Brain-stem and Adrenal Abnormalities in the Sudden-infant-death Syndrome

Naeye, Richard L.

doi:10.1093/ajcp/66.3.526

Cited by 220 publications

(92 citation statements)

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“…The greater increase in ventilation with Con found in aborted SIDS infants at 3 and 4 months of age is consistent with this hypothesis because it has been shown experimentally that acutely injected epinephrine or norepinephrine in adult man causes a greater increase in ventilation in response to C 0 2 (4, 7, 9). Additional support for this hypothesis is provided by the postmortem observation demonstrating hypertrophy of the chromaffin cell layer of the adrenal medulla in victims of SIDS (25).…”

Section: Resting Ventilation In Aborted Slds Infantsmentioning

confidence: 88%

Ventilation and Ventilatory Pattern During Sleep in Aborted Sudden Infant Death Syndrome

et al. 1981

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SummaryT o assess ventilatory control during sleep in infants at risk for the sudden infant death syndrome (SIDS), we made serial measurements of resting tidal volume (Vt), respiratory cycle time (Ttot), and the ventilatory changes resulting from inhalation of 2% Con in aborted S l D S infants in rapid eye movement and quiet sleep and compared them to a group of normal infants during the first 4 months of life. Ventilation was measured by the barometric method, and sleep was staged using electroencephalogram, electrooculogram, and electromyogram and behavioral criteria.Although resting instantaneous minute ventilation (Vt/Ttot) was virtually the same in both groups of infants, Vt tended to be smaller (by up to 50% in the first 2 months) and Ttot tended to be shorter in aborted S l D S than in normal infants in both rapid eye movement and quiet sleep. The increase in the mean Vt/Ttot with 2% COz is greater by about 5 to 20% in aborted SIDS than in normal infants at 3 and 4 months of age in both sleep states. These findings, together with our previous findings that aborted S l D S infants have an increase in heart rate and a shortening of the QT interval, provide indirect evidence that infants a t high risk for S l D S may have increased sympathoadrenal activity.

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Section: Resting Ventilation In Aborted Slds Infantsmentioning

confidence: 88%

Ventilation and Ventilatory Pattern During Sleep in Aborted Sudden Infant Death Syndrome

et al. 1981

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“…12 He concluded that these changes were caused by hypoxia and were not the cause of SIDS. Kinney and colleagues 15 also found gliosis in 22% of their SIDS victims and instituted studies of neurotransmitter systems in the brainstem, particularly muscarinic and serotenergic systems.…”

Section: Discussionmentioning

confidence: 99%

“…6 Naeye reported in 1976 significant proliferation of astroglial fibers in the brainstem of half of his SIDS cases 12 ; the other half had no more nor less astrogliosis than did controls who had died of trauma or acute asphyxia. (Because 4 days or more are required to develop astrogliosis, 13 its presence cannot be attributed to a single acute episode ending in death.)…”

Section: Vulnerable Infantmentioning

confidence: 99%

The Triple Risk Hypotheses in Sudden Infant Death Syndrome

2002

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ABSTRACT. Sudden infant death syndrome (SIDS) victims were regarded as normal as a matter of definition (Beckwith 1970) until 1952 when Kinney and colleagues argued for elimination of the clause, "unexpected by history." They argued that "not all SIDS victims were normal," and referred to their hypothesis that SIDS results from brain abnormalities, which they postulated "to originate in utero and lead to sudden death during a vulnerable postnatal period." Bergman (1970) Interest in the brainstem of SIDS victims began with Naeye's 1976 report of astrogliosis in 50% of all victims. He concluded that these changes were caused by hypoxia and were not the cause of SIDS. He noted an absence of astrogliosis in some older SIDS victims, compatible with a single, terminal episode of hypoxia without previous hypoxic episodes, prenatal or postnatal.Kinney and colleagues (1983) reported gliosis in 22% of their SIDS victims. Subsequently, they instituted studies of neurotransmitter systems in the brainstem, particularly the muscarinic (1995) and serotenergic systems (2001). The major issue is when did the brainstem abnormalities, astrogliosis, or neurotransmitter changes occur and whether either is specific to SIDS. There is no published method known to us of determining the time of origin of these markers except that the injury causing astrogliosis must have occurred at least 4 days before death (Del Bigio and Becker, 1994). Because the changes in neurotransmitter systems found in the arcuate nucleus in SIDS victims were also found in the chronic controls with known hypoxia, specificity of these markers for SIDS has not been established. It seems likely that the "acute control" group of Kinney et al (1995) died too quickly to develop gliosis or severe depletion of the neurotransmitter systems. We can conclude that the acute controls had no previous episodes of severe hypoxia, unlike SIDS or their "chronic controls." Although the average muscarinic cholinergic receptor level in the SIDS victim was significantly less than in the acute controls, the difference was only 27%, and only 21 of 41 SIDS victims had values below the mean of the acute controls. The study of the medullary serotonergic network by Kinney et al (2001) revealed greater reductions in the SIDS victims than in acute controls, but the questions of cause versus effect of the abnormalities, and whether they occurred prenatally or postnatally, remain unanswered. Hypoplasia of the arcuate nucleus was stated to occur in 5% of their SIDS cases by Kinney et al (2001), but this is a "primary developmental defect" according to Matturri et al (2002) with a larger series, many of whom were stillbirths. These cases should not be included under the rubric of SIDS, by definition.There are difficulties with Filiano and Kinney's (1994) explanation of the age at death distribution of SIDS. They postulate that the period between 1 and 6 months represents an unstable time for virtually all physiologic systems. However, this period demonstrates much less instability than does the...

