS-specific negative correlation between the density of gliosis in the dorsal vagus nucleus in the medulla oblongata and the frequency of obstructive apnea (p=0.022) was found. CONCLUSIONS: A significant SIDS-specific correlation with gliosis in the dorsal vagus nucleus and the characteristics of sleep apnea might invite the cardiorespiratory changes in SIDS.

Pathological data on apoptosis in the brainstem and physiological data on sleep apnea in SIDS victims.

UNLABELLED: The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death and its cause is still unknown. A chronic hypoxic situation has been shown to exist in the brains of SIDS victims and apoptosis has been demonstrated in hypoxic situations. In this study, the correlation between apoptotic neurons or glias and sleep apnea in SIDS was investigated in the brainstem of SIDS victims. MATERIALS AND METHODS: In a cohort of 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age. They included 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed. The brainstem material was collected and terminal-deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method was carried out. The density of TUNEL-positive neurons or glias was measured quantitatively. Correlation analyses were carried out between the apoptosis-associated pathological data and the physiological data of sleep apnea. RESULTS: No significant negative or positive correlation between the density of TUNEL-positive neurons or glias and the characteristics of sleep apnea was observed in SIDS victims. No statistically significant differences associated with apoptotic neurons and glias were observed between SIDS and non-SIDS. CONCLUSIONS: The pathological findings of apoptosis were not in agreement with the hypothesis refer to apnea and arousal phenomenon in pathophysiology of SIDS.

Investigation into the correlation in SIDS victims between Alzheimer precursor protein A4 in the brainstem and sleep apnea.

BACKGROUND: Recently, the appearance of beta-amyloid precursor protein (APP) has been demonstrated in the neonatal brain following hypoxic-ischaemic injury. As chronic hypoxia is one of the favoured theories of causation in the sudden infant death syndrome (SIDS), the correlation between APP in the brainstem and sleep apnea in SIDS was investigated. MATERIALS AND METHODS: Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age, which included 26 cases of SIDS. All the infants had been recorded during one night in a pediatric sleep laboratory, some 3 to 12 weeks before death. The frequency and duration of sleep apnea were analyzed. The brainstem material was collected and immunohistochemistry with anti-Alzheimer precursor protein A4 (APP) was carried out. The density of APP-positive elements was measured semi-quantitatively. Correlation analyses were carried out between the density of APP-positive elements and the data on sleep apnea. RESULTS: No correlation was found. CONCLUSION: No correlation between pathological data of APP and physiological data of sleep apnea was not in agreement with the association of sleep apnea in pathophysiology of SIDS.

The correlation between serotonergic neurons in the brainstem and sleep apnea in SIDS victims.

BACKGROUND: In the Sudden Infant Death Syndrome (SIDS), a medullary serotonergic network deficiency theory has been proposed, amongst many other hypotheses. The correlation between serotonergic neurons or dendritic spines in the brainstem of SIDS and sleep apnea was investigated here. MATERIALS AND METHODS: Twenty-seven thousand infants were studied prospectively to characterize their sleep-wake behavior. Of these, 38 infants died under 6 months of age, including 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected and immunohistochemistry for tryptophan hydroxylase (TrypH) carried out. The density of TrypH-positive neurons was measured quantitatively. Correlation analyses were carried out between the TrypH-associated pathological data and the physiological data of sleep apnea. RESULTS: One significant positive correlation between the density of TrypH-positive neurons in the dorsal raphe nucleus of the midbrain and the duration of central apnea (p=0.027) was found in SIDS victims. CONCLUSIONS: Some of serotonergic facts could be involved in the pathophysiology of SIDS.

The correlation between ubiquitin in the brainstem and sleep apnea in SIDS victims.

