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Sudden Infant Death Syndrome: A Literature Review w th Chiropractic Implications

BRAD D. BANKS, B.H.K., RANDY W. BECK, B Sc
MICHAEL COLUMBUS,
PAUL M. GOLD, B.Sc
F. STUART KINSINGER, B.Sc., D.C.
MICHEL A. LALONDE, B.Sc

ABSTRACT

Sudden infant death syndrome is the term applied to the sudden death of an infant or young child that is unexpected by history and for which a thorough postmortem examination fails to demonstrate an adequate cause of death. It is widely believed that sudden infant death syndrome is not an expression of a single cause and effect, but rather a multifactorial phenomenon. This paper gives an overview of recent developments in sudden infant death syndrome research presenting the various hypotheses regarding sudden infant death. Functional disturbances in the brainstem and cervical spinal cord areas related to the reurophysiology of respiration may contribute to the clinical findings associated with sudden infant death syndrome. Parturitional factors, which include maternal (labor and delivery) and extrinsic factors (obstetrical procedures) have received attention. Work has also been done on the development of those neuroanatomical structures associated with respiration. It is postulated that human development progresses through stages with a critical period at 2-4 months. Immaturity of the brainstem and cervical cord is characterized, histologically, by the presence of reticular dendritic spines on the neurons as well as a proliferation of astrocytes and glial cells. Any process, whether genetic, biochemical, biomechanical or traumatic, that alters normal development of the respiratory control centers related to spinal constriction and compression following birth trauma may be contributory to sudden infant death syndrome. (J Manipulative Physiol Ther 1987; 10:246-252) Key Indexing Terms: Sudden Infant Death Syndrome ,(SIDS), Chiropractic. INTRODUCTION Sudden infant death syndrome (SIDS) is the 'term applied to the sudden death of an infant or young child which is unexpected by history and for which a thorough autopsy examination fails to demonstrate an adequate cause of death (1, 2). SIDS results in the deaths of 1500 infants/yr in the United Kingdom (4/day) and 8000 infants/yr in the United States (22/day) (3) giving a frequency of 2.5-3/1000 live births (4). Similar frequencies have been reported in Canada, Holland, Sweden and New Zealand, making SIDS the number one cause of death in children from 2 months to 1 yr of age and second only to accidents as the leading cause of death in childhood (8 days to 14 years) (5). Many previous attempts have been made to identify the causative factors in SIDS, using many experimental approaches ranging from gross and histological autopsy of victims, physiological studies of infants who have previously shown a tendency for apnea (high risk infants), studies of the siblings and parents of SIDS victims and experiments on animal models. Thus many hypotheses regarding the cause of SIDS have been proposed. It is now believed, however, that SIDS is not an exp:. ion of a single cause-effect relationship, but is of multifactorial origin. Historically, cervical spinal cord injury was reported by the Egyptians 3000 years B.C. (6). D. D. Palmer fIrSt associated it with fetal death in 1910 (7), followed by similar reports from Crothers(8) in 1923. This paper reviews recent developments in SIDS research and presents a new hypothesis; il chiropractic model with implications for research and therapeutics. DISCUSSION Typically, the infants tend to die at night, asleep, in any position, between the ages of I and 4 months (9), and more often in the winter months (10). SIDS occurs more frequently in infants of poor families (II i, whose parents are young (less than 20 yr old) (12), unmarried (11), are ill during pregnancy (13), have a history of previous fetal loss (13), and who are smokers or abusers of narcotics (14, IS). Smoking has also been associated with placenta previa, abruptio placentae, pretenD birth and infants who are small for their gestional age (14, 16). The contribution of passive smoke inhalation to the above conditions has yet to be identified. No differences in death raies between breast fed and bottle fed infants have n shown (10, 17). Various papers repo.rt that the risk for SIDS is significantly higher in subsequent siblings of SIDS infants (14, 18-20), although no data to support a genetic component relating to SIDS have been presented (21, 22). Kelly and Shannon (21) have suggested that the iIb-ease of SIDS in some families is due to a deficiency in intrauterine or extrauterine environment. Autonomic breathing centers are constantl.' monitoring the metabolic condition of the organism via afferent connections from chemoreceptors and neuro-receplors, which supply feedback information necessary for the control of respiratory activity (23). Thus, the possibility exists that structural or functional abnormalities of these receptors could result in the sudden death of infants. The carotid body normally responds strongly to hypoxia, hypercapnia and acidosis by increasing respiratory drive through reflex action of medullary respiratory neurons, and normally responds to chronic hypoxia in humans and experimental animals by increasing the volume of its chemoreceptor cells (24). The carotid body of SIDS victims does not seem to react to hypoxia in the same way as a normal person's carotid body. Couriel and Olinsky (22) concluded that peripheral chemoreceptor