Neuronal Control of Neonatal Respiration - Sleep Apnea and the Sudden Infant Death Syndrome

Abstract

During the last decade evidence has been accumulated that there might be a continuum from normally occurring short spells of apnea during sleep to life threatening long lasting respiratory pauses with marked bradycardia or even cardiac arrest from which, however, the infant could be resuscitated - the so-called Near Miss for Sudden Infant Death Event - and finally, to the Sudden Infant Death Syndrome (SIDS). There are still many missing links between these three phenomena and it seems likely that the connection between all three is not a straight matter in degree of immature dysfunction of cardiorespiratory control mechanisms. However, no other concept has shead so much light on SIDS and - most probably - no other concept with its consequence of continuous home monitoring has already salvaged so many babies as research into the different sleep apnea syndromes during infancy. However, for the final evaluation of the above mentioned hypothesis two issues urgently need clarification: a) How much apnea is normal at different ages and in different risk groups of infants. b) Can "near miss infants" or future victims of SIDS be identified on the basis of the amount of apnea prior to the event. In the first part of this survey brain mechanisms possibly underlying both, sleep apnea and serious apneic events will be discussed. In the second part new normative data on the amount of apnea will be presented together with 2 extraordinary cases who could be studied by means of longterm polygraphic sleep recordings prior to a definitely serious near miss event in one case and a crib death in another.

Auditory Brainstem Response (ABR) in Congenital Central Alveolar Hypoventilation

“…The ventilatory CO 2 response was found to be markedly diminished; awake: 7.4, asleep: 0.68 ml/min/torr/kg; normative value: 13.6 ± 3.9 ml/min/torr/kg. As frequently found in CCH patients beyond the age offour months (Shannon 1980) automatie respiratory failure usually became apparent as a gradual reduction in respiratory rate and tidal volurne, and occasionally apneic spells of central type (Schulte et al 1982) were observed.…”

“…For obstruetive apnea normal ABRs have been reported (Mosko et al 1981, Stockard 1982, Karnaze et al 1984 and for eentral apnea ABR abnormalities have been found only in eases who revealed clinieal evidenee of brain stern dysfunetion not restrieted to the respiratory system (Stockard 1982, Peled et al 1983, Karnaze et al 1984, Long and Allen 1984. The equivoeal ABR findings reported for near-miss sudden infant death syndrome (Orlowski etal 1979, Gupta etal 1981, Stockard 1982), a phenomenon whieh in terms of pathogenesis is related to sleep apnea (Schulte et al 1982), may be beeause groups with varied brain stern abnormalities~ere investigated.…”

“…Sieep apnea syndromes are generally divided into three eategories: Central (inaetive) apnea, obstruetive apnea and mixed eentral and obstruetive apnea (Schulte et al 1982). Central sleep apnea syndromes (sometimes referred to as "Ondine's Curse"; Severinghaus and Milchell 1962), whieh result from brainstem disorders afTeeting the metabolie eontrol system of breathing (Milchell andBerger 1975, Guilleminault andDement 1978) oeeur in an aequired and a eongenital form, the latter being the ease for our patient.…”

Mechanical Trauma and Classification of Wounds

“…Though the precise cause of the SID phenomenon is still unknown, a series of systematic morphological studies suggests that CNS involvement plays a central role in sudden infant death syndrome (SIDS). The fatal process underlying SID involves a disturbance of respiratory regulation that results in clinically observable apnoea attacks (Schulte et al 1982) and functional impairment of hypoxemiainjured neurons. Clinical evidence suggests that prenatal stress may alter the course of neurological maturation.…”

Lungenger�stver�nderungen beim pl�tzlichen Kindestod (SIDS)

“…Verl~ngerung der apnoischen Phasen im REM-Schlaf mit subletalen, transienten hypoxischen Episoden (Steinschneider 1972;Gould 1977;Guilleminault et al 1975;Schulte et al 1982;Avery und Frantz 1983;Durand et al 1983;Spitzer et al 1984;Jeffrey et al 1981;Albani et al 1985). Verl~ngerung der apnoischen Phasen im REM-Schlaf mit subletalen, transienten hypoxischen Episoden (Steinschneider 1972;Gould 1977;Guilleminault et al 1975;Schulte et al 1982;Avery und Frantz 1983;Durand et al 1983;Spitzer et al 1984;Jeffrey et al 1981;Albani et al 1985).…”