BACKGROUND: The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death and its etiology has stimulated many competing theories, among which is the role of hypoxia and brainstem abnormalities. One report claims an increased in ubiquitin in the liver of SIDS victims, ubiquitin being one of the heat-shock proteins. The correlation between ubiquitin in the brainstem and sleep apnea in SIDS was investigated here. MATERIALS AND METHODS: Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age, including 26 cases of SIDS. All the infants had been recorded during one night in a pediatric sleep laboratory some 3-12 weeks before death. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected at autopsy and examined immunohistochemically for ubiquitin. The density of ubiquitin-positive elements was measured semiquantitatively. Correlation analyses were carried out between the density of ubiquitin-positive elements and the data on sleep apnea. RESULTS: In the victims of SIDS, a statistically significant positive correlation was found between the density of ubiquitin-positive neuronal factors in the pons and the frequency of obstructive apnea (p=0.001) and statistically significant negative correlations were seen between the density of ubiquitin-positive cells in the ependyma in the pons and the duration of obstructive apnea (p=0.044) and between the density of ubiquitin-positive cells in the subependyma in the medulla and the frequency of central apnea (p=0.024). CONCLUSIONS: It was found that three significant associations existed between the pathological data referring to ubiquitin and physiological data in SIDS victims. These facts are in agreements with the association of sleep apnea in SIDS.

The correlation between microtubule-associated protein 2 in the brainstem of SIDS victims and physiological data on sleep apnea.

BACKGROUND: Microtubule-associated protein 2(MAP2), a cytoskeletal protein of the neuron, is a marker of early ischemic neuronal damage. As a chronic hypoxic situation exists in the brains of victims of the sudden infant death syndrome (SIDS), the correlation between MAP2-positive neurons or dendritic spines in the brainstem and sleep apnea was investigated in SIDS, which is still the main cause of postneonatal infant death. MATERIALS AND METHODS: 27,000 infants were studied prospectively to characterize their sleep-wake behavior and amongst these, 38 infants died under 6 months of age. They included 26 cases of SIDS. The frequency and duration of sleep apneae were analyzed. The brainstem material was collected and immunohistochemistry of MAP2 was carried out. The density of MAP2-positive neurons, dendrites and dendritic spines were measured quantitatively. Correlation analyses were carried out between the MAP2-associated pathological data and the physiological data of sleep apnea. RESULTS: One negative correlation between the density of MAP2-positive dendrites in the pars compacta of pedunculo-pontine tegmentum nucleus (PPTNc) and the duration of obstructive apnea (p=0.017) and two SIDS-specific positive correlations between the density of MAP2-positive dendrites in the pars dissipata of pedunculo-pontine tegmentum nucleus (PPTNd) and the duration of central apnea (p=0.005) and between the dorsal raphe and the frequency of obstructive apnea were found in SIDS victims. The density of MAP2-positive dendritic spines in PPTNc was significantly higher in SIDS than in control (p=0.034). CONCLUSIONS: The significant correlations with the MAP2-positive findings in the midbrain arousal pathway and the characteristics of sleep apnea in SIDS victims were in agreement with the association with apnea and arousal-deficiency in SIDS.

The correlation between tau protein in the brainstem and sleep apnea in SIDS victims.

BACKGROUND: Recently, it has been reported that neuronal plasticity in the brainstem arousal pathway is related to the sudden infant death syndrome (SIDS). Tau protein may contribute to axonal development and neural plasticity; therefore, the correlation between tau protein in the brainstem and sleep apnea in SIDS was investigated here. MATERIALS AND METHODS: Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age, including 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed on all the infants, having been recorded during one night in a pediatric sleep laboratory some 3-12 weeks before death. The brainstem material was collected and immunohistochemistry of tau was carried out. The density of tau-positive elements was measured semiquantitatively. Correlation analyses were carried out between the density of tau-positive elements and the data of sleep apnea. RESULTS: In the 26 SIDS cases, tau-positive findings were observed in the sub-pia mater in two cases, in the colloid plexus in one case, in the ependyma and subependyma in five cases, in neurons in two cases and as a general diffusion in one case. In 12 control cases, tau-positive findings were observed in the sub-pia mater in one case and in neuronal elements in three cases. No correlation was found on analysis. CONCLUSIONS: There was no correlation between the finding of tau in the brainstem of SIDS victims and the incidence of sleep apnea.