function is unlikely to play an important hereditary role in the pathogenesis of SIDS. A form of spinal control over the axial ml:scles of respiration (composed of catecholamine and indolamine-re.easing neurons) (25), may exist in the brainstem. These monominergic neurons send their fibers down the spinal cord in several bulbo-spinal pathways. The noradrenergic fibers are more diffusely represented, but also appear primarily in the ventral and lateral funiculus. Both of these fiber systems have terminals in the anterior horn cells throughout the length of the spinal cord and especially so in the thoracic spinal area (25). The maturational characteristics of these two neuronal systems have been studied by Golden (25), utilizing fetal mice. He found that even in immature animals at birth, these systems are present and are functionally organized. A further supraspinal control may be present in the cerebellum, where it may integrate the dual autonomic and somatic char. cteristics observed in brainstem lower motor neurons, since these activities are influenced by cerebellar stimulation (25). It has been suggested that the developmental interrelationship of maturing brainstem neuronal systems may plan an important role in the pathogenesis of SIDS (25). If a maturational mismatch develops between the different excitatory and inhibitory neurons, activity may become confused, resulting in a period of high risk to the infant until the systems equilibrate their development. Any functional disturbances of areas controlling respiration may result in or contribute to the clinical symptoms associated with SIDS (26, 27). Many theories have been advanced as the cause of these disturbances. Intrinsic and extrinsic parturitional factors, although shown to be of importance in many SIDS cases, have received attention from a limited number of researchers. Intrinsic (maternal) factors include muscular atonia and arrhythmia,:uring labor, and pelvic inadequacies, both of which str. the anatomical and biomecbanical integrity of the cervical spine.in the neonate. Extrinsic (obstetrical) factors include spinal traction, forceps application and delivery procedures that use the infant's mandibular apex (symphysis. menti) or hard palate as a lever. Towbin (26) suggested that physical damage of the spinal cord structures occurs frequently when forcefullongitudinal spinal traction is applied during complicated delivery, resulting in spinal epidural hemorrhage termed "spinal shock." Spinal shock, he proposed, was an important cause of acute and possible chronic neonatal spinal injury. He stresses that these lesions, which include meningeal dural lacerations, spinal nerve root lesions, vertebral subluxation and spinal cord compression, often escape detection at autopsy, and almost invariably occur in the cervical spine (27). Other investigators including Belmusto (28), Visser (29), and Bland (30), suggest that cervical spinal abnormalities, sOl h as compression of the spinal cord by the ondontoic process, spinal hemorrhage, anterior displacement of atlas on axis and fIXation of the atlas on C2 may be at fault. According to Towbin (27), seven out of eight SIDS victims suffered cervical spinal injuries which resulted in the neuropathophysiology that was the death of the infant. As a result of this research, some chiropractors have advanced screening procedures for high risk infants (31). Gilles et al. (32) suggested that a size discrepancy b tween the foramen magnum and the atlas allows the atlas to enter the foramen magnum during hyperextension of the head, resulting in bilateral occlusion of the verebral arteries leading to hypoxia of the spinal structure responsible for respiration. . Autopsy examination has been utilized to large extent in recent years as a method of obtaining information relating to the cause ofSIDS. Some conditions may not show definite changes recognizable at autopsy, such as marked decrease in peripheral vascular resistance, cardiac asystole, extreme bradycardia, or protracted epileptic convulsions (33). Autopsy, using X-ray data, may also be unable to determine histological changes that result in physiological dysfunction such microcompression injuries; thus, conclusions drawn from such data sources must be considered somewhat incomplete. However, many pathological findings are related to hypoxia or ischemia. These findings, however, fail to demonstrate a relationship to the cause of SIDS. Much of SIDS research to this' :late has focused on periodic apnea and airway obstruction during sleep. Two factions have emerged from this research: those who believe that apnea has a major causative role in SIDS,' and those who believe that there is no, or very little, relationship between the two. Airway obstruction has been suggested by Kravitz and Scherz (34) as a cause of SIDS. They suggest that oropharyngeal airway obstruction due to pharyngeal relaxation may occur in the supine position during REM sleep. Equally, in the prone position, a hypermobile mandible might be displaced by the weight of the infant, pushing the tongue and soft palate back far enough to obstruct the airway. This is possible during REM sleep, since skeletal muscle tone, including the pharyngeal constructors and tongue, is inhibited (35). However, apnea has been observed in tracheostomized infants, indicating that laryngeal obstruction is an unlikely cause of the apnea observed (36). Two major hypotheses have been proposed to explain the possible cause(s) of central apnea. The first, proposed by Rigatto and 