Arousal is considered to be an important response to a life-threatening stimulus. Recently, it has been shown that the infant arousal response to an elevated inspired CO2 level occurs as a sequence of events involving presumptive brain stem responses before awakening (A. Lijowska, N. Reed, B. Chiodini, and B. T. Thach. Am. J. Respir. Crit. Care Med. 151: A151, 1995; A. S. Lijowska, N. W. Reed, B. A. Mertins Chiodini, and B. T. Thach. J. Appl. Physiol. 83: 219-228, 1997). We wanted to further evaluate the relationship of subcortical reflexes to cortical arousal in infants. We used a nonrespiratory (tactile) stimulus to elicit arousal in infants during non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. We found that a tactile stimulus elicited an arousal sequence that commenced with a spinal withdrawal reflex, was followed by brain stem responses (respiratory and startle responses), and ended in a cortical arousal. The entire pathway or part of it in the order of spinal to cortical responses could be elicited. REM and NREM responses were similar except for significant differences in the latencies of spinal and subcortical reflexes. These observations suggest that the infant arousal response to a tactile stimulus involves a progression of central nervous system activation from the spinal to cortical levels. The different components of the arousal pathway may be important for an infant to respond appropriately to stimuli during sleep without necessarily disturbing sleep.
During obstructive sleep apnea (OSA) in adults upper airway reopening coincides with a sudden burst in activity of pharyngeal dilating muscles. This has been attributed to arousal from sleep as indicated by increased EEG activity. Recovery from OSA in infants often occurs in the absence of cortical arousal. To investigate mechanisms involved in recovery, we performed experimental airway occlusions in sleeping infants. Based on past work, our hypothesis was that a sleep startle combined with an augmented breath and heart rate acceleration would occur during the occlusion, and that such brainstem mediated reflexes might provide an explanation for recovery from OSA in the absence of cortical arousal. However, this is contrary to expectations, since lung inflation is believed to be necessary for occurrence of an augmented breath. We studied 16 healthy infants during sleep. We recorded EEG, EOG, ECG, oxygen saturation, diaphragmatic, nuchal and limb electromyograms, face mask pressure, and airflow. A startle, accompanied by neck extension, limb and nuchal EMG activation, as well as heart rate acceleration occurred during all airway occlusions. The startle occurred simultaneously with a large biphasic inspiratory effort, having characteristics of an augmented breath (sigh). In more than a third of cases, this occurred without any evidence of cortical arousal activity. The magnitude of startles as well as the increase in heart rate correlated positively with peak airway negative pressure, indicating that arousal processes are graded in intensity. We conclude that the neck extension and pharyngeal dilating muscle activity associated with the startle and augmented breath may account for recovery of airway patency in infants as they do adults. Lung inflation is not a prerequisite for the reflex to occur.
Metachromatic leukodystrophy refers to a group of genetic neurologic diseases caused by deficiencies of the enzyme arylsulfatase A and the resulting accumulation of sulfatides in white matter. Bone marrow transplantation has been advocated as a treatment in an attempt to correct the enzyme deficiency. Such a transplant was performed in 1991 in a 16-year-old girl with a form of late juvenile metachromatic leukodystrophy caused by a homozygous P426L mutation in the arylsulfatase A gene. Engraftment was prompt and resulted in constant enzymatic normalization of circulating lymphocytes. The elevated urinary excretion of sulfatides remained unaffected. Clinical findings up until transplantation consisted of gait disturbances, impairment of cognitive functioning, and deterioration in school performance over several years. During a 6-year follow-up period, the patient's condition was subject to major fluctuations but, on the whole, findings showed slow neurologic and neurophysiologic deterioration. The clinical course observed after bone marrow transplantation probably more or less reflects the natural course expected in this form of late-onset metachromatic leukodystrophy.
The extra- vs intrauterine development of both visual and auditory cortical evoked response patterns was compared at 33, 37 and 40 weeks conceptional age. The maturation of visual cortical evoked responses is retarded in infants at 37 and 40 weeks conceptional age when born with a gestational age of less than 32 weeks, which thus implies a long extrauterine life span. The maturation of the auditory cortical evoked responses is not influenced by premature exposure to the extrauterine environment. The results are explained on the basis of the particular central nervous system growth spurt periods and a thus defined vulnerable period of different brain structures.
Defective arousal mechanisms are viewed as contributory to sleep hypopnea disorders and sudden infant death syndrome. Sighs (i.e. augmented breaths) as well as startles have not traditionally been viewed as arousal-related phenomena in infants. We hypothesized that, if sighs and startles are the initial event in a sequential arousal process, then they might be associated with specific EEG activity changes, because activation of the arousal-related ascending reticular activating system can suppress thalamus-generated sigma spindle oscillations. We studied spontaneous sighs and startles and those elicited by briefly occluding the infants face mask airway in 12 normal infants (age 10-19 wk) during non-rapid eye movement sleep. We recorded EEG (C3-P3), ECG, O2 saturation, diaphragmatic electromyography, limb electromyography, and video of the infant. The startle intensity was scored on a scale of 0 to 3 based on video recorded movements. Sleep spindle periodicity was analyzed by using a threshold over a compressed spectral band array. Spontaneous sighs and sleep startles were immediately followed by an interspindle interval prolongation from (mean +/- SEM) 8.0 +/- 0.16 s (control period) to 17.9 +/- 1.45 s after spontaneous sighs, to 23.8 +/- 1.26 s after spontaneous sighs accompanied by startles and to 26.5 +/- 1.45 s after occlusion-related sighs and startles. Furthermore, the intensity of occlusion-evoked startles was positively correlated with the interspindle interval prolongation (p < 0.01). We conclude that spontaneous as well as evoked sighs and startles are immediately followed by a transient sleep spindle suppression. This phenomenon indicates a close linkage between sighs, startles, and reticular formation-related arousal mechanisms.
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