Not exact matches
Abnormalities of the
brainstem serotonergic system in the sudden
infant death syndrome: A review.
Serotonergenic
brainstem abnormalities in Northern Plains Indians with the sudden
infant death syndrome.
Multiple serotonergenic
brainstem abnormalities in sudden
infant death syndrome.
Our hearing testing offerings include diagnostic audiology services, intra-operative testing, auditory
brainstem response (ABR) testing, inner ear evaluations, specialized screening for newborns,
infants and toddlers and patients with cancer.
The health risks associated with formula feeding for premature
infants include increased incidence of necrotizing enterocolitis, 5 delayed
brainstem maturation, 6 decreased scoring on cognitive and developmental tests,7 - 10 and decreased visual development.11, 12 Thus, human - milk feeding of premature
infants is desirable, and effective strategies to increase breastfeeding rates in this population are needed.
Brainstem abnormalities that involve the medullary serotonergic (5 - hydroxytryptamine [5 - HT]-RRB- system in up to 70 % of infants who die from SIDS are the most robust and specific neuropathologic findings associated with SIDS and have been confirmed in several independent data sets and laboratories.37, — , 40 This area of the brainstem plays a key role in coordinating many respiratory, arousal, and autonomic functions and, when dysfunctional, might prevent normal protective responses to stressors that commonly occur duri
Brainstem abnormalities that involve the medullary serotonergic (5 - hydroxytryptamine [5 - HT]-RRB- system in up to 70 % of
infants who die from SIDS are the most robust and specific neuropathologic findings associated with SIDS and have been confirmed in several independent data sets and laboratories.37, — , 40 This area of the
brainstem plays a key role in coordinating many respiratory, arousal, and autonomic functions and, when dysfunctional, might prevent normal protective responses to stressors that commonly occur duri
brainstem plays a key role in coordinating many respiratory, arousal, and autonomic functions and, when dysfunctional, might prevent normal protective responses to stressors that commonly occur during sleep.
Postmortem studies of Northern Plains American Indian
infants revealed that prenatal cigarette smoking was significantly associated with decreased serotonin receptor binding in the
brainstem.
In animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the
brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a
brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human
infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the
brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm
infants, 32 decreases heart rate variability in preterm33 and term34
infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover,
infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an
infant's vulnerability to SIDS.
Brainstem mechanisms underlying the sudden
infant death syndrome: evidence from human pathologic studies
Developmental neurotransmitter pathology in the
brainstem of sudden
infant death syndrome: a review and sleep position
Serotoninergic receptor 1A in the sudden
infant death syndrome
brainstem medulla and associations with clinical risk factors