9O11eagues (37,' 38) suggests that hypoxemia, which freciuently accompanies respiratory failure, may depress the respiratory centers leading to irregular breathing and apnea. Schulte (40) implies that immaturity of the CNS may result in a decrease in afferent traffic to the reticular formation and lead to a reduction of respiratory center output. Histologically, this mmaturity is reflected by a decreased number of synaptic connections and dendritic arborizations as well as poor CNS myelination. Many authors agree that a central dysfunction in the. control of breathing, from whatever cause, and not hypoxemia is the most likely cause of apnea (39,41-43). The maturational development of central mspiratory controls is closely related to the development of sleep patterns in the newborn infant (44). The infant's behavior in the 2-3 month age period reflects rapid maturati9n of the nervous system, apparent in the ability of the child to sustain longer periods of sleep, the development of a diurnal cycle and major changes in developmental psychology, all attributable to anatomical changes in the brain (45). A fundamental change in EEG pattern of non-REM sleep occurs at 2-3 months of age, from a burst-suppression pattern to the true slow wave pattern (46), paralleling the development of all CNS neurons also occurring at this time. The development of sleep patterns, especially REM (patterns) takes on increasing importance in SIDS research, considering that most of the apneic episodes in premature infants occur during the period of REM sleep (47). Most cases of SIDS occur in the 1-4 month period (9); the same period that major sleep pattern changes occur (9, 45, 47). A possible explanation for the increased numbers of apneic episodes during REM sleep is that during this stage of sleep, the brainstem reflexes are profoundly inhitited. Facilitation of certain brainstem reflexes is d in an infant at 3 months of age, resulting in a decieased ability to respond to an apneic episode (45). Presumably, in normal development, a complex integrative neuronal network between the brainstem and higher centers is functional during this critical period and is effective in maintaining respiration (9). However, immaturity of the control centers leave the infant vulnerable to apneic episodes. With respect to brainstem and cervical cord-related apneic episodes, there is evidence that compression of these areas can produce an apneic response. This has been documented in children with a disease involving abnormal formation of fetal cartilage (achondroplasia) where compression due to narrowing of the foramen magnum or basicranium is suspected as the cause of severe apneic episodes leading to death (26, 29, 30, 48). The hypothesis that apnea is the final common pathway to SIDS 'does have considerable support (49-51). However, some research suggests that this may not be the CC)Se. Richards et al. (52) found no evidence to link prolonged apnea in near-miss infants with a greater risk of subsequent death than in control infants. Southall et al. (3) found that they could not predict the occurrence of SIDS by measuring the apneic periods from 24-hr recordings and found that approximately 1 % of healthy babies experienced cardiac arrythmias during the first 6 weeks of life without succumbing to death. As a result of these inconclusive findings, various authors have suggested that the term "infant apnea syndrome" be used instead of "near miss" or "high risk" for SIDS infant designations. At this time, there is no direct evidence that apneic episodes are truly a warning sign of impending death (53). However, most authors agree that some maturation maldevelopment of the central control mechanisms of respiration is responsible for SIDS. Maturation of the respiratory regulatory structures is integrated with the rest of the neurological development in normal infants. Various authors have found that stability of respiration was achieved, in correlation with other indications of increased neurological maturation, such as a diminution of incidental motions of the eyes and the body as a whole in infants between 36 weeks gestational age and 8 months postpartum (54, 55). At 3-5 months of age, infants develop fine motor skills and greater attention and alertness as measured by specific pediatric examination (45). This implies that a more mature nervous system has been established. Although this maturation progresses with the age of the child, the progression may not be a smooth, continuous process, but may occur in stages. Weathall (56) found that the development of the respiratory contr:>ls in the rabbit occur in stages, which progress from pnmitive to advanced, with a high risk period between the primitive and mature stage of control. Sutton et al. (57) found that infant monkeys were more sensitive to superior laryngeal nerve stimulation than older monkeys and adults. Superior laryngeal nerve stimulation in young infants leads to prolonged apnea, whereas stimulation on older infants'produces mild apnea, and in adults, there was an ailsence of apneic response. This demonstrates that the development of the respiratory control in animals becomes mOrt; stable as the animal matures. Hasselmeyer (58) reported that the peak incidence of SIDS is consistently found to be between the second and fourth month of life with few cases reported either in the period < 1 month and the period >4 months, suggesting further that human infant respiratory development also progresses through stages of development with 'a critical stage