Cerebrospinal fluid adenosine 3',5'-monophosphate, 5-hydroxyindoleacetic acid and homovanillic acid in patients with sleep apnoea syndrome

Cramer, H.; Jm, Warter; Renaud, Bertrand; Krieger, J; Ch, Marescaux; Hammers, Ronald

doi:10.1136/jnnp.44.12.1165

Cited by 20 publications

(8 citation statements)

References 10 publications

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“…Therefore, it is possible that daytime somnolence might be responsible, at least in part, for abnormal ERP fi ndings in OSAS. It has been suggested that one possible explanation for the observed changes in cognitive evoked potentials could be the presence of changes in neurotransmitter metabolism associated with sleep apnea (Rumbach et al , 1991 ); in fact, it has been shown that 5-hydroxyindoleacetic acid levels were increased in the cerebrospinal fl uid of OSAS patients (Cramer et al , 1981 ), and that P3 latencies may be modifi ed by drugs acting on various neurotransmitters (Kales et al , 1985 ). There is also a report of signifi cant correlations between P3 amplitude and sleep stage 1, sleep effi ciency, MSLT and MWT scores (Sangal and Sangal , 1997a ).…”

Section: Response To Treatment Studiesmentioning

confidence: 99%

Cognitive evoked potentials in obstructive sleep apnea syndrome: a review of the literature

Raggi

Ferri

2012

Reviews in the Neurosciences

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Cognitive functions may be altered in patients with obstructive sleep apnea syndrome (OSAS) and it has been proposed that vigilance and attention changes play a fundamental role in all aspects of cognitive deficits noted in this disease. The use of event-related potentials (ERPs) is a high-time resolution technique that can be used to explore the presence of cognitive dysfunction. We review 23 empirical articles on ERPs in OSAS in order to contribute to the clarification of the pattern of cognitive deficits that are specific to this disease and to see whether there might be an improvement of abnormal psychophysiological findings with continuous positive airway pressure (CPAP) treatment. We conclude that ERP studies have contributed to demonstrating changes in cognitive attentive processing in OSAS, mainly in association with altered functioning of the prefrontal cortex, and that CPAP treatment may improve vigilance and attention and generally improve cerebral information processing in these patients. The remaining deficits during sufficient CPAP therapy may, however, reflect irreversible hypoxic cerebral damage.

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Section: Response To Treatment Studiesmentioning

confidence: 99%

Cognitive evoked potentials in obstructive sleep apnea syndrome: a review of the literature

Raggi

Ferri

2012

Reviews in the Neurosciences

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“…16 18 In support of terminal exhaustion of serotonin are the findings of increased levels of serotonin metabolites in the cerebrospinal fluid. 19 Cann-Moisan 20 found that several neurotransmitters and metabolites were increased in the cerebrospinal fluid of SIDS victims compared with living controls; they also found high levels of these in cerebrospinal fluid in infants after they had survived severe asphyxia.…”

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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“…In patients suffering from sleep obstructive apnoea, increases in the levels of the inactive catabolite (5-hydroxyindoleacetic acid) were reported to occur (Cramer, Warter, Renaud, Krieger, Marescaux & Hammers, 1981) and might be attributable to an abnormally high level of 5-HT release. Furthermore, 5-HT has been assumed to play a role in sleep regulation, since tryptophan may restore the capacity to sleep in animals with 5-HT-depleted raphe neurons (for review see Vogt, 1982) and 5-HT2 antagonist modifies human sleep (Idzikowski, Mills & Glennard, 1986).…”

Section: Indirect Effectsmentioning

confidence: 99%

Compared effects of serotonin on cervical and hypoglossal inspiratory activities: an in vitro study in the newborn rat.

Morin

Monteau

Hilaire

1992

The Journal of Physiology

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SUMMARY1. Experiments were performed on the brain stem-spinal cord preparation of newborn rats, in which the phrenic and hypoglossal nerves continue to show rhythmic respiratory activity in vitro, in order to compare the effects of serotonin (5-HT) on both activities and to analyse the mechanisms responsible for the depression by 5-HT of the hypoglossal activity.2. Under control conditions, simultaneous recordings of the inspiratory discharges of hypoglossal and cervical roots showed that the two bursts did not start simultaneously and had different patterns (time-to-peak and peak values); this suggests that both pools of motoneurons did not share the same central drive(s).3. Adding 5-HT and related agents to the bathing medium delayed and depressed the hypoglossal inspiratory discharge via activation of 5-HT2 receptors since these effects were elicited by 5-HT2 agonists (a-methyl-5-HT and 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane-HCl (DOI)) but not by 5-HT1 agonists (RU 24969 and (± )-8-hydroxy-2-(di-N-propylamino)tetralin hydrobromide (8-OH-DPAT)). The 5-HT depression of the hypoglossal discharge was prevented by applying a pretreatment with a specific 5-HT2 antagonist (ketanserin). Parallel to the hypoglossal discharge decrease, 5-HT elicited a permanent cervical root discharge along with a persistent inspiratory bursting. Adding the 5-HT precursor L-tryptophan to the bathing medium depressed the hypoglossal (XII) discharge without affecting the cervical one.4. Local application of 5-HT within the hypoglossal motor nucleus decreased the hypoglossal output, revealing that the 5-HT depression of the hypoglossal discharge was at least partly mediated by the 5-HT effects at the level of the motoneurons. Local application of 5-HT within the cervical motor nucleus elicited a permanent firing in the cervical root with a persistent inspiratory bursting.5. Intracellular analysis confirmed the existence of differences in central respiratory drive between cervical and hypoglossal motoneurons under control conditions, as well as differences in response to 5-HT. All the hypoglossal motoneurons became silent under 5-HT bathing, and showed no change in the input membrane resistance, a moderate depolarization, and a delayed central respiratory MS 9503 D. MORIN, R. MONTEA U AND 0. HILAIRE drive with a decreased amplitude. The cervical motoneurons became more active during inspiration, despite a decrease in the amplitude of the central respiratory drive, which was compensated for by a large depolarization and an increased input membrane resistance. Some cervical motoneurons even fired at a low rate during expiration.6. Taken as a whole, these results suggest that the hypoglossal depression induced by 5-HT was due to the activation of 5-HT2 receptors located within the hypoglossal nucleus but the exact mechanisms whereby 5-HT modulates the hypoglossal outputs are still open to debate. The functional significance of the effects of 5-HT on hypoglossal inspiratory activity is discussed with reference to the obstructive apno...

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Cerebrospinal fluid adenosine 3',5'-monophosphate, 5-hydroxyindoleacetic acid and homovanillic acid in patients with sleep apnoea syndrome

Abstract: SUMMARY Adenosine 3',5'-monophosphate (cyclic AMP), 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA)

Cited by 20 publications

References 10 publications

Cognitive evoked potentials in obstructive sleep apnea syndrome: a review of the literature

Cognitive evoked potentials in obstructive sleep apnea syndrome: a review of the literature

The Triple Risk Hypotheses in Sudden Infant Death Syndrome

Compared effects of serotonin on cervical and hypoglossal inspiratory activities: an in vitro study in the newborn rat.

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