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“…Understanding the role of medullary 5-HT neurons in sleep and thermoregulation may help us determine mechanisms involved in sudden infant death syndrome (SIDS), where abnormalities in thermoregulation and arousal have been implicated (21,22,38,39,57,83,91). Almost 75% of SIDS infants studied have decreased binding to 5-HT 1A receptors and increased numbers of 5-HT neurons in all of the medullary serotonergic nuclei, including the medullary raphé and PGCL (41-43, 65, 69), groups of neurons homologous to those that have been found to be important in thermoregulation and sleep in animals (12,17,53).…”

Section: Methoxyphenyl)-1-piperazinyl]-mentioning

confidence: 99%

Activation of 5-HT_1Areceptors in medullary raphé disrupts sleep and decreases shivering during cooling in the conscious piglet

Brown¹,

Sirlin²,

Benoit³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Activation of 5-HT 1A receptors in the medullary raphé decreases sympathetically mediated brown adipose tissue (BAT) thermogenesis and peripheral vasoconstriction when previously activated with leptin, LPS, prostaglandins, or cooling. It is not known whether shivering is also modulated by medullary raphé 5-HT 1A receptors. We previously showed in conscious piglets that activation of 5-HT 1A receptors with (Ϯ)-8-hydroxy-2-(dipropylamino)-tetralin (8-OH-DPAT) in the paragigantocellularis lateralis (PGCL), a medullary region lateral to the raphé that contains substantial numbers of 5-HT neurons, eliminates rapid eye movement (REM) sleep and decreases shivering in a cold environment, but does not attenuate peripheral vasoconstriction. Hoffman JM, Brown JW, Sirlin EA, Benoit AM, Gill WH, Harris MB, Darnall RA. Am J Physiol Regul Integr Comp Physiol 293: R518 -R527, 2007. We hypothesized that, during cooling, activation of 5-HT 1A receptors in the medullary raphé would also eliminate REM sleep and, in contrast to activation of 5-HT 1A receptors in the PGCL, would attenuate both shivering and peripheral vasoconstriction. In a continuously cool environment, dialysis of 8-OH-DPAT into the medullary raphé resulted in alternating brief periods of non-REM sleep and wakefulness and eliminated REM sleep, as observed when 8-OH-DPAT is dialyzed into the PGCL. Moreover, both shivering and peripheral vasoconstriction were significantly attenuated after 8-OH-DPAT dialysis into the medullary raphé. The effects of 8-OH-DPAT were prevented after dialysis of the selective 5-HT 1A receptor antagonist WAY-100635. We conclude that, during cooling, exogenous activation of 5-HT 1A receptors in the medullary raphé decreases both shivering and peripheral vasoconstriction. Our data are consistent with the hypothesis that neurons expressing 5-HT 1A receptors in the medullary raphé facilitate spinal motor circuits involved in shivering, as well as sympathetic stimulation of other thermoregulatory effector mechanisms. thermoregulation; serotonin; brain stem; raphé; the sudden infant death syndrome MANY NEURONS IN THE MEDULLARY raphé, including serotonergic (5-HT) neurons, project to the intermediolateral cell column (IML) of the spinal cord and modulate sympathetic outflow to thermoregulatory effector mechanisms, including brown adipose tissue (BAT) thermogenesis, vasoconstriction of thermoregulatory cutaneous vascular beds, and heart rate (HR) (14,53,58,86,89). Studies in anesthetized and conscious animals have shown that activation of 5-HT 1A receptors in the medullary raphé with the selective agonist, (Ϯ)-8-hydroxy-2-(dipropylamino)-tetralin (8-OH-DPAT), attenuates sympathetic outflow to BAT and peripheral vessels when previously elevated by LPS, leptin, or cooling (11,52,59,63,64).There is mounting evidence that medullary raphé 5-HT neurons modulate sympathetically mediated thermoregulatory mechanisms; however, little is known about the role of medullary raphé 5-HT neurons in shivering thermogenesis. Shivering is an involuntary tremor that i...

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Brain-stem and Adrenal Abnormalities in the Sudden-infant-death Syndrome

Cited by 220 publications

References 0 publications

Ventilation and Ventilatory Pattern During Sleep in Aborted Sudden Infant Death Syndrome

Ventilation and Ventilatory Pattern During Sleep in Aborted Sudden Infant Death Syndrome

The Triple Risk Hypotheses in Sudden Infant Death Syndrome

Activation of 5-HT_1Areceptors in medullary raphé disrupts sleep and decreases shivering during cooling in the conscious piglet

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Brain-stem and Adrenal Abnormalities in the Sudden-infant-death Syndrome

Cited by 220 publications

References 0 publications

Ventilation and Ventilatory Pattern During Sleep in Aborted Sudden Infant Death Syndrome

Ventilation and Ventilatory Pattern During Sleep in Aborted Sudden Infant Death Syndrome

The Triple Risk Hypotheses in Sudden Infant Death Syndrome

Activation of 5-HT1Areceptors in medullary raphé disrupts sleep and decreases shivering during cooling in the conscious piglet

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Activation of 5-HT_1Areceptors in medullary raphé disrupts sleep and decreases shivering during cooling in the conscious piglet