between 2 and 4 months. The infant requires a certain level of development at this stage in order to sustain life. As well, more histological evidence suggests that SIDS infants possess an immature respiratory nervous system, in which neurons exhibit reticular dendritic spines. Gunby (59) and Quattrochi (60) reveal that 84% of SIDS infants studied had retained dendritic spines, such as would be expected in prematurely born infants. The retention of dendritic spines is considered to be characteristic of immaturity of the brainstem and cervical spine (14, 59-61). CONCLUSION The normal infant passes through a sequence of respiratory maturation that develops concurrently with the whole of the nervous system, in keeping with the increased demands of the developing child. Since the well-being of the newborn infant is governed by appropriate integrity and function of the vital centers in the brainstem and spinal cord (54), any process that alters normal development of the respiratory control centers will be detrimental to the infant's survival. Normally, the child must progress through one or possibly several critical high risk stages before functiOllal stability is established. It is during these high risk stages that the development and function of the respiratory centers is challenged. The consequences of underdevelopment at these critical hi, h risk stages may be grave. The maturatio al lag of the respiratory centers is caused by several factors, Including biochemical imbalances, genetic abnormalities, adverse maternal influences (aberrant life-style) and biomechanical stress (trauma), all of which will retard the proper development of the respiratory nervous system (10, 36, 4, 56, 58). Much evidence demons tes that nerve constriction and compression following trauma to the brainstem and cervical spinal cord results in retarded development of the respiratory nervous system. Axonal constriction and compression results in a decrease in axoplasmic flow (62), which results in decreased neurotransmitter release, decreased myelination, degeneration of the axon distal to the obstruction and a decreased trophic influence on the innervated cells and neural tissue (62, 63). Compression of either central or peripheral axons results in a conduction block that ceases stimulation (64). Compress; -.n also results in a failure of axoplasmic transport, caush g a damming of materials proximal to the lesion, and '1 depletion distally (65-67). Sharpless (68) has shown that compression of axons produces a conduction block and this conduction block becomes progressively more severe as the block is maintained. As little as 10 mm Hg pressure maintained for 10 min reduces the compound action potential activity of dorsal nerve roots of half their normal values. Furthermore, compression sensitivity is much greater in spinal nerve roots than peripheral nerves. Slight nerve compression causes decreased nerve activity without degeneration of the neuron. This decreased neuronal activity results in the retention of dendritic spines in order to maintain neuronal impulse flow at a constant rate as the maturational demand on the neuron is surpassed by the functional demand. Not only is there decreased nerve activity following trauma, but glial cells and astrocytes proliferate, both of which are consistent pathological findings in SIDS infants (14, 62, 63, 69-72). The victims of SIDS were originally thought to be normal, healthy babies who suddenly died without any pathogenesis evident. We hypothesize that these children have been subject to stress caused by developmental immaturity of their respiratory nervous systems as a result of spinal constriction and compression. The evidence of this is manifested in the variety of clinical signs and symptoms associated with SIDS infants, such as hypoxia, abnormal sleep patterns, altered cardiopulmonary function and tissue oxygen utilization, postnatal growth retardation and aberrant behavioral patterns (1, 14, 45, 61). We further hypothesize that the common denominator underlying these manifestations is an immature and underdeveloped nervous system due to the spinal constriction and compression (26-30, 57, 73-75). Stiga (76) theorizes that cervical traction applied at birth results in vagal aberration caused by pressure exerted on the hindbrain and vagal nucleus by the occiput. This may occur in all types of presentations and deliveries. During labor and delivery, the cervical rotational and long axis traction forces may affect the inferior cervical sympathetic ganglh and the phrenic nerve, thus inhibiting diaphragmatic breathing. Trauma causing underdevelopment and immaturity of the neuronal network controlling respiration leads to respiratory dysfunction. Traumatic underdevelopment of other neuronal networks will result in other types of neurological disorders seen in newborns such as paraplegia, quadraplegia, hypotonia and muscular tremors, as well as subsequent developmental abnormalities (20, 32, 77-79). Based on the information gathered, infantile neural compression can lead to the pathophysiological state responsible for sudden infant death syndrome. Furthermore, this neural compression may be very closely related to the biomechanical and neurological integrity of the upper cervical spine of the infant. Further investigations required to develop an appropriate animal model, screening orocedures and effective therapeutics for this tragic syndrome. REFEI .;NCES I. Bergfuan AB, Beckwith JB, Ray CE, eds. 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